Check Your Understanding 16, 18, 19, 20
A patient is diagnosed with cardiogenic shock. The patient is hyperventilating and is therefore at risk for the respiratory complication of respiratory acidosis. T/F?
False. A patient diagnosed with cardiogenic shock who is hyperventilating is at risk for respiratory alkalosis.
High blood pressure increases the workload of the left ventricle, because it increases: A. Afterload B. Preload C. Blood volume D. Stroke volume
A. Afterload Hypertension reflects an elevation in SVR; rising afterload increases myocardial oxygen demand and overall cardiac workload. The workload of the left ventricle does not increase the stroke volume, blood volume, or preload.
Constrictive pericarditis is associated with: A. Impaired cardiac filling B. Cardiac hypertrophy C. Increased cardiac preload D. Elevated myocardial oxygen consumption
A. Impaired cardiac filling Constrictive pericarditis results in a fibrous scarred pericardium that restricts cardiac filling. Chronic pericarditis may be the result of a previous cardiac surgery. Pericarditis is associated with increased workload of the heart because contraction is opposed by the surrounding structures. The constrictive process includes symptoms of exercise intolerance, weakness, and fatigue.
Hypertrophy of the RV is a compensatory response to: A. Pulmonary stenosis B. Aortic regurgitation C. Tricuspid stenosis D. Aortic stenosis
A. Pulmonary stenosis Right ventricular hypertrophy is the direct result of pulmonary disorders that increase pulmonary vascular resistance and impose a high afterload on the right ventricle. Aortic stenosis does not lead to right ventricular hypertrophy. Aortic regurgitation is not associated with right ventricular hypertrophy. Hypertrophy of the right ventricle is not a compensatory response to tricuspid stenosis.
Myocarditis should be suspected in a patient who presents with: A. Acute onset of LV dysfunction. B. Murmur and abnormal valves on echocardiogram. C. Family history of cardiomyopathy. D. Chest pain and ST elevation.
A. Acute onset of LV dysfunction. Acute myocarditis is commonly characterized by left ventricular dysfunction or general dilation of all four heart chambers. Chest pain and ST elevation is indicative of myocardial infarction. Myocarditis is associated with viral infections. Dilated cardiomyopathy runs in families and has a genetic basis.
A patient with significant aortic stenosis is likely to experience: A. Syncope B. Increased pulse pressure C. Peripheral edema D. Hypertension
A. Syncope In the patient with aortic stenosis, syncope and "greying out" episodes may occur when cerebral perfusion is inadequate. Low systolic blood pressure is a common sign of aortic stenosis. Faint pulses are a common sign of aortic stenosis. Peripheral edema is not associated with aortic stenosis.
An elderly patient's BP is measured at 160/98. How would the patient's LV function be affected by this level of BP? A. LV workload is increased with high afterload. B. High BP enhances LV perfusion during systole. C. This is an expected BP in the elderly and has little effect on LV function. D. High-pressure workload leads to LV atrophy.
A. LV workload is increased with high afterload. Activation of the sympathetic nervous system increases the heart rate, contractility, blood pressure, and fluid retention by the kidney. Unfortunately, these compensatory efforts impose a greater workload on the heart. A blood pressure of 160/90 mm Hg is a higher than expected blood pressure in an elderly patient. High blood pressure does not enhance ventricular perfusion. Greater workload on the heart may contribute to further ischemic damage.
Hypotension associated with neurogenic and anaphylactic shock is because of? A. Peripheral pooling of blood B. Poor cardiac contractility C. High afterload D. Hypovolemia
A. Peripheral pooling of blood Profound peripheral vasodilation of both arterioles and veins leads to peripheral pooling of blood and hypotension. Decreased venous return to the heart results in decreased cardiac output and hypotension. Hypovolemia is not the source of the hypotension involved in neurogenic and anaphylactic shock. Cardiac output is generally adequate in neurogenic and anaphylactic shock. Hypotension in neurogenic and anaphylactic shock is not related to high afterload.
