Fisdap Cardiology Review (Paramedic)

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congestive heart failure

when the heart is unable to pump powerfully or fast enough to empty its chambers which results in blood backing up into the systemic circuit, the pulmonary circuit, or both

pericarditis

inflammation of the pericardial sac as the result of an infection or trauma. Positional chest pain (alleviated by sitting forward), shortness of breath, and history of recent infection or fever. Diffuse ST-segment elevation and a depressed PR segment, and concave ST segment (never any reciprocal changes)

rheumatic fever

inflammatory disease caused by streptococcal bacteria that can cause a stenosis of the mitral or aortic valve, leading to heart complications

tunica intima

innermost layer of blood vessels; smooth inner lining that is only one cell thick

Modifiable risk factors for heart disease

hypertension, elevated cholesterol level, smoking, poor diet, obesity, sedentary lifestyle, oral contraceptives, hormone replacement therapy, and high stress.

endocarditis

infection of the inner lining of the heart characterized by inflammation of the inside lining of the heart chambers including the valves; almost exclusively caused by the straph or strep virus

myocarditis

inflammation of the myocardium caused by viral, bacterial and fungal infections (can also be caused by trauma)

Coronary sinus

large vessel in the posterior part of the coronary sulcus where venous blood empties; it ends at the right atrium.

veins

vessels that carry blood to the heart; generally deoxygenated blood (except the pulmonary veins). The largest are the inferior and superior vena cava

thrill

vibration the occurs frequently and remains constant

pulse deficit

when a palpated radial pulse is less than an apical pulse

Frank-Starling mechanism

when cardiac muscle is stretched it contracts with a greater force in order to ensure complete emptying and increase the SV resulting in higher CO

cardiac tamponade

when excessive fluid accumulates within the pericardium, limiting the hearts ability to expand fully after each contraction and resulting in reduced CO. Diagnosed with gradual dyspnea and weakness or traumatic chest pain. There will be an initial systolic drop then the diastolic will slowly rise (narrowing pulse pressure) followed by an increase in heart rate and muffled heart sounds. May have JVD.

cardiogenic shock

when the heart is so damaged that it can no longer pump a volume of blood sufficient for tissue perfusion

In addition to CPR, the recommended treatment sequence for an unresponsive, apneic, and pulseless patient with a regular, wide-complex cardiac rhythm at a rate of 40 beats/min includes:

1 mg of epinephrine every 3 to 5 minutes and treating reversible causes. Pulseless electrical activity (PEA) exists when an unresponsive, apneic, pulseless patient presents with a regular cardiac rhythm. Treatment for PEA includes immediate high-quality CPR with minimal interruptions, obtaining vascular access (IV or IO), 1 mg of epinephrine every 3 to 5 minutes, advanced airway management (ie, ET tube, multilumen or supraglottic airway), and assessing for and treating reversible causes (Hs and Ts). Vasopressin, in a one-time dose of 40 units, can be given to replace the first or second dose of epinephrine, but not both. There are insufficient data to recommend transcutaneous pacing (TCP) for patients with bradycardic PEA or asystole, and the routine use of calcium chloride during cardiac arrest is not recommended.

Which of the following represents the MOST appropriate initial drug and dose that is given to all adult patients in cardiac arrest?

10 mL of epinephrine 1:10,000 every 3 to 5 minutes. Once vascular access has been obtained (IV or IO), the first drug and dose given to all patients in cardiac arrest—regardless of the rhythm on the cardiac monitor—is epinephrine 1 mg (10 mL) of a 1:10,000 solution, repeated every 3 to 5 minutes. You may consider a one-time dose of vasopressin (40 units) to replace the first or second dose of epinephrine, but not both. Higher doses of epinephrine may be necessary if special circumstances exist (ie, severe beta-blocker toxicity). Consult with medical control as needed.

A clinically unstable patient presents with an irregular narrow-complex tachycardia at a rate of 170 per minute. What is the recommended initial energy setting for synchronized cardioversion?

120 to 200 joules. If a patient has a heart rate that is greater than 150 per minute, and he or she is clinically unstable because of the cardiac rhythm, synchronized cardioversion should be performed. The following initial energy settings are recommended by current emergency cardiac care (ECC) guidelines: narrow and regular, 50 to 100 joules (biphasic or monophasic); narrow and irregular, 120 to 200 joules biphasic (200 joules monophasic); wide and regular, 100 joules (biphasic or monophasic); wide and irregular, defibrillation dose (NOT synchronized). If the initial energy dose is unsuccessful, increase in a stepwise fashion.

The initial dose of diltiazem for a 165-pound patient is approximately:

19. Diltiazem hydrochloride (Cardizem) is a calcium channel blocking drug that is used to treat rapid ventricular rates associated with atrial fibrillation or atrial flutter. It can also be used after adenosine to treat refractory reentry supraventricular tachycardia in hemodynamically stable patients. The initial dose of diltiazem is 0.25 mg/kg IV over 2 minutes; the average initial dose is 15 to 20 mg. It may be repeated in 15 minutes in a dose of 0.35 mg/kg IV over 2 minutes; the average second dose is 20 to 25 mg. A 165-pound patient weighs 75 kg. Therefore, the initial dose of diltiazem for a patient of this weight would be 18.75 mg (approximately 19 mg), and the second dose would be 26.25 mg (approximately 26 mg).

What is the correct initial dose and rate of administration of amiodarone for a patient with refractory ventricular fibrillation?

300 mg via rapid IV or IO push. The correct initial dose and rate of administration of amiodarone for a patient with refractory ventricular fibrillation or pulseless ventricular tachycardia is 300 mg rapid IV or IO push. You may repeat amiodarone one time in 5 minutes at a dose of 150 mg rapid IV or IO push. For patients with hemodynamically stable narrow or wide-complex tachycardias, the correct dose and rate of administration for amiodarone is 150 mg given over 10 minutes.

A 145-pound man requires a dopamine infusion at 15 µg/kg/min for severe hypotension. You have a premixed bag containing 800 mg of dopamine in 500 mL of normal saline. If you are using a microdrip administration set (60 gtts/mL), how many drops per minute should you deliver to achieve the required dose?

36. First, convert the patient's weight from pounds to kilograms: 145 ÷ 2.2 = 66 kg. Next, determine the desired dose: 15 µg/kg/min × 66 kg = 990 µg/min. The next step is to determine the concentration of dopamine on hand: 800 mg ÷ 500 mL = 1.6 mg/mL (1,600 µg/mL [1.6 × 1,000 = 1,600]). Now, you must determine the number of mL to be delivered per minute: 990 µg/min [desired dose] ÷ 1,600 µg/mL [concentration on hand] = 0.6 mL/min. The final step is to determine the number of drops per minute that you must set your IV flow rate at: 0.6 mL/min × 60 gtts/mL (drop factor of the microdrip) ÷ 1 (total infusion time in minutes) = 36 gtts/min.

Which of the following cardiac rhythms is associated with bradycardia, and is characterized by regular R-R intervals and a greater ratio of P waves to QRS complexes?

3rd degree AV block. Third-degree AV block is caused by a complete block at the AV node. The SA node initiates impulses as usual; however, when they reach the AV node, they are blocked. Resultantly, the ventricles receive no electrical stimulus from the atria, so they initiate their own impulses, although at a much slower rate. On the ECG, this manifests as a bradycardic rhythm with more P waves than QRS complexes. The P-P intervals are regular (some P waves may not be visible because they are buried in a QRS complex), as are the R-R intervals; however, no relationship exists between a given P wave and QRS complex. Second-degree AV block type I (Wenkebach) is caused by a progressive delay at the AV node until an impulse is blocked from entering the ventricles. On the ECG, this manifests as a progressively lengthening P-R interval until a P wave is blocked (not followed by a QRS complex). At this point, the R-R interval becomes irregular, and the presence of this lone P wave increases the ratio of P waves to QRS complexes. Second-degree AV block type I may or may not be associated with bradycardia. Second-degree AV block type II is caused by an intermittent block at the AV node; it occurs when atrial impulses are not conducted to the ventricles. Unlike a second-degree AV block type I, however, a type II block is characterized by consistent P-R intervals of the P waves that are conducted. First-degree AV block is an abnormal delay at the AV node; on the ECG, this manifests with PR intervals greater than 0.20 seconds (120 ms) in duration. In first-degree AV block, all of the atrial impulses are conducted through the AV node and into the ventricles.

Which of the following represents the correct adult dosing regimen for adenosine?

6 mg, followed by 12 mg in 2 minutes if needed. According to the 2010 guidelines for CPR and emergency cardiac care (ECC), the correct dosing regimen of adenosine for a hemodynamically stable patient with a narrow-complex tachycardia is 6 mg via rapid (over 1 to 3 seconds) IV push. If needed, adenosine can be repeated in 1 to 2 minutes in a dose of 12 mg rapid IV push.

Sudden cardiac arrest in the adult population is MOST often secondary to:

A cardiac dysrhythmia. Most cases of sudden cardiac arrest (SCA) in the adult population are secondary to a cardiac dysrhythmia, usually ventricular fibrillation (V-Fib). This fact underscores the criticality of early defibrillation. Respiratory failure is the most common cause of cardiac arrest in the pediatric population.

Administer up to 325 mg of aspirin. Since oxygen has already been administered to this patient and your partner is attaching the ECG leads, you should administer aspirin (160 to 325 mg, non-enteric-coated). Early administration of aspirin has clearly been shown to reduce mortality and morbidity in patients experiencing an acute coronary syndrome (ACS). After establishing vascular access, you should assess his vital signs and then administer 0.4 mg of nitroglycerin (up to 3 doses, 5 minutes apart), provided that his systolic BP is greater than 90 mm Hg. If 3 doses of nitroglycerin fail to completely relieve his chest discomfort, consider administering 2 to 4 mg of morphine IV, provided that his systolic BP remains above 90 mm Hg.

You are assessing a 50-year-old man with acute chest pressure, diaphoresis, and nausea. The 12-lead ECG tracing reveals 3-mm ST segment elevation in leads V3 through V6. This indicates:

Anterolateral injury. Leads V1 and V2 view the interventricular septum. Leads V3 and V4 view the anterior wall of the left ventricle. Leads I, aVL, V5 and V6 view the lateral wall of the left ventricle. Leads II, III, and aVF view the inferior wall of the left ventricle. Myocardial ischemia manifests on the 12-lead ECG with ST segment depression and/or T-wave inversion, whereas myocardial injury manifests with ST segment elevation that is equal to or greater than 1-mm in two or more contiguous leads. Therefore, 3-mm ST segment elevation in leads V3 through V6 indicates injury to the anterior and lateral wall of the left ventricle (anterolateral injury).

The MOST appropriate initial action for a 54-year-old man who presents with the following cardiac rhythm should consist of:

Assessing the patient's clinical status. When assessing the cardiac rhythm of any patient, you must interpret it in the context of his or her clinical status. Before you reach for atropine or a pacemaker, determine if the bradycardia is causing hemodynamic compromise (ie, hypotension, altered mental status, chest pressure or discomfort, pulmonary edema). If the patient is hemodynamically unstable, treat according to established ACLS guidelines (ie, atropine, pacing, etc.). However, if the patient is hemodynamically stable, simply monitor his or her clinical status and transport to the hospital.

During your SAMPLE history of an elderly man, he tells you that his cardiologist told him that he has an "irregular heartbeat." His medications include warfarin sodium and digoxin. On the basis of this information, what underlying cardiac rhythm should you suspect?

Atrial fibrillation. Patients with atrial fibrillation (A-Fib) are commonly prescribed digoxin (a digitalis preparation) and warfarin sodium (Coumadin), which is a blood thinner. As the atria fibrillate, blood has a tendency to stagnate and form microemboli that can be ejected from the heart and occlude a pulmonary, cerebral, or coronary artery.

You should interpret the following cardiac rhythm as:

Atrial flutter with a fixed block. Because of the typical "sawtooth" flutter (F) waves, this rhythm is interpreted as atrial flutter (A-Flutter). The block is fixed in that the ratio of F waves to QRS complexes is consistent (2:1). A-Flutter with a variable block occurs when the ratio of F waves to QRS complexes is different. Atrial fibrillation (A-Fib) is characterized by an irregularly irregular rhythm with no identifiable P waves. A type II second-degree AV block is characterized by a rhythm in which some P waves are blocked (eg, they are not followed by QRS complexes).

Which of the following signs or symptoms occurs more commonly in patients with stable angina than in those with unstable angina?

Chest pain that begins during exertion. Angina pectoris occurs when the heart's demand for oxygen exceeds it's available supply (ischemia) and is a sign of coronary artery disease (CAD). Angina is classified as being stable or unstable. Stable angina typically follows a predictable pattern (ie, chest pain, pressure, or discomfort induced by exertion), lasts less than 15 minutes, and is usually relieved with rest and/or nitroglycerin. While unstable angina (preinfarction angina) can also occur during exertion, it more commonly occurs when the patient otherwise would not expect it to, such as when he or she is asleep or is otherwise resting. Furthermore, unstable angina is often not relieved by rest and/or nitroglycerin and typically lasts longer than 15 minutes. Chest pressure, tightness, or discomfort occurs in patients with both stable and unstable angina. If a patient is experiencing angina, you would expect to see ST segment depression and/or T wave inversion on the 12-lead ECG as these are indicators of myocardial ischemia. ST segment elevation indicates myocardial injury (eg, acute MI in progress).

On the 12-lead ECG, the high lateral wall of the left ventricle is viewed by leads:

I and aVL. Leads V1 and V2 view the interventricular septum. Leads V3 and V4 view the anterior wall of the left ventricle. Leads V5 and V6 view the low lateral wall of the left ventricle. Leads I and aVL view the high lateral wall of the left ventricle. Leads II, III, and aVF view the inferior wall of the left ventricle. Lead V4R views the right ventricle.

A 44-year-old man presents with the rhythm shown below. He complains of nausea, but denies vomiting. He is conscious and alert with a BP of 122/62 mm Hg, a pulse rate of 98 beats/min, and respirations of 16 breaths/min and unlabored. Treatment for this patient would MOST likely include:

Ondansetron, 4 mg. Unless associated with a fast rate (> 100 beats/min) and hemodynamic compromise (eg, hypotension, altered mental status, pulmonary edema), treatment for atrial flutter is usually not necessary in the prehospital setting. Administer supplemental oxygen if indicated, transport, and monitor the patient's hemodynamic status en route. For this patient, you should treat his nausea with an antiemetic, such as ondansetron (Zofran), 4 mg; or promethazine (Phenergan), 12.5 to 25 mg.

Which of the following ECG findings indicates a pathologic delay at the AV node?

P-R interval of 0.28 seconds. Normally, there is a physiologic delay of an impulse at the AV node that allows the atria to empty into the ventricles. On the ECG, this manifests as a P-R interval—the period of time that includes atrial depolarization and the delay at the AV node—that is between 0.12 and 0.20 seconds (120 to 200 ms). A pathologic delay at the AV node, such as what occurs with a first-degree AV block, would manifest with a P-R interval that is greater than 0.12 seconds (120 ms) in duration. By contrast, A P-R interval that is less than 0.12 seconds indicates that an impulse is traversing the AV node too fast or is bypassing it altogether, such as what occurs with Wolff-Parkinson-White (WPW) syndrome, a preexcitation syndrome in which the electrical impulse follows accessory pathways around the AV node (bundle of Kent) and prematurely depolarizes the ventricles. A wide (> 0.12 seconds [120 ms]) QRS complex indicates an intraventricular conduction delay, such as a bundle branch block. P waves that vary in morphology (appearance) indicate more than one atrial pacemaker site; an example of this is an ectopic atrial rhythm.

A 35-year-old female experienced a syncopal episode shortly after complaining of palpitations. She was reportedly unconscious for less than 10 seconds. Upon your arrival, she is conscious and alert, denies any injuries, and states that she feels fine. She further denies any significant medical history. Her vital signs are stable and the cardiac monitor reveals a sinus rhythm with frequent premature atrial complexes. On the basis of this information, what MOST likely caused her syncopal episode?

Paroxysmal supraventricular tachycardia. Syncope (fainting) of cardiac origin is caused by a sudden decrease in cerebral perfusion secondary to a decrease in cardiac output. This is usually the result of an acute bradydysrhythmia or tachydysrhythmia. In this particular patient, the presence of frequent premature atrial complexes (PACs), which indicates atrial irritability, suggests paroxysmal supraventricular tachycardia (PSVT) as the underlying dysrhythmia that caused her syncopal episode. In PSVT, the heart is beating so fast that ventricular filling and cardiac output decrease, which results in a transient decrease in cerebral perfusion. Not all patients with PSVT experience syncope. Many experience an acute onset of palpitations and/or lightheadedness that spontaneously resolves.

A patient experiencing a right ventricular infarction would be expected to present with:

ST elevation in leads II, III, and aVF. A right ventricular infarction (RVI) should be suspected when a patient presents with ECG changes indicative of an inferior wall injury pattern (equal to or greater than 1-mm ST elevation in leads II, III, and aVF; reciprocol ST depression and T wave inversion in leads I and aVL) AND has equal to or greater than 1-mm ST elevation in lead V4R when a right-sided 12-lead ECG is obtained. Patients experiencing an RVI are preload dependent and often present with hypotension; therefore, vasodilators (eg, nitroglycerin, morphine) should be avoided. Instead, IV fluid boluses should be given to maintain adequate perfusion. Other signs of an RVI include jugular venous distention and peripheral edema. Pulmonary edema and coughing up blood (hemoptysis) are indicative of left ventricular failure.

If a patient was experiencing acute injury involving the interventricular septum and anterior wall of the left ventricle, you would expect the 12-lead ECG to reveal:

ST segment elevation in leads V1 through V4. ST segment elevation that is equal to or greater than 1-mm in two or more contiguous leads indicates myocardial injury (eg, an acute MI in progress). ST segment depression and/or dynamic T wave inversion indicates myocardial ischemia. Leads V1 and V2 view the interventricular septum; leads V3 and V4 view the anterior wall of the left ventricle; leads V5, V6, I, and aVL view the lateral wall of the left ventricle; and leads II, III, and aVF view the inferior wall of the left ventricle. Therefore, if a patient is experiencing acute injury involving the interventricular septum and anterior wall of the left ventricle (anteroseptal injury), you would expect the 12-lead ECG tracing to reveal ST segment elevation is leads V1 through V4. It is important to note, however, that an absence of ST elevation does not definitively rule out acute myocardial infarction.

A 65-year-old man with difficulty breathing and palpitations presents with the cardiac rhythm shown below, which you should interpret as:

Supraventricular tachycardia. Since this rhythm has narrow (less than 0.12 seconds) QRS complexes and a rate greater than 150 beats/min, it should be interpreted as supraventricular tachycardia (SVT), which means that its site of origin is above (supra) the level of the ventricles. SVT can be either atrial or junctional in origin. Atrial fibrillation is characterized by an irregularly irregular rhythm and no discernable P waves. Atrial flutter is characterized by flutter (F) waves that resemble a saw tooth. Ventricular tachycardia (V-Tach), in contrast to SVT, is characterized by wide (greater than 0.12 seconds) QRS complexes and no visible P waves.

Ventilate at a rate of 10 to 12 breaths/min, support blood pressure, and consider therapeutic hypothermia. The 2010 guidelines for CPR and emergency cardiac care (ECC) have added a fifth link to the chain of survival, integrated post-arrest care. In addition to supporting the patient's airway and ventilatory status and supporting his or her blood pressure with IV fluid boluses or an inotropic agent (ie, dopamine), you should assess for and correct any glucose abnormalities. If the patient is unable to follow verbal commands or remains comatose following return of spontaneous circulation (ROSC), therapeutic hypothermia (89.6°F to 93.2°F [32°C to 34°C]) has been shown to improve neurologic recovery and should be considered (follow your local protocols regarding therapeutic hypothermia). Once ROSC has been established, you should continue to ventilate the adult patient at a rate of 10 to 12 breaths/min (one breath every 5 to 6 seconds) if he or she remains apneic. DO NOT hyperventilate the patient as this may impair venous return to the heart and compromise cardiac output. If the patient is able to follow verbal commands following ROSC, obtain a 12-lead ECG tracing and assess for signs of acute MI (ie, ST elevation). Depending on your transport time, you may consider starting a maintenance infusion of the antidysrhythmic drug that was administered during the arrest, which in this case, would be amiodarone (1 mg/min).

depolarization

process by which muscle fibers are stimulated to contract.

tunica adventitia

protective outer layer of fibrous tissue that provides blood vessels with the strength needed to withstand high pressure against their walls

blood pressure

the pressure exerted by the blood against the arterial walls generated by repeated forceful contractions of the left ventricle which keeps blood flowing through the body. Magnitude is influenced by caridac output, blood volume and relative constriction/dilation of the arteries

opening snap

sound indicative of a noncompliant valve

role of magnesium in cardiac function

stabilizes the cell membrane; acts with potassium and opposes the actions of calcium

pulsus alterans

the pulse alternates between strong and weak beats; typically indicates left ventricular systolic damage

Palpitations

the sensation of an abnormally fast or irregular heart beat

pericardium

the tough, fibrous sac surrounding the heart in order to protect it and provide lubrication between the heart and surrounding structures.

systole

the period of time when the atria or ventricles are contracting

nitrates

these drugs decrease the workload of the heart thereby decreasing the heart's need for oxygen and the anginal pain is dissipated. Can also cause significant vasodilation.

arteries

thick-walled, muscular vessels that carry blood away from the heart. Usually oxygenated blood except the pulmonary arteries

epicardium

thin membrane that forms the outermost layer of the heart

endocardium

thin membrane that lines the inside of the hearts cavities and forms the valves; vital to reduction of turbulance.

intraventricular septum

thin wall that separates the left and right sides of the heart

Purkinje fibers

thousands of fibrils distributed through the ventricular muscle; during electrical impulse conduction here the ventricles contract simultaneously. 20-40 beats per minute

pericardial friction rub

to-and-fro sound indicating pericarditis

Pediatric atropine dose

0.02mg/kg

Fentanyl Citrate

-Binds to opiate receptors, producing analgesia and euphoria

J point

the junction point at the beginning of the ST segment

lumen

the opening within a blood vessel

Coronary arteries

transport oxygenated blood to the heart; divided into left and right and they brance off the aorta at the coronary ostia.

Atropine Sulfate

-Inhibits the action of acetylcholine at postganglionic parasympathetic neuroeffector sites -Increases heart rate in life-threatening bradycardic dysrhythmias

How can hyperkalemia be treated?

Albuterol, calcium, sodium bicarbonate

Treatment of ventricular fibrillation

BLS, IV/IO, Defibrillation, Epi/vasopressin, amio/lido

The cardiac cell required for cardiac muscle contraction which favors slow channels

Calcium

The morphology of univocal PVCs is

Constant configuration

Dub-Aortic and pulmonic valves close

Cranial nerve 1

Olfactory nerve

What is the cause of carpopedal spasms

Hyperventilation

McBurney's point

Pain in RLQ with appendicitis

The left arm lead on an ECG is what (-/+)

Positive

Tricuspid valve

Separates the right atrium and the right ventricle

What ion is responsible for depolarization of the myocardium?

Sodium

How to calculate minute volume

Tidal volume X Respiratory rate

When is therapeutic hypothermia indicated?

When your PT gets ROSC and is still unconscious

when are coronary arteries perfused?

ventricular diastole

A 66-year-old woman is diagnosed with cardiomyopathy. What does this indicate? A: Progressive cardiac weakening B: An occluded coronary artery C: An enlarged myocardium D: Strengthening of the ventricles

*A: Progressive cardiac weakening* Reason: Cardiomyopathy is a progressive weakening of the myocardium. This condition is commonly the result of chronic hypertension or a history of multiple myocardial infarctions. An enlarged myocardium is called cardiomegaly.

Which of the following represents the correct adult dosing regimen for adenosine? A: 12 mg, followed by 12 mg in 2 minutes if needed B: 6 mg, followed by 12 mg in 2 minutes if needed C: 36 mg, divided in 12 mg increments 2 minutes apart D: 6 mg, followed by 6 mg in 2 minutes if needed

*B: 6 mg, followed by 12 mg in 2 minutes if needed* Reason: According to the 2010 guidelines for CPR and emergency cardiac care (ECC), the correct dosing regimen of adenosine for a hemodynamically stable patient with a narrow-complex tachycardia is 6 mg via rapid (over 1 to 3 seconds) IV push. If needed, adenosine can be repeated in 1 to 2 minutes in a dose of 12 mg rapid IV push.

On the 12-lead ECG, the high lateral wall of the left ventricle is viewed by leads: A: III and aVF. B: I and aVL. C: V1 and V2. D: V5 and V6.

*B: I and aVL* Reason: Leads V1 and V2 view the interventricular septum. Leads V3 and V4 view the anterior wall of the left ventricle. Leads V5 and V6 view the low lateral wall of the left ventricle. Leads I and aVL view the high lateral wall of the left ventricle. Leads II, III, and aVF view the inferior wall of the left ventricle. Lead V4R views the right ventricle.

Which of the following represents the MOST appropriate initial drug and dose that is given to all adult patients in cardiac arrest? A: 10 mL of epinephrine 1:10,000 every 3 to 5 minutes B: 0.1 mg/kg of epinephrine every 3 to 5 minutes C: 1 mg of epinephrine 1:1,000 every 3 to 5 minutes D: 40 units of vasopressin every 3 to 5 minutes

*A: 10 mL of epinephrine 1:10,000 every 3 to 5 minutes* Reason: Once vascular access has been obtained (IV or IO), the first drug and dose given to all patients in cardiac arrest—regardless of the rhythm on the cardiac monitor—is epinephrine 1 mg (10 mL) of a 1:10,000 solution, repeated every 3 to 5 minutes. You may consider a one-time dose of vasopressin (40 units) to replace the first or second dose of epinephrine, but not both. Higher doses of epinephrine may be necessary if special circumstances exist (ie, severe beta-blocker toxicity). Consult with medical control as needed.

The initial dose of diltiazem for a 165-pound patient is approximately: A: 19 mg. B: 17 mg. C: 25 mg. D: 22 mg.

*A: 19 mg.* Reason: Diltiazem hydrochloride (Cardizem) is a calcium channel blocking drug that is used to treat rapid ventricular rates associated with atrial fibrillation or atrial flutter. It can also be used after adenosine to treat refractory reentry supraventricular tachycardia in hemodynamically stable patients. The initial dose of diltiazem is 0.25 mg/kg IV over 2 minutes; the average initial dose is 15 to 20 mg. It may be repeated in 15 minutes in a dose of 0.35 mg/kg IV over 2 minutes; the average second dose is 20 to 25 mg. A 165-pound patient weighs 75 kg. Therefore, the initial dose of diltiazem for a patient of this weight would be 18.75 mg (approximately 19 mg), and the second dose would be 26.25 mg (approximately 26 mg).

Morphine Sulfate

-Alleviates pain through CNS action -Increases peripheral venous capacitance and decreases venous return -Decreases preload, afterload and myocadial oxygen demand

Which of the following clinical presentations is MOST consistent with dissection of the ascending aorta? A: Acute tearing pain in between the scapulae, blood pressure discrepancy between arms, maximal pain severity from the onset B: Tearing abdominal pain unrelieved by analgesia, pulse deficit in the femoral arteries, lightheadedness, blood in the stool C: Gradual onset of chest pressure that increases in severity over time, hypotension, tachycardia, bilaterally weak radial pulses D: Sudden onset of lower back pain that radiates to the groin, urge to defecate, pain is constant and moderate in severity

*A: Acute tearing pain in between the scapulae, blood pressure discrepancy between arms, maximal pain severity from the onset* Reason: Aortic dissection occurs when the layers of the aorta undergo destructive changes, resulting in an aneurysm (weakening and ballooning of the arterial wall). In dissection of the ascending aorta, the patient typically experiences an acute onset of ripping, tearing, or stabbing pain in the anterior chest or in between the scapulae. In some patients, it may be difficult to differentiate the pain of acute aortic dissection from that of acute myocardial infarction (AMI); however, a number of distinctive features may help. The pain of an AMI is often preceded by prodromal symptoms (eg, nausea, weakness, sweating). Although pain from an AMI is acute, it gradually intensifies over time and is typically described as a squeezing or pressure sensation. By contrast, the pain of aortic dissection is acute, is of maximal intensity from the onset, and is usually described as a ripping, tearing, or stabbing feeling. Other signs and symptoms depend on the extent and location of the dissection. In dissections of the ascending aorta, one or more of the vessels of the aortic arch may be compromised. Disruption of blood flow through the innominate artery, for example, is likely to produce a difference in blood pressure between the arms. The onset and pain characteristics of abdominal aortic dissection are similar to those of ascending aortic dissection; however, the pain typically begins in the abdomen or lower back. Pulse deficits in the femoral arteries may be present, and if the aneurysm is leaking blood into the retroperitoneal space, the patient may complain of an urge to defecate and exhibit signs of shock.

You are transporting a 60-year-old woman with chest discomfort and diaphoresis. The 12-lead ECG indicates an acute anterior wall MI. The patient is receiving oxygen and an IV has been established. You have administered 324 mg of aspirin, 3 sublingual nitroglycerin, and 5 mg of morphine. Which of the following should concern you the MOST during transport? A: An acute cardiac dysrhythmia B: Severe hypotension C: Completely relieving her pain D: Respiratory depression

*A: An acute cardiac dysrhythmia* Reason: More than 500,000 deaths occur each year as the result of acute myocardial infarction (AMI). Sixty to seventy percent of these deaths occur outside the hospital, usually during the first few hours after the onset of symptoms. Of all deaths from AMI, 90% are due to dysrhythmias—usually ventricular fibrillation—which typically occur during the early hours of the infarct; this should be your primary concern. Many patients experiencing an anterior wall MI are hyperdynamic—that is, they are hypertensive and tachycardic; hypotension is not as common. Depression of the CNS (respiratory depression, bradycardia, and hypotension) should be a concern any time you administer a narcotic analgesic (ie, morphine); however, most patients do not experience significant CNS depression with 5 mg of morphine. Pain relief is an important aspect in the management of the patient with AMI; minimizing pain minimizes anxiety, which can limit the size of the infarct.

Which of the following pain descriptions is MOST consistent with a cardiac problem? A: Crushing B: Sharp C: Tearing D: Intermittent

*A: Crushing* Reason: Chest pain of cardiac origin is most often described as crushing, dull, pressure, or as a feeling of heaviness or discomfort. The pain is typically constant, not intermittent, and is usually not palliated or exacerbated by movement. Bear in mind that these are typical pain descriptions. The paramedic should not rule out a cardiac problem if the patient describes the pain differently. Sharp (pleuritic) pain is often associated with conditions such as pleurisy, pulmonary embolism, or spontaneous pneumothorax. A tearing sensation should alert you to the possibility of acute aortic dissection.

What is the therapeutic effect of aspirin when administered to a patient experiencing an acute coronary syndrome (ACS)? A: Decreased thromboxane A2 production, which inhibits platelet aggregation B: Destruction of platelets by increasing thromboxane A2 production C: Destruction of a blood clot in a coronary artery by destroying fibrin D: Decreased platelet production and coronary artery vasoconstriction

*A: Decreased thromboxane A2 production, which inhibits platelet aggregation* Reason: Thromboxane A2 is produced by activated platelets. It is a potent vasoconstrictor, it stimulates activation of new platelets, and it increases platelet aggregation. Aspirin (acetylsalicylic acid [ASA]) blocks the production of thromboxane A2, which inhibits vasoconstriction, inhibits activation of new platelets, and inhibits platelet aggregation (ie, it makes the platelets less "sticky"). Aspirin does not destroy a clot in a coronary artery—it prevents it from getting larger. Furthermore, by inhibiting local coronary vasoconstriction, it may enhance blood flow around the clot. Fibrinolytic agents (ie, alteplase [Activase], streptokinase [Streptase], tenecteplase [TNKase]) convert the body's own clot-dissolving enzyme from its inactive form, plasminogen, to its active form, plasmin. Plasmin then destroys the fibrin matrix of the clot—hence the term "fibrinolysis."

You are preparing to defibrillate a patient in cardiac arrest with a manual biphasic defibrillator, but are unsure of the appropriate initial energy setting. What should you do? A: Deliver one shock with 200 joules and resume CPR. B: Continue CPR and shock with 360 joules in 2 minutes. C: Contact medical control for further guidance. D: Deliver three sequential shocks with 120 joules.

*A: Deliver one shock with 200 joules and resume CPR* Reason: Energy settings for manual biphasic defibrillators are device-specific—typically 120 joules (rectilinear) or 150 joules (truncated). However, if the appropriate initial energy setting is unknown, you should defibrillate with 200 joules. For subsequent shocks, use the same or higher energy setting. Whether you are using a monophasic or biphasic defibrillator, you should only perform 1 shock, followed immediately by CPR (starting with chest compressions).

Which of the following ECG lead configurations is correct? A: To assess lead II, place the negative lead on the right arm and the positive lead on the left leg. B: To assess lead III, place the negative lead on the right arm and the positive lead on the left leg. C: To assess lead III, place the negative lead on the left leg and the positive lead on the right arm. D: To assess lead I, place the positive lead on the right arm and the negative lead on the left arm.

*A: To assess lead II, place the negative lead on the right arm and the positive lead on the left leg.* Reason: According to the Einthoven triangle, lead I is assessed by placing the negative (white) lead on the right arm and the positive (red) lead on the left arm. Lead II is assessed by placing the negative lead on the right arm and the positive lead on the left leg. Lead III is assessed by placing the negative lead on the left arm and the positive lead on the left leg.