Which dysrhythmia is thought to be associated with reentrant mechanisms? A. Preexcitation syndrome tachycardia (Wolf-Parkinson-White syndrome) B. Sinus bradycardia C. Junctional escape D. Second-degree AV block
A. Preexcitation syndrome tachycardia (Wolf-Parkinson-White syndrome) Reentry is a complex process in which a cardiac impulse continues to depolarize in a part of the heart after the main impulse has finished its path and the majority of the fibers have repolarized. Wolff-Parkinson-White syndrome is caused by accessory pathways that originate in the atria, bypass the AV node, and enter a site in the ventricular myocardium. This causes the ventricles to contract prematurely, resulting in a reentrant tachycardia. Second-degree block is a conduction failure between the sinus impulse and its ventricular response. Sinus bradycardia is a slowed impulse generation by the sinus node. A junctional escape rhythm originates in the AV node.
An abnormally wide (more than 0.10 second) QRS complex is a characteristic of: A. Premature ventricular complexes. B. Supraventricular tachycardia. C. Junctional escape rhythm. D. Paroxysmal atrial tachycardia.
A. Premature ventricular complexes. The QRS of the premature complex is prolonged (greater than 0.10 second) and bizarre in appearance. Paroxysmal atrial tachycardia does not display a QRS complex that is greater than 0.10 seconds. Supraventricular tachycardia does not display a wide QRS complex. Escape rhythms may have a P wave that is inverted and located before, during, or after the QRS.
Cardiogenic shock is characterized by: A. Reduced CO. B. Reduced systemic vascular resistance. C. Elevated SvO2. D. Hypovolemia.
A. Reduced CO. Cardiogenic shock occurs primarily as a result of severe dysfunction of the left or right ventricles, or both, that results in inadequate cardiac pumping. The low cardiac output state is associated with a high left ventricular diastolic filling pressure. Cardiogenic shock is not manifested by hypovolemia. Sympathetic activation leads to increases in heart rate, vasoconstriction, and a narrow pulse pressure. Low cardiac output leads to reduced SvO 2.
A patient with a history of myocardial infarction continues to complain of intermittent chest pain brought on by exertion and relieved by rest. The likely cause of this pain is: A. Stable angina. B. Myocardial infarction. C. Unstable angina. D. Coronary vasospasm.
A. Stable angina. Stable angina is the most common form of chest pain and is characterized by pain that is caused under conditions of increased myocardial workload, such as physical exertion or emotional strain. Pain related to myocardial infarction is not relieved by rest. Coronary vasospasm is characterized by unpredictable attacks of angina pain. A patient with unstable angina presents with symptoms similar to myocardial infarction.
Massive release of histamine with consequent vasodilation and hypotension occurs with what type of shock? A. Hypovolemic B. Anaphylactic C. Neurogenic D. Cardiogenic
B. Anaphylactic Exposure to a specific antigen causes receptors on mast cells and basophils to cross-link and activate histamine. The release of histamine along with other vasoactive chemicals produces bronchoconstriction. Cardiogenic shock is not associated with histamine release. Hypovolemic shock is not associated with histamine release. Histamine release does not occur with neurogenic shock.
In which dysrhythmias should treatment be instituted immediately? A. Premature atrial complexes occurring every 20 seconds. B. Atrial fibrillation with a ventricular rate of 220 beats/minute. C. Fever-induced tachycardia at 122 beats/minute. D. Asymptomatic sinus bradycardia at a heart rate of 50 beats/minute.
B. Atrial fibrillation with a ventricular rate of 220 beats/minute. Atrial fibrillation is a completely disorganized and irregular atrial rhythm accompanied by an irregular ventricular rhythm of variable rate. Atrial fibrillation causes the atria to quiver rather than to contract forcefully. This allows blood to become stagnant in the atria and may lead to formation of thrombi. This condition requires resuscitation because of the reduction in cardiac output. The cause of the bradycardia should be investigated, but is not treated emergently when an individual is not exhibiting any symptoms. Fever-induced tachycardia will correct itself once the fever is lowered. Dysrhythmias are treated if they produce significant symptoms or are expected to progress to a more serious level.
Hypotension, distended neck veins, and muffled heart sounds are classic manifestations of: A. Congestive heart failure B. Cardiac tamponade C. Myocardial infarction D. Cardiomyopathy
B. Cardiac tamponade The three classic symptoms of cardiac tamponade are hypotension, distended neck veins, and muffled heart sounds. There are many other manifestations as well. Myocardial infarction is not exhibited by the symptoms described. Classic symptoms of cardiac tamponade are hypotension, distended neck veins, and muffled heart sounds. Symptoms of CHF may include jugular venous distention. Cardiomyopathy is not exhibited by the symptoms described.
A loud pansystolic murmur that radiated to the axilla is most likely a result of: A. Mitral stenosis B. Mitral regurgitation C. Aortic regurgitation D. Aortic stenosis
B. Mitral regurgitation The murmur of mitral regurgitation usually occurs throughout ventricular systole (pansystolic), radiates toward the left axilla, and has a high-pitched blowing character. Aortic insufficiency is characterized by a high-pitched blowing murmur during ventricular diastole. A characteristic murmur of aortic stenosis occurs during ventricular systole and varies in intensity, progressively getting louder and then diminishing (crescendo-decrescendo). The murmur of aortic stenosis generally radiates to the neck. Blood rushing through the narrowed mitral valve during ventricular diastole can sometimes be heard as a low-pitched, rumbling diastolic murmur at the heart's apex.
Beta-blockers are advocated in the management of heart failure because they: A. Increase CO B. Reduce CO C. Reduce blood flow to the kidneys. D. Enhance sodium absorption.
B. Reduce CO Beta-blockers are advocated in the management of heart failure to inhibit the cardiac effects of sympathetic activation. These drugs are negative inotropes and have the potential to reduce cardiac output. The goal with the use of beta-blockers in heart failure is to reduce cardiac output. Beta-blockers do not affect sodium reabsorption. Angiotensin II and aldosterone enhance sodium and water reabsorption by the kidney, contributing to an elevated blood volume.
The majority of tachydysrhythmias are believed to occur because of: A. Enhanced automaticity B. Reentry mechanisms C. Triggered activity D. Defective gap junctions
B. Reentry mechanisms Reentry is thought to be the culprit in most tachydysrhythmias. Reentry is a complex process in which a cardiac impulse continues to depolarize in a part of the heart after the main impulse has finished its path. Triggered activity occurs when an impulse is generated during or just after repolarization. Alterations in automaticity create electrolyte imbalances. Defective gap junctions are not related to tachydysrhythmias.
Pulse pressure is defined as: A. Systolic + Diastolic B. Systolic - Diastolic C. 2/3 Systolic + Diastolic D. Systolic x Systemic Resistance
B. Systolic - Diastolic Pulse pressure is defined as the difference between systolic and diastolic blood pressure. Pulse pressure is the difference between systolic and diastolic pressure. Pulse pressure is not the sum of the systolic and diastolic pressures. Systemic resistance is not involved in determining the pulse pressure.
The progressive stage of hypovolemic shock is characterized by: A. Hypertension B. Tachycardia C. Lactic acidosis D. Cardiac failure
B. Tachycardia In the progressive stage of hypovolemic shock, the patient is anxious and confused, with decreased blood pressure and heart rate greater than 120 beats/minute. In this stage of shock, the blood pressure is decreased. Lactic acidosis does not occur in the progressive stage of hypovolemic shock. Cardiac failure is not likely to occur in the earlier stages of hemorrhagic shock.