Beta Blockers (lol's)

-Bind to beta-adrenoceptors and thereby block the binding of of norepinephrine and epinephrine to these receptors -Inhibits normal sympathetic effects that act through these receptors (sympatholytic)

You respond to a residence for a 68-year-old male with nausea, vomiting, and blurred vision. As you are assessing him, he tells you that he has congestive heart failure and atrial fibrillation, and takes numerous medications. The cardiac monitor reveals atrial fibrillation with a ventricular rate of 50 beats/min. Which of the following medications is MOST likely responsible for this patient's clinical presentation? A: Digoxin B: Furosemide C: Vasotec D: Warfarin

*A: Digoxin* Reason: This patient has classic signs of digitalis toxicity. Digoxin is commonly prescribed to patients with congestive heart failure and atrial fibrillation (A-Fib) or atrial flutter (A-Flutter). Its positive inotropic effects increase cardiac contractility and maintain cardiac output, while its negative chronotropic effects control the ventricular rate of the A-Fib or A-Flutter. Digitalis preparations (ie, Lanoxin, Digoxin) have a narrow therapeutic index—that is, there is a fine line between a therapeutic and toxic dose. You should suspect digitalis toxicity in any patient who takes Digoxin or Lanoxin and presents with complaints such as nausea, vomiting, abdominal pain, anorexia, or blurred/yellow vision. Additionally, virtually any cardiac dysrhythmia can be caused by the toxic effects of digitalis. Treatment involves the administration of Digibind, which is given at the hospital.

You are treating a 68-year-old woman with chest pressure and shortness of breath that started 2 days ago. Her BP is 76/52 mm Hg and her pulse is 130 beats/min and weak. The cardiac monitor reveals sinus tachycardia with occasional PVCs and auscultation of her lungs reveals diffuse coarse crackles. Which of the following treatment interventions is MOST appropriate for this patient? A: Dopamine, 2 to 20 µg/kg/min. B: Nitroglycerin, 10 to 20 µg/min. C: Amiodarone, 150 mg over 10 min. D: Normal saline, 20 mL/kg rapid bolus.

*A: Dopamine, 2 to 20 µg/kg/min.* Reason: Your patient's history and clinical presentation is consistent with cardiogenic shock. She has had chest pressure and shortness of breath for 2 days and is now significantly hypotensive with weak pulses. Because of its positive inotropic effect of increasing myocardial contractility, dopamine is the drug of choice for non-hypovolemic shock (eg, cardiogenic shock) and may improve perfusion. Typically, dopamine for cardiogenic shock is started at 2 µg/kg/min and titrated upwards as needed to improve blood pressure and perfusion. At doses of greater than 10 µg/kg/min, dopamine acts predominantly as a vasopressor, which results in systemic vasoconstriction. Clearly, nitroglycerin is contraindicated in any patient with shock; its potent vasodilatory effects would further lower the patient's blood pressure and worsen her condition. Amiodarone is not the drug of choice for this patient; it is given in a dose of 150 mg over 10 minutes for hemodynamically stable patients with wide or narrow-complex tachycardias that exceed 150 beats/min. Caution must be used if you consider giving a normal saline bolus; the coarse crackles in her lungs indicate pulmonary edema, which could easily be exacerbated by large fluid boluses. Her problem is heart failure, not hypovolemia.

Which of the following interventions has the greatest impact on patient survival from sudden cardiac arrest? A: Early CPR and defibrillation B: Cardiac medication administration C: Identifying the cause D: Advanced airway control

*A: Early CPR and defibrillation* Reason: Early CPR and defibrillation are the two interventions that will have the greatest impact on patient survival from sudden cardiac arrest (SCA). Early, effective CPR maintains perfusion to the body's vital organs until defibrillation can be provided. The most common initial cardiac rhythm observed during SCA is ventricular fibrillation (V-Fib). Early defibrillation, in conjunction with early CPR, greatly enhances the chance of establishing return of spontaneous circulation (ROSC). The probability of successful defibrillation decreases over time, especially if CPR is delayed. For each minute that V-Fib persists, the patient's chance of survival decreases by approximately 7% to 10%.

Which of the following findings is MOST suggestive of right-sided heart failure? A: Engorged jugular veins B: Persistent orthopnea C: Nocturnal dyspnea D: Blood-tinged sputum

*A: Engorged jugular veins* As the right side of the heart fails, blood is not effectively ejected into the pulmonary circulation; therefore, it backs up beyond the right atrium and into the systemic venous system. This is most noticeable by the presence of engorged or distended jugular veins. Orthopnea, nocturnal dyspnea, and coughing up blood-tinged sputum are indicators of left-sided heart failure as they all indicate fluid in the lungs.

You are assessing a man with a acute chest pain. As you are inquiring about the quality of his pain, he clenches his fist. This is called __________ sign and nonverbally conveys a feeling of: A: Levine's, pressure. B: Cullen's, dullness. C: Beck's, impending doom. D: Grey-Turner's, fluttering.

*A: Levine's, pressure* Reason: Patients with an acute coronary syndrome (ACS)—that is, unstable angina or acute myocardial infarction—often clench their fist when describing the quality of their chest pain or discomfort. This is called Levine's sign, and it conveys a feeling of pressure in the chest. The pain associated with ACS may also be described as a dull or aching sensation or as a feeling of heaviness. An ACS patient who complains of fluttering in the chest should make you suspicious for a cardiac dysrhythmia (ie, SVT, V-Tach). Cullen's sign is characterized by periumbilical bruising and indicates blood in the peritoneal space. Grey-Turner's sign—bruising to the flank area—also indicates blood in the peritoneal space. Beck's triad is a trio of clinical findings that indicates a cardiac tamponade; it includes jugular venous distention, muffled or distant heart sounds, and a narrowing pulse pressure.

Which of the following ECG findings indicates a pathologic delay at the AV node? A: P-R interval of 0.28 seconds B: P waves of varying morphologies C: P-R interval less than 0.12 seconds D: QRS complex of 0.16 seconds

*A: P-R interval of 0.28 seconds* Reason: Normally, there is a physiologic delay of an impulse at the AV node that allows the atria to empty into the ventricles. On the ECG, this manifests as a P-R interval—the period of time that includes atrial depolarization and the delay at the AV node—that is between 0.12 and 0.20 seconds (120 to 200 ms). A pathologic delay at the AV node, such as what occurs with a first-degree AV block, would manifest with a P-R interval that is greater than 0.12 seconds (120 ms) in duration. By contrast, A P-R interval that is less than 0.12 seconds indicates that an impulse is traversing the AV node too fast or is bypassing it altogether, such as what occurs with Wolff-Parkinson-White (WPW) syndrome, a preexcitation syndrome in which the electrical impulse follows accessory pathways around the AV node (bundle of Kent) and prematurely depolarizes the ventricles. A wide (> 0.12 seconds [120 ms]) QRS complex indicates an intraventricular conduction delay, such as a bundle branch block. P waves that vary in morphology (appearance) indicate more than one atrial pacemaker site; an example of this is an ectopic atrial rhythm.

You are evaluating a regular cardiac rhythm in lead II. The rate is 90 beats/min, the QRS complexes consistently measure 0.16 seconds, and inverted P waves are seen immediately following each QRS complex. The rhythm described is MOST characteristic of a/an: A: accelerated junctional rhythm with ventricular aberrancy. B: second-degree AV block with abnormal ventricular conduction. C: wandering atrial pacemaker with a bundle branch block. D: ectopic atrial rhythm with a ventricular conduction delay.

*A: accelerated junctional rhythm with ventricular aberrancy.* Reason: A junctional rhythm is characterized by inverted P waves in lead II. If seen, the inverted P waves precede or follow the QRS complex. At a rate of 90 beats/min, the rhythm is further defined as an accelerated junctional rhythm. QRS complexes greater than 0.12 seconds (120 ms) indicate aberrant (abnormal) ventricular conduction (ie, bundle branch block). A wandering atrial pacemaker is characterized by P waves that precede each QRS complex, but vary in morphology. An ectopic atrial rhythm is also characterized by P waves of varying morphologies as well as varying PR intervals. A second- or third-degree AV block should be suspected when there are more P waves than QRS complexes.

Side effects of atropine sulfate may include: A: acute urinary retention. B: pupillary constriction. C: hypersalivation. D: hypotension.

*A: acute urinary retention* Reason: Side effects of atropine sulfate may include thirst, dry mouth, pupillary dilation (mydriasis), tachycardia, hypertension, and urinary retention. Acute urinary retention is especially common in older men with benign prostatic hyperplasia (BPH), also known as an enlarged prostate gland.

A transmural myocardial infarction is defined as: A: an MI that involves the entire thickness of the left ventricular wall from endocardium to epicardium. B: multiple areas of myocardial necrosis confined to the inner one third to one half of the left ventricular wall. C: an MI that occurs without gross ST segment elevation or the presence of a pathologic Q wave. D: any area of infarcted myocardium that is caused by focal areas of acute coronary vasospasm.

*A: an MI that involves the entire thickness of the left ventricular wall from endocardium to epicardium* Reason: A transmural myocardial infarction involves the entire thickness of the left ventricular wall from endocardium to epicardium; it is associated with ST-segment elevation and, eventually, the development of pathologic Q waves. A subendocardial infarction involves multiple areas of myocardial necrosis confined to the inner one third to one half of the left ventricular wall; subendocardial infarctions are also referred to as non-Q-wave infarctions. Myocardial ischemia caused by focal areas of spontaneous coronary vasospasm, which may lead to infarction, is called Prinzmetal's (variant) angina; the exact cause of this spontaneous coronary vasospasm is largely unknown.

You are assessing a 50-year-old man with acute chest pressure, diaphoresis, and nausea. The 12-lead ECG tracing reveals 3-mm ST segment elevation in leads V3 through V6. This indicates: A: anterolateral injury. B: inferior injury. C: anteroseptal ischemia. D: lateral ischemia.

*A: anterolateral injury.* Reason: Leads V1 and V2 view the interventricular septum. Leads V3 and V4 view the anterior wall of the left ventricle. Leads I, aVL, V5 and V6 view the lateral wall of the left ventricle. Leads II, III, and aVF view the inferior wall of the left ventricle. Myocardial ischemia manifests on the 12-lead ECG with ST segment depression and/or T-wave inversion, whereas myocardial injury manifests with ST segment elevation that is equal to or greater than 1-mm in two or more contiguous leads. Therefore, 3-mm ST segment elevation in leads V3 through V6 indicates injury to the anterior and lateral wall of the left ventricle (anterolateral injury).

You are called to a local supermarket where a customer collapsed. When you arrive, two bystanders are performing CPR on the patient. You should: A: assess the patient to confirm pulselessness and apnea. B: immediately assess the patient's cardiac rhythm. C: verify the effectiveness of the bystander's CPR. D: perform a precordial thump and assess for a carotid pulse.

*A: assess the patient to confirm pulselessness and apnea* Reason: When you arrive at a scene and find bystanders performing CPR, you should briefly pause and confirm that the patient is pulseless and apneic. In some cases, you will find CPR being performed on patients who do not require it. Once cardiac arrest is confirmed, resume high-quality CPR and assess the patient's cardiac rhythm as soon as possible. According to the 2010 guidelines for CPR and emergency cardiac care (ECC), the precordial thump should not be used for unwitnessed out-of-hospital cardiac arrest. However, it may be considered for patients with witnessed, monitored unstable ventricular tachycardia, including pulseless ventricular tachycardia, if a defibrillator is not immediately ready for use.

A middle-aged man is found unresponsive, pulseless, and apneic. His cardiac arrest was not witnessed, although his skin is still warm to the touch. You should: A: begin immediate high-quality CPR. B: administer a precordial thump. C: insert an advanced airway device. D: assess his need for defibrillation.

*A: begin immediate high-quality CPR* Reason: The first and most crucial intervention for any patient in cardiac arrest is immediate high-quality CPR. With CPR ongoing, you or your partner can apply the defibrillation pads and assess the patient's cardiac rhythm. If a shock is indicated, deliver it and immediately resume CPR, starting with chest compressions. During the 2-minute cycles of CPR, vascular access can be obtained, cardiac drugs can be administered, and the patient's airway can be secured with an advanced device if necessary. It is absolutely critical to minimize interruptions in chest compressions; if you must interrupt compressions, do so for no longer than 10 seconds. The precordial thump is not indicated for unwitnessed cardiac arrest; it may be considered for patients with witnessed V-Tach, however, but has a low success rate.

In the context of an acute coronary syndrome, the presence of dyspnea should make you MOST suspicious for: A: pulmonary congestion. B: severe anxiety. C: cor pulmonale. D: diffuse bronchospasm.

*A: pulmonary congestion.* Reason: Dyspnea that occurs in the context of an acute coronary syndrome (ACS)—that is, unstable angina or acute myocardial infarction—should be assumed to be the result of left side congestive heart failure with resultant pulmonary congestion/edema. The majority of myocardial infarctions involve the left ventricle. The damage may be so extensive that myocardial contractility is impaired and blood backs up into the lungs. Cor pulmonale—acute right heart failure secondary to pulmonary hypertension—typically presents with systemic venous congestion (ie, JVD, peripheral edema), not pulmonary congestion. Anxiety is very common with ACS, and can potentially exacerbate the patient's condition due to increases in myocardial oxygen consumption and demand. In the interest of the patient, however, assume that any complaint of dyspnea in conjunction with ACS is the result of the worst case scenario—pulmonary edema and impaired oxygenation.

A 56-year-old man complains of chest discomfort, shortness of breath, and is profusely diaphoretic. His blood pressure is 84/64 mm Hg and his radial pulses are barely palpable. You should: A: consider sedation and perform cardioversion. B: defibrillate with 200 biphasic joules. C: prepare for immediate cardiac pacing. D: give 150 mg of amiodarone over 10 minutes.

*A: consider sedation and perform cardioversion* Reason: Your patient has a narrow-complex tachycardia, probably supraventricular tachycardia (SVT). Furthermore, he is hemodynamically unstable as evidenced by his hypotension, respiratory distress, and chest discomfort. Heart rates greater than 150 beats/min often cause hemodynamic compromise because they impair ventricular filling and subsequent cardiac output. Patients with unstable tachycardias require synchronized cardioversion. For the patient with a regular narrow-complex tachycardia (ie, SVT), start with 50 to 100 joules. Consider sedating the patient prior to cardioversion only if doing so does not delay the procedure. If the initial cardioversion attempt is unsuccessful, repeat the cardioversion, increasing the energy setting in a stepwise fashion, and search for potentially reversible underlying causes. Defibrillation is indicated for patients with V-Fib and pulseless V-Tach. Transcutaneous cardiac pacing (TCP) is indicated for patients with hemodynamically unstable bradycardia. Amiodarone, in a dose of 150 mg over 10 minutes, is indicated for patients with stable narrow or wide-complex tachycardias.

You and your team are performing CPR on a middle-aged male who presented with asystole. After 2 minutes of CPR, you reassess him and note that his cardiac rhythm has changed to ventricular fibrillation. You should: A: defibrillate and then resume CPR. B: assess for a carotid pulse for 5 seconds. C: defibrillate after 2 more minutes of CPR. D: make sure the leads are still attached.

*A: defibrillate and then resume CPR.* Reason: CPR alone rarely, if ever, converts asystole—or any other cardiac arrest rhythm—to a perfusing rhythm. Furthermore, if one of the leads detaches from the patient's chest, you will more likely see something that resembles massive artifact, not ventricular fibrillation (V-Fib). If you see V-Fib on the cardiac monitor, defibrillate one time with 360 monophasic joules (or equivalent biphasic) and then immediately resume CPR, starting with chest compressions. Assessing for a carotid pulse in a patient who is clearly in V-Fib wastes time; it delays defibrillation and CPR. After 2 minutes of CPR, reassess the patient's cardiac rhythm; if V-fib is still present, defibrillate one time and immediately resume CPR. If you see an organized cardiac rhythm, assess for a pulse for at least 5 seconds but no more than 10 seconds, and then resume CPR if indicated.

A 59-year-old woman presents with a regular, narrow-complex tachycardia at a rate of 180 beats/min. She is conscious and alert, but complains of chest discomfort and has a blood pressure of 86/56 mm Hg. In addition to giving her supplemental oxygen, you should: A: have her chew and swallow 325 mg of aspirin. B: administer 12 mg of adenosine rapid IV push. C: give her up to 3 sublingual doses of nitroglycerin. D: administer 150 mg of amiodarone over 10 min.

*A: have her chew and swallow 325 mg of aspirin* Reason: A regular, narrow complex tachycardia at a rate greater than 150 beats/min is consistent with supraventricular tachycardia (SVT). Although the patient is conscious and alert, she is complaining of chest discomfort and is hypotensive. Since she could be experiencing an acute coronary syndrome (ACS), you should instruct her to chew and swallow up to 325 mg of aspirin. Aspirin should be given to any patient suspected of experiencing an ACS, provided there are no contraindications (eg, allergy); it will not affect her blood pressure. Nitroglycerin, however, may exacerbate her hypotension and should be avoided. You can consider administering adenosine; however, the initial dose is 6 mg rapid IV push. Amiodarone, in a dose of 150 mg over 10 minutes, is appropriate for patients with hemodynamically stable wide-complex tachycardias (ie, V-Tach). Closely monitor this patient and be prepared to perform synchronized cardioversion.

An older man is suddenly awakened in the middle of the night, gasping for air. He is extremely restless and pale, and is coughing up blood. His clinical presentation is MOST consistent with: A: left side heart failure. B: unstable angina. C: right side heart failure. D: gastrointestinal bleed.

*A: left side heart failure.* Reason: Waking up in the middle of the night with severe difficulty breathing (paroxysmal nocturnal dyspnea [PND]) and coughing up blood or blood-tinged sputum (hemoptysis) are consistent with left-sided heart failure and pulmonary edema. Right-sided heart failure typically does not present with respiratory distress; it commonly manifests with jugular venous distention and peripheral edema. Shortness of breath and hemoptysis are not consistent with a gastrointestinal (GI) bleed; signs of a GI bleed include abdominal pain, vomiting up blood (hematemesis), which may be bright red or have a coffee-ground appearance; dark, tarry stools (melena); or bright red blood in the stool (hematochezia). Because left-sided heart failure can be caused by other factors, such as a long history of poorly-controlled hypertension, angina may or may not be present.

Ventricular ejection fraction is defined as the: A: percentage of blood in the ventricle pumped out during a contraction. B: volume of blood pumped into the left ventricle from the left atrium. C: amount of blood pumped out from either ventricle per contraction. D: amount of blood pumped from either ventricle each minute.

*A: percentage of blood in the ventricle pumped out during a contraction.* Reason: Ejection fraction (EF) is the percentage of blood that is pumped from the ventricle per contraction. The total volume of blood pumped out of the ventricle per contraction is called the stroke volume (SV). If the ventricle contains 100 mL of blood before a contraction, but only ejects 55 mL when it contracts (SV), the ejection fraction is 55% (100 mL × 0.55 = 55 mL). Ejection fraction should be at least 65% in the adult. Cardiac output (CO) is the volume of blood ejected from the left ventricle each minute, and is calculated by multiplying the stroke volume by the heart rate; in the adult, this is typically 5 to 6 L/min

*B: 36* Reason: First, convert the patient's weight from pounds to kilograms: 145 ÷ 2.2 = 66 kg. Next, determine the desired dose: 15 µg/kg/min × 66 kg = 990 µg/min. The next step is to determine the concentration of dopamine on hand: 800 mg ÷ 500 mL = 1.6 mg/mL (1,600 µg/mL [1.6 × 1,000 = 1,600]). Now, you must determine the number of mL to be delivered per minute: 990 µg/min [desired dose] ÷ 1,600 µg/mL [concentration on hand] = 0.6 mL/min. The final step is to determine the number of drops per minute that you must set your IV flow rate at: 0.6 mL/min × 60 gtts/mL (drop factor of the microdrip) ÷ 1 (total infusion time in minutes) = 36 gtts/min.

You are transporting a 62-year-old male who called EMS because of nausea and diarrhea. His past medical history includes high cholesterol, for which he takes Lipitor; he denies any other medical history. His blood pressure is 132/78 mm Hg, pulse is 68 beats/min, and respirations are 16 breaths/min. He is receiving oxygen via nasal cannula and has a patent IV line established. He has been in a normal sinus rhythm, but is now experiencing occasional premature ventricular complexes (PVCs). After noting the PVCs, you should: A: reassess and continue monitoring him. B: administer 1.5 mg/kg of lidocaine. C: contact the receiving facility immediately. D: give a 250-500 mL normal saline bolus.

*A: reassess and continue monitoring him* Reason: The patient in this scenario is hemodynamically stable. Premature ventricular complexes (PVCs) are generally not a cause for concern unless they are frequent (> 6 per minute) or occur in the context of acute coronary syndrome (ACS) or hemodynamic compromise. Nonetheless, any change in the patient's condition warrants reassessment. Continue monitoring the ECG and his vital signs. If the PVCs become more frequent, or if his condition deteriorates, an antidysrhythmic (eg, lidocaine, amiodarone) may be indicated. The patient's current vital signs are not suggestive of hypovolemia; therefore, a fluid bolus is not indicated at this point. Call your radio report to the receiving facility as usual and report your findings at that time; there is no need to contact them "immediately."

Immediately following return of spontaneous circulation, the paramedic should: A: reassess the patient's ventilatory status. B: induce therapeutic hypothermia. C: provide a bolus of normal saline solution. D: assess the patient's blood pressure

*A: reassess the patient's ventilatory status* Reason: Immediately following return of spontaneous circulation (ROSC), as evidenced by the presence of a pulse, the paramedic should reassess the patient's ventilatory status and continue to treat accordingly. Remember, if an advanced airway is placed during cardiac arrest, ventilations are given at a rate of one breath every 6 to 8 seconds (8 to 10 breaths/min) with continuous chest compressions. However, if ROSC occurs and the patient remains apneic, you should deliver one breath every 5 to 6 seconds (10 to 12 breaths/min) for the adult, or one breath every 3 to 5 seconds (12 to 20 breaths/min) for infants and children. Next, assess the patient's BP and use crystalloid fluid boluses or an inotropic drug (eg, dopamine) to treat hypotension and maintain adequate perfusion. If the patient remains comatose following ROSC, therapeutic hypothermia should be considered. Follow your local protocols.

A 30-year-old man complains of nausea and one episode of vomiting. He is conscious and alert and states that he has a slight headache. He denies chest pain or shortness of breath, and his skin is pink, warm, and dry. His BP is 136/88 mm Hg, pulse is 44 beats/min and strong, and respirations are 14 breaths/min and unlabored. The cardiac monitor reveals sinus bradycardia. Treatment for this patient should include: A: supportive care and transport to the hospital. B: high-flow oxygen and 0.5 mg atropine IV push. C: high-flow oxygen and a 20 mL/kg fluid bolus. D: 2 to 10 µg/min of epinephrine via IV infusion.

*A: supportive care and transport to the hospital* Reason: Although the patient's heart rate is slow, he is hemodyamically stable; therefore, pharmacological or electrical intervention aimed at increasing his heart rate is not indicated at this point. Provide supportive care (ie, oxygen as needed, IV set to a KVO/TKO rate) and transport him to the hospital. Consider administering an antiemetic drug, such as ondansetron (Zofran) or promethazine (Phenergan). If his clinical status deteriorates (ie, chest pain, dyspnea, altered mental status, hypotension), atropine sulfate (0.5 mg) or transcutaneous cardiac pacing (TCP) will be necessary. IV fluid boluses are not indicated at this point because there is no evidence of hypovolemia.

When administering epinephrine to a patient in cardiac arrest, the MAIN desired effect is: A: vasoconstriction, which improves coronary and cerebral perfusion. B: beta-1 receptor stimulation, which increases cardiac contractility. C: bronchodilation, which facilitates positive-pressure ventilation. D: coronary artery dilation, which decreases the myocardial workload.

*A: vasoconstriction, which improves coronary and cerebral perfusion.* Reason: Epinephrine stimulates alpha and beta receptors. However, it is used during cardiac arrest because of its vasopressor effects that result from stimulation of alpha-1 receptors. In conjunction with high-quality CPR, epinephrine's vasoconstrictive effects improve coronary and cerebral perfusion, thus keeping these organs viable until the underlying cardiac dysrhythmia can be terminated.

You are attempting to resuscitate a 50-year-old man in cardiac arrest. The patient has a history of congestive heart failure, hypertension, and cirrhosis of the liver. The cardiac monitor reveals a slow, wide complex rhythm. CPR is ongoing and the patient has been intubated. In addition to looking for potentially reversible causes of the patient's condition, further treatment should include: A: ventilations at a rate of 8 to 10 breaths/min and 1 mg of epinephrine 1:10,000 every 3 to 5 minutes. B: hyperventilation for presumed acidosis and 1 mg of epinephrine 1:10,000 every 3 to 5 minutes. C: one breath every 5 to 6 seconds, 40 units of vasopressin every 5 minutes, and transcutaneous pacing. D: one breath every 3 to 5 seconds, a 2-liter normal saline bolus, a vasopressor, and a dopamine infusion.

*A: ventilations at a rate of 8 to 10 breaths/min and 1 mg of epinephrine 1:10,000 every 3 to 5 minutes* Reason: Pulseless electrical activity (PEA) refers to the presence of an organized cardiac rhythm (except V-Tach), despite the absence of a pulse; it can result from a variety of conditions, such as hypovolemia, overdose, hypothermia, and trauma, among others. Treatment for PEA includes high-quality CPR with minimal interruptions, 1 mg of epinephrine 1:10,000 every 3 to 5 minutes, advanced airway management, and treating potentially reversible causes. A one-time 40-unit dose of vasopressin can be given to replace the first or second dose of epinephrine, but not both. After an advanced airway device is in place, perform asynchronous CPR; the compressor delivers at least 100 compressions/min and the ventilator provides 8 to 10 breaths/min (one breath every 6 to 8 seconds). Do not hyperventilate the patient; doing so may impair venous return to the heart and decrease cardiac output. A ventilation rate of 12 to 20 breaths/min is appropriate for infants and children who are apneic, but have a pulse. An apneic adult with a pulse should be ventilated at a rate of 10 to 12 breaths/min. Dopamine is not indicated for patients in cardiac arrest, and current evidence does not support the use of transcutaneous cardiac pacing (TCP) in patients with PEA or asystole.

The appropriate second dose and method of administration of amiodarone for a patient with refractory ventricular fibrillation is: A: 150 mg given over 10 minutes. B: 150 mg via rapid IV/IO push. C: 300 mg via rapid IV/IO push. D: 300 mg given over 10 minutes.

*B: 150 mg via rapid IV/IO push.* Reason: The initial dose of amiodarone for a patient with refractory ventricular fibrillation or pulseless ventricular tachycardia is 300 mg via rapid IV or IO push. A second dose of 150 mg via rapid IV or IO push may be repeated one time in 5 minutes. For supraventricular tachycardia or ventricular tachycardia with a pulse, amiodarone should be given in a dose of 150 mg over 10 minutes; this same dose may be repeated as needed.

What is the correct initial dose and rate of administration of amiodarone for a patient with refractory ventricular fibrillation? A: 150 mg via rapid IV or IO push B: 300 mg via rapid IV or IO push C: 150 mg given over 10 minutes D: 300 mg given over 10 minutes

*B: 300 mg via rapid IV or IO push* Reason: The correct initial dose and rate of administration of amiodarone for a patient with refractory ventricular fibrillation or pulseless ventricular tachycardia is 300 mg rapid IV or IO push. You may repeat amiodarone one time in 5 minutes at a dose of 150 mg rapid IV or IO push. For patients with hemodynamically stable narrow or wide-complex tachycardias, the correct dose and rate of administration for amiodarone is 150 mg given over 10 minutes.

Calcium Channel Blockers (pine's)

-Block calcium entry into cardiac cells causing vascular smooth muscle relaxation, decreased myocardial force generation, decreased heart rate, and decreased conduction velocity particularly at the AV node

You are assessing a 59-year-old woman who complains of chest pressure. When you are looking at her list of medications, you note that she takes Vasotec. What type of medication is this? A: Parasympathetic blocker B: ACE inhibitor C: Calcium channel blocker D: Beta-blocker

*B: ACE inhibitor* Reason: Enalapril maleate (Vasotec) is an ACE (angiotensin converting enzyme) inhibitor that is used to treat hypertension. Angiotensin II, a potent chemical produced by the kidneys that causes vasoconstriction, is formed from angiotensin I in the blood by the angiotensin converting enzyme. ACE inhibitors inhibit the activity of this enzyme, which decreases the production of angiotensin II. As a result, the blood vessels dilate and blood pressure is reduced. Beta blockers, which are also used to treat hypertension, include drugs such as metoprolol (Lopressor), propranolol (Inderal), and atenolol (Tenormin), among others. Calcium channel blockers are also used to treat hypertension, and include drugs such as diltiazem (Cardizem), verapamil (Calan; Isoptin), and amlodipine (Norvasc), among others. Atropine sulfate is a parasympathetic blocker (vagolytic) that is used to treat patients with hemodynamically unstable bradycardia.

*B: Atrial fibrillation* Reason: Patients with atrial fibrillation (A-Fib) are commonly prescribed digoxin (a digitalis preparation) and warfarin sodium (Coumadin), which is a blood thinner. As the atria fibrillate, blood has a tendency to stagnate and form microemboli that can be ejected from the heart and occlude a pulmonary, cerebral, or coronary artery.

Which of the following electrolytes moves slowly into the cardiac cell and maintains the depolarized state of the cell membrane? A: Magnesium B: Calcium C: Sodium D: Potassium

*B: Calcium* Reason: The process of depolarization begins as sodium ions rush into the cell. At the same time, calcium ions enter the cell—albeit more slowly and through specialized channels—to help maintain the depolarized state of the cell membrane and to supply calcium ions for contraction of cardiac muscle tissue. During repolarization, the sodium and calcium channels close, thus stopping the rapid influx of these ions. Then, special potassium channels open, allowing potassium ions to rapidly exit the cell. This helps restore the inside of the cell to its negative charge; the proper electrolyte distribution is then reestablished by pumping sodium ions out of the cell and potassium ions back in. After the potassium channels close, the sodium-potassium pump helps move sodium and potassium ions back to their respective locations. For every three sodium ions the pump moves out of the cell, it moves two potassium ions into the cell, thereby maintaining the polarity of the cell membrane

When assessing a patient with suspected cardiac-related chest pain, which of the following questions would be MOST appropriate to ask? A: Does the pain move to your arms? B: Can you describe the quality of the pain? C: Were you at rest when the pain began? D: Is the pain crushing or dull in nature?

*B: Can you describe the quality of the pain?* Reason: Patient assessment involves simple questioning techniques. You should ask open-ended questions, whenever possible; this is especially true when determining the onset and quality of a patient's pain. Asking a leading question, such as "Do you have sharp chest pain?" will often lead the patient to say "yes," even though that is not the true quality of his or her pain. Allow the patient to use his or her own words when describing symptoms.

Which of the following signs or symptoms occurs more commonly in patients with stable angina than in those with unstable angina? A: Chest pressure, tightness, or discomfort B: Chest pain that begins during exertion C: Pain that lasts more than 15 minutes D: ST segment elevation on the 12-lead ECG

*B: Chest pain that begins during exertion* Reason: Angina pectoris occurs when the heart's demand for oxygen exceeds it's available supply (ischemia) and is a sign of coronary artery disease (CAD). Angina is classified as being stable or unstable. Stable angina typically follows a predictable pattern (ie, chest pain, pressure, or discomfort induced by exertion), lasts less than 15 minutes, and is usually relieved with rest and/or nitroglycerin. While unstable angina (preinfarction angina) can also occur during exertion, it more commonly occurs when the patient otherwise would not expect it to, such as when he or she is asleep or is otherwise resting. Furthermore, unstable angina is often not relieved by rest and/or nitroglycerin and typically lasts longer than 15 minutes. Chest pressure, tightness, or discomfort occurs in patients with both stable and unstable angina. If a patient is experiencing angina, you would expect to see ST segment depression and/or T wave inversion on the 12-lead ECG as these are indicators of myocardial ischemia. ST segment elevation indicates myocardial injury (eg, acute MI in progress).

You are treating a 68-year-old woman with chest pressure and shortness of breath that started 2 days ago. Her BP is 76/52 mm Hg and her pulse is 130 beats/min and weak. The cardiac monitor reveals sinus tachycardia with occasional PVCs and auscultation of her lungs reveals diffuse coarse crackles. Which of the following treatment interventions is MOST appropriate for this patient? A: Nitroglycerin, 10 to 20 µg/min. B: Dopamine, 2 to 20 µg/kg/min. C: Amiodarone, 150 mg over 10 min. D: Normal saline, 20 mL/kg rapid bolus.

*B: Dopamine, 2 to 20 µg/kg/min* Reason: Your patient's history and clinical presentation is consistent with cardiogenic shock. She has had chest pressure and shortness of breath for 2 days and is now significantly hypotensive with weak pulses. Because of its positive inotropic effect of increasing myocardial contractility, dopamine is the drug of choice for non-hypovolemic shock (eg, cardiogenic shock) and may improve perfusion. Typically, dopamine for cardiogenic shock is started at 2 µg/kg/min and titrated upwards as needed to improve blood pressure and perfusion. At doses of greater than 10 µg/kg/min, dopamine acts predominantly as a vasopressor, which results in systemic vasoconstriction. Clearly, nitroglycerin is contraindicated in any patient with shock; its potent vasodilatory effects would further lower the patient's blood pressure and worsen her condition. Amiodarone is not the drug of choice for this patient; it is given in a dose of 150 mg over 10 minutes for hemodynamically stable patients with wide or narrow-complex tachycardias that exceed 150 beats/min. Caution must be used if you consider giving a normal saline bolus; the coarse crackles in her lungs indicate pulmonary edema, which could easily be exacerbated by large fluid boluses. Her problem is heart failure, not hypovolemia.

Furosemide (Lasix)

-Blocks absorption of sodium and chloride at the distal and proximal tubules and the loop of Henle, causing increased urine output

Where is the point of maximal impulse (PMI) located in most people? A: Directly over the sternum, approximately 1" to the left of the angle of Louis B: Left anterior chest, in the midclavicular line, at the fifth intercostal space C: Left anterior chest, on the left sternal border, at the fourth intercostal space D: Left anterolateral chest, in the midaxillary line, at the fifth intercostal space

*B: Left anterior chest, in the midclavicular line, at the fifth intercostal space*

*B: Paroxysmal supraventricular tachycardia* Reason: Syncope (fainting) of cardiac origin is caused by a sudden decrease in cerebral perfusion secondary to a decrease in cardiac output. This is usually the result of an acute bradydysrhythmia or tachydysrhythmia. In this particular patient, the presence of frequent premature atrial complexes (PACs), which indicates atrial irritability, suggests paroxysmal supraventricular tachycardia (PSVT) as the underlying dysrhythmia that caused her syncopal episode. In PSVT, the heart is beating so fast that ventricular filling and cardiac output decrease, which results in a transient decrease in cerebral perfusion. Not all patients with PSVT experience syncope. Many experience an acute onset of palpitations and/or lightheadedness that spontaneously resolves.

A patient experiencing a right ventricular infarction would be expected to present with: A: hypertension and tachycardia. B: ST elevation in leads II, III, and aVF. C: severe pulmonary edema and hemoptysis. D: greater than 2-mm ST depression in lead V1.

*B: ST elevation in leads II, III, and aVF.* Reason: A right ventricular infarction (RVI) should be suspected when a patient presents with ECG changes indicative of an inferior wall injury pattern (equal to or greater than 1-mm ST elevation in leads II, III, and aVF; reciprocol ST depression and T wave inversion in leads I and aVL) AND has equal to or greater than 1-mm ST elevation in lead V4R when a right-sided 12-lead ECG is obtained. Patients experiencing an RVI are preload dependent and often present with hypotension; therefore, vasodilators (eg, nitroglycerin, morphine) should be avoided. Instead, IV fluid boluses should be given to maintain adequate perfusion. Other signs of an RVI include jugular venous distention and peripheral edema. Pulmonary edema and coughing up blood (hemoptysis) are indicative of left ventricular failure.

Which of the following is an absolute contraindication for fibrinolytic therapy? A: Current use of anticoagulant medication B: Subdural hematoma 3 years ago C: BP of 170/100 mm Hg on presentation D: Ischemic stroke within the last 6 months

*B: Subdural hematoma 3 years ago* Reason: According to current emergency cardiac care (ECC) guidelines, absolute contraindications for fibrinolytic therapy include ANY prior intracranial hemorrhage (ie, subdural, epidural, intracerebral hematoma); known structural cerebrovascular lesion (ie, arteriovenous malformation); known malignant intracranial tumor (primary or metastatic); ischemic stroke within the past 3 months, EXCEPT for acute ischemic stroke within the past 3 hours; suspected aortic dissection; active bleeding or bleeding disorders (except menses); and significant closed head trauma or facial trauma within the past 3 months. Relative contraindications (eg, the physician may deem fibrinolytic therapy appropriate under certain circumstances) include, a history of chronic, severe, poorly-controlled hypertension; severe uncontrolled hypertension on presentation (SBP > 180 mm Hg or DBP > 110 mm Hg); ischemic stroke greater than 3 months ago; dementia; traumatic or prolonged (> 10 minutes) CPR or major surgery within the past 3 weeks; recent (within 2 to 4 weeks) internal bleeding; noncompressible vascular punctures; pregnancy; prior exposure (> 5 days ago) or prior allergic reaction to streptokinase or anistreplase; active peptic ulcer; and current use of anticoagulants (ie, Coumadin).

In which of the following situations is transcutaneous cardiac pacing (TCP) clearly indicated? A: Pulseless electrical activity at a rate of 50 beats/min. B: Third-degree AV block in a patient with pulmonary edema. C: First-degree AV block in a patient with abdominal pain. D: Asystole, but only after 10 minutes of adequate CPR.

*B: Third-degree AV block in a patient with pulmonary edema.* Reason: Because third-degree AV block (complete heart block)—an inherently slow cardiac dysrhythmia—represents total atrioventricular dissociation, it is associated with hemodynamic compromise in most cases and should be treated with immediate transcutaneous cardiac pacing (TCP). Signs of hemodynamic compromise include ongoing chest pain, pulmonary edema, decreased level of consciousness, shortness of breath, and hypotension. First-degree AV block is typically a benign rhythm and is not commonly associated with hemodynamic compromise. Evidence has shown TCP to be of little or no benefit to patients with PEA or asystole, and it is clearly of no benefit to patients with prolonged asystole.

A patient's medication regimen includes fluoxetine, Toprol, Proscar, lansoprazole, and Klonopin. Which of these medications is used to treat cardiovascular disorders? A: fluoxetine B: Toprol C: lansoprazole D: Proscar

*B: Toprol* Reason: Toprol (metaprolol) is a commonly prescribed beta-blocker used to treat various cardiovascular conditions, including hypertension and tachydysrhythmias. Proscar (finasteride) is used to treat benign prostatic hyperplasia (BPH). Fluoxetine (Prozac) is a selective serotonin reuptake inhibitor (SSRI) antidepressant. It is used to treat conditions such as depression, generalized anxiety disorder, and obsessive-compulsive disorder (OCD). Lansoprazole (Prevacid)—a proton pump inhibitor—is used to treat conditions such as heartburn, acid reflux disease, and ulcers. Clonazepam (Klonopin) is a benzodiazepine sedative-hypnotic; it is used to treat anxiety.

Sudden cardiac arrest in the adult population is MOST often secondary to:Sudden cardiac arrest in the adult population is MOST often secondary to: A: respiratory failure. B: a cardiac dysrhythmia. C: massive hypovolemia. D: accidental electrocution.

*B: a cardiac dysrhythmia.* Reason: Most cases of sudden cardiac arrest (SCA) in the adult population are secondary to a cardiac dysrhythmia, usually ventricular fibrillation (V-Fib). This fact underscores the criticality of early defibrillation. Respiratory failure is the most common cause of cardiac arrest in the pediatric population.

Amiodarone

-Blocks sodium channels and myocardial potassium channels, delaying repolarization and increasing the duration of action potential

You and your team are attempting to resuscitate a 66-year-old man in cardiac arrest. The cardiac monitor reveals a slow, wide-complex rhythm. The patient has been successfully intubated and an IV line has been established. As CPR is ongoing, you should: A: give 40 units of vasopressin every 3 to 5 minutes. B: administer 10 mL of epinephrine 1:10,000 IV. C: ventilate the patient at a rate of 24 breaths/min. D: attempt transcutaneous pacing to increase the heart rate.

*B: administer 10 mL of epinephrine 1:10,000 IV* Reason: The first drug given to any patient in cardiac arrest is epinephrine in a dose of 1 mg (10 mL of a 1:10,000 solution) via the IV or IO route. This dose should be repeated every 3 to 5 minutes. Alternatively, a one-time dose of vasopressin (40 units) can be given to replace the first or second dose of epinephrine, but not both. Do NOT hyperventilate the patient as doing so increases intrathoracic pressure and can impair venous return (preload) and cardiac output, which would decrease the effectiveness of chest compressions. After an advanced airway has been placed during cardiac arrest, deliver one breath every 6 to 8 seconds (8 to 10 breaths/min) and ensure that chest compressions are uninterrupted. There is presently no evidence to support the efficacy of transcutaneous cardiac pacing (TCP) in patients with bradycardic PEA or asystole.

You arrive approximately 8 minutes after a 51-year-old male collapsed at a family event. After determining that he is unresponsive and apneic, you should: A: begin CPR, starting with chest compressions. B: assess for a carotid pulse for 5 to 10 seconds. C: immediately assess the patient's cardiac rhythm. D: give 2 rescue breaths and check for a pulse.

*B: assess for a carotid pulse for 5 to 10 seconds* Reason: After determining that an adult patient is unresponsive and apneic, you should assess for a carotid pulse for at least 5 seconds but no more than 10 seconds. If the patient has a pulse, open the airway and provide rescue breathing. If the patient does not have a pulse, begin CPR (starting with chest compressions), then open the airway and give 2 rescue breaths. Assess the patient's cardiac rhythm as soon as a monitor/defibrillator is available.

Immediately after establishing a return of spontaneous circulation in a woman with ventricular fibrillation of short duration, you should: A: obtain a 12-lead ECG to assess for cardiac damage. B: assess her ventilatory status and treat accordingly. C: assess her blood pressure and treat if needed. D: establish vascular access and give amiodarone.

*B: assess her ventilatory status and treat accordingly.* Reason: Your first action after establishing return of spontaneous circulation (ROSC) in a patient—regardless of his or her arrest rhythm and duration—is to assess the patient's ventilatory status. If the patient is not breathing or is breathing inadequately, provide ventilatory support. After assessing and managing airway and breathing, assess the patient's blood pressure and stabilize it if it is low. Airway and circulatory support are critical following ROSC; inadequate ventilation and/or hypotension following cardiac arrest may lead to a recurrence of cardiac arrest. Depending on your local protocols, IV amiodarone may be given following ROSC. After assessing and maintaining respiratory and circulatory functions, obtain a 12-lead ECG if time allows. If the patient remains comatose following ROSC, consider inducing therapeutic hypothermia.

A 60-year-old female presents with confusion, shortness of breath, and diaphoresis. Her blood pressure is 70/40 mm Hg and her heart rate is 40 beats/min. The cardiac monitor reveals a slow, wide complex rhythm with dissociated P waves. After applying supplemental oxygen, you should: A: give her up to 325 mg of baby aspirin. B: begin immediate transcutaneous pacing. C: start an IV and give a rapid fluid bolus. D: start an IV and give 0.5 mg of atropine.

*B: begin immediate transcutaneous pacing*

A 56-year-old man has had chest pain for the past 2 days, but refused to go to the hospital. His wife called EMS when she noticed that he was not acting right. He is conscious, but confused, and is diaphoretic. His BP is 80/40 mm Hg and his pulse is rapid and weak. The patient's history and your assessment findings are MOST consistent with: A: unstable angina pectoris. B: cardiogenic hypoperfusion. C: acute myocardial infarction. D: acute ischemic stroke.

*B: cardiogenic hypoperfusion.* Reason: The patient most likely experienced an acute myocardial infarction (AMI); however, since he did not receive timely treatment, extensive myocardial damage has resulted in pump failure. His low BP; weak, rapid pulses; and altered mental status indicate that he is systemically hypoperfused. Hypoperfusion (shock) secondary to a cardiac etiology (ie, pump failure, fast or slow heart rate) is called cardiogenic shock. True cardiogenic shock, which occurs when the myocardium is extensively and permanently damaged and can no longer meet the metabolic needs of the body, has a high mortality rate.

You have defibrillated a patient who presented with ventricular fibrillation. After 2 minutes of CPR, you reassess the patient's cardiac rhythm and see a wide-complex tachycardia. You should: A: defibrillate and then immediately resume chest compressions. B: check for a carotid pulse and defibrillate if a pulse is absent. C: administer 300 mg of amiodarone via rapid IV or IO push. D: cardiovert with the energy setting you used to defibrillate

*B: check for a carotid pulse and defibrillate if a pulse is absent* Reason: Cardiac rhythm checks should be performed after every 2 minutes of CPR. If you note a change in the patient's cardiac rhythm after 2 minutes, especially if it is an organized rhythm, you should check for a carotid pulse for 5 to 10 seconds. In this case, the patient has converted from V-Fib to a wide-complex tachycardia, which is probably V-Tach. If the patient has a pulse, perform synchronized cardioversion with the same energy setting that you used for defibrillation. If the patient is pulseless, however, you should defibrillate and immediately resume CPR, starting with chest compressions. During the 2-minute period of CPR, you can administer epinephrine, if 3 to 5 minutes have passed, or 300 mg of amiodarone via rapid IV or IO push.

A middle-aged man presents with chest discomfort, shortness of breath, and nausea. You give him supplemental oxygen and continue your assessment. As your partner is attaching the ECG leads, you should: A: establish vascular access. B: administer 0.4 mg of nitroglycerin. C: administer up to 325 mg of aspirin. D: administer 2 to 4 mg of morphine IM.

*C: administer up to 325 mg of aspirin* Reason: Since oxygen has already been administered to this patient and your partner is attaching the ECG leads, you should administer aspirin (160 to 325 mg, non-enteric-coated). Early administration of aspirin has clearly been shown to reduce mortality and morbidity in patients experiencing an acute coronary syndrome (ACS). After establishing vascular access, you should assess his vital signs and then administer 0.4 mg of nitroglycerin (up to 3 doses, 5 minutes apart), provided that his systolic BP is greater than 90 mm Hg. If 3 doses of nitroglycerin fail to completely relieve his chest discomfort, consider administering 2 to 4 mg of morphine IV, provided that his systolic BP remains above 90 mm Hg.

A 50-year-old woman is pulseless and apneic. Your partner and an emergency medical responder are performing well-coordinated CPR. After 2 minutes of CPR, the cardiac monitor reveals coarse ventricular fibrillation. You should: A: shock the patient three times with 360 monophasic joules. B: deliver a single shock and immediately resume CPR. C: defibrillate at once and then reassess the rhythm and pulse. D: assess for a carotid pulse for no longer than 10 seconds.

*B: deliver a single shock and immediately resume CPR.* Reason: A single shock (360 monophasic joules or the biphasic equivalent) should be administered to the patient with V-Fib or pulseless V-Tach cardiac arrest. Immediately following this single shock, begin or resume CPR, starting with chest compressions. Assessing the patient's cardiac rhythm and pulse immediately following defibrillation causes an unnecessary delay in CPR, and delays in CPR have been directly linked to poor patient outcomes. Most patients who are defibrillated—especially if their arrest interval is prolonged—remain in V-Fib/pulseless V-Tach or convert to another non-perfusing rhythm (ie, asystole, PEA). Either way, the patient is still in cardiac arrest and needs immediate CPR. After 2 minutes of CPR, reassess the patient's rhythm, and if necessary, a pulse (if an organized cardiac rhythm appears), and repeat defibrillation (single shock) if indicated, followed immediately by CPR.

When attempting transcutaneous cardiac pacing (TCP), you will know that electrical capture has been achieved when: A: the patient's inherent heart rate spontaneously increases. B: each pacemaker spike is followed by a wide QRS complex. C: the milliamp setting is at least 40 and the patient is in pain. D: you see an increase in the number of narrow QRS complexes.

*B: each pacemaker spike is followed by a wide QRS complex* Reason: Transcutaneous cardiac pacing (TCP) involves passing small, repetitive electrical currents through the patient's skin (transcutaneous) across the heart between one externally placed pacing pad and another. The pacemaker is set at a specific rate, usually 60 to 80/min. The energy is then increased—usually by 10 to 20 milliamps (mA) every few seconds—until the heart begins to respond to the electrical stimulus. Electrical capture has been achieved when the stimulus depolarizes the ventricles; this appears as a wide QRS complex immediately following each pacemaker spike. If the QRS complex is not present, the pacemaker current is not depolarizing the ventricles and electrical capture has not been achieved. Mechanical capture is achieved when the patient's palpated pulse rate corresponds with the paced rate on the ECG.

You are treating a patient with ventricular fibrillation. As the defibrillator is charging, you should: A: check the defibrillator to ensure the synchronizer is activated. B: ensure that CPR is continuing until the defibrillator is charged. C: visually confirm that nobody is touching the patient. D: ask your partner to ventilate the patient at 20 breaths/min.

*B: ensure that CPR is continuing until the defibrillator is charged* Reason: A major emphasis is placed on minimizing interruptions in CPR. Evidence has shown that even a brief pause in chest compressions can result in a significant decrease in coronary and cerebral perfusion. Therefore, CPR should be continuing—even as the defibrillator is charging. When the defibrillator is charged, ensure (visually and verbally) that nobody is touching the patient, and then deliver the shock. When defibrillating a patient with V-Fib, you must ensure that the synchronizer is off; the synchronizer will not be able to identify an R wave in V-Fib due to the chaotic nature of the dysrhythmia. Cardiac arrest patients (adults, children, and infants) should be ventilated at a rate of 8 to 10 breaths/min after an advanced airway device has been placed (eg, ET tube, multilumen airway, supraglottic airway). Excessive ventilation rates should be avoided; they cause increased intrathoracic pressure, which may impair venous return and cardiac output.

*B: ensure that CPR is continuing until the defibrillator is charged.* Reason: A major emphasis is placed on minimizing interruptions in CPR. Evidence has shown that even a brief pause in chest compressions can result in a significant decrease in coronary and cerebral perfusion. Therefore, CPR should be continuing—even as the defibrillator is charging. When the defibrillator is charged, ensure (visually and verbally) that nobody is touching the patient, and then deliver the shock. When defibrillating a patient with V-Fib, you must ensure that the synchronizer is off; the synchronizer will not be able to identify an R wave in V-Fib due to the chaotic nature of the dysrhythmia. Cardiac arrest patients (adults, children, and infants) should be ventilated at a rate of 8 to 10 breaths/min after an advanced airway device has been placed (eg, ET tube, multilumen airway, supraglottic airway). Excessive ventilation rates should be avoided; they cause increased intrathoracic pressure, which may impair venous return and cardiac output.

A 59-year-old woman presents with a regular, narrow-complex tachycardia at a rate of 180 beats/min. She is conscious and alert, but complains of chest discomfort and has a blood pressure of 86/56 mm Hg. In addition to giving her supplemental oxygen, you should: A: administer 150 mg of amiodarone over 10 min. B: have her chew and swallow 325 mg of aspirin. C: give her up to 3 sublingual doses of nitroglycerin. D: administer 12 mg of adenosine rapid IV push.

*B: have her chew and swallow 325 mg of aspirin* Reason: A regular, narrow complex tachycardia at a rate greater than 150 beats/min is consistent with supraventricular tachycardia (SVT). Although the patient is conscious and alert, she is complaining of chest discomfort and is hypotensive. Since she could be experiencing an acute coronary syndrome (ACS), you should instruct her to chew and swallow up to 325 mg of aspirin. Aspirin should be given to any patient suspected of experiencing an ACS, provided there are no contraindications (eg, allergy); it will not affect her blood pressure. Nitroglycerin, however, may exacerbate her hypotension and should be avoided. You can consider administering adenosine; however, the initial dose is 6 mg rapid IV push. Amiodarone, in a dose of 150 mg over 10 minutes, is appropriate for patients with hemodynamically stable wide-complex tachycardias (ie, V-Tach). Closely monitor this patient and be prepared to perform synchronized cardioversion.

*D: 36*

Sodium Bicarbonate

-Buffers metabolic acidosis and lactic acid buildup in the body caused by anaerobic metabolism secondary to severe hypoxia by reacting with hydrogen ions to form water and carbon dioxide

After performing synchronized cardioversion on an unstable patient with a wide-complex tachycardia, you look at the monitor and see coarse ventricular fibrillation. The patient is unresponsive, apneic, and pulseless. You should: A: prepare to intubate the patient as your partner begins CPR. B: start CPR, ensure the synchronize mode is off, and defibrillate. C: begin CPR, establish vascular access, and give amiodarone. D: perform CPR for 2 minutes and then cardiovert with 100 joules.

*B: start CPR, ensure the synchronize mode is off, and defibrillate* Reason: If a patient develops ventricular fibrillation (V-Fib) or pulseless ventricular tachycardia (V-Tach) following synchronized cardioversion, immediately begin CPR (even if it's just for a short period of time), ensure that the monitor/defibrillator is not in synchronize mode, and defibrillate as soon as possible. CPR should be ongoing as the defibrillator is charging in order to avoid unnecessary delays in performing chest compressions. The synchronize mode must be turned off prior to defibrillation or the device will not deliver a shock; this is because there are no R waves to synchronize with in V-Fib. Vascular access (IV or IO), advanced airway management, and pharmacologic therapy should be performed during the 2-minute cycles of CPR; they are not an immediate priority during early cardiac arrest.

You are assessing a 75-year-old male who experienced a sudden onset of slurred speech, a right-sided facial droop, and left-sided hemiparesis approximately 45 minutes ago. His blood pressure is 170/94 mm Hg, pulse rate is 68 beats/min and irregular, and respirations are 14 breaths/min and unlabored. His oxygen saturation is 94% on room air. The MOST appropriate treatment for this patient includes: A: oxygen via nonrebreathing mask, an IV of normal saline, cardiac monitoring, 5 mg of labetalol to lower his BP, blood glucose assessment, and rapid transport. B: supplemental oxygen via nasal cannula, cardiac monitoring, blood glucose assessment, an IV of normal saline set to keep the vein open, and prompt transport. C: assisted ventilation with a bag-mask device, cardiac monitoring, an IV of normal saline, IV dextrose if his blood glucose level is less than 80 mg/dL, and transport. D: 160 to 325 mg of aspirin, supplemental oxygen via nasal cannula, cardiac monitoring, blood glucose assessment, an IV of an isotonic crystalloid, and transport.

*B: supplemental oxygen via nasal cannula, cardiac monitoring, blood glucose assessment, an IV of normal saline set to keep the vein open, and prompt transport* Reason: The patient is likely experiencing an acute ischemic stroke. Determining the time of onset of his symptoms is critical; fibrinolytic therapy must be administered within the first 3 hours following a stroke in order to be of maximum benefit. Treatment includes supplemental oxygen (a nasal cannula is appropriate, given his room air oxygen saturation), blood glucose assessment (hypoglycemia can mimic certain signs of a stroke), vascular access, cardiac monitoring, and prompt transport with early notification of the receiving facility. Do not give aspirin to suspected stroke patients in the field; it can cause further harm to the patient with a hemorrhagic stroke. Aspirin may be given at the hospital after a hemorrhagic stroke is ruled out with a computed tomography (CT) scan of the brain. Antihypertensive therapy should also be avoided in the field; it should be performed in the controlled setting of a hospital, where the patient has invasive hemodynamic monitoring. Lowering a patient's BP in the field is dangerous and can have disastrous effects; inadvertently inducing hypotension in the stroke patient may exacerbate cerebral ischemia.

A 27-year-old female complains of palpitations. The cardiac monitor reveals a narrow-complex tachycardia at 180/min. She denies any other symptoms, and states that this has happened to her before, but it typically resolves on its own. Her blood pressure is 126/66 mm Hg, pulse is 180 beats/min, and respirations are 16 breaths/min. After attempting vagal maneuvers and giving two doses of adenosine, her cardiac rhythm and vital signs remain unchanged. You should: A: infuse 150 mg of amiodarone over 10 minutes, reassess her, and repeat the amiodarone if needed. B: transport at once, reassess her frequently, and perform synchronized cardioversion if necessary. C: administer 5 mg of midazolam and perform synchronized cardioversion starting with 50 joules. D: administer 0.35 mg/kg of diltiazem over 2 minutes and then reassess her hemodynamic status.

*B: transport at once, reassess her frequently, and perform synchronized cardioversion if necessary.* Reason: Although the patient is in supraventricular tachycardia (SVT), she remains stable following your initial efforts to slow her heart rate with vagal maneuvers and adenosine. Her failure to respond to initial treatment does not automatically make her unstable. Simply transport her, closely monitor her en route, and be prepared to cardiovert her if she does become unstable (ie, hypotension, altered mental status, chest pain). Unless specified in your local protocols, pharmacologic therapy beyond adenosine (ie, calcium channel blockers, amiodarone) is typically not indicated in the field for stable patients with SVT, although these medications may be given in the emergency department. However, if your protocols or medical control call for the administration of diltiazem (Cardizem), the initial dose is 0.25 mg/kg.

When administering epinephrine to a patient in cardiac arrest, the MAIN desired effect is: A: beta-1 receptor stimulation, which increases cardiac contractility. B: vasoconstriction, which improves coronary and cerebral perfusion. C: bronchodilation, which facilitates positive-pressure ventilation. D: coronary artery dilation, which decreases the myocardial workload.

*B: vasoconstriction, which improves coronary and cerebral perfusion*

A clinically unstable patient presents with an irregular narrow-complex tachycardia at a rate of 170 per minute. What is the recommended initial energy setting for synchronized cardioversion? A: 50 to 100 joules B: 320 to 360 joules C: 120 to 200 joules D: 200 to 300 joules

*C: 120 to 200 joules* Reason: If a patient has a heart rate that is greater than 150 per minute, and he or she is clinically unstable because of the cardiac rhythm, synchronized cardioversion should be performed. The following initial energy settings are recommended by current emergency cardiac care (ECC) guidelines: narrow and regular, 50 to 100 joules (biphasic or monophasic); narrow and irregular, 120 to 200 joules biphasic (200 joules monophasic); wide and regular, 100 joules (biphasic or monophasic); wide and irregular, defibrillation dose (NOT synchronized). If the initial energy dose is unsuccessful, increase in a stepwise fashion.

You are preparing to defibrillate a patient in cardiac arrest with a manual biphasic defibrillator, but are unsure of the appropriate initial energy setting. What should you do? A: Continue CPR and shock with 360 joules in 2 minutes. B: Contact medical control for further guidance. C: Deliver one shock with 200 joules and resume CPR. D: Deliver three sequential shocks with 120 joules.

*C: Deliver one shock with 200 joules and resume CPR.* Reason: Energy settings for manual biphasic defibrillators are device-specific—typically 120 joules (rectilinear) or 150 joules (truncated). However, if the appropriate initial energy setting is unknown, you should defibrillate with 200 joules. For subsequent shocks, use the same or higher energy setting. Whether you are using a monophasic or biphasic defibrillator, you should only perform 1 shock, followed immediately by CPR (starting with chest compressions).

Which of the following interventions has the greatest impact on patient survival from sudden cardiac arrest? A: Identifying the cause B: Cardiac medication administration C: Early CPR and defibrillation D: Advanced airway control

*C: Early CPR and defibrillation* Reason: Early CPR and defibrillation are the two interventions that will have the greatest impact on patient survival from sudden cardiac arrest (SCA). Early, effective CPR maintains perfusion to the body's vital organs until defibrillation can be provided. The most common initial cardiac rhythm observed during SCA is ventricular fibrillation (V-Fib). Early defibrillation, in conjunction with early CPR, greatly enhances the chance of establishing return of spontaneous circulation (ROSC). The probability of successful defibrillation decreases over time, especially if CPR is delayed. For each minute that V-Fib persists, the patient's chance of survival decreases by approximately 7% to 10%.

Calcium Gluconate

-Counteracts the toxicity of hyperkalemia by stabilizing the membranes of the cardiac cells, reducing the likelihood of fibrillation

You and your team are performing CPR on a 70-year-old male. The cardiac monitor reveals a slow, organized rhythm. His wife tells you that he goes to dialysis every day, but has missed his last three treatments. She also tells you that he has high blood pressure, hyperthyroidism, and has had several cardiac bypass surgeries. Based on the patient's medical history, which of the following conditions is the MOST likely underlying cause of his condition? A: Coronary thrombus B: Drug toxicity C: Hyperkalemia D: Hypovolemia

*C: Hyperkalemia* Reason: Although any of the listed conditions could be causing this patient's condition, the fact that he missed his last three dialysis treatments should make you most suspicious for hyperkalemia. Dialysis filters metabolic waste products from the blood in patients with renal insufficiency or failure. If the patient is not dialyzed, these waste products, including potassium and other electrolytes, accumulate to toxic levels in the blood. In addition to performing high-quality CPR, managing the airway, and administering epinephrine, your protocols may call for the administration of calcium chloride and sodium bicarbonate if hyperkalemia is suspected. Albuterol also has been shown to be effective in treating patients with hyperkalemia becauses it causes potassium to shift back into the cells; it can be nebulized down the ET tube or administered intravenously. Follow your local protocols regarding the treatment for suspected hyperkalemia.

Which of the following causes of pulseless electrical activity (PEA) would be the MOST likely to respond to immediate treatment in the prehospital setting? A: Lactic acidosis B: Hypokalemia C: Hypovolemia D: Drug overdose

*C: Hypovolemia* Reason: Hypovolemia is the most easily correctable cause of PEA, provided that immediate treatment is given in the prehospital setting. In addition to CPR, airway management, and epinephrine, fluid boluses are repeatedly given, followed by a reassessment of the patient's condition. Remember, myocardial contraction is dependent on electricity and pressure. This pressure is caused as blood fills the heart. If there is no blood, the heart will not pump, even though electrical activity continues. Drug overdose is the underlying cause of asystole that would most likely respond to immediate prehospital treatment, especially in younger patients. Hypokalemia is treated with potassium chloride, which is not administered in the prehospital setting. Lactic acidosis is treated with effective ventilation first, and then sodium bicarbonate if local protocol permits. While sodium bicarbonate can be given in the prehospital setting, paramedics do not have the ability to quantify the pH or bicarbonate level of the patient's blood; this requires arterial blood gas analysis.

What are the therapeutic effects of morphine sulfate when administered to a patient with cardiogenic pulmonary edema? A: Systemic venous pooling of blood and increased afterload B: Decreased venous capacitance and increased inotropy C: Increased venous capacitance and decreased preload D: Increased cardiac inotropy and increased cardiac output

*C: Increased venous capacitance and decreased preload* Reason: In patients with cardiogenic pulmonary edema (ie, congestive heart failure [CHF]), morphine sulfate causes systemic pooling of blood, which increases venous capacitance and decreases preload (the volume of blood returned to the heart). The net effect is to minimize the volume of fluid that accumulates in the lungs. Note that morphine is not a diuretic and will not remove fluid from the body. This is accomplished by administering furosemide (Lasix), which may be considered for patients with CHF and pulmonary edema.

Which of the following represents the correct medication sequence when treating a patient with a suspected acute coronary syndrome? A: Oxygen, aspirin, morphine, and nitroglycerin B: Oxygen, nitroglycerin, aspirin, and morphine C: Oxygen, aspirin, nitroglycerin, and morphine D: Oxygen, morphine, aspirin, and nitroglycerin

*C: Oxygen, aspirin, nitroglycerin, and morphine* Reason: The mnemonic "MONA" is used to help remember the medications given to patients who are experiencing an acute coronary syndrome (ACS). Although it does not represent the correct sequence in which the medications should be given, it is a useful mnemonic to remember. The appropriate sequence of medications is oxygen (as needed to maintain an SpO2 of greater than 94%), aspirin (160 to 325 mg), nitrogylcerin (0.4 mg up to 3 times), and morphine (2 to 4 mg) if the nitroglycerin does not relieve the chest pain. Pain relief is very important in patients experiencing ACS (eg, unstable angina or AMI) because it reduces anxiety and subsequent oxygen consumption and demand.

*C: Paroxysmal supraventricular tachycardia* Reason: Syncope (fainting) of cardiac origin is caused by a sudden decrease in cerebral perfusion secondary to a decrease in cardiac output. This is usually the result of an acute bradydysrhythmia or tachydysrhythmia. In this particular patient, the presence of frequent premature atrial complexes (PACs), which indicates atrial irritability, suggests paroxysmal supraventricular tachycardia (PSVT) as the underlying dysrhythmia that caused her syncopal episode. In PSVT, the heart is beating so fast that ventricular filling and cardiac output decrease, which results in a transient decrease in cerebral perfusion. Not all patients with PSVT experience syncope. Many experience an acute onset of palpitations and/or lightheadedness that spontaneously resolves.

What are the physiologic effects of nitroglycerin when given to patients with cardiac-related chest pain, pressure, or discomfort? A: Increased venous return to the right side of the heart B: Increased afterload and vascular constriction C: Smooth muscle relaxation and decreased preload D: Analgesia, vasoconstriction, and increased preload

*C: Smooth muscle relaxation and decreased preload* Reason: Nitroglycerin (NTG) is a vasodilator. It relaxes the smooth muscle of the vascular walls, which promotes systemic venous pooling of blood. As a result, venous return to the right atrium (preload) is decreased; this decreases the cardiac workload. The amount of resistance that the left ventricle must contract against (afterload) is also decreased secondary to vasodilation. By dilating the coronary arteries, NTG increases blood supply to ischemic myocardium and may relieve the chest pain, pressure, or discomfort associated with acute coronary syndrome (ACS). Nitroglycerin is not an analgesic; if it relieves the patient's pain, it is because myocardial oxygen supply and demand have been rebalanced.

Lidocaine Hydrochloride

-Decreases automaticity by slowing the rate of spontaneous phase 4 depolarization

What occurs at the beginning of ventricular contraction? A: Increased ventricular pressure causes the ventricular walls to stretch. B: The pulmonic and aortic valves close and the tricuspid and mitral valves open. C: The atrioventricular valves close and the semilunar valves are forced open. D: Additional blood fills the ventricles secondary to atrial kick.

*C: The atrioventricular valves close and the semilunar valves are forced open* Reason: As ventricular contraction begins, the atrioventricular valves (tricuspid and mitral) close and the semilunar valves (pulmonic and aortic) are forced open. As a result, blood moves from the right ventricle through the pulmonary arteries and from the left ventricle through the aorta and into the systemic circulation. The majority of ventricular filling occurs by gravity. Atrial kick is the volume of blood that the atria contribute to ventricular filling; this occurs before ventricular contraction. Increased pressure within the myocardium (ie, increased blood volume) causes stretching of the myocardial walls, thus increasing the force of its contraction (Starling effect); this process precedes ventricular contraction.

In which of the following situations is transcutaneous cardiac pacing (TCP) clearly indicated? A: First-degree AV block in a patient with abdominal pain. B: Pulseless electrical activity at a rate of 50 beats/min. C: Third-degree AV block in a patient with pulmonary edema. D: Asystole, but only after 10 minutes of adequate CPR.