A patient is exhibiting severe dyspnea and anxiety. The patient also has bubbly crackles in all lung fields with pink, frothy sputum. This patient is most likely experiencing: A. Cardiomyopathy B. Right-sided heart failure C. Acute cardiogenic pulmonary edema D. A medication reaction
C. Acute cardiogenic pulmonary edema. Acute cardiogenic pulmonary edema is a life-threatening condition requiring immediate treatment. It is associated with left ventricular failure that severely impairs gas exchange, and produces dramatic signs and symptoms including anxiety, severe dyspnea, an upright posture to breathe effectively, and pink frothy sputum. Right-sided heart failure produces systemic venous congestion. Cardiomyopathy is not associated with bubbly crackles and pink frothy sputum. A medication reaction is not the reason for the patient to exhibit severe dyspnea, anxiety, bubbly crackles, and frothy sputum
The majority of cases of anaphylactic shock occur when a sensitized individual comes in contact with: A. Perfumes B. Animal proteins or dander C. Antibiotics D. Incompatible blood products
C. Antibiotics Anaphylactic shock is most frequently associated with antibiotic therapy. Contact with perfumes is not the most frequent cause of anaphylactic shock. Incompatible blood products do not lead to anaphylactic shock. Animal dander may lead to an anaphylactic reaction, but does so less commonly than antibiotics.
In which stage of shock is a patient who has lost 1200 mL of blood, who has normal BP when supine, but who exercises orthostatic hypotension upon standing? A. Class III, Progressive Stage B. Class IV, Refractory Stage C. Class II, Compensated Stage D. Class I, Initial Stage
C. Class II, Compensated Stage In compensated stage hemorrhage (Class II), the blood loss is between 750 and 1500 mL. Blood pressure remains normal when the patient is supine but decreases upon standing. In initial stage hemorrhage (Class I) blood loss is up to 750 mL, and the patient's vital signs remain normal. Class III hemorrhage (progressive stage) is blood loss of 1500 and 2000 mL. Vital signs are changing. Severe Class IV hemorrhage (refractory stage) occurs when more than 2000 mL is lost. The patient is lethargic, with severe hypotension.
Angiotensin-converting enzyme (ACE) inhibitors block the: A. Effect of aldosterone on the kidney. B. Conversion of angiotensinogen to angiotensin I. C. Conversion of angiotensin I to angiotensin II. D. Release of renin.
C. Conversion of angiotensin I to angiotensin II. Angiotensin I is converted into angiotensin II while it is circulating through the pulmonary vessels, by the angiotensin-converting enzyme. ACE inhibitors block the conversion of angiotension I to angiotension II. Renin plays a role in the regulation of arterial blood pressure. ACE inhibitors do not block the conversion of angiotensinogen to angiotensin or the effect of aldosterone on the kidney.
Administration of a vasodilator to a patient in shock would be expected to: A. Decrease vascular resistance B. Increase tissue perfusion C. Decrease left ventricular afterload D. Increase contractility
C. Decrease left ventricular afterload Vasodilators are used to decrease the workload of the heart by decreasing left ventricular afterload. Nitroprusside and nitroglycerin are examples of vasodilators. Dobutamine is used to decrease vascular resistance. Positive inotropic drugs are used to increase contractility. Positive inotropes include β-adrenergic agonists, which have the ability to increase tissue perfusion.
The therapy that most directly improves cardiac contractility in a patient with systolic heart failure is: A. Preload reduction B. Afterload reduction C. Digitalis D. Beta-antagonist agents
C. Digitalis Digitalis may be used for symptom management of heart failure. Cardiac glycosides directly inhibit the sodium-potassium pump present in the cell membrane of all cells. The intracellular changes allow more calcium to remain in the cell, thus strengthening myocardial contraction. Contractility is not improved through afterload reduction. Beta-blockers inhibit the effects of sympathetic activation and have the potential to reduce cardiac output. Preload reduction is not the therapy of choice in improving cardiac contractility.