*C: Third-degree AV block in a patient with pulmonary edema* Reason: Because third-degree AV block (complete heart block)—an inherently slow cardiac dysrhythmia—represents total atrioventricular dissociation, it is associated with hemodynamic compromise in most cases and should be treated with immediate transcutaneous cardiac pacing (TCP). Signs of hemodynamic compromise include ongoing chest pain, pulmonary edema, decreased level of consciousness, shortness of breath, and hypotension. First-degree AV block is typically a benign rhythm and is not commonly associated with hemodynamic compromise. Evidence has shown TCP to be of little or no benefit to patients with PEA or asystole, and it is clearly of no benefit to patients with prolonged asystole.

When assessing a patient's pulse, you note that it is fast and has an irregularly irregular pattern. On the basis of these findings, which of the following cardiac rhythms would MOST likely be seen on the cardiac monitor? A: Supraventricular tachycardia B: Ventricular tachycardia C: Uncontrolled atrial fibrillation D: Second-degree AV block type 1

*C: Uncontrolled atrial fibrillation* Reason: Of the cardiac rhythms listed, atrial fibrillation (A-Fib) is the only one that is irregularly irregular. In fact, A-Fib is never seen as a regular rhythm. At a rate of less than 100 beats/min, A-Fib is said to be controlled. Uncontrolled A-Fib, or A-Fib with a rapid ventricular rate (RVR), occurs when the ventricular rate exceeds 100 beats/min. Second-degree AV block type I has a pattern that is regularly irregular; the P-R interval progressively lengthens until a P wave is blocked. Ventricular tachycardia (V-Tach) and supraventricular tachycardia (SVT) are typically regular rhythms.

During resuscitation of a 60-year-old man with ventricular fibrillation, you restore spontaneous circulation following CPR, defibrillation, two doses of epinephrine, and one dose of amiodarone. The patient remains unresponsive and apneic. Which of the following represents the MOST appropriate post-arrest care for this patient? A: Ventilate at a rate of 20 breaths/min, begin an epinephrine infusion to maintain perfusion, and keep the patient warm B: Ventilate at a rate of 8 to 10 breaths/min, support blood pressure, and give 150 mg of amiodarone over 10 minutes C: Ventilate at a rate of 10 to 12 breaths/min, support blood pressure, and consider therapeutic hypothermia D: Hyperventilate the patient, administer a normal saline bolus, and begin an amiodarone infusion at 0.5 mg/min

*C: Ventilate at a rate of 10 to 12 breaths/min, support blood pressure, and consider therapeutic hypothermia* Reason: The 2010 guidelines for CPR and emergency cardiac care (ECC) have added a fifth link to the chain of survival, integrated post-arrest care. In addition to supporting the patient's airway and ventilatory status and supporting his or her blood pressure with IV fluid boluses or an inotropic agent (ie, dopamine), you should assess for and correct any glucose abnormalities. If the patient is unable to follow verbal commands or remains comatose following return of spontaneous circulation (ROSC), therapeutic hypothermia (89.6°F to 93.2°F [32°C to 34°C]) has been shown to improve neurologic recovery and should be considered (follow your local protocols regarding therapeutic hypothermia). Once ROSC has been established, you should continue to ventilate the adult patient at a rate of 10 to 12 breaths/min (one breath every 5 to 6 seconds) if he or she remains apneic. DO NOT hyperventilate the patient as this may impair venous return to the heart and compromise cardiac output. If the patient is able to follow verbal commands following ROSC, obtain a 12-lead ECG tracing and assess for signs of acute MI (ie, ST elevation). Depending on your transport time, you may consider starting a maintenance infusion of the antidysrhythmic drug that was administered during the arrest, which in this case, would be amiodarone (1 mg/min).

Side effects of atropine sulfate may include: A: hypotension. B: pupillary constriction. C: acute urinary retention. D: hypersalivation.

*C: acute urinary retention.* Reason: Side effects of atropine sulfate may include thirst, dry mouth, pupillary dilation (mydriasis), tachycardia, hypertension, and urinary retention. Acute urinary retention is especially common in older men with benign prostatic hyperplasia (BPH), also known as an enlarged prostate gland.

When treating an adult patient with a blood pressure of 60/40 mm Hg, confusion, a heart rate of 40 beats/min, and sinus bradycardia on the cardiac monitor, you should administer supplemental oxygen, establish vascular access, and then: A: acquire a 12-lead ECG, which may reveal signs of acute myocardial ischemia or injury. B: administer sequential crystalloid fluid boluses until his BP is greater than 100 mm Hg. C: administer 0.5 mg of atropine sulfate and consider transcutaneous cardiac pacing. D: begin a dopamine infusion to increase blood pressure and improve cerebral perfusion.

*C: administer 0.5 mg of atropine sulfate and consider transcutaneous cardiac pacing* Reason: A patient who presents with or develops symptomatic bradycardia needs to be treated in a manner that will increase the heart rate, thus improving cardiac output, blood pressure, and mental status. Altered mental status, hypotension, chest pain or pressure, and shortness of breath are indications for treatment of the bradycardic patient. After ensuring adequate oxygenation and ventilation, establish vascular access and give 0.5 mg of atropine; this may be repeated every 3 to 5 minutes to a maximum dose of 3 mg. If the patient is severely compromised or does not respond to atropine, begin transcutaneous cardiac pacing (TCP) without delay. If the patient is in a second-degree type II or third-degree AV block, TCP is the first-line treatment. Atropine and TCP-refractory bradycardia may require a sympathomimetic infusion, such as epinephrine or dopamine. The body's normal physiologic response to hypovolemia is tachycardia, not bradycardia. Therefore, fluid boluses are not the initial treatment for the hypotensive, bradycardic patient. In fact, they may cause further harm to the patient. With a slow heart rate and decreased cardiac output, a sudden increase in preload may result in acute pulmonary edema. After stabilizing the patient's heart rate and improving perfusion, obtain a 12-lead ECG to assess for signs of acute myocardial ischemia or injury.

A 70-year-old man presents with an acute onset of confusion, slurred speech, and left side weakness. According to his daughter, he has high blood pressure and has had several "small strokes" over the past 6 months. Your partner applies supplemental oxygen; assesses his vital signs, which are stable; and assesses his blood glucose level, which reads 35 mg/dL. You attempt to perform the Cincinnati Prehospital Stroke test, but the patient is unable to understand your instructions. After establishing IV access, you should: A: administer oral glucose, place him in a semi-sitting position, monitor his cardiac rhythm, and transport. B: monitor his cardiac rhythm, withhold glucose in case he is having a hemorrhagic stroke, and transport. C: administer 50% dextrose, monitor his cardiac rhythm, protect his impaired extremities, and transport. D: give 324 mg of baby aspirin, place him in a supine position, monitor his cardiac rhythm, and transport.

*C: administer 50% dextrose, monitor his cardiac rhythm, protect his impaired extremities, and transport. Reason: This patient's clinical presentation and his history of hypertension and transient ischemic attacks (TIAs) suggest acute ischemic stroke. However, his blood glucose level (BGL) is significantly low and must be treated. Untreated hypoglycemia may cause irreversible brain damage or death. Appropriate treatment for this patient involves administering 50% dextrose (consider giving 12.5 g) and then reassessing his BGL to determine the need for additional glucose. Because the patient is confused, and because some patients with acute ischemic stroke lose protective airway reflexes, oral glucose should be avoided. He may not be able to swallow it, which may result in aspiration. Further treatment includes protecting his impaired extremities from injury, monitoring his cardiac rhythm, and transporting him to the hospital. Notify the receiving facility early. Aspirin should be avoided in the prehospital setting for patients with signs and symptoms of a stroke. A CT scan of the head must be performed first to rule out intracranial hemorrhage.

ACE Inhibitors (pril's)

-Dilate arteries and veins by blocking angiotensin II formation and inhibiting bradykinin metabolism -Reduces preload, afterload and myocardial oxygen demand

Epinephrine

-Direct-acting alpha and beta agonist -Blocks histamine receptors

Assessment and treatment of a responsive adult with a suspected acute coronary syndrome (ACS) might include all of the following, EXCEPT: A: administering 2 to 5 mg of morphine sulfate. B: asking the patient if she has a cardiac history. C: administering lidocaine at a dose of 1.5 mg/kg. D: obtaining a 12-lead electrocardiogram.

*C: administering lidocaine at a dose of 1.5 mg/kg* Reason: Lidocaine is not given prophylactically to patients suspected of experiencing an acute coronary syndrome (ACS). In addition to assessing the responsive patient's ABCs and vital signs, you should obtain a 12-lead ECG as early as possible and promptly notify the receiving facility of your findings. Obtaining a SAMPLE history may provide you with additional information that may affect your treatment. Treatment includes supplemental oxygen (maintain an SpO2 of greater than or equal to 94%), 160 to 325 mg of baby aspirin, IV access, up to three doses of nitroglycerin (if the systolic BP is greater than 90 mm Hg), and 2 to 5 mg of morphine sulfate if nitroglycerin fails to completely relieve the patient's chest pain or discomfort and his or her systolic BP remains above 90 mm Hg. Transport the patient as soon as possible, obtain additional 12-lead tracings en route to the hospital, and monitor his or her vital signs and level of pain.

You are assessing a 50-year-old man with acute chest pressure, diaphoresis, and nausea. The 12-lead ECG tracing reveals 3-mm ST segment elevation in leads V3 through V6. This indicates: A: lateral ischemia. B: anteroseptal ischemia. C: anterolateral injury. D: inferior injury.

*C: anterolateral injury* Reason: Leads V1 and V2 view the interventricular septum. Leads V3 and V4 view the anterior wall of the left ventricle. Leads I, aVL, V5 and V6 view the lateral wall of the left ventricle. Leads II, III, and aVF view the inferior wall of the left ventricle. Myocardial ischemia manifests on the 12-lead ECG with ST segment depression and/or T-wave inversion, whereas myocardial injury manifests with ST segment elevation that is equal to or greater than 1-mm in two or more contiguous leads. Therefore, 3-mm ST segment elevation in leads V3 through V6 indicates injury to the anterior and lateral wall of the left ventricle (anterolateral injury).

You arrive approximately 8 minutes after a 51-year-old male collapsed at a family event. After determining that he is unresponsive and apneic, you should: A: begin CPR, starting with chest compressions. B: immediately assess the patient's cardiac rhythm. C: assess for a carotid pulse for 5 to 10 seconds. D: give 2 rescue breaths and check for a pulse.

*C: assess for a carotid pulse for 5 to 10 seconds.* Reason: After determining that an adult patient is unresponsive and apneic, you should assess for a carotid pulse for at least 5 seconds but no more than 10 seconds. If the patient has a pulse, open the airway and provide rescue breathing. If the patient does not have a pulse, begin CPR (starting with chest compressions), then open the airway and give 2 rescue breaths. Assess the patient's cardiac rhythm as soon as a monitor/defibrillator is available.

A 54-year-old man presents with chest pressure, confusion, and profuse diaphoresis. As your partner administers supplemental oxygen, you apply the cardiac monitor. In lead II, you observe a wide QRS complex rhythm with dissociated P waves and a ventricular rate of 35 beats/min. You should: A: immediately obtain a 12-lead ECG. B: start an IV and give 0.5 mg of atropine. C: begin transcutaneous pacing at once. D: obtain a complete set of vital signs.

*C: begin transcutaneous pacing at once* Reason: The patient in this scenario is in a third-degree (complete) AV block, which is causing his signs and symptoms. Complete heart block should be treated with immediate transcutaneous cardiac pacing (TCP). Given the patient's clinical presentation, it is clear that he is hemodynamically unstable; obtaining a complete set of vital signs will yield very little, if any, additional information. A 12-lead ECG should be obtained, but not before addressing the most immediate problem of hemodynamic compromise. Atropine should be avoided in patients with high-grade AV heart blocks (eg, second-degree AV block type II and third-degree AV block). Atropine may worsen the patient's condition—especially in cases of third-degree AV block—by increasing sinus node discharge without any effect on the ventricles. Remember, if the rhythm is perfusing, but is slow and wide, begin TCP without delay.

When administering a sympathomimetic medication, you must be alert for: A: acute hypotension. B: severe bradycardia. C: cardiac arrhythmias. D: acute respiratory failure.

*C: cardiac arrhythmias* Reason: Sympathomimetic medications, such as epinephrine and norepinephrine, cause increases in myocardial oxygen demand and consumption. If given to patients with hypoxemia or acute coronary syndrome (eg, unstable angina, acute myocardial infarction), this effect can result in cardiac arrhythmias. Therefore, you should monitor the cardiac rhythm of any patient who receives a sympathomimetic drug. Sympathomimetic drugs cause an increase in heart rate, not a decrease. Hypotension and respiratory failure are not common following the administration of a sympathomimetic drug.

Unlike a second-degree AV block type I, a second-degree AV block type II is characterized by: A: a progressive lengthening of the P-R interval. B: dissociation of the P waves and QRS complexes. C: consistent P-R intervals following conducted P waves. D: a ventricular rate that is less than 50 beats/min.

*C: consistent P-R intervals following conducted P waves* Reason: A second-degree AV block Mobitz Type II (classic second-degree AV block) is characterized by more P waves than QRS complexes. However, the P-R intervals of the conducted complexes (P waves that are followed by a QRS complex)—whether shortened, normal, or prolonged—are consistent. By contrast, a second-degree AV block Mobitz Type I (Wenkebach) is characterized by a progressive lengthening of the P-R interval until a P wave is blocked (not followed by a QRS complex). The ventricular rate of a second-degree AV block may be normal or slow. Dissociation of the P waves and QRS complexes is characteristic of a third-degree (complete) AV block.

On the 12-lead ECG, the high lateral wall of the left ventricle is viewed by leads: A: V1 and V2. B: V5 and V6. C: III and aVF. D: I and aVL.

*D: I and aVL* Reason: Leads V1 and V2 view the interventricular septum. Leads V3 and V4 view the anterior wall of the left ventricle. Leads V5 and V6 view the low lateral wall of the left ventricle. Leads I and aVL view the high lateral wall of the left ventricle. Leads II, III, and aVF view the inferior wall of the left ventricle. Lead V4R views the right ventricle.

Dopamine Hydrochloride

-Immediate metabolic precursor to norepinephrine -Produces positive inotropic and chronotropic effects -Dilates renal and splanchnic vasculature -Constricts systemic vasculature, increasing blood pressure and preload -Increases myocardial contractility and stroke volume

Calcium Chloride

-Increases cardiac contractile state (positive inotropic effect) -May enhance ventricular automaticity

A 50-year-old woman is pulseless and apneic. Your partner and an emergency medical responder are performing well-coordinated CPR. After 2 minutes of CPR, the cardiac monitor reveals coarse ventricular fibrillation. You should: A: defibrillate at once and then reassess the rhythm and pulse. B: shock the patient three times with 360 monophasic joules. C: deliver a single shock and immediately resume CPR. D: assess for a carotid pulse for no longer than 10 seconds.

*C: deliver a single shock and immediately resume CPR* Reason: A single shock (360 monophasic joules or the biphasic equivalent) should be administered to the patient with V-Fib or pulseless V-Tach cardiac arrest. Immediately following this single shock, begin or resume CPR, starting with chest compressions. Assessing the patient's cardiac rhythm and pulse immediately following defibrillation causes an unnecessary delay in CPR, and delays in CPR have been directly linked to poor patient outcomes. Most patients who are defibrillated—especially if their arrest interval is prolonged—remain in V-Fib/pulseless V-Tach or convert to another non-perfusing rhythm (ie, asystole, PEA). Either way, the patient is still in cardiac arrest and needs immediate CPR. After 2 minutes of CPR, reassess the patient's rhythm, and if necessary, a pulse (if an organized cardiac rhythm appears), and repeat defibrillation (single shock) if indicated, followed immediately by CPR.

The main purpose of listening to heart sounds is to: A: evaluate the location of the point of maximal impulse (PMI). B: assess the rate, regularity, and quality of the heartbeat. C: determine if the cardiac valves are functioning properly. D: assess for an S4 sound, which indicates a weak left ventricle.

*C: determine if the cardiac valves are functioning properly*

According to the Los Angeles Prehospital Stroke Screen (LAPSS), the likelihood that a conscious patient with an acute atraumatic neurologic complaint is experiencing a stroke is HIGHEST if he or she: A: is normally bedridden or wheelchair bound. B: has a blood glucose level of 750 mg/dL. C: does not have a history of seizures. D: has a symmetrical face upon smiling.

*C: does not have a history of seizures.* Reason: The Los Angeles Prehospital Stroke Screen (LAPSS) is a useful tool for indentifying patients who are possibly experiencing a stroke. It requires the paramedic to rule out other causes of abnormal neurologic signs (eg, seizures, hypoglycemia). There are six components to the LAPSS. If any one of these items is checked "yes" or "unknown," you should notify the receiving facility as soon as possible and inform them that the patient is potentially experiencing a stroke. Bear in mind, however, that some patients who are experiencing a stroke may have unremarkable findings on the LAPSS (eg, all components of the LAPSS are checked "no"). Following are the six components of the LAPSS: (1) Age > 45 years; (2) History of seizures is absent; (3) Patient is not normally bedridden or confined to a wheelchair; (4) Blood glucose level is between 60 and 400 mg/dL; (5) Symptom duration is < 24 hours; (6) Unilateral asymmetry in any of the following categories: Facial smile/grimace, Grip strength, or Arm strength (eg, arm drift).

When assessing lead II in a patient with a heart rate of 70 beats/min, the Q-T interval is considered prolonged if it is: A: twice the width of the QRS complex. B: three times the length of the P-R interval. C: greater than one half of the R-R interval. D: consistently greater than 0.20 seconds.

*C: greater than one half of the R-R interval.* Reason: The Q-T interval represents the time from the beginning of ventricular depolarization to the end of ventricular repolarization, and is measured from the start of the QRS complex to the end of the T wave. In a patient with a heart rate between 60 and 100 beats/min, the Q-T interval in lead II is considered to be prolonged if it is greater than one half the distance between any two R waves (R-R interval). If the Q-T interval is prolonged, the patient is at increased risk for developing a lethal dysrhythmia; an electrical impulse may fire during the relative refractory period (downslope of the T-wave), resulting in monomorphic or polymorphic ventricular tachycardia (with or without a pulse) or ventricular fibrillation. If lead II suggests Q-T prolongation, a 12-lead ECG should be obtained to quantify this finding. In a normocardic patient (heart rate of 60 to 100 beats/min), the corrected Q-T interval (QTc) should range between 0.36 and 0.44 seconds (360 to 440 milliseconds) on the 12-lead ECG. The Q-T interval is corrected based on the patient's heart rate. The faster the heart rate, the narrower the Q-T interval; the slower the heart rate, the wider the Q-T interval.

A 47-year-old male took two of his prescribed nitroglycerin tablets prior to calling EMS. When you arrive at the scene, the patient tells you that he has a throbbing headache and is still experiencing chest pain. Your MOST immediate suspicion should be that: A: his chest pain is probably not of a cardiac origin. B: permanent myocardial damage has already occurred. C: he is experiencing continued myocardial ischemia. D: his nitroglycerin is outdated or has lost its potency

*C: he is experiencing continued myocardial ischemia* Reason: When a patient reports taking nitroglycerin (NTG) for chest pain, you should determine how many tablets or sprays he or she took, and whether or not the NTG relieved his or her pain. Failure of NTG to relieve cardiac-related chest pain can occur for one of two reasons—the pain is of extraordinary severity, such as that associated with acute myocardial infarction, or the NTG has been open too long and has lost its potency. Fresh, potent NTG has certain distinct side effects, including a throbbing headache, a burning sensation under the tongue, and a bitter taste. If the patent did not experience any of these side effects, chances are the drug was outdated or had lost its potency. However, if the patient experienced any of these side effects, but is still experiencing chest pain, you should suspect that he or she is experiencing continued myocardial ischemia and is in the process of having an acute myocardial infarction. A 12-lead ECG and other diagnostic tests (ie, echocardiography) are required to determine if permanent myocardial damage has occurred.

You are assessing a 67-year-old female with chest discomfort when she becomes unresponsive, apneic, and pulseless. The cardiac monitor reveals coarse ventricular fibrillation. You achieve return of spontaneous circulation after 6 minutes and the cardiac monitor now reveals a narrow complex rhythm. The patient is still unresponsive, has occasional respirations, a blood pressure of 70/40 mm Hg, and a weak pulse of 70 beats/min. The MOST appropriate postresuscitation care for this patient includes: A: high-flow oxygen via nonrebreathing mask, vascular access, a lidocaine infusion, and an adequate volume of normal saline solution to increase her blood pressure. B: prompt insertion of a multilumen airway device, ventilatory assistance, vascular access, 150 mg of amiodarone over 10 minutes, and 0.5 mg of atropine sulfate. C: insertion of an airway adjunct, assisted ventilation, vascular access, a 500-mL crystalloid bolus, an antidysrhythmic, and consideration for induced hypothermia. D: preoxygenation with a bag-mask device and high-flow oxygen, endotracheal intubation, vascular access, 300 mg of amiodarone, and a dopamine infusion.

*C: insertion of an airway adjunct, assisted ventilation, vascular access, a 500-mL crystalloid bolus, an antidysrhythmic, and consideration for induced hypothermia.* Reason: If return of spontaneous circulation (ROSC) occurs, you must focus on preventing recurrent cardiac arrest and providing optimal conditions that enhance neurologic recovery. Immediately following ROSC, reassess the patient's airway and breathing and treat accordingly. For this patient, you should insert an airway adjunct and assist her ventilations with a bag-mask device and high-flow oxygen. If her breathing does not improve, and she remains unresponsive, an advanced airway device should be considered. Her heart rate (70 beats/min) does not require treatment, although you must closely monitor it. Her blood pressure, however, is low and should be treated. Marked hypotension must be corrected in order to minimize cerebral ischemia; this is usually accomplished initially with crystalloid fluid boluses. If fluid boluses are unsuccessful, an inotropic drug (eg, dopamine) should be considered. Because the patient is still unresponsive, you should consider inducing therapeutic hypothermia, depending on your local protocols. The induction of hypothermia following ROSC has been shown to improve neurologic recovery. The postresuscitation cardiac rhythm should be stabilized to the extent possible. If the arrest rhythm was V-Fib or pulseless V-Tach, consider an antidysrhythmic bolus (eg, lidocaine, amiodarone), followed by an infusion of that same drug.

You are assessing the cardiac rhythm of a woman with respiratory distress. The rhythm is irregularly irregular with a rate of 120 beats/min. The QRS complexes measure 0.10 seconds in duration, the P wave to QRS ratio is 1:1, and the P waves vary in shape. This cardiac rhythm is MOST likely: A: atrial fibrillation. B: atrial flutter with aberrancy. C: multifocal atrial tachycardia. D: a wandering atrial pacemaker.

*C: multifocal atrial tachycardia.* Reason: In multifocal atrial tachycardia (MAT), the pacemaker of the heart moves within various areas of the atria. MAT is characterized by a ventricular rate that is greater than 100 beats/min. MAT is irregularly irregular, with variation between R-R intervals based on the site of the pacemaker for that particular complex. P waves are present, upright, and precede each QRS complex; however, the shapes of the P waves vary as an indication of their different sites of origin. The P-R interval generally measures between 0.12 and 0.20 seconds, but also varies slightly based on the origin of the particular complex. Atrial fibrillation (A-Fib) is also an irregularly irregular rhythm; however, there are no discernable P waves. A wandering atrial pacemaker essentially contains all the components of MAT; unlike MAT, however, the ventricular rate is typically less than 100 beats/min. Atrial flutter (A-Flutter) has characteristic flutter waves (F waves) that resemble a saw tooth. If accompanied by aberrancy, A-flutter has QRS complexes that are greater than 0.12 seconds in duration, which indicates abnormal (aberrant) ventricular conduction.

Atropine sulfate exerts its therapeutic effect by: A: increasing cardiac contractility. B: blocking sympathetic activity. C: opposing the vagus nerve. D: stimulating alpha receptors.

*C: opposing the vagus nerve* Reason: Atropine sulfate is a parasympathetic blocker (parasympatholytic, vagolytic). It is used to increase the heart rate by opposing the vagus nerve when excessive parasympathetic (vagal) tone causes symptomatic bradycardia. Alpha adrenergic agonists, such as norepinephrine (Levophed), primarily stimulate alpha-1 receptors and cause vasoconstriction. Drugs such as propranolol (Inderal) and prazosin (Minipress) block sympathetic nervous system activity by binding to beta and alpha receptors, respectively. Beta receptor blockade causes a decrease in heart rate (negative chronotropy), a decrease in contractility (negative inotropy), and a decrease in electrical conduction velocity (negative dromotropy). Alpha receptor blockade causes vasodilation, and a subsequent decrease in blood pressure. Drugs that increase cardiac contractility, such as dopamine (Intropin), do so through their positive inotropic effects.

Ventricular ejection fraction is defined as the: A: amount of blood pumped out from either ventricle per contraction. B: volume of blood pumped into the left ventricle from the left atrium. C: percentage of blood in the ventricle pumped out during a contraction. D: amount of blood pumped from either ventricle each minute.

*C: percentage of blood in the ventricle pumped out during a contraction* Reason: Ejection fraction (EF) is the percentage of blood that is pumped from the ventricle per contraction. The total volume of blood pumped out of the ventricle per contraction is called the stroke volume (SV). If the ventricle contains 100 mL of blood before a contraction, but only ejects 55 mL when it contracts (SV), the ejection fraction is 55% (100 mL × 0.55 = 55 mL). Ejection fraction should be at least 65% in the adult. Cardiac output (CO) is the volume of blood ejected from the left ventricle each minute, and is calculated by multiplying the stroke volume by the heart rate; in the adult, this is typically 5 to 6 L/min.

ECG indicators of Wolff-Parkinson-White (WPW) syndrome include: A: tall P waves, QT interval prolongation, and tachycardia. B: narrow QRS complexes and peaked T waves. C: short PR intervals, delta waves, and QRS widening. D: delta waves, flattened T waves, and bradycardia.

*C: short PR intervals, delta waves, and QRS widening* Reason: Wolff-Parkinson-White (WPW) syndrome is a condition in which accessory pathways—called the bundle of Kent—bypass the atrioventricular (AV) node, causing the ventricles to depolarize earlier than normal (preexcitation). Because the normal delay at the AV node does not occur, the PR intervals in patients with WPW are usually less than 0.12 seconds (120 ms). When conduction occurs down the AV node and simultaneously along the bundle of Kent in an anterograde fashion, the two waves of depolarization meet (fusion). This manifests on the ECG as a delta wave—slurring or notching at the beginning of the QRS complex—which may cause QRS widening. The bundle of Kent is a potential site for a reentry circuit because it allows continued transmission of an electrical impulse from the atria to the ventricles. Therefore, patients with WPW are prone to reentry tachycardias—most notably, AV reentry supraventricular tachycardia (SVT).

Occlusion of the right coronary artery would MOST likely result in: A: ectopic ventricular complexes. B: sudden cardiac arrest. C: sinoatrial node failure. D: an increase in atrial kick

*C: sinoatrial node failure* Reason: The sinoatrial (SA) node is the dominant cardiac pacemaker; it sets the inherent rate at which the heart beats. The SA node receives blood from the right coronary artery (RCA); therefore, if the RCA is occluded (ie, acute myocardial infarction), the SA node will become ischemic and may cease functioning. If this occurs, the atrioventricular (AV) node would likely assume the role of the primary pacemaker, although at an inherently slower rate. If the SA node fails, the flow of electricity throughout the atria would likely suffer as well; this would result in a decrease in atrial kick—the volume of blood (about 20%) that is ejected from the atria to the ventricles (the other 80% fills the ventricles by gravity). Sudden cardiac arrest is more likely to occur following occlusion of the left main coronary artery. Ectopic ventricular complexes (eg, PVCs), although benign in many cases, may indicate irritability in the ventricles.

In addition to CPR, the recommended treatment sequence for an unresponsive, apneic, and pulseless patient with a regular, wide-complex cardiac rhythm at a rate of 40 beats/min includes: A: transcutaneous cardiac pacing and 1 mg of epinephrine every 3 to 5 minutes. B: 1 mg of epinephrine every 3 to 5 minutes and 1 gram of calcium chloride. C: 40 units of vasopressin every 10 minutes and treating reversible causes. D: 1 mg of epinephrine every 3 to 5 minutes and treating reversible causes.

*D: 1 mg of epinephrine every 3 to 5 minutes and treating reversible causes* Reason: Pulseless electrical activity (PEA) exists when an unresponsive, apneic, pulseless patient presents with a regular cardiac rhythm. Treatment for PEA includes immediate high-quality CPR with minimal interruptions, obtaining vascular access (IV or IO), 1 mg of epinephrine every 3 to 5 minutes, advanced airway management (ie, ET tube, multilumen or supraglottic airway), and assessing for and treating reversible causes (Hs and Ts). Vasopressin, in a one-time dose of 40 units, can be given to replace the first or second dose of epinephrine, but not both. There are insufficient data to recommend transcutaneous pacing (TCP) for patients with bradycardic PEA or asystole, and the routine use of calcium chloride during cardiac arrest is not recommended.

A 71-year-old male presents with chest pain and shortness of breath. He is conscious, but confused, and is profusely diaphoretic. He has weakly palpable radial pulses, a BP of 70/40 mm Hg, and diffuse crackles in all lung fields. You administer high-flow oxygen and apply the cardiac monitor, which reveals sinus tachycardia. The closest appropriate hospital is 40 miles away. Which of the following is the MOST appropriate next action? A: Give 20 mL/kg fluid boluses. B: Obtain a 12-lead ECG tracing. C: Perform a head-to-toe exam. D: Begin an infusion of dopamine

*D: Begin an infusion of dopamine* Reason: The patient in this scenario has likely experienced an acute myocardial infarction and is now in cardiogenic shock (pump failure). Cardiogenic shock is characterized by general signs of shock (eg, tachycardia, diaphoresis), hypotension, altered mental status, and pulmonary congestion—a sign of significant left ventricular damage and decreased stroke volume. After ensuring airway patency and adequate oxygenation and ventilation, your priority is to improve perfusion. Crystalloid fluid boluses, at least not large fluid boluses (ie, 20 mL/kg), are not appropriate for this patient; they may exacerbate his pulmonary edema and further impair pulmonary respiration. Dopamine is a more appropriate intervention. In a dosing range of 5 to 10 µg/kg/min, dopamine possesses positive inotropic effects, which increases myocardial contractility and may improve cardiac output. Rapid transport for this patient is essential; because of your extended transport time, start the dopamine infusion en route. Unfortunately, true cardiogenic shock has a high mortality rate.

Which of the following electrolytes moves slowly into the cardiac cell and maintains the depolarized state of the cell membrane? A: Potassium B: Magnesium C: Sodium D: Calcium

*D: Calcium* Reason: The process of depolarization begins as sodium ions rush into the cell. At the same time, calcium ions enter the cell—albeit more slowly and through specialized channels—to help maintain the depolarized state of the cell membrane and to supply calcium ions for contraction of cardiac muscle tissue. During repolarization, the sodium and calcium channels close, thus stopping the rapid influx of these ions. Then, special potassium channels open, allowing potassium ions to rapidly exit the cell. This helps restore the inside of the cell to its negative charge; the proper electrolyte distribution is then reestablished by pumping sodium ions out of the cell and potassium ions back in. After the potassium channels close, the sodium-potassium pump helps move sodium and potassium ions back to their respective locations. For every three sodium ions the pump moves out of the cell, it moves two potassium ions into the cell, thereby maintaining the polarity of the cell membrane

Which of the following clinical presentations is MOST consistent with an acute ischemic stroke involving the left cerebral hemisphere? A: Dysphasia, confusion, left side hemiparesis, right side facial droop B: Decerebrate posturing, asymmetric pupils, hypertension, bradycardia C: Aphasia, lethargy, right side hemiparalysis, right side facial droop D: Dysarthria, confusion, right side hemiparesis, left side facial droop

*D: Dysarthria, confusion, right side hemiparesis, left side facial droop* Reason: Acute ischemic strokes represent approximately 75% of all strokes. Each cerebral hemisphere controls functions on the contralateral (opposite) side of the body; therefore, sensory and motor deficits (ie, hemiparesis, hemiparalysis) are observed on the side of the body opposite the stroke. However, because the facial nerves do not decussate (cross as they leave the cerebral cortex, move through the brainstem, and arrive at the spinal cord), facial droop is typically observed on the ipsilateral (same) side as the stroke. Pupillary changes, if present, will also occur on the same side as the stroke because of optic nerve crossover in the brain. Other common signs of acute ischemic stroke include dysarthria (slurred speech), dysphasia (difficulty speaking or understanding), aphasia (inability to speak or understand), and mental status changes. In contrast to acute ischemic stroke, acute hemorrhagic stroke (caused by a ruptured cerebral artery) typically presents with more ominous signs, which include a sudden, severe headache that is followed by a rapid decline in level of consciousness. Because bleeding is occurring within the brain, intracranial pressure increases, resulting in signs such as decorticate (flexor) or decerebrate (extensor) posturing, asymmetric or bilaterally dilated pupils, and Cushing's triad (hypertension, bradycardia, abnormal respiratory pattern).

You and your team are performing CPR on a 70-year-old male. The cardiac monitor reveals a slow, organized rhythm. His wife tells you that he goes to dialysis every day, but has missed his last three treatments. She also tells you that he has high blood pressure, hyperthyroidism, and has had several cardiac bypass surgeries. Based on the patient's medical history, which of the following conditions is the MOST likely underlying cause of his condition? A: Drug toxicity B: Coronary thrombus C: Hypovolemia D: Hyperkalemia

*D: Hyperkalemia* Reason: Although any of the listed conditions could be causing this patient's condition, the fact that he missed his last three dialysis treatments should make you most suspicious for hyperkalemia. Dialysis filters metabolic waste products from the blood in patients with renal insufficiency or failure. If the patient is not dialyzed, these waste products, including potassium and other electrolytes, accumulate to toxic levels in the blood. In addition to performing high-quality CPR, managing the airway, and administering epinephrine, your protocols may call for the administration of calcium chloride and sodium bicarbonate if hyperkalemia is suspected. Albuterol also has been shown to be effective in treating patients with hyperkalemia becauses it causes potassium to shift back into the cells; it can be nebulized down the ET tube or administered intravenously. Follow your local protocols regarding the treatment for suspected hyperkalemia.

*D: Hypovolemia* Reason: Hypovolemia is the most easily correctable cause of PEA, provided that immediate treatment is given in the prehospital setting. In addition to CPR, airway management, and epinephrine, fluid boluses are repeatedly given, followed by a reassessment of the patient's condition. Remember, myocardial contraction is dependent on electricity and pressure. This pressure is caused as blood fills the heart. If there is no blood, the heart will not pump, even though electrical activity continues. Drug overdose is the underlying cause of asystole that would most likely respond to immediate prehospital treatment, especially in younger patients. Hypokalemia is treated with potassium chloride, which is not administered in the prehospital setting. Lactic acidosis is treated with effective ventilation first, and then sodium bicarbonate if local protocol permits. While sodium bicarbonate can be given in the prehospital setting, paramedics do not have the ability to quantify the pH or bicarbonate level of the patient's blood; this requires arterial blood gas analysis.

*D: Paroxysmal supraventricular tachycardia* Reason: Syncope (fainting) of cardiac origin is caused by a sudden decrease in cerebral perfusion secondary to a decrease in cardiac output. This is usually the result of an acute bradydysrhythmia or tachydysrhythmia. In this particular patient, the presence of frequent premature atrial complexes (PACs), which indicates atrial irritability, suggests paroxysmal supraventricular tachycardia (PSVT) as the underlying dysrhythmia that caused her syncopal episode. In PSVT, the heart is beating so fast that ventricular filling and cardiac output decrease, which results in a transient decrease in cerebral perfusion. Not all patients with PSVT experience syncope. Many experience an acute onset of palpitations and/or lightheadedness that spontaneously resolves.

What are the therapeutic effects of aspirin when given to patients experiencing an acute coronary syndrome? A: Increases platelet production B: Direct blood-thinning effect C: Dilates the coronary arteries D: Prevents platelet aggregation

*D: Prevents platelet aggregation* Reason: Aspirin (acetylsalicylic acid [ASA]) blocks the formation of thromboxane A2, thus minimizing local coronary vasoconstriction and preventing platelet aggregation. Therefore, aspirin helps prevent an existing clot from getting any larger. Aspirin has clearly been shown to reduce mortality and morbidity from acute coronary syndrome (ACS), and should be given as soon as possible. Examples of blood thinners (anticoagulants) include warfarin sodium (Coumadin) and heparin. Aspirin is not an anticoagulant, nor does it dilate the coronary arteries; nitroglycerin (NTG) does this.

You are assessing a middle-aged female who complains of chest discomfort. She is conscious, alert, and oriented. Her skin is diaphoretic. Her blood pressure is 122/72 mm Hg, her pulse rate is 120 beats/min, and her respirations are 20 breaths/min. On the basis of her chief complaint, which of your assessment findings is the MOST significant? A: Mental status B: Diaphoresis C: Elevated respiratory rate D: Pulse rate of 120 beats/min

*D: Pulse rate of 120 beats/min* Reason: Your patient has signs and symptoms of an acute coronary syndrome (ACS)—a spectrum of cardiac diseases that includes unstable angina pectoris and acute myocardial infarction. In ACS, tachycardia increases myocardial oxygen consumption and demand, and may exacerbate myocardial ischemia or injury. Therefore, her heart rate of 120 beats/min is the most significant clinical finding. Stimulation of the sympathetic nervous system increases the production of sweat, resulting in diaphoresis. Although this is a clinically significant finding, it is not detrimental to the patient. The patient's mental status—conscious, alert, and oriented—indicates that her brain is adequately perfused; obviously, this is a positive sign. Her respiratory rate of 20 breaths/min is consistent with the upper limit of normal for an adult.

Which of the following 12-lead ECG findings signifies a left bundle branch block? A: QRS duration of 122 ms; terminal S wave in lead V6 B: QRS duration of 126 ms; terminal S wave in lead aVL C: QRS duration of 128 ms; terminal R wave in lead V1 D: QRS duration of 124 ms; terminal S wave in lead V1

*D: QRS duration of 124 ms; terminal S wave in lead V1* Reason: A QRS duration of greater than 120 ms (0.12 seconds [3 small boxes]) signifies an intraventricular conduction delay (IVCD), such as a bundle branch block. A left bundle branch block (LBBB) is characterized by a QRS duration of greater than 120 ms and a terminal S wave in lead V1 (the second half of the QRS complex terminates in an S wave); terminal R waves are seen in leads I, aVL, and V6. A right bundle branch block (RBBB) is characterized by a QRS duration of greater than 120 ms and a terminal R wave in lead V1 (the second half of the QRS complex terminates in an R wave); terminal S waves are seen in leads I, aVL, and V6.

Cardioversion involves delivering a shock that is synchronized to occur during the: A: P wave. B: downslope of the T wave. C: upslope of the T wave. D: R wave.

*D: R wave.* Reason: Cardioversion involves delivering a shock that is synchronized to occur during the R wave, which is when the heart is absolutely refractory. This prevents the shock from occurring during the relative refractory period (the downslope of the T wave). Depolarization that occurs during the relative refractory period may induce a non-perfusing ventricular dysrhythmia, such as pulseless V-Tach or V-Fib. Synchronized cardioversion is indicated for patients with supraventricular or ventricular tachycardia who have a pulse, but are hemodynamically unstable.

Which of the following statements regarding right ventricular failure (RVF) is correct? A: Fluid boluses are contraindicated in patients with RVF. B: RVF most often leads to pulmonary hypertension. C: Morphine is the drug of choice for patients with RVF. D: Sacral and pedal edema are common signs of RVF.

*D: Sacral and pedal edema are common signs of RVF* Reason: The most common cause of right ventricular failure (RVF) is left ventricular failure (LVF). When the left ventricle fails, blood backs up into the lungs and eventually into the pulmonary circulation, resulting in pulmonary hypertension. Because the right ventricle must work harder to overcome the increased resistance in the pulmonary circulation, it eventually fails as an effective forward pump. As a result, blood backs up into the systemic circulation, resulting in jugular venous distention, hepatomegaly (enlarged liver), and peripheral edema—especially to dependent areas of the body (eg, extremities, the sacrum in bedridden patients). In patients with severe RVF, total body edema (anasarca) may be present. Hypotension may be observed in patients with RVF, and commonly occurs as the result of right ventricular infarction (RVI). Treat the hypotensive patient with crystalloid fluid boluses (250 to 500 mL), which will increase preload and may improve contractility via the Starling effect. Vasodilators (ie, morphine, nitroglycerin) should not be administered to patients with RVF; they may induce or exacerbate hypotension.

A 61-year-old male presents with chest pressure that woke him up from his nap 30 minutes ago. He is diaphoretic, anxious, and rates his pain as an an 8 over 10. His past medical history is significant for hypertension, type II diabetes, and coronary stent placement 2 months ago. He takes lisinopril, Plavix, and Glucophage, and is wearing a medical alert bracelet stating "allergic to salicylates." His blood pressure is 160/100 mm Hg, pulse is 110 beats/min, and respirations are 22 breaths/min. The 12-lead ECG shows sinus tachycardia with 3-mm ST segment elevation in leads V1 through V5. Which of the following treatment modalities is MOST appropriate for this patient? A: 325 mg of baby aspirin, supplemental oxygen, vascular access, up to three doses of nitroglycerin, and up to 10 mg of morphine if his systolic BP is greater than 120 mm Hg and he is still in pain B: 325 mg of baby aspirin; high-flow oxygen via nonrebreathing mask; vascular access; and 1 µg/kg of fentanyl to relieve his pain, treat his anxiety, and lower his BP C: High-flow oxygen via nonrebreathing mask, a right-sided 12-lead ECG, vascular access, 0.25 mg/kg of diltiazem, and application of pacing pads in case he becomes bradycardic D: Supplemental oxygen, vascular access, up to three 0.4 mg doses of nitroglycerin, and 2 to 4 mg of morphine sulfate if his systolic BP is greater than 90 mm Hg and he is still experiencing pain

*D: Supplemental oxygen, vascular access, up to three 0.4 mg doses of nitroglycerin, and 2 to 4 mg of morphine sulfate if his systolic BP is greater than 90 mm Hg and he is still experiencing pain* Reason: The patient is experiencing an acute coronary syndrome (ACS). His 12-lead ECG indicates anteroseptal injury with lateral extension (ST elevation in leads V1 through V5). Appropriate treatment includes oxygen (maintain an SpO2 of greater than 94%), vascular access, up to three 0.4 mg doses of nitroglycerin (NTG), and 2 to 4 mg of morphine if NTG fails to relieve his pain and his systolic BP is above 90 mm Hg. Some EMS systems may use fentanyl (Sublimaze) for analgesia. Aspirin, a salicylate, is also given to patients with ACS; however, this patient is allergic to salicylates. Obtain a right-sided 12-lead ECG in patients with signs of inferior wall injury (ST elevation in leads II, III, aVF). Inferior wall infarctions may involve the right ventricle; a right-sided 12-lead ECG will help confirm this. Apply the multi-pads to the patient, not because he is at risk for bradycardia (more common with inferior infarctions), but because he is at risk for cardiac arrest due to V-Fib or pulseless V-Tach.

Which of the following cardiac rhythms is associated with bradycardia, and is characterized by regular R-R intervals and a greater ratio of P waves to QRS complexes? A: First-degree AV block B: Second-degree AV block type I C: Second-degree AV block type II D: Third-degree AV block

*D: Third-degree AV block* Reason: Third-degree AV block is caused by a complete block at the AV node. The SA node initiates impulses as usual; however, when they reach the AV node, they are blocked. Resultantly, the ventricles receive no electrical stimulus from the atria, so they initiate their own impulses, although at a much slower rate. On the ECG, this manifests as a bradycardic rhythm with more P waves than QRS complexes. The P-P intervals are regular (some P waves may not be visible because they are buried in a QRS complex), as are the R-R intervals; however, no relationship exists between a given P wave and QRS complex. Second-degree AV block type I (Wenkebach) is caused by a progressive delay at the AV node until an impulse is blocked from entering the ventricles. On the ECG, this manifests as a progressively lengthening P-R interval until a P wave is blocked (not followed by a QRS complex). At this point, the R-R interval becomes irregular, and the presence of this lone P wave increases the ratio of P waves to QRS complexes. Second-degree AV block type I may or may not be associated with bradycardia. Second-degree AV block type II is caused by an intermittent block at the AV node; it occurs when atrial impulses are not conducted to the ventricles. Unlike a second-degree AV block type I, however, a type II block is characterized by consistent P-R intervals of the P waves that are conducted. First-degree AV block is an abnormal delay at the AV node; on the ECG, this manifests with PR intervals greater than 0.20 seconds (120 ms) in duration. In first-degree AV block, all of the atrial impulses are conducted through the AV node and into the ventricles.

Which of the following statements regarding the use of vasopressin in cardiac arrest is correct? A: Vasopressin should be given every 3 to 5 minutes throughout the arrest B: Vasopressin is highly effective in treating pediatric cardiac arrest patients C: Vasopressin is superior to epinephrine and should be used when possible D: Vasopressin can be used to replace the first or second dose of epinephrine

*D: Vasopressin can be used to replace the first or second dose of epinephrine* Reason: According to the 2010 guidelines for CPR and emergency cardiac care (ECC), vasopressin, in a one-time dose of 40 units, can be given to replace the first OR second dose of epinephrine for adult patients in cardiac arrest. There are no definitive data to support superiority of vasopressin over epinephrine. There are insufficient data to make a recommendation for or against the use of vasopressin in pediatric cardiac arrest.

Sudden cardiac arrest in the adult population is MOST often secondary to: A: massive hypovolemia. B: respiratory failure. C: accidental electrocution. D: a cardiac dysrhythmia.

*D: a cardiac dysrhythmia* Reason: Most cases of sudden cardiac arrest (SCA) in the adult population are secondary to a cardiac dysrhythmia, usually ventricular fibrillation (V-Fib). This fact underscores the criticality of early defibrillation. Respiratory failure is the most common cause of cardiac arrest in the pediatric population.

You are evaluating a regular cardiac rhythm in lead II. The rate is 90 beats/min, the QRS complexes consistently measure 0.16 seconds, and inverted P waves are seen immediately following each QRS complex. The rhythm described is MOST characteristic of a/an: A: second-degree AV block with abnormal ventricular conduction. B: wandering atrial pacemaker with a bundle branch block. C: ectopic atrial rhythm with a ventricular conduction delay. D: accelerated junctional rhythm with ventricular aberrancy.

*D: accelerated junctional rhythm with ventricular aberrancy* Reason: A junctional rhythm is characterized by inverted P waves in lead II. If seen, the inverted P waves precede or follow the QRS complex. At a rate of 90 beats/min, the rhythm is further defined as an accelerated junctional rhythm. QRS complexes greater than 0.12 seconds (120 ms) indicate aberrant (abnormal) ventricular conduction (ie, bundle branch block). A wandering atrial pacemaker is characterized by P waves that precede each QRS complex, but vary in morphology. An ectopic atrial rhythm is also characterized by P waves of varying morphologies as well as varying PR intervals. A second- or third-degree AV block should be suspected when there are more P waves than QRS complexes.

A 49-year-old male complains of generalized weakness that began about a week ago. He is conscious and alert and is breathing adequately. His blood pressure is 138/78 mm Hg, pulse is 130 beats/min and irregular, and respirations are 14 breaths/min. You administer supplemental oxygen and apply the cardiac monitor, which reveals atrial fibrillation; a 12-lead ECG tracing reveals the same. The patient denies any significant medical problems and takes no medications. After establishing IV access, you should: A: sedate with midazolam and perform synchronized cardioversion. B: attempt vagal maneuvers and then give 6 mg of adenosine IV push. C: give 150 mg of amiodarone over 10 minutes and transport. D: administer 0.25 mg/kg of diltiazem and transport for evaluation.

*D: administer 0.25 mg/kg of diltiazem and transport for evaluation.* Reason: In the absence of any significant medical history, this patient's weakness probably signaled the onset of his atrial fibrillation (A-Fib). New-onset A-Fib of greater than 48 hours' duration should not be treated with synchronized cardioversion until the patient is adequately anticoagulated first (ie, Coumadin). Blood can stagnate in the fibrillating atria, which increases the risk of clot formation; cardioversion may dislodge these clots, resulting in a stroke, pulmonary embolism, or myocardial infarction. Furthermore, this patient is hemodynamically stable and is not in need of electrical therapy. Appropriate treatment for a patient with A-Fib or atrial flutter (A-Flutter) with a rapid ventricular rate (RVR) involves controlling the ventricular rate with a calcium-channel blocker. Diltiazem (Cardizem) is the most common drug used for this purpose. The initial dose is 0.25 mg/kg, which may be repeated in 15 minutes in a dose of 0.35 mg/kg. Amiodarone may be used to terminate new-onset A-Fib or A-Flutter, but is uncommonly given for this purpose in the prehospital setting. Vagal maneuvers and adenosine are indicated for narrow-complex tachycardias in an attempt to slow the ventricular rate so you can identify the underlying rhythm. You have already identified this patient's rhythm.

Assessment and treatment of a responsive adult with a suspected acute coronary syndrome (ACS) might include all of the following, EXCEPT: A: administering 2 to 5 mg of morphine sulfate. B: obtaining a 12-lead electrocardiogram. C: asking the patient if she has a cardiac history. D: administering lidocaine at a dose of 1.5 mg/kg.

*D: administering lidocaine at a dose of 1.5 mg/kg.* Reason: Lidocaine is not given prophylactically to patients suspected of experiencing an acute coronary syndrome (ACS). In addition to assessing the responsive patient's ABCs and vital signs, you should obtain a 12-lead ECG as early as possible and promptly notify the receiving facility of your findings. Obtaining a SAMPLE history may provide you with additional information that may affect your treatment. Treatment includes supplemental oxygen (maintain an SpO2 of greater than or equal to 94%), 160 to 325 mg of baby aspirin, IV access, up to three doses of nitroglycerin (if the systolic BP is greater than 90 mm Hg), and 2 to 5 mg of morphine sulfate if nitroglycerin fails to completely relieve the patient's chest pain or discomfort and his or her systolic BP remains above 90 mm Hg. Transport the patient as soon as possible, obtain additional 12-lead tracings en route to the hospital, and monitor his or her vital signs and level of pain.

A 72-year-old male presents with an acute onset of confusion, slurred speech, and decreased movement of his right arm. The patient's wife tells you that this began about 20 minutes ago, and that he was fine before that. He has type II diabetes, hypertension, and atrial fibrillation. Given this patient's clinical presentation and past medical history, you should be MOST suspicious that he has: A: a space-occupying intracranial lesion. B: acute hypoglycemia. C: an acute epidural hemorrhage. D: an occluded cerebral artery

*D: an occluded cerebral artery* Reason: Acute ischemic stroke, which is caused by an occluded cerebral artery, is characterized by an acute onset of confusion, slurred speech, facial droop, and unilateral weakness (hemiparesis), among other signs. This patient has two major risk factors for a stroke: hypertension and atrial fibrillation (A-Fib). Although hypertension could be a contributing factor, it is more likely that his A-Fib resulted in the stroke. In A-Fib, a small blood clot can dislodge from the wall of the fibrillating atria, enter the systemic circulation, and occlude a cerebral artery. An epidural hemorrhage is unlikely; it is generally the result of blunt head trauma—most often to the temporal lobe. Furthermore, patients with an epidural hemorrhage tend to deteriorate rapidly and exhibit signs of increased intracranial pressure. Epidural hemorrhage is most often the result of injury to the middle meningeal artery, which bleeds rapidly. Hypoglycemia can also present with acute confusion and slurred speech; however, hemiparesis is a less common finding. Clearly, you should assess the blood glucose level of any patient with an altered mental status. Patients with a space-occupying intracranial lesion (eg, brain tumor) typically have a slow onset and insidious progression of symptoms—often over a period of months. In some patients with a brain tumor, a seizure may be the only presenting clinical manifestation.

A 72-year-old male presents with an acute onset of confusion, slurred speech, and decreased movement of his right arm. The patient's wife tells you that this began about 20 minutes ago, and that he was fine before that. He has type II diabetes, hypertension, and atrial fibrillation. Given this patient's clinical presentation and past medical history, you should be MOST suspicious that he has: A: an acute epidural hemorrhage. B: acute hypoglycemia. C: a space-occupying intracranial lesion. D: an occluded cerebral artery.

*D: an occluded cerebral artery.* Reason: Acute ischemic stroke, which is caused by an occluded cerebral artery, is characterized by an acute onset of confusion, slurred speech, facial droop, and unilateral weakness (hemiparesis), among other signs. This patient has two major risk factors for a stroke: hypertension and atrial fibrillation (A-Fib). Although hypertension could be a contributing factor, it is more likely that his A-Fib resulted in the stroke. In A-Fib, a small blood clot can dislodge from the wall of the fibrillating atria, enter the systemic circulation, and occlude a cerebral artery. An epidural hemorrhage is unlikely; it is generally the result of blunt head trauma—most often to the temporal lobe. Furthermore, patients with an epidural hemorrhage tend to deteriorate rapidly and exhibit signs of increased intracranial pressure. Epidural hemorrhage is most often the result of injury to the middle meningeal artery, which bleeds rapidly. Hypoglycemia can also present with acute confusion and slurred speech; however, hemiparesis is a less common finding. Clearly, you should assess the blood glucose level of any patient with an altered mental status. Patients with a space-occupying intracranial lesion (eg, brain tumor) typically have a slow onset and insidious progression of symptoms—often over a period of months. In some patients with a brain tumor, a seizure may be the only presenting clinical manifestation.

A 60-year-old man presents with chest discomfort, diaphoresis, and dyspnea. The 12-lead ECG reveals 4-mm ST segment elevation in leads V1 through V4. You should suspect: A: anterolateral infarct. B: inferoseptal ischemia. C: anterolateral injury. D: anteroseptal injury.

*D: anteroseptal injury.* Reason: The precordial (chest) leads view the following aspects of the heart: V1 and V2, interventricular septum; V3 and V4, anterior wall; V5 and V6, lateral wall. ST segment depression and/or T wave inversion in two or more contiguous leads indicates ischemia. ST segment that is equal to or greater than 1-mm in two or more contiguous leads indicates injury. A developing Q wave may be seen in conjunction with ST segment elevation associated with myocardial injury. Therefore, 4-mm ST segment elevation in leads V1 through V4 indicates an anteroseptal injury pattern (acute MI in progress). Infarcted (dead [necrotic]) myocardium is characterized by poor R wave progression in the precordial leads and/or the presence of a pathologic Q wave in two or more contiguous leads. By definition, a pathologic Q wave is wider than 0.04 seconds (40 ms) or deeper than one third the height of the R wave that follows it.

Appropriate treatment for asystole includes: A: vasopressin every 3 to 5 minutes and tracheal intubation. B: supraglottic airway placement and antidysrhythmic therapy. C: transcutaneous cardiac pacing and epinephrine 1:10,000. D: epinephrine 1:10,000 and advanced airway management.

*D: epinephrine 1:10,000 and advanced airway management.* Reason: Appropriate treatment for a patient in asystole includes high-quality CPR with minimal interruptions, vascular access, 1 mg of epinephrine 1:10,000 every 3 to 5 minutes, advanced airway management (eg, ET tube, multilumen airway, supraglottic airway), and assessing for and ruling out potentially reversible causes (Hs and Ts). Vasopressin may be given in a one-time dose of 40 units to replace the first or second dose of epinephrine, but not both. Transcutaneous cardiac pacing (TCP) has not shown to be beneficial for patients in asystole and is not recommended. Antidysrhythmic drugs, such as amiodarone and lidocaine, are indicated for patients with ventricular fibrillation or pulseless ventricular tachycardia; they are not given to patients with asystole.

In contrast to unstable angina, stable angina occurs when a patient: A: complains of chest pain at the same time of the day for more than 2 weeks. B: presents with chest pain or discomfort during periods of low oxygen demand. C: needs more than two nitroglycerin treatments to relieve his or her chest pain. D: experiences chest discomfort after a certain, predictable amount of exertion.

*D: experiences chest discomfort after a certain, predictable amount of exertion.* Reason: Angina pectoris is a sign of coronary artery disease (CAD), and is the result of an imbalance in myocardial oxygen supply and demand. Stable angina occurs when the patient experiences chest pain or discomfort after a certain, predictable amount of exertion. Furthermore, the patient with stable angina typically knows what actions to take to relieve the pain (ie, rest, nitroglycerin). By contrast, unstable angina is characterized by noticeable changes in the frequency, severity, and degree of chest pain or discomfort. The patient experiences symptoms, which are often not relieved with rest and/or nitroglycerin, when myocardial oxygen demand is otherwise low (ie, sleep, rest). Unstable angina indicates advanced CAD; it is commonly referred to as preinfarction angina.

When obtaining a 12-lead ECG, lead V1 should be placed: A: approximately 1 inch to the right of the angle of Louis. B: in the second intercostal space just inferior to the second rib. C: on the upper right shoulder just above the clavicle. D: in the fourth intercostal space just to the right of the sternum

*D: in the fourth intercostal space just to the right of the sternum* Reason: Correct lead placement is critical in obtaining an accurate 12-lead ECG tracing. Lead V1—the first precordial (chest) lead—is placed in the fourth intercostal space, just to the right of the sternum. Lead V2 is placed in the fourth intercostal space, just to the left of the sternum.

When assessing a patient with sinus tachycardia at a rate of 135 beats/min, you should recall that: A: a heart rate greater than 130 beats/min often causes significant hemodynamic compromise. B: tachycardia in a patient with cardiac ischemia is beneficial in that it improves coronary perfusion. C: the preferred treatment for tachycardia less than 150 beats/min is a calcium channel blocker. D: rate-related symptoms are uncommon in patients with a heart rate less than 150 beats/min.

*D: rate-related symptoms are uncommon in patients with a heart rate less than 150 beats/min* Reason: Sinus tachycardia in the adult—that is, a heart rate less than 150 beats/min—is usually a manifestation of an underlying problem, such as hypovolemia or hypoxia. Therefore, the treatment for sinus tachycardia should focus on treating the underlying cause (ie, fluid boluses, oxygen). Rate-related hemodynamic compromise is uncommon in patients with a heart rate less than 150 beats/min. Tachycardia in the patient with myocardial ischemia is NOT good; it increases myocardial oxygen demand and consumption, which can exacerbate ischemia. Calcium channel blockers (eg, diltiazem [Cardizem]) are commonly used for ventricular rate control in patients with atrial fibrillation or atrial flutter. Synchronized cardioversion is indicated for patients with hemodynamic compromise secondary to supraventricular tachycardia (narrow complex; heart rate > 150 beats/min) and ventricular tachycardia (wide complex; rate > 100 beats/min [often > 200 beats/min]).

You are transporting a 62-year-old male who called EMS because of nausea and diarrhea. His past medical history includes high cholesterol, for which he takes Lipitor; he denies any other medical history. His blood pressure is 132/78 mm Hg, pulse is 68 beats/min, and respirations are 16 breaths/min. He is receiving oxygen via nasal cannula and has a patent IV line established. He has been in a normal sinus rhythm, but is now experiencing occasional premature ventricular complexes (PVCs). After noting the PVCs, you should: A: give a 250-500 mL normal saline bolus. B: administer 1.5 mg/kg of lidocaine. C: contact the receiving facility immediately. D: reassess and continue monitoring him.

*D: reassess and continue monitoring him* Reason: The patient in this scenario is hemodynamically stable. Premature ventricular complexes (PVCs) are generally not a cause for concern unless they are frequent (> 6 per minute) or occur in the context of acute coronary syndrome (ACS) or hemodynamic compromise. Nonetheless, any change in the patient's condition warrants reassessment. Continue monitoring the ECG and his vital signs. If the PVCs become more frequent, or if his condition deteriorates, an antidysrhythmic (eg, lidocaine, amiodarone) may be indicated. The patient's current vital signs are not suggestive of hypovolemia; therefore, a fluid bolus is not indicated at this point. Call your radio report to the receiving facility as usual and report your findings at that time; there is no need to contact them "immediately."

ECG indicators of Wolff-Parkinson-White (WPW) syndrome include: A: tall P waves, QT interval prolongation, and tachycardia. B: narrow QRS complexes and peaked T waves. C: delta waves, flattened T waves, and bradycardia. D: short PR intervals, delta waves, and QRS widening.

*D: short PR intervals, delta waves, and QRS widening* Reason: Wolff-Parkinson-White (WPW) syndrome is a condition in which accessory pathways—called the bundle of Kent—bypass the atrioventricular (AV) node, causing the ventricles to depolarize earlier than normal (preexcitation). Because the normal delay at the AV node does not occur, the PR intervals in patients with WPW are usually less than 0.12 seconds (120 ms). When conduction occurs down the AV node and simultaneously along the bundle of Kent in an anterograde fashion, the two waves of depolarization meet (fusion). This manifests on the ECG as a delta wave—slurring or notching at the beginning of the QRS complex—which may cause QRS widening. The bundle of Kent is a potential site for a reentry circuit because it allows continued transmission of an electrical impulse from the atria to the ventricles. Therefore, patients with WPW are prone to reentry tachycardias—most notably, AV reentry supraventricular tachycardia (SVT).

In older adults, an S3 heart sound: A: is considered a normal variant. B: is generally very pronounced. C: indicates mitral valve closure. D: signifies moderate heart failure.

*D: signifies moderate heart failure* Reason: The S3 or third heart sound is a soft, low-pitched sound that is caused by vibrations of the ventricular walls, resulting from the rapid filling period of the ventricle during the beginning of diastole. An S3 sound should occur 120 to 170 milliseconds after S2, if it is heard at all. An S3 sound may be a normal clinical finding in children and young adults, although a cardiac evaluation should be performed to determine this. When it is heard in older adults, however, it signifies moderate to severe heart failure. S1 is heard near the beginning of ventricular contraction (systole), when the tricuspid and mitral valves close. S2 is heard near the beginning of ventricular relaxation (diastole), when the pulmonic and aortic valves close.

A 59-year-old male with a monomorphic wide-complex tachycardia at a rate of 220/min, a blood pressure of 80/50 mm Hg, and a decreased level of consciousness, should be treated with: A: 150 mg of amiodarone IV. B: 2 g of magnesium sulfate. C: monophasic defibrillation. D: synchronized cardioversion.

*D: synchronized cardioversion* Reason: The patient in this scenario is likely in ventricular tachycardia (V-Tach). Approximately 90% of wide-complex tachycardias are ventricular in origin. Furthermore, he is hypotensive and has a decreased level of consciousness—signs of hemodynamic compromise. To prevent his condition from deteriorating further, immediate synchronized cardioversion, starting with 100 joules, is indicated. Monophasic (or biphasic equivalent) defibrillation is indicated for patients with pulseless V-Tach and ventricular fibrillation (V-Fib). Amiodarone (150 mg over 10 minutes) is indicated for patients with V-Tach who have a pulse, but are hemodynamically stable; it may also be used as an adjunct for patients with unstable V-Tach when cardioversion alone is not effective. Magnesium sulfate (1 to 2 g) is indicated for patients with torsade de pointes—a variant of polymorphic V-Tach.

A 39-year-old female presents with an acute onset of lightheadedness. The cardiac monitor reveals a tachycardic rhythm at 170 beats/min with QRS complexes that measure 0.08 seconds in duration. Despite vagal maneuvers and adenosine, her cardiac rhythm remains unchanged. She is conscious and alert, has a blood pressure of 118/72 mm Hg, and denies shortness of breath or chest discomfort. You should: A: administer 150 mg of amiodarone over 10 minutes. B: consider that her rhythm is ventricular in origin. C: perform synchronized cardioversion with 50 joules. D: transport immediately and monitor her en route.

*D: transport immediately and monitor her en route* Reason: The patient in this scenario is in supraventricular tachycardia (SVT); her heart rate is 170 beats/min and her QRS complexes are narrow (< 0.12 seconds). Despite appropriate treatment for her rhythm (ie, vagal maneuvers, adenosine), her rhythm remains unchanged, although she remains hemodynamically stable. Lightheadedness is common in patients with SVT, but it is not a clinical indicator of hemodynamic instability. A cardiac rhythm of ventricular origin (eg, ventricular tachycardia) is characterized by QRS complexes that are greater than 0.12 seconds in duration; this patient's QRS complexes are 0.08 seconds in duration. If vagal maneuvers and adenosine are unsuccessful in converting her rhythm, transport immediately without further treatment (other than oxygen); her present condition indicates that she is tolerating the cardiac rhythm. However, if signs of hemodynamic instability are noted (ie, hypotension, decreased level of consciousness, chest pain, shortness of breath), perform synchronized cardioversion at 50 to 100 joules without delay.

Aspirin

-Prevents platelets from clumping together, or aggregating, and forming emboli

Magnesium Sulfate

-Reduces striated muscle contractions and blocks peripheral neuromuscular transmission by reducing acetylcholine release at the myoneural junction -Can cause bronchodilation after beta-agonists and anti-cholinergics have been administered

Diltiazem

-Slow calcium channel blocker that blocks calcium ion influx during depolarization of cardiac and vascular smooth muscle -Decreases peripheral vascular resistance and causes relaxation of the vascular smooth muscle, resulting in a decrease of both systolic and diastolic blood pressure -Reduces preload, afterload and myocardial oxygen demand

Adenosine

-Slows conduction through the AV Node -Can interrupt reentrant pathways -Slows heart by acting directly on the sinus pacemaker cells by slowing impulse formation -Can be used diagnostically for stable, wide-complex tachycardia of unknown origin after two doses of lidocaine

Nitroglycerin

-Smooth muscle relaxant acting on vasculature, bronchial, uterine, intestinal smooth muscle -Dilation of arterioles and veins in periphery -Reduces preload, afterload and myocardial oxygen demand

Vasopressin

-Stimulation of smooth muscle receptors -Potent vasoconstrictor when given in high doses -Alternative vasopressor to the first or second dose of epinephrine in cardiac arrest, alternative to epinephrine in asystole, PEA

Glucagon

-Unknown mechanism of stabilizing cardiac rhythm in beta blocker overdose -Minimal positive inotropic and chronotropic response

What is the PR interval in a NSR

.12-.20

Pediatric adenosine dose

0.1 mg/kg MR 0.2mg/kg

The dosage of cardizem

0.25mg/kg to a max of 10 mg slow IV push

The initial dose for pediatric cardioversion is

0.5-1J/kg

relaxation phase

0.52 seconds; left atrium fills passively with blood under venous pressure and about 80% of ventricular filling occurs as flood flows through the open tricuspid and mitral valves.

The appropriate second dose and method of administration of amiodarone for a patient with refractory ventricular fibrillation is:

150 mg via rapid IV/IO push. The initial dose of amiodarone for a patient with refractory ventricular fibrillation or pulseless ventricular tachycardia is 300 mg via rapid IV or IO push. A second dose of 150 mg via rapid IV or IO push may be repeated one time in 5 minutes. For supraventricular tachycardia or ventricular tachycardia with a pulse, amiodarone should be given in a dose of 150 mg over 10 minutes; this same dose may be repeated as needed.

Using a macrodrip drop set how many drops is 1ml?

10 drops

How to calculate how much traction to pull on a fractured femur

10% of their body weight in lbs to a max of 15lbs

A disaster has _____ or more patients

100

Junctional tachycardia rate

100+

How long does a 12 lead ekg record?