Critically ill patients may have parenterally administered vasoactive drugs that are adjusted according to their ___________ pressure. A. Pulse B. Diastolic C. Mean arterial D. Systolic
C. Mean arterial The mean arterial pressure is used to make incremental adjustments to vasoactive drugs. The MAP is the calculated average pressure within the circulatory system throughout the cardiac cycle. The systolic pressure is a part of the calculation but is not the data element used in adjustment of vasoactive medications. The diastolic reading is involved in calculating the MAP, but is not the number used in titration of vasoactive medications. The pulse pressure is the difference between the systolic and diastolic pressure.
Atherosclerotic plaque with large lipid cored are prone to: A. Dislodgement B. Binding C. Rupture D. Attachment
C. Rupture In compensated stage hemorrhage (Class II), the blood loss is between 750 and 1500 mL. Blood pressure remains normal when the patient is supine but decreases upon standing. In initial stage hemorrhage (Class I) blood loss is up to 750 mL, and the patient's vital signs remain normal. Class III hemorrhage (progressive stage) is blood loss of 1500 and 2000 mL. Vital signs are changing. Severe Class IV hemorrhage (refractory stage) occurs when more than 2000 mL is lost. The patient is lethargic, with severe hypotension.
The effect of nitric oxide on systemic arterioles is: A. Opposed by nitrate drugs. B. Vasoconstriction C. Vasodilation D. Not significant
C. Vasodilation Nitric oxide causes vasodilation in the systemic arterioles. Vasoconstriction is not associated with nitric oxide. There is a significant effect on the systemic arterioles related to nitric oxide. The effects of nitric oxide are not known to be opposed by nitrate drugs.
An example of acyanotic heart defect is: A. Tetraology of Fallot. B. All right-to-left shunt defects. C. Ventricular septal defect. D. Transposition of the great arteries.
C. Ventricular septal defect. An example of an acyanotic heart defect is a ventricular septal defect. In this condition, blood from the left ventricle leaks into the right ventricle because of a defect in the ventricular wall. This leakage causes extra pressure in the right ventricle resulting in pulmonary hypertension. Tetralogy of Fallot is a cyanotic congenital defect. Transposition of the great vessels is a cyanotic congenital defect. The category of cyanotic congenital defects refers to those that are right-to-left shunts.
Tachycardia is an early sign of low cardiac output that occurs because of: A. Anxiety B. Tissue hypoxia C. Acidosis D. Baroreceptor activity
D. Baroreceptor activity A number of compensatory responses are set in motion to restore tissue perfusion and oxygenation in the early stage of shock. Baroreceptors located in the aorta and carotid arteries quickly sense the decrease in pressure and transmit signals to the vasomotor center in the brainstem medulla. The sympathetic nervous system stimulates β1 receptors, which respond by increasing the heart rate in an attempt to increase cardiac output. Tachycardia is not caused initially by tissue hypoxia. An early sign of low cardiac output is not anxiety. Tachycardia does not occur because of acidosis.
Patients with structural evidence of heart failure who exhibit no signs or symptoms are classified into which NY Heart Association heart failure class? A. Class IV B. Class III C. Class II D. Class I
D. Class I Patients who have structural heart disease but no signs or symptoms of heart failure are placed in Class I of the NYHA Classes. Class II patients have current or previous symptoms of heart failure. Class III patients have current or previous symptoms of heart failure, such as dyspnea or fatigue. Class IV patients have advanced structural heart disease and marked symptoms at rest.
A patient presents to the emergency department with a diastolic BP of 132 mmHg, retinopathy, and symptoms of ischemic stroke. This symptomology is likely the result of: A. Myocardial infarction B. Arthrosclerosis C. Angina D. Hypertensive crisis
D. Hypertensive crisis Hypertensive crisis is characterized by a diastolic blood pressure of greater than 120 mm Hg, and symptoms of end-organ damage such as retinopathy and ischemic stroke. Blood pressure is not an indication of arthrosclerosis. Angina may accompany hypertensive crisis, but the question stem relates directly to hypertensive crisis. The patient may be having a myocardial infarction, but the addition of end-organ damage symptoms points to hypertensive crisis.