12 seconds

Normal fetal heart rate

120-160

How many mEq in calcium chloride

13.6

Dopamine alpha dose

15-20mcg/kg/min

stage 2 hemorrhage

15-30% blood loss

To be classified as an organ it must have Howe many layers of tissue

Treatment for a PT with GI bleeding includes

2 L fluid bolus infusion in adults, 20 ml/kg in children. High flow 02 and pneumatic anti-shock garments should be considered

The dose of an epi drip

2-10mcg/min

The second dose for pediatric cardioversion is

2J/kg

What is the ratio of fluid replacement to fluid loss in shock patients?

3:1

How many mEq in calcium gluconate

4.6

Vasopressin dose

40 U

The AV node typically beats

40-60bpm

The proper flow rate of a blow by NRB mask

5 LPM

Pediatric amiodarone cardiac arrest dose

5 mg/kg

How many mL of blood is typically well tolerated by a mother post delivery?

500

Using a microdrip set how many drops is 1ml?

60 drops

Accelerated junctional rhythm hasn't a rate of

60-100

If a patient has a carotid pulse but not a radial what can you expect her b/p to be?

60-70

How to set up and epi drip

8mg epi(1:1,000) in 1L NS

posterior ECG

evaluates the electrical activity of the posterior wall of the left ventricle

right-sided ECG

evaluates the electrical activity of the right ventricle (generally lead V4R is the most indicative of right ventricular AMI)

Signs and symptoms of an upper GI bleed

A black, tarry stool(melena) often indicates an upper GI bleed

How is Addison's disease caused by

A deficiency of corticosteroid hormones cortisol and aldosterone

Signs and symptoms of a brown recluse spider bite

A lesion may be surrounded by a red halo known as the "bull's eye,'' symptoms include fever chills malaise N/V generalized rash and the development of hemolytic anemia.

Treatment of a PT in A Fib

administration of a calcium channel blocker such as cardizem or a beta blocker

Nonmodifiable risk factors for heart disease

advanced age, family history, carbohydrate intolerance, Type A personality traits

You are assessing a 59-year-old woman who complains of chest pressure. When you are looking at her list of medications, you note that she takes Vasotec. What type of medication is this?

ACE inhibitor. Enalapril maleate (Vasotec) is an ACE (angiotensin converting enzyme) inhibitor that is used to treat hypertension. Angiotensin II, a potent chemical produced by the kidneys that causes vasoconstriction, is formed from angiotensin I in the blood by the angiotensin converting enzyme. ACE inhibitors inhibit the activity of this enzyme, which decreases the production of angiotensin II. As a result, the blood vessels dilate and blood pressure is reduced. Beta blockers, which are also used to treat hypertension, include drugs such as metoprolol (Lopressor), propranolol (Inderal), and atenolol (Tenormin), among others. Calcium channel blockers are also used to treat hypertension, and include drugs such as diltiazem (Cardizem), verapamil (Calan; Isoptin), and amlodipine (Norvasc), among others. Atropine sulfate is a parasympathetic blocker (vagolytic) that is used to treat patients with hemodynamically unstable bradycardia.

The primary neurotransmitter of the parasympathetic nervous system

Acetylcholine

melena

black tarry stool which indicates and upper GI bleed

ventricular contraction

AV valves close; two ventricles contract and the semilunar valves are forced open. Blood squeezed out of the right ventricle moves forward into the pulmonary arteries and blood from the left ventricle is pushed through the aorta. Systole takes half the time as ventricular filling (~.28seconds)

Aadminister 10 mL of epinephrine 1:10,000 IV. The first drug given to any patient in cardiac arrest is epinephrine in a dose of 1 mg (10 mL of a 1:10,000 solution) via the IV or IO route. This dose should be repeated every 3 to 5 minutes. Alternatively, a one-time dose of vasopressin (40 units) can be given to replace the first or second dose of epinephrine, but not both. Do NOT hyperventilate the patient as doing so increases intrathoracic pressure and can impair venous return (preload) and cardiac output, which would decrease the effectiveness of chest compressions. After an advanced airway has been placed during cardiac arrest, deliver one breath every 6 to 8 seconds (8 to 10 breaths/min) and ensure that chest compressions are uninterrupted. There is presently no evidence to support the efficacy of transcutaneous cardiac pacing (TCP) in patients with bradycardic PEA or asystole.

3rd trimester dark red vaginal bleeding with severe pain

Abruptio placenta

This type of seizure is described as a brief LOC without loss of posture

Absence seizure(petit mal)

Accelerated junctional rhythm with ventricular aberrancy. A junctional rhythm is characterized by inverted P waves in lead II. If seen, the inverted P waves precede or follow the QRS complex. At a rate of 90 beats/min, the rhythm is further defined as an accelerated junctional rhythm. QRS complexes greater than 0.12 seconds (120 ms) indicate aberrant (abnormal) ventricular conduction (ie, bundle branch block). A wandering atrial pacemaker is characterized by P waves that precede each QRS complex, but vary in morphology. An ectopic atrial rhythm is also characterized by P waves of varying morphologies as well as varying PR intervals. A second- or third-degree AV block should be suspected when there are more P waves than QRS complexes.

Which of the following clinical presentations is MOST consistent with dissection of the ascending aorta?

Acute tearing pain in between the scapulae, blood pressure discrepancy between arms, maximal pain severity from the onset. Aortic dissection occurs when the layers of the aorta undergo destructive changes, resulting in an aneurysm (weakening and ballooning of the arterial wall). In dissection of the ascending aorta, the patient typically experiences an acute onset of ripping, tearing, or stabbing pain in the anterior chest or in between the scapulae. In some patients, it may be difficult to differentiate the pain of acute aortic dissection from that of acute myocardial infarction (AMI); however, a number of distinctive features may help. The pain of an AMI is often preceded by prodromal symptoms (eg, nausea, weakness, sweating). Although pain from an AMI is acute, it gradually intensifies over time and is typically described as a squeezing or pressure sensation. By contrast, the pain of aortic dissection is acute, is of maximal intensity from the onset, and is usually described as a ripping, tearing, or stabbing feeling. Other signs and symptoms depend on the extent and location of the dissection. In dissections of the ascending aorta, one or more of the vessels of the aortic arch may be compromised. Disruption of blood flow through the innominate artery, for example, is likely to produce a difference in blood pressure between the arms. The onset and pain characteristics of abdominal aortic dissection are similar to those of ascending aortic dissection; however, the pain typically begins in the abdomen or lower back. Pulse deficits in the femoral arteries may be present, and if the aneurysm is leaking blood into the retroperitoneal space, the patient may complain of an urge to defecate and exhibit signs of shock.

Side effects of atropine sulfate may include:

Acute urinary retention. Side effects of atropine sulfate may include thirst, dry mouth, pupillary dilation (mydriasis), tachycardia, hypertension, and urinary retention. Acute urinary retention is especially common in older men with benign prostatic hyperplasia (BPH), also known as an enlarged prostate gland.

Administer 0.25 mg/kg of diltiazem and transport for evaluation. In the absence of any significant medical history, this patient's weakness probably signaled the onset of his atrial fibrillation (A-Fib). New-onset A-Fib of greater than 48 hours' duration should not be treated with synchronized cardioversion until the patient is adequately anticoagulated first (ie, Coumadin). Blood can stagnate in the fibrillating atria, which increases the risk of clot formation; cardioversion may dislodge these clots, resulting in a stroke, pulmonary embolism, or myocardial infarction. Furthermore, this patient is hemodynamically stable and is not in need of electrical therapy. Appropriate treatment for a patient with A-Fib or atrial flutter (A-Flutter) with a rapid ventricular rate (RVR) involves controlling the ventricular rate with a calcium-channel blocker. Diltiazem (Cardizem) is the most common drug used for this purpose. The initial dose is 0.25 mg/kg, which may be repeated in 15 minutes in a dose of 0.35 mg/kg. Amiodarone may be used to terminate new-onset A-Fib or A-Flutter, but is uncommonly given for this purpose in the prehospital setting. Vagal maneuvers and adenosine are indicated for narrow-complex tachycardias in an attempt to slow the ventricular rate so you can identify the underlying rhythm. You have already identified this patient's rhythm.

Administer 0.5 mg of atropine sulfate and consider transcutaneous cardiac pacing. A patient who presents with or develops symptomatic bradycardia needs to be treated in a manner that will increase the heart rate, thus improving cardiac output, blood pressure, and mental status. Altered mental status, hypotension, chest pain or pressure, and shortness of breath are indications for treatment of the bradycardic patient. After ensuring adequate oxygenation and ventilation, establish vascular access and give 0.5 mg of atropine; this may be repeated every 3 to 5 minutes to a maximum dose of 3 mg. If the patient is severely compromised or does not respond to atropine, begin transcutaneous cardiac pacing (TCP) without delay. If the patient is in a second-degree type II or third-degree AV block, TCP is the first-line treatment. Atropine and TCP-refractory bradycardia may require a sympathomimetic infusion, such as epinephrine or dopamine. The body's normal physiologic response to hypovolemia is tachycardia, not bradycardia. Therefore, fluid boluses are not the initial treatment for the hypotensive, bradycardic patient. In fact, they may cause further harm to the patient. With a slow heart rate and decreased cardiac output, a sudden increase in preload may result in acute pulmonary edema. After stabilizing the patient's heart rate and improving perfusion, obtain a 12-lead ECG to assess for signs of acute myocardial ischemia or injury.

A transmural myocardial infarction is defined as:

An MI that involves the entire thickness of the left ventricular wall from endocardium to epicardium. A transmural myocardial infarction involves the entire thickness of the left ventricular wall from endocardium to epicardium; it is associated with ST-segment elevation and, eventually, the development of pathologic Q waves. A subendocardial infarction involves multiple areas of myocardial necrosis confined to the inner one third to one half of the left ventricular wall; subendocardial infarctions are also referred to as non-Q-wave infarctions. Myocardial ischemia caused by focal areas of spontaneous coronary vasospasm, which may lead to infarction, is called Prinzmetal's (variant) angina; the exact cause of this spontaneous coronary vasospasm is largely unknown.

Administer 50% dextrose, monitor his cardiac rhythm, protect his impaired extremities, and transport. This patient's clinical presentation and his history of hypertension and transient ischemic attacks (TIAs) suggest acute ischemic stroke. However, his blood glucose level (BGL) is significantly low and must be treated. Untreated hypoglycemia may cause irreversible brain damage or death. Appropriate treatment for this patient involves administering 50% dextrose (consider giving 12.5 g) and then reassessing his BGL to determine the need for additional glucose. Because the patient is confused, and because some patients with acute ischemic stroke lose protective airway reflexes, oral glucose should be avoided. He may not be able to swallow it, which may result in aspiration. Further treatment includes protecting his impaired extremities from injury, monitoring his cardiac rhythm, and transporting him to the hospital. Notify the receiving facility early. Aspirin should be avoided in the prehospital setting for patients with signs and symptoms of a stroke. A CT scan of the head must be performed first to rule out intracranial hemorrhage.

Assessment and treatment of a responsive adult with a suspected acute coronary syndrome (ACS) might include all of the following, EXCEPT:

Administering lidocaine at a dose of 1.5 mg/kg. Lidocaine is not given prophylactically to patients suspected of experiencing an acute coronary syndrome (ACS). In addition to assessing the responsive patient's ABCs and vital signs, you should obtain a 12-lead ECG as early as possible and promptly notify the receiving facility of your findings. Obtaining a SAMPLE history may provide you with additional information that may affect your treatment. Treatment includes supplemental oxygen (maintain an SpO2 of greater than or equal to 94%), 160 to 325 mg of baby aspirin, IV access, up to three doses of nitroglycerin (if the systolic BP is greater than 90 mm Hg), and 2 to 5 mg of morphine sulfate if nitroglycerin fails to completely relieve the patient's chest pain or discomfort and his or her systolic BP remains above 90 mm Hg. Transport the patient as soon as possible, obtain additional 12-lead tracings en route to the hospital, and monitor his or her vital signs and level of pain.

Treatment of right ventricular failure

Administration of a 250 mL IV bolus over 5-10 minutes

Treatment of croup

Administration of cool mist or humidified or nebulized oxygen

These types of laws are created by different govement agencies

Administrative

Hyperventilation syndrome causes respiratory ___________________

Alkalosis

Signs, symptoms, and history that indicate a myocardial infarction and cardiogenic shock

Along with signs and symptoms of MI, the PT will present with hypotension(usually <80 systolic), pulmonary congestion(crackles), altered LOC, cool and clammy skin, and JVD

An acute cardiac dysrhythmia. More than 500,000 deaths occur each year as the result of acute myocardial infarction (AMI). Sixty to seventy percent of these deaths occur outside the hospital, usually during the first few hours after the onset of symptoms. Of all deaths from AMI, 90% are due to dysrhythmias—usually ventricular fibrillation—which typically occur during the early hours of the infarct; this should be your primary concern. Many patients experiencing an anterior wall MI are hyperdynamic—that is, they are hypertensive and tachycardic; hypotension is not as common. Depression of the CNS (respiratory depression, bradycardia, and hypotension) should be a concern any time you administer a narcotic analgesic (ie, morphine); however, most patients do not experience significant CNS depression with 5 mg of morphine. Pain relief is an important aspect in the management of the patient with AMI; minimizing pain minimizes anxiety, which can limit the size of the infarct.

An occluded cerebral artery. Acute ischemic stroke, which is caused by an occluded cerebral artery, is characterized by an acute onset of confusion, slurred speech, facial droop, and unilateral weakness (hemiparesis), among other signs. This patient has two major risk factors for a stroke: hypertension and atrial fibrillation (A-Fib). Although hypertension could be a contributing factor, it is more likely that his A-Fib resulted in the stroke. In A-Fib, a small blood clot can dislodge from the wall of the fibrillating atria, enter the systemic circulation, and occlude a cerebral artery. An epidural hemorrhage is unlikely; it is generally the result of blunt head trauma—most often to the temporal lobe. Furthermore, patients with an epidural hemorrhage tend to deteriorate rapidly and exhibit signs of increased intracranial pressure. Epidural hemorrhage is most often the result of injury to the middle meningeal artery, which bleeds rapidly. Hypoglycemia can also present with acute confusion and slurred speech; however, hemiparesis is a less common finding. Clearly, you should assess the blood glucose level of any patient with an altered mental status. Patients with a space-occupying intracranial lesion (eg, brain tumor) typically have a slow onset and insidious progression of symptoms—often over a period of months. In some patients with a brain tumor, a seizure may be the only presenting clinical manifestation.

calcium channel blockers

block the influx of calcium ions into cadiac muscle and relieve angina by preventing coronary artery spasms and weakening cardiac contraction thereby decreasing myocardial oxygen demand.

A 60-year-old man presents with chest discomfort, diaphoresis, and dyspnea. The 12-lead ECG reveals 4-mm ST segment elevation in leads V1 through V4. You should suspect:

Anteroseptal injury. The precordial (chest) leads view the following aspects of the heart: V1 and V2, interventricular septum; V3 and V4, anterior wall; V5 and V6, lateral wall. ST segment depression and/or T wave inversion in two or more contiguous leads indicates ischemia. ST segment that is equal to or greater than 1-mm in two or more contiguous leads indicates injury. A developing Q wave may be seen in conjunction with ST segment elevation associated with myocardial injury. Therefore, 4-mm ST segment elevation in leads V1 through V4 indicates an anteroseptal injury pattern (acute MI in progress). Infarcted (dead [necrotic]) myocardium is characterized by poor R wave progression in the precordial leads and/or the presence of a pathologic Q wave in two or more contiguous leads. By definition, a pathologic Q wave is wider than 0.04 seconds (40 ms) or deeper than one third the height of the R wave that follows it.

The 3 components to the pediatric assessments

Appearance, work of breathing and circulation

What cartilage is an important visual landmark for endotracheal intubation

Arytenoid

You arrive approximately 8 minutes after a 51-year-old male collapsed at a family event. After determining that he is unresponsive and apneic, you should:

Assess for a carotid pulse for 5 to 10 seconds. After determining that an adult patient is unresponsive and apneic, you should assess for a carotid pulse for at least 5 seconds but no more than 10 seconds. If the patient has a pulse, open the airway and provide rescue breathing. If the patient does not have a pulse, begin CPR (starting with chest compressions), then open the airway and give 2 rescue breaths. Assess the patient's cardiac rhythm as soon as a monitor/defibrillator is available.

Immediately after establishing a return of spontaneous circulation in a woman with ventricular fibrillation of short duration, you should:

Assess her ventilatory status and treat accordingly. Your first action after establishing return of spontaneous circulation (ROSC) in a patient—regardless of his or her arrest rhythm and duration—is to assess the patient's ventilatory status. If the patient is not breathing or is breathing inadequately, provide ventilatory support. After assessing and managing airway and breathing, assess the patient's blood pressure and stabilize it if it is low. Airway and circulatory support are critical following ROSC; inadequate ventilation and/or hypotension following cardiac arrest may lead to a recurrence of cardiac arrest. Depending on your local protocols, IV amiodarone may be given following ROSC. After assessing and maintaining respiratory and circulatory functions, obtain a 12-lead ECG if time allows. If the patient remains comatose following ROSC, consider inducing therapeutic hypothermia.

You are called to a local supermarket where a customer collapsed. When you arrive, two bystanders are performing CPR on the patient. You should:

Assess the patient to confirm pulselessness and apnea. When you arrive at a scene and find bystanders performing CPR, you should briefly pause and confirm that the patient is pulseless and apneic. In some cases, you will find CPR being performed on patients who do not require it. Once cardiac arrest is confirmed, resume high-quality CPR and assess the patient's cardiac rhythm as soon as possible. According to the 2010 guidelines for CPR and emergency cardiac care (ECC), the precordial thump should not be used for unwitnessed out-of-hospital cardiac arrest. However, it may be considered for patients with witnessed, monitored unstable ventricular tachycardia, including pulseless ventricular tachycardia, if a defibrillator is not immediately ready for use.

When arriving on scene of a scene with a possible hazmat situation how many feet should you park away from the scene?

At least 100 feet

This type of seizure is described as an abrupt loss of muscle tone, sudden collapse and is sometimes known as a "drop attack"

Atonic seizure

Atrial contraction

The first drug of choice in an organophosphate poisoning

Atropine should always be used first

The parkland burn formula

BSA x 4ml x kg body weight

Begin an infusion of dopamine. The patient in this scenario has likely experienced an acute myocardial infarction and is now in cardiogenic shock (pump failure). Cardiogenic shock is characterized by general signs of shock (eg, tachycardia, diaphoresis), hypotension, altered mental status, and pulmonary congestion—a sign of significant left ventricular damage and decreased stroke volume. After ensuring airway patency and adequate oxygenation and ventilation, your priority is to improve perfusion. Crystalloid fluid boluses, at least not large fluid boluses (ie, 20 mL/kg), are not appropriate for this patient; they may exacerbate his pulmonary edema and further impair pulmonary respiration. Dopamine is a more appropriate intervention. In a dosing range of 5 to 10 µg/kg/min, dopamine possesses positive inotropic effects, which increases myocardial contractility and may improve cardiac output. Rapid transport for this patient is essential; because of your extended transport time, start the dopamine infusion en route. Unfortunately, true cardiogenic shock has a high mortality rate.

A middle-aged man is found unresponsive, pulseless, and apneic. His cardiac arrest was not witnessed, although his skin is still warm to the touch. You should:

Begin immediate high-quality CPR. The first and most crucial intervention for any patient in cardiac arrest is immediate high-quality CPR. With CPR ongoing, you or your partner can apply the defibrillation pads and assess the patient's cardiac rhythm. If a shock is indicated, deliver it and immediately resume CPR, starting with chest compressions. During the 2-minute cycles of CPR, vascular access can be obtained, cardiac drugs can be administered, and the patient's airway can be secured with an advanced device if necessary. It is absolutely critical to minimize interruptions in chest compressions; if you must interrupt compressions, do so for no longer than 10 seconds. The precordial thump is not indicated for unwitnessed cardiac arrest; it may be considered for patients with witnessed V-Tach, however, but has a low success rate.

Begin immediate transcutaneous pacing. The cardiac rhythm described is a third-degree (complete) AV block, and the patient is clinically unstable (ie, hypotension, altered mental status, shortness of breath). Third-degree AV block is characterized by a slow ventricular rate and no P-to-QRS relationship (AV dissociation). Patients with high-grade AV blocks (eg, second-degree type II, third-degree) are often clinically unstable and require immediate transcutaneous cardiac pacing (TCP). Atropine is an appropriate drug for clinically unstable patients with sinus bradycardia and bradycardia associated with low-grade AV blocks (eg, first-degree, second-degree type I); it is not recommended for high-grade AV blocks. If TCP is unsuccessful for this patient, consider an epinephrine infusion (2 to 10 µg/min) or a dopamine infusion (5 to 10 µg/kg/min), either of which may increase her heart rate and blood pressure. The patient's hypotension is secondary to severe bradycardia, not hypovolemia; therefore, a rapid IV fluid bolus is not indicated. If you have reason to suspect that the patient is experiencing an acute coronary syndrome (ACS), aspirin should be given.

Begin transcutaneous pacing at once. The patient in this scenario is in a third-degree (complete) AV block, which is causing his signs and symptoms. Complete heart block should be treated with immediate transcutaneous cardiac pacing (TCP). Given the patient's clinical presentation, it is clear that he is hemodynamically unstable; obtaining a complete set of vital signs will yield very little, if any, additional information. A 12-lead ECG should be obtained, but not before addressing the most immediate problem of hemodynamic compromise. Atropine should be avoided in patients with high-grade AV heart blocks (eg, second-degree AV block type II and third-degree AV block). Atropine may worsen the patient's condition—especially in cases of third-degree AV block—by increasing sinus node discharge without any effect on the ventricles. Remember, if the rhythm is perfusing, but is slow and wide, begin TCP without delay.

Eccymosis

Bruising that looks identical to a contusion, but is not the result of internal bleeding.

If a patient was experiencing acute injury involving the interventricular septum and anterior wall of the left ventricle, you would expect the 12-lead ECG to reveal: A: Inverted T waves in all of the precordial leads. B: ST segment elevation in leads V5, V6, I, and aVL. C: ST segment elevation in leads V1 through V4. D: ST segment depression in leads II, III, and aVF.

C: ST segment elevation in leads V1 through V4. Reason: ST segment elevation that is equal to or greater than 1-mm in two or more contiguous leads indicates myocardial injury (eg, an acute MI in progress). ST segment depression and/or dynamic T wave inversion indicates myocardial ischemia. Leads V1 and V2 view the interventricular septum; leads V3 and V4 view the anterior wall of the left ventricle; leads V5, V6, I, and aVL view the lateral wall of the left ventricle; and leads II, III, and aVF view the inferior wall of the left ventricle. Therefore, if a patient is experiencing acute injury involving the interventricular septum and anterior wall of the left ventricle (anteroseptal injury), you would expect the 12-lead ECG tracing to reveal ST segment elevation is leads V1 through V4. It is important to note, however, that an absence of ST elevation does not definitively rule out acute myocardial infarction.

The major extra cellular anion in the body

Calcium

What ion is responsible for contraction of the myocardium?

Calcium

Which of the following electrolytes moves slowly into the cardiac cell and maintains the depolarized state of the cell membrane?

Calcium. The process of depolarization begins as sodium ions rush into the cell. At the same time, calcium ions enter the cell—albeit more slowly and through specialized channels—to help maintain the depolarized state of the cell membrane and to supply calcium ions for contraction of cardiac muscle tissue. During repolarization, the sodium and calcium channels close, thus stopping the rapid influx of these ions. Then, special potassium channels open, allowing potassium ions to rapidly exit the cell. This helps restore the inside of the cell to its negative charge; the proper electrolyte distribution is then reestablished by pumping sodium ions out of the cell and potassium ions back in. After the potassium channels close, the sodium-potassium pump helps move sodium and potassium ions back to their respective locations. For every three sodium ions the pump moves out of the cell, it moves two potassium ions into the cell, thereby maintaining the polarity of the cell membrane

When assessing a patient with suspected cardiac-related chest pain, which of the following questions would be MOST appropriate to ask?

Can you describe the quality of the pain? Patient assessment involves simple questioning techniques. You should ask open-ended questions, whenever possible; this is especially true when determining the onset and quality of a patient's pain. Asking a leading question, such as "Do you have sharp chest pain?" will often lead the patient to say "yes," even though that is not the true quality of his or her pain. Allow the patient to use his or her own words when describing symptoms.

When administering a sympathomimetic medication, you must be alert for:

Cardiac arrhythmias. Sympathomimetic medications, such as epinephrine and norepinephrine, cause increases in myocardial oxygen demand and consumption. If given to patients with hypoxemia or acute coronary syndrome (eg, unstable angina, acute myocardial infarction), this effect can result in cardiac arrhythmias. Therefore, you should monitor the cardiac rhythm of any patient who receives a sympathomimetic drug. Sympathomimetic drugs cause an increase in heart rate, not a decrease. Hypotension and respiratory failure are not common following the administration of a sympathomimetic drug.

Cardiogenic hypoperfusion. The patient most likely experienced an acute myocardial infarction (AMI); however, since he did not receive timely treatment, extensive myocardial damage has resulted in pump failure. His low BP; weak, rapid pulses; and altered mental status indicate that he is systemically hypoperfused. Hypoperfusion (shock) secondary to a cardiac etiology (ie, pump failure, fast or slow heart rate) is called cardiogenic shock. True cardiogenic shock, which occurs when the myocardium is extensively and permanently damaged and can no longer meet the metabolic needs of the body, has a high mortality rate.

Hyperventilation causes what effects on the body?

Cerebrovascular constriction, reduced cerebral perfusion

You have defibrillated a patient who presented with ventricular fibrillation. After 2 minutes of CPR, you reassess the patient's cardiac rhythm and see a wide-complex tachycardia. You should:

Check for a carotid pulse and defibrillate if a pulse is absent. Cardiac rhythm checks should be performed after every 2 minutes of CPR. If you note a change in the patient's cardiac rhythm after 2 minutes, especially if it is an organized rhythm, you should check for a carotid pulse for 5 to 10 seconds. In this case, the patient has converted from V-Fib to a wide-complex tachycardia, which is probably V-Tach. If the patient has a pulse, perform synchronized cardioversion with the same energy setting that you used for defibrillation. If the patient is pulseless, however, you should defibrillate and immediately resume CPR, starting with chest compressions. During the 2-minute period of CPR, you can adminster epinephrine, if 3 to 5 minutes have passed, or 300 mg of amiodarone via rapid IV or IO push.

A 56-year-old man presents with the cardiac rhythm shown below. He complains of chest discomfort, shortness of breath, and is profusely diaphoretic. His blood pressure is 84/64 mm Hg and his radial pulses are barely palpable. You should:

Consider sedation and perform cardioversion. Your patient has a narrow-complex tachycardia, probably supraventricular tachycardia (SVT). Furthermore, he is hemodynamically unstable as evidenced by his hypotension, respiratory distress, and chest discomfort. Heart rates greater than 150 beats/min often cause hemodynamic compromise because they impair ventricular filling and subsequent cardiac output. Patients with unstable tachycardias require synchronized cardioversion. For the patient with a regular narrow-complex tachycardia (ie, SVT), start with 50 to 100 joules. Consider sedating the patient prior to cardioversion only if doing so does not delay the procedure. If the initial cardioversion attempt is unsuccessful, repeat the cardioversion, increasing the energy setting in a stepwise fashion, and search for potentially reversible underlying causes. Defibrillation is indicated for patients with V-Fib and pulseless V-Tach. Transcutaneous cardiac pacing (TCP) is indicated for patients with hemodynamically unstable bradycardia. Amiodarone, in a dose of 150 mg over 10 minutes, is indicated for patients with stable narrow or wide-complex tachycardias.

A 70-year-old man presents with the cardiac rhythm shown below. He is confused, is slow to answer your questions, and is profusely diaphoretic. His blood pressure is 76/54 mm Hg, his pulse is rapid and weak, and his respirations are 22 breaths/min and labored. He is receiving high-flow oxygen and your partner has established a patent IV line. You should:

Consider sedation and then cardiovert with 100 joules. This patient is in ventricular tachycardia (V-Tach). Furthermore, he is hemodynamically unstable as evidenced by his confusion, hypotension, and labored breathing. Therefore, he requires prompt synchronized cardioversion, starting with 100 joules. Consider sedation with midazolam (Versed) or diazepam (Valium), but do not allow this to delay cardioversion. Amiodarone would be an appropriate intervention if the patient was hemodynamically stable. Vagal maneuvers and adenosine are appropriate for stable patients with narrow complex tachycardias (eg, SVT). Fluid boluses will likely not improve the patient's blood pressure; his hypotension is the result of inadequate ventricular filling and decreased cardiac output due to his cardiac rhythm—not hypovolemia.

Unlike a second-degree AV block type I, a second-degree AV block type II is characterized by:

Consistent P-R intervals following conducted P waves. A second-degree AV block Mobitz Type II (classic second-degree AV block) is characterized by more P waves than QRS complexes. However, the P-R intervals of the conducted complexes (P waves that are followed by a QRS complex)—whether shortened, normal, or prolonged—are consistent. By contrast, a second-degree AV block Mobitz Type I (Wenkebach) is characterized by a progressive lengthening of the P-R interval until a P wave is blocked (not followed by a QRS complex). The ventricular rate of a second-degree AV block may be normal or slow. Dissociation of the P waves and QRS complexes is characteristic of a third-degree (complete) AV block.

How is Hep B transmitted?

Contact with infectious blood, semen, or other body fluids, also perinatal

Symptoms of Lupus

butterfly shaped rash on chin & cheeks, pericarditis, pleuritis, extreme fatigue, painful or swollen joints, and kidney problems.

Treatment of stable monomorphic V Tach

Procainamide, amiodarone

Which of the following pain descriptions is MOST consistent with a cardiac problem?

Crushing. Chest pain of cardiac origin is most often described as crushing, dull, pressure, or as a feeling of heaviness or discomfort. The pain is typically constant, not intermittent, and is usually not palliated or exacerbated by movement. Bear in mind that these are typical pain descriptions. The paramedic should not rule out a cardiac problem if the patient describes the pain differently. Sharp (pleuritic) pain is often associated with conditions such as pleurisy, pulmonary embolism, or spontaneous pneumothorax. A tearing sensation should alert you to the possibility of acute aortic dissection.

A 38-year-old woman who is experiencing abnormal weight gain in her neck/upper back and growth of facial hair could possibly have which condition?

Cushing's syndrome

A 66-year-old woman is diagnosed with cardiomyopathy. What does this indicate?

Progressive cardiac weakening. Cardiomyopathy is a progressive weakening of the myocardium. This condition is commonly the result of chronic hypertension or a history of multiple myocardial infarctions. An enlarged myocardium is called cardiomegaly.

MAP calculation

DBP + 1/3 (SBP - DBP)

Dah- ventricles filling(abnormal and may indicate a failing heart)

A 70-year-old woman was suddenly awakened with the feeling that she was suffocating. She is anxious, is laboring to breathe, and has dried blood on her lips. The ECG shows the cardiac rhythm below. Which of the following pathophysiologies BEST explains her clinical presentation?

Decreased stroke volume with left heart failure. Paroxysmal nocturnal dyspnea (PND), the sudden awakening from sleep with the feeling of being suffocated, along with the dried blood around the patient's lips (likely due to coughing up blood-tinged sputum), are classic indicators of left-sided congestive heart failure (CHF). In left-sided CHF, stroke volume (the amount of blood ejected from the ventricle per contraction) is decreased secondary to a weakened or damaged myocardium. Decreased stroke volume causes blood to regurgitate into the upper chamber of the heart and ultimately backs up into the lungs and causes pulmonary edema.

What is the therapeutic effect of aspirin when administered to a patient experiencing an acute coronary syndrome (ACS)?

Decreased thromboxane A2 production, which inhibits platelet aggregation. Thromboxane A2 is produced by activated platelets. It is a potent vasoconstrictor, it stimulates activation of new platelets, and it increases platelet aggregation. Aspirin (acetylsalicylic acid [ASA]) blocks the production of thromboxane A2, which inhibits vasoconstriction, inhibits activation of new platelets, and inhibits platelet aggregation (ie, it makes the platelets less "sticky"). Aspirin does not destroy a clot in a coronary artery—it prevents it from getting larger. Furthermore, by inhibiting local coronary vasoconstriction, it may enhance blood flow around the clot. Fibrinolytic agents (ie, alteplase [Activase], streptokinase [Streptase], tenecteplase [TNKase]) convert the body's own clot-dissolving enzyme from its inactive form, plasminogen, to its active form, plasmin. Plasmin then destroys the fibrin matrix of the clot—hence the term "fibrinolysis."

Defibrillate and then resume CPR. CPR alone rarely, if ever, converts asystole—or any other cardiac arrest rhythm—to a perfusing rhythm. Furthermore, if one of the leads detaches from the patient's chest, you will more likely see something that resembles massive artifact, not ventricular fibrillation (V-Fib). If you see V-Fib on the cardiac monitor, defibrillate one time with 360 monophasic joules (or equivalent biphasic) and then immediately resume CPR, starting with chest compressions. Assessing for a carotid pulse in a patient who is clearly in V-Fib wastes time; it delays defibrillation and CPR. After 2 minutes of CPR, reassess the patient's cardiac rhythm; if V-fib is still present, defibrillate one time and immediately resume CPR. If you see an organized cardiac rhythm, assess for a pulse for at least 5 seconds but no more than 10 seconds, and then resume CPR if indicated.

Deliver a single shock and immediately resume CPR. A single shock (360 monophasic joules or the biphasic equivalent) should be administered to the patient with V-Fib or pulseless V-Tach cardiac arrest. Immediately following this single shock, begin or resume CPR, starting with chest compressions. Assessing the patient's cardiac rhythm and pulse immediately following defibrillation causes an unnecessary delay in CPR, and delays in CPR have been directly linked to poor patient outcomes. Most patients who are defibrillated—especially if their arrest interval is prolonged—remain in V-Fib/pulseless V-Tach or convert to another non-perfusing rhythm (ie, asystole, PEA). Either way, the patient is still in cardiac arrest and needs immediate CPR. After 2 minutes of CPR, reassess the patient's rhythm, and if necessary, a pulse (if an organized cardiac rhythm appears), and repeat defibrillation (single shock) if indicated, followed immediately by CPR.

You are preparing to defibrillate a patient in cardiac arrest with a manual biphasic defibrillator, but are unsure of the appropriate initial energy setting. What should you do?

Deliver one shock with 200 joules and resume CPR. Energy settings for manual biphasic defibrillators are device-specific—typically 120 joules (rectilinear) or 150 joules (truncated). However, if the appropriate initial energy setting is unknown, you should defibrillate with 200 joules. For subsequent shocks, use the same or higher energy setting. Whether you are using a monophasic or biphasic defibrillator, you should only perform 1 shock, followed immediately by CPR (starting with chest compressions).

The main purpose of listening to heart sounds is to:

Determine if the cardiac valves are functioning properly. In general patient assessment, the main purpose of listening to heart sounds is to identify the "lub-dub" that indicates the cardiac valves are functioning properly. S1 (lub) occurs near the beginning of ventricular contraction, when the tricuspid and mitral valves close. S2 (dub) occurs near the end of the ventricular contraction, when the pulmonary and aortic valves close. Although cardiac rate and regularity can be assessed by listening to heart sounds (apical pulse), the quality of the heartbeat can only be assessed by palpating the pulse. The point of maximal impulse (PMI)—also called the apical thrust—is not heard, but rather seen. The PMI, which is normally located on the left anterior part of the chest in the midclavicular line at the fifth intercostal space, occurs when the heart's apex rotates forward with systole and gently beats against the chest wall, producing a visible pulsation.

Conjugate gaze

Deviation of both eyes to either side at rest which implies damage to brain tissue

dysconjugate gaze

Deviation of the eyes to the opposite sides at rest implies damage to the brainstem

Digoxin. This patient has classic signs of digitalis toxicity. Digoxin is commonly prescribed to patients with congestive heart failure and atrial fibrillation (A-Fib) or atrial flutter (A-Flutter). Its positive inotropic effects increase cardiac contractility and maintain cardiac output, while its negative chronotropic effects control the ventricular rate of the A-Fib or A-Flutter. Digitalis preparations (ie, Lanoxin, Digoxin) have a narrow therapeutic index—that is, there is a fine line between a therapeutic and toxic dose. You should suspect digitalis toxicity in any patient who takes Digoxin or Lanoxin and presents with complaints such as nausea, vomiting, abdominal pain, anorexia, or blurred/yellow vision. Additionally, virtually any cardiac dysrhythmia can be caused by the toxic effects of digitalis. Treatment involves the administration of Digibind, which is given at the hospital.

The most common cause of lower GI bleed

Diverticulosis

According to the Los Angeles Prehospital Stroke Screen (LAPSS), the likelihood that a conscious patient with an acute atraumatic neurologic complaint is experiencing a stroke is HIGHEST if he or she:

Does not have a history of seizures. The Los Angeles Prehospital Stroke Screen (LAPSS) is a useful tool for indentifying patients who are possibly experiencing a stroke. It requires the paramedic to rule out other causes of abnormal neurologic signs (eg, seizures, hypoglycemia). There are six components to the LAPSS. If any one of these items is checked "yes" or "unknown," you should notify the receiving facility as soon as possible and inform them that the patient is potentially experiencing a stroke. Bear in mind, however, that some patients who are experiencing a stroke may have unremarkable findings on the LAPSS (eg, all components of the LAPSS are checked "no"). Following are the six components of the LAPSS: (1) Age > 45 years; (2) History of seizures is absent; (3) Patient is not normally bedridden or confined to a wheelchair; (4) Blood glucose level is between 60 and 400 mg/dL; (5) Symptom duration is < 24 hours; (6) Unilateral asymmetry in any of the following categories: Facial smile/grimace, Grip strength, or Arm strength (eg, arm drift).

Dopamine, 2 to 20 µg/kg/min. Your patient's history and clinical presentation is consistent with cardiogenic shock. She has had chest pressure and shortness of breath for 2 days and is now significantly hypotensive with weak pulses. Because of its positive inotropic effect of increasing myocardial contractility, dopamine is the drug of choice for non-hypovolemic shock (eg, cardiogenic shock) and may improve perfusion. Typically, dopamine for cardiogenic shock is started at 2 µg/kg/min and titrated upwards as needed to improve blood pressure and perfusion. At doses of greater than 10 µg/kg/min, dopamine acts predominantly as a vasopressor, which results in systemic vasoconstriction. Clearly, nitroglycerin is contraindicated in any patient with shock; its potent vasodilatory effects would further lower the patient's blood pressure and worsen her condition. Amiodarone is not the drug of choice for this patient; it is given in a dose of 150 mg over 10 minutes for hemodynamically stable patients with wide or narrow-complex tachycardias that exceed 150 beats/min. Caution must be used if you consider giving a normal saline bolus; the coarse crackles in her lungs indicate pulmonary edema, which could easily be exacerbated by large fluid boluses. Her problem is heart failure, not hypovolemia.

Which of the following clinical presentations is MOST consistent with an acute ischemic stroke involving the left cerebral hemisphere?

Dysarthria, confusion, right side hemiparesis, left side facial droop. Acute ischemic strokes represent approximately 75% of all strokes. Each cerebral hemisphere controls functions on the contralateral (opposite) side of the body; therefore, sensory and motor deficits (ie, hemiparesis, hemiparalysis) are observed on the side of the body opposite the stroke. However, because the facial nerves do not decussate (cross as they leave the cerebral cortex, move through the brainstem, and arrive at the spinal cord), facial droop is typically observed on the ipsilateral (same) side as the stroke. Pupillary changes, if present, will also occur on the same side as the stroke because of optic nerve crossover in the brain. Other common signs of acute ischemic stroke include dysarthria (slurred speech), dysphasia (difficulty speaking or understanding), aphasia (inability to speak or understand), and mental status changes. In contrast to acute ischemic stroke, acute hemorrhagic stroke (caused by a ruptured cerebral artery) typically presents with more ominous signs, which include a sudden, severe headache that is followed by a rapid decline in level of consciousness. Because bleeding is occurring within the brain, intracranial pressure increases, resulting in signs such as decorticate (flexor) or decerebrate (extensor) posturing, asymmetric or bilaterally dilated pupils, and Cushing's triad (hypertension, bradycardia, abnormal respiratory pattern).

Side effects of an ACE inhibitor

Hypertension, edema and CHF

During ventricular systole what is the blood pumped through?

Pulmonary and aortic valve

When attempting transcutaneous cardiac pacing (TCP), you will know that electrical capture has been achieved when:

Each pacemaker spike is followed by a wide QRS complex. Transcutaneous cardiac pacing (TCP) involves passing small, repetitive electrical currents through the patient's skin (transcutaneous) across the heart between one externally placed pacing pad and another. The pacemaker is set at a specific rate, usually 60 to 80/min. The energy is then increased—usually by 10 to 20 milliamps (mA) every few seconds—until the heart begins to respond to the electrical stimulus. Electrical capture has been achieved when the stimulus depolarizes the ventricles; this appears as a wide QRS complex immediately following each pacemaker spike. If the QRS complex is not present, the pacemaker current is not depolarizing the ventricles and electrical capture has not been achieved. Mechanical capture is achieved when the patient's palpated pulse rate corresponds with the paced rate on the ECG.

Which of the following interventions has the greatest impact on patient survival from sudden cardiac arrest?

Early CPR and defibrillation. Early CPR and defibrillation are the two interventions that will have the greatest impact on patient survival from sudden cardiac arrest (SCA). Early, effective CPR maintains perfusion to the body's vital organs until defibrillation can be provided. The most common initial cardiac rhythm observed during SCA is ventricular fibrillation (V-Fib). Early defibrillation, in conjunction with early CPR, greatly enhances the chance of establishing return of spontaneous circulation (ROSC). The probability of successful defibrillation decreases over time, especially if CPR is delayed. For each minute that V-Fib persists, the patient's chance of survival decreases by approximately 7% to 10%.

3 signs of Becks triad

Elevated pulse pressure, muffled heart tones, and hypotension

Which of the following findings is MOST suggestive of right-sided heart failure?

Engorged jugular veins. As the right side of the heart fails, blood is not effectively ejected into the pulmonary circulation; therefore, it backs up beyond the right atrium and into the systemic venous system. This is most noticeable by the presence of engorged or distended jugular veins. Orthopnea, nocturnal dyspnea, and coughing up blood-tinged sputum are indicators of left-sided heart failure as they all indicate fluid in the lungs.

You are treating a patient with ventricular fibrillation. As the defibrillator is charging, you should:

Ensure that CPR is continuing until the defibrillator is charged. A major emphasis is placed on minimizing interruptions in CPR. Evidence has shown that even a brief pause in chest compressions can result in a significant decrease in coronary and cerebral perfusion. Therefore, CPR should be continuing—even as the defibrillator is charging. When the defibrillator is charged, ensure (visually and verbally) that nobody is touching the patient, and then deliver the shock. When defibrillating a patient with V-Fib, you must ensure that the synchronizer is off; the synchronizer will not be able to identify an R wave in V-Fib due to the chaotic nature of the dysrhythmia. Cardiac arrest patients (adults, children, and infants) should be ventilated at a rate of 8 to 10 breaths/min after an advanced airway device has been placed (eg, ET tube, multilumen airway, supraglottic airway). Excessive ventilation rates should be avoided; they cause increased intrathoracic pressure, which may impair venous return and cardiac output.

Appropriate treatment for asystole includes:

Epinephrine 1:10,000 and advanced airway management. Appropriate treatment for a patient in asystole includes high-quality CPR with minimal interruptions, vascular access, 1 mg of epinephrine 1:10,000 every 3 to 5 minutes, advanced airway management (eg, ET tube, multilumen airway, supraglottic airway), and assessing for and ruling out potentially reversible causes (Hs and Ts). Vasopressin may be given in a one-time dose of 40 units to replace the first or second dose of epinephrine, but not both. Transcutaneous cardiac pacing (TCP) has not shown to be beneficial for patients in asystole and is not recommended. Antidysrhythmic drugs, such as amiodarone and lidocaine, are indicated for patients with ventricular fibrillation or pulseless ventricular tachycardia; they are not given to patients with asystole.

The most common cause of upper GI bleed

Peptic ulcer disease and variceal rupture

Left ventricular heart failure will cause a back flow of blood into which system?

Pulmonary circulation

After determining that an elderly man is pulseless and apneic, you and your team begin CPR and briefly pause to assess his cardiac rhythm, which is shown below. After resuming CPR, you should:

Establish vascular access and give 1 mg of epinephrine. After determining that a patient is in pulseless electrical activity (PEA), you should resume CPR, establish vascular access (IV or IO), and administer 1 mg of epinephrine 1:10,000. Consider inserting an advanced airway (ie, ET tube, multilumen airway, supraglottic airway), but DO NOT interrupt CPR to do this. Focus on ruling out potentially reversible causes (Hs and Ts). Routine administration of sodium bicarbonate during cardiac arrest is not recommended; its administration should be guided by arterial blood gas (ABG) values. Synchronized cardioversion is indicated for hemodynamically unstable patients with wide and narrow complex tachycardias, not PEA.

In contrast to unstable angina, stable angina occurs when a patient:

Experiences chest discomfort after a certain, predictable amount of exertion. Angina pectoris is a sign of coronary artery disease (CAD), and is the result of an imbalance in myocardial oxygen supply and demand. Stable angina occurs when the patient experiences chest pain or discomfort after a certain, predictable amount of exertion. Furthermore, the patient with stable angina typically knows what actions to take to relieve the pain (ie, rest, nitroglycerin). By contrast, unstable angina is characterized by noticeable changes in the frequency, severity, and degree of chest pain or discomfort. The patient experiences symptoms, which are often not relieved with rest and/or nitroglycerin, when myocardial oxygen demand is otherwise low (ie, sleep, rest). Unstable angina indicates advanced CAD; it is commonly referred to as preinfarction angina.

How is Hepatitis A transmitted?

Fecal-oral route

Lupus primarily effects what type of patient?

Females between the ages of 15-45

PT with myasthenia gravis can not receive what drug?

Fentanyl

Semilungar valves

Found at the junction of the ventricles and the pulmonary/systemic circulation

Lefort I fracture

Fracture involving the maxillae

Lefort II

Fractures involving the maxillae and nose

Lefort III

Fractures of the maxillae, nose and orbits Andy will typically be a fracture off of the skull also

Where to approach a helicopter

From the front

Treatment of anaphylaxis

Give Epinephrine to all patients with clinical signs of shock, airway swelling or difficulty breathing.

Patients who are non responsive to epinephrine during an anaphylactic reaction due to beta locker usage may be given what medication?

Glucagon

GHigh altitude illness is directly attributed to exposures of what?

Reduced atmosphere pressure

When assessing lead II in a patient with a heart rate of 70 beats/min, the Q-T interval is considered prolonged if it is:

Greater than one half of the R-R interval. The Q-T interval represents the time from the beginning of ventricular depolarization to the end of ventricular repolarization, and is measured from the start of the QRS complex to the end of the T wave. In a patient with a heart rate between 60 and 100 beats/min, the Q-T interval in lead II is considered to be prolonged if it is greater than one half the distance between any two R waves (R-R interval). If the Q-T interval is prolonged, the patient is at increased risk for developing a lethal dysrhythmia; an electrical impulse may fire during the relative refractory period (downslope of the T-wave), resulting in monomorphic or polymorphic ventricular tachycardia (with or without a pulse) or ventricular fibrillation. If lead II suggests Q-T prolongation, a 12-lead ECG should be obtained to quantify this finding. In a normocardic patient (heart rate of 60 to 100 beats/min), the corrected Q-T interval (QTc) should range between 0.36 and 0.44 seconds (360 to 440 milliseconds) on the 12-lead ECG. The Q-T interval is corrected based on the patient's heart rate. The faster the heart rate, the narrower the Q-T interval; the slower the heart rate, the wider the Q-T interval.

Pain and bruising in the flank area

Grey turners sign

coronary sulcus

Groove where the arteries and the main coronary vein cross the heart that separates atria from the ventricles.

How to calculate cardiac output

HR x SV

Have her chew and swallow 325 mg of aspirin. A regular, narrow complex tachycardia at a rate greater than 150 beats/min is consistent with supraventricular tachycardia (SVT). Although the patient is conscious and alert, she is complaining of chest discomfort and is hypotensive. Since she could be experiencing an acute coronary syndrome (ACS), you should instruct her to chew and swallow up to 325 mg of aspirin. Aspirin should be given to any patient suspected of experiencing an ACS, provided there are no contraindications (eg, allergy); it will not affect her blood pressure. Nitroglycerin, however, may exacerbate her hypotension and should be avoided. You can consider administering adenosine; however, the initial dose is 6 mg rapid IV push. Amiodarone, in a dose of 150 mg over 10 minutes, is appropriate for patients with hemodynamically stable wide-complex tachycardias (ie, V-Tach). Closely monitor this patient and be prepared to perform synchronized cardioversion.

He is experiencing continued myocardial ischemia. When a patient reports taking nitroglycerin (NTG) for chest pain, you should determine how many tablets or sprays he or she took, and whether or not the NTG relieved his or her pain. Failure of NTG to relieve cardiac-related chest pain can occur for one of two reasons—the pain is of extraordinary severity, such as that associated with acute myocardial infarction, or the NTG has been open too long and has lost its potency. Fresh, potent NTG has certain distinct side effects, including a throbbing headache, a burning sensation under the tongue, and a bitter taste. If the patent did not experience any of these side effects, chances are the drug was outdated or had lost its potency. However, if the patient experienced any of these side effects, but is still experiencing chest pain, you should suspect that he or she is experiencing continued myocardial ischemia and is in the process of having an acute myocardial infarction. A 12-lead ECG and other diagnostic tests (ie, echocardiography) are required to determine if permanent myocardial damage has occurred.

Hyperkalemia. Although any of the listed conditions could be causing this patient's condition, the fact that he missed his last three dialysis treatments should make you most suspicious for hyperkalemia. Dialysis filters metabolic waste products from the blood in patients with renal insufficiency or failure. If the patient is not dialyzed, these waste products, including potassium and other electrolytes, accumulate to toxic levels in the blood. In addition to performing high-quality CPR, managing the airway, and administering epinephrine, your protocols may call for the administration of calcium chloride and sodium bicarbonate if hyperkalemia is suspected. Albuterol also has been shown to be effective in treating patients with hyperkalemia becauses it causes potassium to shift back into the cells; it can be nebulized down the ET tube or administered intravenously. Follow your local protocols regarding the treatment for suspected hyperkalemia.

Which of the following causes of pulseless electrical activity (PEA) would be the MOST likely to respond to immediate treatment in the prehospital setting?

Hypovolemia. Hypovolemia is the most easily correctable cause of PEA, provided that immediate treatment is given in the prehospital setting. In addition to CPR, airway management, and epinephrine, fluid boluses are repeatedly given, followed by a reassessment of the patient's condition. Remember, myocardial contraction is dependent on electricity and pressure. This pressure is caused as blood fills the heart. If there is no blood, the heart will not pump, even though electrical activity continues. Drug overdose is the underlying cause of asystole that would most likely respond to immediate prehospital treatment, especially in younger patients. Hypokalemia is treated with potassium chloride, which is not administered in the prehospital setting. Lactic acidosis is treated with effective ventilation first, and then sodium bicarbonate if local protocol permits. While sodium bicarbonate can be given in the prehospital setting, paramedics do not have the ability to quantify the pH or bicarbonate level of the patient's blood; this requires arterial blood gas analysis.

How to measure CPP

ICP subtracted by MAP

Treatment of unstable V Tach

Immediate synchronized cardioversion at 100 J

When obtaining a 12-lead ECG, lead V1 should be placed:

In the fourth intercostal space just to the right of the sternum. Correct lead placement is critical in obtaining an accurate 12-lead ECG tracing. Lead V1—the first precordial (chest) lead—is placed in the fourth intercostal space, just to the right of the sternum. Lead V2 is placed in the fourth intercostal space, just to the left of the sternum.

Normal changes in pregnant vital signs include

Increase in heart rate, respiratory rate, and blood volume and a decrease in blood pressure

A patient with acute chest discomfort displays the cardiac rhythm shown below. Which of the following is the MOST detrimental effect that this rhythm can have on the patient?

Increased myocardial oxygen demand. The rhythm shown is sinus tachycardia. Any increase in cardiac workload, such as an increase in heart rate, contractility, or blood pressure, will increase the amount of oxygen that the myocardium demands and consumes. In patients experiencing an acute coronary syndrome (ie, unstable angina [UA], acute myocardial infarction [AMI]), this could extend the area of ischemia or infarction.

What are the therapeutic effects of morphine sulfate when administered to a patient with cardiogenic pulmonary edema?

Increased venous capacitance and decreased preload. In patients with cardiogenic pulmonary edema (ie, congestive heart failure [CHF]), morphine sulfate causes systemic pooling of blood, which increases venous capacitance and decreases preload (the volume of blood returned to the heart). The net effect is to minimize the volume of fluid that accumulates in the lungs. Note that morphine is not a diuretic and will not remove fluid from the body. This is accomplished by administering furosemide (Lasix), which may be considered for patients with CHF and pulmonary edema.

Treating a patient who overdosed on a tricyclic antidepressant drug

Per medical direction, sodium bicarb may begin to reverse cardiac toxicity. Airway, ventilatory and circulatory support; IV access, ECG monitoring.

The T wave represents

Repolarization of the ventricles

Insertion of an airway adjunct, assisted ventilation, vascular access, a 500-mL crystalloid bolus, an antidysrhythmic, and consideration for induced hypothermia. If return of spontaneous circulation (ROSC) occurs, you must focus on preventing recurrent cardiac arrest and providing optimal conditions that enhance neurologic recovery. Immediately following ROSC, reassess the patient's airway and breathing and treat accordingly. For this patient, you should insert an airway adjunct and assist her ventilations with a bag-mask device and high-flow oxygen. If her breathing does not improve, and she remains unresponsive, an advanced airway device should be considered. Her heart rate (70 beats/min) does not require treatment, although you must closely monitor it. Her blood pressure, however, is low and should be treated. Marked hypotension must be corrected in order to minimize cerebral ischemia; this is usually accomplished initially with crystalloid fluid boluses. If fluid boluses are unsuccessful, an inotropic drug (eg, dopamine) should be considered. Because the patient is still unresponsive, you should consider inducing therapeutic hypothermia, depending on your local protocols. The induction of hypothermia following ROSC has been shown to improve neurologic recovery. The postresuscitation cardiac rhythm should be stabilized to the extent possible. If the arrest rhythm was V-Fib or pulseless V-Tach, consider an antidysrhythmic bolus (eg, lidocaine, amiodarone), followed by an infusion of that same drug.

Battery `

Is the act of causing harm to someone

Assault

Is threatening harm to someone

Pathology of altitude illness

It is attributed directly to exposure to reduced atmospheric pressure

How is Cushing syndrome caused

It is caused by an abnormally high circulating level of corticosteroid hormone

cholecystitis is more common in which type of patient?

It is more common in women age 30-50

Becks Triad signs

JVD, narrowing pulse pressure, hypotension and muffled heart tones

Where is the point of maximal impulse (PMI) located in most people?

Left anterior chest, in the midclavicular line, at the fifth intercostal space. On visualization of the chest, you may be able to see the apical thrust, or point of maximal impulse (PMI). The PMI is normally located on the left anterior part of the chest, in the midclavicular line, at the fifth intercostal space. This thrust occurs when the apex of the heart rotates forward during systole, gently beating against the chest wall and producing a visible pulsation.

systemic circulation

consists of all blood vessels between the left ventricle and left atrium

An older man is suddenly awakened in the middle of the night, gasping for air. He is extremely restless and pale, and is coughing up blood. His clinical presentation is MOST consistent with:

Left side heart failure. Waking up in the middle of the night with severe difficulty breathing (paroxysmal nocturnal dyspnea [PND]) and coughing up blood or blood-tinged sputum (hemoptysis) are consistent with left-sided heart failure and pulmonary edema. Right-sided heart failure typically does not present with respiratory distress; it commonly manifests with jugular venous distention and peripheral edema. Shortness of breath and hemoptysis are not consistent with a gastrointestinal (GI) bleed; signs of a GI bleed include abdominal pain, vomiting up blood (hematemesis), which may be bright red or have a coffee-ground appearance; dark, tarry stools (melena); or bright red blood in the stool (hematochezia). Because left-sided heart failure can be caused by other factors, such as a long history of poorly-controlled hypertension, angina may or may not be present.

You are assessing a man with a acute chest pain. As you are inquiring about the quality of his pain, he clenches his fist. This is called __________ sign and nonverbally conveys a feeling of:

Levine's, pressure. Patients with an acute coronary syndrome (ACS)—that is, unstable angina or acute myocardial infarction—often clench their fist when describing the quality of their chest pain or discomfort. This is called Levine's sign, and it conveys a feeling of pressure in the chest. The pain associated with ACS may also be described as a dull or aching sensation or as a feeling of heaviness. An ACS patient who complains of fluttering in the chest should make you suspicious for a cardiac dysrhythmia (ie, SVT, V-Tach). Cullen's sign is characterized by periumbilical bruising and indicates blood in the peritoneal space. Grey-Turner's sign—bruising to the flank area—also indicates blood in the peritoneal space. Beck's triad is a trio of clinical findings that indicates a cardiac tamponade; it includes jugular venous distention, muffled or distant heart sounds, and a narrowing pulse pressure.

Driving code 3

Lights and sirens, the most dangerous way of driving

How is hypoxic drive stimulated

Low PaO2 levels

Lub-Tricuspid and Mitral valve close

Signs and symptoms of meningitis

Malaise, low grade fever, projectile vomiting, petechial rash, headache and a stiff neck.

Excessive menstrual flow is known as what?

Menorrhagia

pulmonary circulation

consists of all blood vessels between the right ventricle and left atrium

Multifocal atrial tachycardia. In multifocal atrial tachycardia (MAT), the pacemaker of the heart moves within various areas of the atria. MAT is characterized by a ventricular rate that is greater than 100 beats/min. MAT is irregularly irregular, with variation between R-R intervals based on the site of the pacemaker for that particular complex. P waves are present, upright, and precede each QRS complex; however, the shapes of the P waves vary as an indication of their different sites of origin. The P-R interval generally measures between 0.12 and 0.20 seconds, but also varies slightly based on the origin of the particular complex. Atrial fibrillation (A-Fib) is also an irregularly irregular rhythm; however, there are no discernable P waves. A wandering atrial pacemaker essentially contains all the components of MAT; unlike MAT, however, the ventricular rate is typically less than 100 beats/min. Atrial flutter (A-Flutter) has characteristic flutter waves (F waves) that resemble a saw tooth. If accompanied by aberrancy, A-flutter has QRS complexes that are greater than 0.12 seconds in duration, which indicates abnormal (aberrant) ventricular conduction.

Signs and symptoms of a black widow spider bite

Muscle cramps and spasms, abdominal rigidity and intense pain, pain in the muscles of the shoulders, back and chest. Headache, dizziness, N/V, and edema of the eyelids

This type of seizure is described as brief muscle contractions that usually occur at the same time on both sides of the body

Myoclonic seizures

The right arm lead on an ECG is what (-/+)

Negative

Driving code 1

No lights or sirens And also the safest

An overdose on what medication could result in bradycardia and hypertension in the patient?

Norepinephrine

The primary neurotransmitter of the sympathetic nervous system

Norepinephrine

Preexisting conditions for HHNK

Often occurs in older patients with type 2 diabetes

Which type of patient is most likely to experience HHNS?

Older patients with type 2 diabetes or patients with undiagnosed diabetes

Atropine sulfate exerts its therapeutic effect by:

Opposing the vagus nerve. Atropine sulfate is a parasympathetic blocker (parasympatholytic, vagolytic). It is used to increase the heart rate by opposing the vagus nerve when excessive parasympathetic (vagal) tone causes symptomatic bradycardia. Alpha adrenergic agonists, such as norepinephrine (Levophed), primarily stimulate alpha-1 receptors and cause vasoconstriction. Drugs such as propranolol (Inderal) and prazosin (Minipress) block sympathetic nervous system activity by binding to beta and alpha receptors, respectively. Beta receptor blockade causes a decrease in heart rate (negative chronotropy), a decrease in contractility (negative inotropy), and a decrease in electrical conduction velocity (negative dromotropy). Alpha receptor blockade causes vasodilation, and a subsequent decrease in blood pressure. Drugs that increase cardiac contractility, such as dopamine (Intropin), do so through their positive inotropic effects.

In a patient with a tension pneumothorax the trachea will deviate toward which side?

Opposite

signs and symptoms of HHNS

Orthostatic hypotension, dry mucous membranes, tachycardia

Which of the following represents the correct medication sequence when treating a patient with a suspected acute coronary syndrome?

Oxygen, aspirin, nitroglycerin, and morphine. The mnemonic "MONA" is used to help remember the medications given to patients who are experiencing an acute coronary syndrome (ACS). Although it does not represent the correct sequence in which the medications should be given, it is a useful mnemonic to remember. The appropriate sequence of medications is oxygen (as needed to maintain an SpO2 of greater than 94%), aspirin (160 to 325 mg), nitrogylcerin (0.4 mg up to 3 times), and morphine (2 to 4 mg) if the nitroglycerin does not relieve the chest pain. Pain relief is very important in patients experiencing ACS (eg, unstable angina or AMI) because it reduces anxiety and subsequent oxygen consumption and demand.

Signs, symptoms, and history that indicate an acute myocardial infarction

PT usually have a history of atherosclerosis, some PT only have symptoms of dyspnea, syncope, or confusion, however 70-90% have substernal chest pain. Other signs and symptoms are anxiety, cyanosis, N/V, weakness and palpitations

Murphy's sign

Pain with palplation of gall bladder (seen with cholecystitis)

Ventricular ejection fraction is defined as the:

Percentage of blood in the ventricle pumped out during a contraction. Ejection fraction (EF) is the percentage of blood that is pumped from the ventricle per contraction. The total volume of blood pumped out of the ventricle per contraction is called the stroke volume (SV). If the ventricle contains 100 mL of blood before a contraction, but only ejects 55 mL when it contracts (SV), the ejection fraction is 55% (100 mL × 0.55 = 55 mL). Ejection fraction should be at least 65% in the adult. Cardiac output (CO) is the volume of blood ejected from the left ventricle each minute, and is calculated by multiplying the stroke volume by the heart rate; in the adult, this is typically 5 to 6 L/min.

You are transporting a 44-year-old man with shortness of breath. He is conscious alert and is receiving supplemental oxygen. A patent IV line has been established. Suddenly, he develops the rhythm shown below. He is now responsive to pain only; is profusely diaphoretic; and has weak radial pulses. You should:

Perform synchronized cardioversion with 100 joules. The patient is in monomorphic ventricular tachycardia with a pulse. He is clinically unstable, as evidenced by his decreased level of consciousness, profuse diaphoresis, and weak radial pulses. Assessing his BP will yield little additional information; therefore, you should perform synchronized cardioversion with 100 joules. Consider sedating the patient, but do not delay cardioversion. Amiodarone, 150 mg IV over 10 minutes, would be an appropriate intervention if the patient was clinically stable. Adenosine is used for clinically stable patients with narrow-complex tachycardias and can be considered for clinically stable patients with wide-complex monomorphic tachycardias.

3rd trimester bright red and painless vaginal bleeding

Placenta previa

The left lower limb lead on an ECG is what (-/+)

Positive

What ion is responsible for repolarization of the myocardium

Potassium

What is a delivery called that is delivered within the first 3 hours of labor

Precipitous delivery

What are the therapeutic effects of aspirin when given to patients experiencing an acute coronary syndrome?

Prevents platelet aggregation. Aspirin (acetylsalicylic acid [ASA]) blocks the formation of thromboxane A2, thus minimizing local coronary vasoconstriction and preventing platelet aggregation. Therefore, aspirin helps prevent an existing clot from getting any larger. Aspirin has clearly been shown to reduce mortality and morbidity from acute coronary syndrome (ACS), and should be given as soon as possible. Examples of blood thinners (anticoagulants) include warfarin sodium (Coumadin) and heparin. Aspirin is not an anticoagulant, nor does it dilate the coronary arteries; nitroglycerin (NTG) does this.

The pneumonic TICLS stands for what?

Tone Interactivness Consolability Look Speech

The pneumonic TICLS stand still for what?

Tone Interactivnss Consalability

This type of seizure is described as a sudden LOC and loss of organized muscle tone

Tonic-clonic seizure

In the context of an acute coronary syndrome, the presence of dyspnea should make you MOST suspicious for:

Pulmonary congestion. Dyspnea that occurs in the context of an acute coronary syndrome (ACS)—that is, unstable angina or acute myocardial infarction—should be assumed to be the result of left side congestive heart failure with resultant pulmonary congestion/edema. The majority of myocardial infarctions involve the left ventricle. The damage may be so extensive that myocardial contractility is impaired and blood backs up into the lungs. Cor pulmonale—acute right heart failure secondary to pulmonary hypertension—typically presents with systemic venous congestion (ie, JVD, peripheral edema), not pulmonary congestion. Anxiety is very common with ACS, and can potentially exacerbate the patient's condition due to increases in myocardial oxygen consumption and demand. In the interest of the patient, however, assume that any complaint of dyspnea in conjunction with ACS is the result of the worst case scenario—pulmonary edema and impaired oxygenation.

Pulse rate of 120 beats/min. Your patient has signs and symptoms of an acute coronary syndrome (ACS)—a spectrum of cardiac diseases that includes unstable angina pectoris and acute myocardial infarction. In ACS, tachycardia increases myocardial oxygen consumption and demand, and may exacerbate myocardial ischemia or injury. Therefore, her heart rate of 120 beats/min is the most significant clinical finding. Stimulation of the sympathetic nervous system increases the production of sweat, resulting in diaphoresis. Although this is a clinically significant finding, it is not detrimental to the patient. The patient's mental status—conscious, alert, and oriented—indicates that her brain is adequately perfused; obviously, this is a positive sign. Her respiratory rate of 20 breaths/min is consistent with the upper limit of normal for an adult.

bundle branch block

QRS complex with a bizarre appearance and a long duration

Which of the following 12-lead ECG findings signifies a left bundle branch block?

QRS duration of 124 ms; terminal S wave in lead V1 . A QRS duration of greater than 120 ms (0.12 seconds [3 small boxes]) signifies an intraventricular conduction delay (IVCD), such as a bundle branch block. A left bundle branch block (LBBB) is characterized by a QRS duration of greater than 120 ms and a terminal S wave in lead V1 (the second half of the QRS complex terminates in an S wave); terminal R waves are seen in leads I, aVL, and V6. A right bundle branch block (RBBB) is characterized by a QRS duration of greater than 120 ms and a terminal R wave in lead V1 (the second half of the QRS complex terminates in an R wave); terminal S waves are seen in leads I, aVL, and V6.

Cardioversion involves delivering a shock that is synchronized to occur during the:

R wave. Cardioversion involves delivering a shock that is synchronized to occur during the R wave, which is when the heart is absolutely refractory. This prevents the shock from occurring during the relative refractory period (the downslope of the T wave). Depolarization that occurs during the relative refractory period may induce a non-perfusing ventricular dysrhythmia, such as pulseless V-Tach or V-Fib. Synchronized cardioversion is indicated for patients with supraventricular or ventricular tachycardia who have a pulse, but are hemodynamically unstable.