Tumor necrosis factor alpha and interleukin-1 contribute to shock states because they induce production of: A. Catecholamines B. Clotting factors C. Vasopression D. Nitric oxide
D. Nitric oxide In septic shock, tumor necrosis factor-α, interleukin-1, and other inflammatory mediators induce vascular cells to produce excessive amounts of the vasodilator nitric oxide. Catecholamines are not produced by TNF-α and IL-1. The production of clotting factors is not induced by tumor necrosis factor-α and interleukin-1. Vasopressin production is not induced by TNF-α and IL-1.
An erroneously low BP measurement may be caused by: A. Positioning the arm at heart level. B. Measuring the BP after exercise. C. Using a cuff that is too small. D. Positioning the arm above the heart level.
D. Positioning the arm above the heart level. An erroneous blood pressure result could occur with the arm above the level of the heart. It is important to measure blood pressure with the appropriate size cuff. The arm should be positioned at the level of the heart for a more accurate reading. Measuring pressure after exercise yields a higher measurement.
Left-sided heart failure is characterized by: A. Peripheral edema. B. Jugular vein distention. C. Decreased systemic vascular resistance. D. Pulmonary congestion.
D. Pulmonary congestion Left-sided heart failure is characterized by pulmonary congestion and edema. Right-sided heart failure is characterized by congestion in the systemic venous system that increases systemic vascular resistance. Jugular vein distention is a classic sign of right-sided heart failure. Peripheral edema is seen in right-sided failure.
A lab test that should be routinely monitored in patients receiving digitalis therapy is: A. Serum calcium b. Serum sodium C. Albumin level D. Serum potassium
D. Serum potassium Digitalis slows the heart rate through parasympathetic system activation and promotes sodium and water excretion through improved cardiac output to the kidney. Depletion of serum potassium (hypokalemia) may potentiate digitalis toxicity. Sodium and water excretion is activated through the parasympathetic system because of improved cardiac output to the kidneys. Albumin level is not affected by digitalis. Digitalis allows more calcium to remain in the cell through a slowing of the sodium-dependent calcium pump.
Restriction of which electrolytes is recommended in the management of high BP? A. Calcium B. Magnesium C. Potassium D. Sodium
D. Sodium The balance of the intake of water and sodium with their excretion by the kidney remains the central feature of long-term blood pressure maintenance. Sodium is not rapidly eliminated by the kidney like water and adds to the body's fluid volume. It is not necessary to restrict the intake of calcium when managing high blood pressure. Potassium does not need to be restricted in the management of high blood pressure. Magnesium does not play a role in the management of high blood pressure.
A patient who reports dizziness and who has absent P waves, wide QRS complexes, and a heart rate of 38 bpm on an ECG is most likely associated with which rhythm? A. Junctional tachycardia B. Sinus bradycardia C. Third-degree heart block D. Ventricular escape rhythm
D. Ventricular escape rhythm A ventricular escape rhythm originates in the Purkinje fibers, has a rate of 15 to 40 beats/minute, and is characterized by a wide QRS complex. An important clue to identifying escape rhythms is the absence of normal P waves and PR intervals. The rhythm involved in third-degree heart block includes regularly occurring P waves. Junctional tachycardia has a heart rate between 70 and 140 beats/minute. P waves are preceding, following, or buried in the QRS complex. Sinus bradycardia has a normal pattern on the ECG, but with a rate of less than 60 beats/minute.
Lactated Ringer solution and normal saline are commonly used crystalloid solutions that contain electrolytes. T/F?
True. Lactated Ringer solution and normal saline are commonly used crystalloid solutions that contain electrolytes.