Appendicitis S/S

RLQ abdominal pain or cramping, nausea, vomiting, chills, low grade fever

When assessing a patient with sinus tachycardia at a rate of 135 beats/min, you should recall that:

Rate-related symptoms are uncommon in patients with a heart rate less than 150 beats/min. Sinus tachycardia in the adult—that is, a heart rate less than 150 beats/min—is usually a manifestation of an underlying problem, such as hypovolemia or hypoxia. Therefore, the treatment for sinus tachycardia should focus on treating the underlying cause (ie, fluid boluses, oxygen). Rate-related hemodynamic compromise is uncommon in patients with a heart rate less than 150 beats/min. Tachycardia in the patient with myocardial ischemia is NOT good; it increases myocardial oxygen demand and consumption, which can exacerbate ischemia. Calcium channel blockers (eg, diltiazem [Cardizem]) are commonly used for ventricular rate control in patients with atrial fibrillation or atrial flutter. Synchronized cardioversion is indicated for patients with hemodynamic compromise secondary to supraventricular tachycardia (narrow complex; heart rate > 150 beats/min) and ventricular tachycardia (wide complex; rate > 100 beats/min [often > 200 beats/min]).

Reassess and continue monitoring him. The patient in this scenario is hemodynamically stable. Premature ventricular complexes (PVCs) are generally not a cause for concern unless they are frequent (> 6 per minute) or occur in the context of acute coronary syndrome (ACS) or hemodynamic compromise. Nonetheless, any change in the patient's condition warrants reassessment. Continue monitoring the ECG and his vital signs. If the PVCs become more frequent, or if his condition deteriorates, an antidysrhythmic (eg, lidocaine, amiodarone) may be indicated. The patient's current vital signs are not suggestive of hypovolemia; therefore, a fluid bolus is not indicated at this point. Call your radio report to the receiving facility as usual and report your findings at that time; there is no need to contact them "immediately."

Immediately following return of spontaneous circulation, the paramedic should:

Reassess the patient's ventilatory status. Immediately following return of spontaneous circulation (ROSC), as evidenced by the presence of a pulse, the paramedic should reassess the patient's ventilatory status and continue to treat accordingly. Remember, if an advanced airway is placed during cardiac arrest, ventilations are given at a rate of one breath every 6 to 8 seconds (8 to 10 breaths/min) with continuous chest compressions. However, if ROSC occurs and the patient remains apneic, you should deliver one breath every 5 to 6 seconds (10 to 12 breaths/min) for the adult, or one breath every 3 to 5 seconds (12 to 20 breaths/min) for infants and children. Next, assess the patient's BP and use crystalloid fluid boluses or an inotropic drug (eg, dopamine) to treat hypotension and maintain adequate perfusion. If the patient remains comatose following ROSC, therapeutic hypothermia should be considered. Follow your local protocols.

What is the most important extrauterine function?

Respiration

What are physiological effects of hyperventilation?

Respiratory alkalosis, which lowers PC02 and C02

Cushing's syndrome character appearance

Round and red face, fat trunk, thin limbs

Pulmonary embolisms will typically present with this finding on an ECG

S1Q3T3

pulmonary embolism

S1Q3T3 pattern, new RBBB and ST- segment depression V1-V3. Pattern means deep S wave in lead 1, deep narrow Q wave in lead 3, and T-wave inversion lead 3.

Which of the following statements regarding right ventricular failure (RVF) is correct?

Sacral and pedal edema are common signs of RVF. The most common cause of right ventricular failure (RVF) is left ventricular failure (LVF). When the left ventricle fails, blood backs up into the lungs and eventually into the pulmonary circulation, resulting in pulmonary hypertension. Because the right ventricle must work harder to overcome the increased resistance in the pulmonary circulation, it eventually fails as an effective forward pump. As a result, blood backs up into the systemic circulation, resulting in jugular venous distention, hepatomegaly (enlarged liver), and peripheral edema—especially to dependent areas of the body (eg, extremities, the sacrum in bedridden patients). In patients with severe RVF, total body edema (anasarca) may be present. Hypotension may be observed in patients with RVF, and commonly occurs as the result of right ventricular infarction (RVI). Treat the hypotensive patient with crystalloid fluid boluses (250 to 500 mL), which will increase preload and may improve contractility via the Starling effect. Vasodilators (ie, morphine, nitroglycerin) should not be administered to patients with RVF; they may induce or exacerbate hypotension.

atrioventricular (AV) valves

Separates the atria from the ventricles and prevents backflow during ventricular contraction.

How will pancreatitis present?

Severe epigastric pain radiating from the mid-umbilicus to the patients back and shoulders , nausea, vomiting and in severe cases the patient has fever, tachycardia, and signs of generalized sepsis and shock.

Signs and symptoms of thyroid storm

Severe tachycardia, heart failure, dysrhythmias, shock, hyperthermia, abdominal pain

ECG indicators of Wolff-Parkinson-White (WPW) syndrome include:

Short PR intervals, delta waves, and QRS widening. Wolff-Parkinson-White (WPW) syndrome is a condition in which accessory pathways—called the bundle of Kent—bypass the atrioventricular (AV) node, causing the ventricles to depolarize earlier than normal (preexcitation). Because the normal delay at the AV node does not occur, the PR intervals in patients with WPW are usually less than 0.12 seconds (120 ms). When conduction occurs down the AV node and simultaneously along the bundle of Kent in an anterograde fashion, the two waves of depolarization meet (fusion). This manifests on the ECG as a delta wave—slurring or notching at the beginning of the QRS complex—which may cause QRS widening. The bundle of Kent is a potential site for a reentry circuit because it allows continued transmission of an electrical impulse from the atria to the ventricles. Therefore, patients with WPW are prone to reentry tachycardias—most notably, AV reentry supraventricular tachycardia (SVT).

In older adults, an S3 heart sound:

Signifies moderate heart failure. The S3 or third heart sound is a soft, low-pitched sound that is caused by vibrations of the ventricular walls, resulting from the rapid filling period of the ventricle during the beginning of diastole. An S3 sound should occur 120 to 170 milliseconds after S2, if it is heard at all. An S3 sound may be a normal clinical finding in children and young adults, although a cardiac evaluation should be performed to determine this. When it is heard in older adults, however, it signifies moderate to severe heart failure. S1 is heard near the beginning of ventricular contraction (systole), when the tricuspid and mitral valves close. S2 is heard near the beginning of ventricular relaxation (diastole), when the pulmonic and aortic valves close.

Occlusion of the right coronary artery would MOST likely result in:

Sinoatrial node failure. The sinoatrial (SA) node is the dominant cardiac pacemaker; it sets the inherent rate at which the heart beats. The SA node receives blood from the right coronary artery (RCA); therefore, if the RCA is occluded (ie, acute myocardial infarction), the SA node will become ischemic and may cease functioning. If this occurs, the atrioventricular (AV) node would likely assume the role of the primary pacemaker, although at an inherently slower rate. If the SA node fails, the flow of electricity throughout the atria would likely suffer as well; this would result in a decrease in atrial kick—the volume of blood (about 20%) that is ejected from the atria to the ventricles (the other 80% fills the ventricles by gravity). Sudden cardiac arrest is more likely to occur following occlusion of the left main coronary artery. Ectopic ventricular complexes (eg, PVCs), although benign in many cases, may indicate irritability in the ventricles.

An elderly man is apneic and pulseless. The ECG shows the following rhythm, which you should interpret as:

Sinus tachycardia. The rhythm shown is sinus tachycardia at a rate of approximately 100 to 110 beats/min. First-degree AV block is characterized by a PR interval that is greater than 0.20 seconds, the normal being 0.12 to 0.20 seconds (120 to 200 milliseconds). The fact that the patient does not have a pulse indicates pulseless electrical activity (PEA). PEA is not a specific rhythm; it is a condition in which a pulseless, apneic patient presents with an organized cardiac rhythm (except for pulseless V-Tach).

What are the physiologic effects of nitroglycerin when given to patients with cardiac-related chest pain, pressure, or discomfort?

Smooth muscle relaxation and decreased preload. Nitroglycerin (NTG) is a vasodilator. It relaxes the smooth muscle of the vascular walls, which promotes systemic venous pooling of blood. As a result, venous return to the right atrium (preload) is decreased; this decreases the cardiac workload. The amount of resistance that the left ventricle must contract against (afterload) is also decreased secondary to vasodilation. By dilating the coronary arteries, NTG increases blood supply to ischemic myocardium and may relieve the chest pain, pressure, or discomfort associated with acute coronary syndrome (ACS). Nitroglycerin is not an analgesic; if it relieves the patient's pain, it is because myocardial oxygen supply and demand have been rebalanced.

The ion that rushes into cardiac cells which is responsible for rapid depolarization

Sodium

While assessing a middle-aged man who complains of nausea and weakness, he suddenly becomes unresponsive. The cardiac monitor displays the rhythm shown below. After determining that he is apneic and pulseless, you should:

Start CPR and prepare to defibrillate. You witnessed your patient's deterioration to cardiac arrest, and he is now in ventricular fibrillation (V-Fib). You should immediately start CPR and defibrillate as soon as possible. Deliver a single shock with 360 monophasic joules or the equivalent biphasic setting, and immediately resume CPR (starting with chest compressions). Perform 5 cycles (about 2 minutes) of CPR and then reassess his cardiac rhythm. If V-Fib persists, defibrillate again and immediately resume CPR, starting with chest compressions. During CPR, establish vascular access (if not already done), and give 1 mg of epinephrine 1:10,000. After 2 minutes of CPR, reassess the patient's cardiac rhythm. If V-Fib persists, defibrillate again and immediately resume CPR, starting with chest compressions. It would then be appropriate to administer 300 mg of amiodarone. Synchronized cardioversion is indicated for patients with narrow or wide-complex tachycardias who are hemodynamically unstable but have a pulse.

Start CPR, ensure the synchronize mode is off, and defibrillate. If a patient develops ventricular fibrillation (V-Fib) or pulseless ventricular tachycardia (V-Tach) following synchronized cardioversion, immediately begin CPR (even if it's just for a short period of time), ensure that the monitor/defibrillator is not in synchronize mode, and defibrillate as soon as possible. CPR should be ongoing as the defibrillator is charging in order to avoid unnecessary delays in performing chest compressions. The synchronize mode must be turned off prior to defibrillation or the device will not deliver a shock; this is because there are no R waves to synchronize with in V-Fib. Vascular access (IV or IO), advanced airway management, and pharmacologic therapy should be performed during the 2-minute cycles of CPR; they are not an immediate priority during early cardiac arrest.

Which of the following is an absolute contraindication for fibrinolytic therapy?

Subdural hematoma 3 years ago. According to current emergency cardiac care (ECC) guidelines, absolute contraindications for fibrinolytic therapy include ANY prior intracranial hemorrhage (ie, subdural, epidural, intracerebral hematoma); known structural cerebrovascular lesion (ie, arteriovenous malformation); known malignant intracranial tumor (primary or metastatic); ischemic stroke within the past 3 months, EXCEPT for acute ischemic stroke within the past 3 hours; suspected aortic dissection; active bleeding or bleeding disorders (except menses); and significant closed head trauma or facial trauma within the past 3 months. Relative contraindications (eg, the physician may deem fibrinolytic therapy appropriate under certain circumstances) include, a history of chronic, severe, poorly-controlled hypertension; severe uncontrolled hypertension on presentation (SBP > 180 mm Hg or DBP > 110 mm Hg); ischemic stroke greater than 3 months ago; dementia; traumatic or prolonged (> 10 minutes) CPR or major surgery within the past 3 weeks; recent (within 2 to 4 weeks) internal bleeding; noncompressible vascular punctures; pregnancy; prior exposure (> 5 days ago) or prior allergic reaction to streptokinase or anistreplase; active peptic ulcer; and current use of anticoagulants (ie, Coumadin).

Supplemental oxygen via nasal cannula, cardiac monitoring, blood glucose assessment, an IV of normal saline set to keep the vein open, and prompt transport. The patient is likely experiencing an acute ischemic stroke. Determining the time of onset of his symptoms is critical; fibrinolytic therapy must be administered within the first 3 hours following a stroke in order to be of maximum benefit. Treatment includes supplemental oxygen (a nasal cannula is appropriate, given his room air oxygen saturation), blood glucose assessment (hypoglycemia can mimic certain signs of a stroke), vascular access, cardiac monitoring, and prompt transport with early notification of the receiving facility. Do not give aspirin to suspected stroke patients in the field; it can cause further harm to the patient with a hemorrhagic stroke. Aspirin may be given at the hospital after a hemorrhagic stroke is ruled out with a computed tomography (CT) scan of the brain. Antihypertensive therapy should also be avoided in the field; it should be performed in the controlled setting of a hospital, where the patient has invasive hemodynamic monitoring. Lowering a patient's BP in the field is dangerous and can have disastrous effects; inadvertently inducing hypotension in the stroke patient may exacerbate cerebral ischemia.

Supplemental oxygen, vascular access, up to three 0.4 mg doses of nitroglycerin, and 2 to 4 mg of morphine sulfate if his systolic BP is greater than 90 mm Hg and he is still experiencing pain. The patient is experiencing an acute coronary syndrome (ACS). His 12-lead ECG indicates anteroseptal injury with lateral extension (ST elevation in leads V1 through V5). Appropriate treatment includes oxygen (maintain an SpO2 of greater than 94%), vascular access, up to three 0.4 mg doses of nitroglycerin (NTG), and 2 to 4 mg of morphine if NTG fails to relieve his pain and his systolic BP is above 90 mm Hg. Some EMS systems may use fentanyl (Sublimaze) for analgesia. Aspirin, a salicylate, is also given to patients with ACS; however, this patient is allergic to salicylates. Obtain a right-sided 12-lead ECG in patients with signs of inferior wall injury (ST elevation in leads II, III, aVF). Inferior wall infarctions may involve the right ventricle; a right-sided 12-lead ECG will help confirm this. Apply the multi-pads to the patient, not because he is at risk for bradycardia (more common with inferior infarctions), but because he is at risk for cardiac arrest due to V-Fib or pulseless V-Tach.

Supportive care and transport to the hospital. Although the patient's heart rate is slow, he is hemodyamically stable; therefore, pharmacological or electrical intervention aimed at increasing his heart rate is not indicated at this point. Provide supportive care (ie, oxygen as needed, IV set to a KVO/TKO rate) and transport him to the hospital. Consider administering an antiemetic drug, such as ondansetron (Zofran) or promethazine (Phenergan). If his clinical status deteriorates (ie, chest pain, dyspnea, altered mental status, hypotension), atropine sulfate (0.5 mg) or transcutaneous cardiac pacing (TCP) will be necessary. IV fluid boluses are not indicated at this point because there is no evidence of hypovolemia.

A 59-year-old male with a monomorphic wide-complex tachycardia at a rate of 220/min, a blood pressure of 80/50 mm Hg, and a decreased level of consciousness, should be treated with:

Synchronized cardioversion. The patient in this scenario is likely in ventricular tachycardia (V-Tach). Approximately 90% of wide-complex tachycardias are ventricular in origin. Furthermore, he is hypotensive and has a decreased level of consciousness—signs of hemodynamic compromise. To prevent his condition from deteriorating further, immediate synchronized cardioversion, starting with 100 joules, is indicated. Monophasic (or biphasic equivalent) defibrillation is indicated for patients with pulseless V-Tach and ventricular fibrillation (V-Fib). Amiodarone (150 mg over 10 minutes) is indicated for patients with V-Tach who have a pulse, but are hemodynamically stable; it may also be used as an adjunct for patients with unstable V-Tach when cardioversion alone is not effective. Magnesium sulfate (1 to 2 g) is indicated for patients with torsade de pointes—a variant of polymorphic V-Tach.

Right ventricular heart failure will cause a back flow of blood into which system?

Systemic circulation

A PT with hyperkalemia will present with what abnormal ecg findings

T wave

A PT with stroke like symptoms that resolve within 24 hours without per any damage is called

TIA

What sign of early shock is frequently overlooked?

Tachycardia

Signs and symptoms of anaphylaxis

The PT may complain of throat tightness and dyspnea, stridor, and wheezing may be present. The PT may also have erythema(redness) and urticaria(hives) and angioedema

The intubation curved blade is designed to be inserted into what structure?

The Vallecula

What occurs at the beginning of ventricular contraction?

The atrioventricular valves close and the semilunar valves are forced open. As ventricular contraction begins, the atrioventricular valves (tricuspid and mitral) close and the semilunar valves (pulmonic and aortic) are forced open. As a result, blood moves from the right ventricle through the pulmonary arteries and from the left ventricle through the aorta and into the systemic circulation. The majority of ventricular filling occurs by gravity. Atrial kick is the volume of blood that the atria contribute to ventricular filling; this occurs before ventricular contraction. Increased pressure within the myocardium (ie, increased blood volume) causes stretching of the myocardial walls, thus increasing the force of its contraction (Starling effect); this process precedes ventricular contraction.

If the pupils are fixed and dilated there has been an injury to which part of the CNS

The brainstem

Treatment of organophosphate poisoning

The drugs currently used as antidotes include, atropine, pralidoxime chloride and diazepam or lorazepam.

The thermoregulagory center in the brain isn't located where

The hypothalamus

Technique for performing a needle thoracostomy (or needle thoracentesis)

The needle can be inserted anteriorly in the second intercostal space in the midclavicular line just above the rib to avoid the nerve, artery, and vein

The treatment of a partial airway obstruction

The treatment is to monitor the patient and to encourage the patient to forcefully cough.

In which of the following situations is transcutaneous cardiac pacing (TCP) clearly indicated?

Third-degree AV block in a patient with pulmonary edema. Because third-degree AV block (complete heart block)—an inherently slow cardiac dysrhythmia—represents total atrioventricular dissociation, it is associated with hemodynamic compromise in most cases and should be treated with immediate transcutaneous cardiac pacing (TCP). Signs of hemodynamic compromise include ongoing chest pain, pulmonary edema, decreased level of consciousness, shortness of breath, and hypotension. First-degree AV block is typically a benign rhythm and is not commonly associated with hemodynamic compromise. Evidence has shown TCP to be of little or no benefit to patients with PEA or asystole, and it is clearly of no benefit to patients with prolonged asystole.

You should interpret the following cardiac rhythm as:

Third-degree AV block. The rhythm is regular, with a ventricular rate of approximately 40 to 50 beats/min. It has wide (greater than 120 ms [0.12 sec]) QRS complexes and more P waves than QRS complexes. Because there is no relationship between any one P wave to a given QRS complex, this is a third-degree AV block, also called complete heart block. First-degree AV block is characterized by P-R intervals that exceed 200 ms (0.20 seconds [5 small boxes]), although there is a consistent 1:1 P-to-QRS ratio; unless ectopic compexes are present, it is usually a regular rhythm. Second-degree AV block type I is characterized by P-R intervals that progressively lengthen until a P wave is blocked (not followed by a QRS complex); it is an irregular rhythm. Second-degree AV block type II, which may be regular or irregular, is characterized by more P waves than QRS complexes; however, the P-R intervals of the conducted complexes are the same.

How is hepatitis c transmitted?

Through receipt of contaminated blood, most commonly through a needle stick injury

Which of the following ECG lead configurations is correct?

To assess lead II, place the negative lead on the right arm and the positive lead on the left leg. According to the Einthoven triangle, lead I is assessed by placing the negative (white) lead on the right arm and the positive (red) lead on the left arm. Lead II is assessed by placing the negative lead on the right arm and the positive lead on the left leg. Lead III is assessed by placing the negative lead on the left arm and the positive lead on the left leg.

A patient's medication regimen includes fluoxetine, Toprol, Proscar, lansoprazole, and Klonopin. Which of these medications is used to treat cardiovascular disorders?

Toprol. Toprol (metaprolol) is a commonly prescribed beta-blocker used to treat various cardiovascular conditions, including hypertension and tachydysrhythmias. Proscar (finasteride) is used to treat benign prostatic hyperplasia (BPH). Fluoxetine (Prozac) is a selective serotonin reuptake inhibitor (SSRI) antidepressant. It is used to treat conditions such as depression, generalized anxiety disorder, and obsessive-compulsive disorder (OCD). Lansoprazole (Prevacid)—a proton pump inhibitor—is used to treat conditions such as heartburn, acid reflux disease, and ulcers. Clonazepam (Klonopin) is a benzodiazepine sedative-hypnotic; it is used to treat anxiety.

Transport at once, reassess her frequently, and perform synchronized cardioversion if necessary. Although the patient is in supraventricular tachycardia (SVT), she remains stable following your initial efforts to slow her heart rate with vagal maneuvers and adenosine. Her failure to respond to initial treatment does not automatically make her unstable. Simply transport her, closely monitor her en route, and be prepared to cardiovert her if she does become unstable (ie, hypotension, altered mental status, chest pain). Unless specified in your local protocols, pharmacologic therapy beyond adenosine (ie, calcium channel blockers, amiodarone) is typically not indicated in the field for stable patients with SVT, although these medications may be given in the emergency department. However, if your protocols or medical control call for the administration of diltiazem (Cardizem), the initial dose is 0.25 mg/kg.

Transport immediately and monitor her en route. The patient in this scenario is in supraventricular tachycardia (SVT); her heart rate is 170 beats/min and her QRS complexes are narrow (< 0.12 seconds). Despite appropriate treatment for her rhythm (ie, vagal maneuvers, adenosine), her rhythm remains unchanged, although she remains hemodynamically stable. Lightheadedness is common in patients with SVT, but it is not a clinical indicator of hemodynamic instability. A cardiac rhythm of ventricular origin (eg, ventricular tachycardia) is characterized by QRS complexes that are greater than 0.12 seconds in duration; this patient's QRS complexes are 0.08 seconds in duration. If vagal maneuvers and adenosine are unsuccessful in converting her rhythm, transport immediately without further treatment (other than oxygen); her present condition indicates that she is tolerating the cardiac rhythm. However, if signs of hemodynamic instability are noted (ie, hypotension, decreased level of consciousness, chest pain, shortness of breath), perform synchronized cardioversion at 50 to 100 joules without delay.

Treatment of a headache

Treatment in the prehospital setting is mostly supportive however a full history should be obtained and a full neurological exam should be performed. Most headaches can be managed with analgesics

Treatment of a delusional patient

Treatment is aimed at correcting the underlying physical disorder to reduce anxiety. Sedatives may be required to manage the PT.

You should interpret the following cardiac rhythm as:

Type I second-degree AV block. The progressive lengthening of the PR interval until a P wave is blocked (not followed by a QRS complex) makes this cardiac rhythm a type I second-degree AV block, also referred to as "Wenckebach." This type of AV heart block represents a progressive delay at the AV node/junction until an electrical impulse is completely blocked from entering the ventricles. A type II second-degree AV block is characterized by more P waves than QRS complexes; however, the P-R intervals of the conducted complexes are consistent. In complete AV dissociation (ie, third-degree AV block), there are more P waves than QRS complexes, and no relationship exists between a given P wave and QRS complex. A wandering atrial pacemaker is characterized by varying morphologies of P waves.

A PT with hypokalemia will present with what abnormal ecg findings

U wave

Uncontrolled atrial fibrillation. Of the cardiac rhythms listed, atrial fibrillation (A-Fib) is the only one that is irregularly irregular. In fact, A-Fib is never seen as a regular rhythm. At a rate of less than 100 beats/min, A-Fib is said to be controlled. Uncontrolled A-Fib, or A-Fib with a rapid ventricular rate (RVR), occurs when the ventricular rate exceeds 100 beats/min. Second-degree AV block type I has a pattern that is regularly irregular; the P-R interval progressively lengthens until a P wave is blocked. Ventricular tachycardia (V-Tach) and supraventricular tachycardia (SVT) are typically regular rhythms.

Treatment of polymorphic v tach

Unsynchronized shocks(defibrillation) and magnesium sulfate

The first intervention in stable SVT

Vagal maneuvers

When administering epinephrine to a patient in cardiac arrest, the MAIN desired effect is:

Vasoconstriction, which improves coronary and cerebral perfusion. Epinephrine stimulates alpha and beta receptors. However, it is used during cardiac arrest because of its vasopressor effects that result from stimulation of alpha-1 receptors. In conjunction with high-quality CPR, epinephrine's vasoconstrictive effects improve coronary and cerebral perfusion, thus keeping these organs viable until the underlying cardiac dysrhythmia can be terminated.

Which of the following statements regarding the use of vasopressin in cardiac arrest is correct?

Vasopressin can be used to replace the first or second dose of epinephrine. According to the 2010 guidelines for CPR and emergency cardiac care (ECC), vasopressin, in a one-time dose of 40 units, can be given to replace the first OR second dose of epinephrine for adult patients in cardiac arrest. There are no definitive data to support superiority of vasopressin over epinephrine. There are insufficient data to make a recommendation for or against the use of vasopressin in pediatric cardiac arrest.

What RSI drug should be used in the presence of trauma?

Vecuronium, succicoline is contra indicated

Tonsillar herniation

When rising ICP causes portions of the brain to herniate through the foreman magnum

Rhabdomyolysis

When the body will break down muscle tissue and release the byproduct into the bloodstream

Ventilations at a rate of 8 to 10 breaths/min and 1 mg of epinephrine 1:10,000 every 3 to 5 minutes. Pulseless electrical activity (PEA) refers to the presence of an organized cardiac rhythm (except V-Tach), despite the absence of a pulse; it can result from a variety of conditions, such as hypovolemia, overdose, hypothermia, and trauma, among others. Treatment for PEA includes high-quality CPR with minimal interruptions, 1 mg of epinephrine 1:10,000 every 3 to 5 minutes, advanced airway management, and treating potentially reversible causes. A one-time 40-unit dose of vasopressin can be given to replace the first or second dose of epinephrine, but not both. After an advanced airway device is in place, perform asynchronous CPR; the compressor delivers at least 100 compressions/min and the ventilator provides 8 to 10 breaths/min (one breath every 6 to 8 seconds). Do not hyperventilate the patient; doing so may impair venous return to the heart and decrease cardiac output. A ventilation rate of 12 to 20 breaths/min is appropriate for infants and children who are apneic, but have a pulse. An apneic adult with a pulse should be ventilated at a rate of 10 to 12 breaths/min. Dopamine is not indicated for patients in cardiac arrest, and current evidence does not support the use of transcutaneous cardiac pacing (TCP) in patients with PEA or asystole.

Signs and symptoms of Guillian Barr syndrome

Weakness or tingling sensations in the legs that may be spread to the arms and upper legs

claudication

a severe pain in the calf muscle caused by a narrowing of the arteries in this muscle and leading to a painfl limp

Prehospital treatment for pneumonia

airway support, oxygen administration, ventilatory assistance as needed, IV fluids to support B/P, and to thin and loosen mucus, cardiac monitoring and sometimes bronchodilator drugs

conductivity

allows cardiac cells to pass an electrical impulse from one cell to another

excitability

allows cardiac cells to respond to an electrical impulse

dromotropic effect

alters the conduction of electrical signals through the heart

inotropic effect

alters the contractility of the heart muscle

chronotropic effect

alters the heart's rate of contraction

murmur

ambiguous sound indicating turbulent blood flow through the valves

Stroke volume

amount of blood pumped out by either ventricle in a single contraction. Normally 60-100mL but a healthy heart may do significantly more

cardiac output

amount of blood that is pumped out by either ventircles. Normal is ~ 5-6L/min. CO= SV X HR

hypertensive encephalopathy

an acute hypertensive crisis marked by a sudden rise in bp >200/130. Usually determined by MAP

pulsus paradoxus

an excessive drop in the systolic blood pressure with each inspired breath

Signs and symptoms of a CVA

aphasia, confusion or coma, convulsions, incontinence, vision change, headache, dizziness or vertigo and ataxia

Becks triad is associated with ___

cardiac tamponade

benign early repolarization

characterized by ST-elevation or fishhook appearance at the J point and concave ST segment often seen exclusively in left precordial leads; there are never any reciprocal changes

right atrial enlargement

characterized by a colossal P wave in lead 2

Wolff-Parkinson White

characterized by a short PR interval, widened QRS and a delta wave

Prinzmetal angina

chest pain at rest caused by coronary artery vasospasm; more common in women in their 50s.

pulmonary veins

collect oxygen-rich blood and return it to the left atrium

inferior vena cava

collects deoxygenated blood from the lower portion of the body

superior vena cava

collects deoxygenated blood from the upper half of the body

Long QT syndrome

condition characterized by a QT interval exceeding 450ms; indicates the heart is experiencing extra long refractory period making the ventricle more vulnerable to dysrhythmias

hypertrophic cardiomyopathy

conditionin which myocardial walls become very thick. Shortness of breath, chest pain, syncope with exercise. Deep narrow Q waves in inferior and high lateral leads and very tall R waves in left precordial

beta blockers

decrease the rate and strength of cardiac contractions thereby decreasing the hearts demand for oxygen

collateral circulation

develops in response to the early stages of coronary heart disease during which the inside diameter of the coronary arteries begins to narrow as plaque deposits on the walls. This is the formation of additional blood vessels connecting arterioles originating in other blood vessels in order to increase oxygenated blood delivery to the myocardium.

path of deoxygenated blood in the heart

enters the right atrium and is pumped into the right ventricle which pumps it into the pulmonary artery for distribution into the lungs

atherosclerosis

fatty material is deposited along the inner wall of arteries usually at points of turbulent blood flow

The classic triad of meningitis includes

fever, altered mental status, and nucahl rigidity.

sympathetic (adrenergic) nervous system

fight or flight nervous system; increases hr, cardiac muscle contractions and provides other responses to ensure that tissues increased oxygen demands are satisfied with increased CO. Commands are conveyed via norepi

hypokalemic ECG changes

flat or apparently absent d waves with a U wave

Role of sodium in cardiac function

flows into cell to initiate depolarization

role of potassium in cardiac function

flows out of the cell to initiate repolarization

Brugada syndrome

genetic disorder involving the sodium channels in the heart; often unaware of condition until sudden onset. Incomplete RBBB and ST-segment elevation that aggressively returns to baseline

pericardial knock

high-pitched sound during the diastole phase indicating a thickened pericardium limiting ventricular expansion

ejection click

high-pitched sound indicating a dilated pulmonary artery or septal defect

limb leads

leads 1,2, 3, avR, aVL, and aVF

precordial leads

leads V1-V6

atrioventricular node

located in the region of the AV junction; serves as the gatekeeper to the ventricles and in general blood from comes from a branch of the RCA (rarely it can come from the LCX). The impulse is delayed briefly to ensure that the atria can empty into the ventricles. 40 to 60 beats per minute

left atrial enlargement

long P wave with a notched appearance and predominantly negative in lead 1

tunica media

middle layer of elastic fibers and muscle that gives strength and contractility to blood vessels. Much thicker and stronger in arteries compared to veins

diuretics

prescribed to patients with chronic fluid overload; these patients frequently develop cardiac dysrhythmias because of hypokalemia

myocardium

muscular middle layer of the heart between the epicardium and endocardium; composed of specialized cardiac fibers that can spontaneously contract.

hematochezia

passage of fresh, bright red blood from the rectum which is a sign of lower GI bleed

ejection fraction

percentage of blood that leaves the heart each time that it contracts. Normal range is 55-70% but may be lower with damage

diastole

period of time when the atria or ventricles are resting

digitalis preparations

prescribed for the treatment of chronic CHF or rapid atrial dysrhthmias by increasing the strength of cardiac coontractions and slowing AV conduction however at least 30% of patients develop toxicity; these patients are sensitive to calcium preparations

An ECG shows a wide complex rhythm at a rate of 36 beats per minute, what part of the heart is this originating

purkinje fibers

QRS complex

represents the depolarization of the ventricles

PR- interval

represents the time required for an impulse to traverse the atria and AV junction and the amount of time the AV node delays transmission of atrial activity to the ventricles

parasympathetic (cholinergic) nervous system

rest and digest nervous system; uses primarily the vagus nerve. When activated things slow down, when blocked things cant. Uses the release of acetycholine to slow the heartl blocked by atropine.

Sick sinus syndrome

rhythms that involve a poorly function SA node; very common in elderly patients.

low-pressure pump

right side of the heart because it pumps against relatively low resistance of pulmonary circulation

role of calcium in cardiac function

role in depolarization of pacemaker cells and myocardial contractility

Mitral valve (bicuspid)

separates the left atrium from the left ventricle

Aortic semilunar valve

separates the left ventricle from the pulmonary artery

pulmonary semilunar valve (pulmonic)

separates the right ventricle from the pulmonary artery; preventing backflow from the artery into the ventricle.

phlebitis

swelling and pain along the veins that can lead to the formation of blood clots called DVTs

hyperkalemia ECG changes

tall, peaked asymmetric T waves and flattened/absent P waves; more severe cases result in wide QRS complexes

Mallory-Weiss syndrome

tear in the distal esophagus from retching in alcoholism or bulimia

automaticity

the ability of heart muscle to generate its own electrical impulses without nerve stimulation

atrial kick

the amount of blood kicked into the ventricles by the atrium

pacemaker

the area of conduction tissue in which the electrical activity arises at any given time that sets the pace for cardiac contraction

atrial contraction

the contents of each atrium is squeezed into the respective ventricle to complete ventricular filling

P-wave

the depolarization of the atria and the brief pause as conduction is momentarily slowed through thr AV junction

sinoatrial node

the dominant pacemaker in the heart; located in the right atrium near the inlet of the superior vena cava. Receives blood from the right coronary artery; if RCA is occluded this node will become ischemic and may fire slowly or not at all. 60 to 100 beats per minute

ST segment

the end of ventricular depolarization and the beginning of ventricular repolarization

afterload

the force of driving blood out of the heart against the high resistance of systemic arteries

preload

the initial stretching of the cardiac myocytes prior to contraction of the left side of the heart

aorta

the largest artery in the body

high pressure pump

the left side of the heart as it pumps oxygen-rich blood into the left atrium; controlled by preload in order to drive blood out against relatively high resistant systemic arteries

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