Dysrhythmia and CV

S26: know the max joules used for cardioversion vs defib. Know which is elective vs emergency, and that the patient in cardioversion is awake, with some sedation, like used for GI diagnostic procedures (review these

, elective cardioversion is the priority intervention when the client is awake and responsive. cardioversion: elective procedure, client is awake and sedated, sycronizes QRS, 50-200 joules, EKG moniture, constant form defib: emergency, vfib/ vtach, no cardiac output, begin with 200 j up to 360 joules, client uncounscious, EKG monituring

1. Know that electrical depolarization in heart happens before the physical/mechanical events in the heart (example: SA node fires and impulse spreads through the atria to the AV node before the atria contract).

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1. MUST KNOW: It is your heart beating that generates the arterial pulse...if no heartbeat, then no pulse, AND therefore no HR. A patient in PEA, for example, has no palpable pulse and therefore no measurable HR.

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1. Reading rhythms and intervening (if appropriate): there will be 4 rhythms on the test (with 2-3 questions for each), where I will show you a rhythm and ask you to identify/name it AND how you need to respond to it - rhythms I will use will be normal sinus rhythm, sinus bradycardia, sinus tachycardia, Atrial fibrillation, Atrial Flutter, Torsades, Ventricular tachycardia, Ventricular fibrillation, Asystole, and PEA - know that for PEA, it LOOKS like a patient has a rhythm BUT they have no pulse when you assess them

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1. S19: be able to recognize Afib vs Aflutter EKG - note the similar s/s in table

Afib: rapid pulse, irregular pulse, dizzy/fainting, palpation, SOB, weakness, chest pain/ tingling, increase chance of blood clot. Aflutter: rapid pulse, can be regular or irregular pulse, dizzy/fainting, palpation, SOB, weakness, chest pain/ tingling, increase chance of blood clot.

1. S135: We have a patient come in with to hospital with a suspected acute cardiac event (let's say MI), we have some labs we get right away to assess cardiac muscle damage and risk factors. Re-read all the lab descriptions on left but I want you to know what are considered elevated lab numbers for Troponin and BNP and what each signifies (in purple table)

BNP > 100 suggests heart failure Troponin > 0.03 suggest myocardial ischemia •Lipid panel (discussed earlier in this ppt) •Cardiac Enzymes (table to the right; Troponin is released by cardiac cells in response to right ventricle damage - most specific cardiac marker for cardiac tissue damage) •Creatine kinase is an isoenzyme that is found in the skeletal muscles, the heart, and the brain. The isoenzyme specific to heart is CK-MB, which can accurately detect tissue necrosis or injury within a few hours of onset. One of the earliest markers of an MI is myoglobin, which begins to rise within 2 hours of injury. However, it is not specific to heart tissues and has limited diagnostic usefulness •B-type Natriuretic Peptide (BNP): released by cardiac muscles in response to elevated pressures in the heart - see effects on the body next slide

1. S128: know the prototype cardiac glycoside and 4 BPs under it. Know Metoprolol is a BB approved for CHF. Know the 2 vasodilators and the point in red about right-sided HF. Know the phosphodiesterase inhibitor Milrinone (watch out - it can cause dysrhythmias)

Cardiac Glycosides: Increase cardiac output by increasing the force of myocardial contraction and slowing heart rate •(prototype: Digoxin); positive inotropic effect •Electrolyte imbalances can change how the body absorbs Digoxin: low K+, low Mg+ and High Ca+ are particularly concerning •Improves symptoms, but no impact on morbidity and mortality •Margin of safety for Digoxin is narrow - N/V/D are EARLY signs of toxicity and should be reported to MD •Adrenergic Blockers: Decrease cardiac workload by slowing heart rate (Beta 1) and decreasing blood pressure (Alpha-1) Only 2 adrenergic blockers approved for CHF treatment: Metoprolol •Vasodilators: Decrease cardiac workload by dilating vessels directly and reducing preload and afterload •Isosorbide dinitrate (Isordil) and Hydralazine (Apresoline) are 2 examples •HOWEVER, decreasing preload CAN make right-sided CHF worse so for these patients, vasodilators not the best option •Phosphodiesterase Inhibitors: Increase cardiac output by increasing the force of myocardial contraction (positive inotropic effect) and cause vasodilation •Milrinone (Primacor) •Adverse effect of dysrhythmias (may occur in 1 of every 10 patients taking the drug) •medication is usually infused over 48-72 hours in a hospital setting; however, home infusion through a central line is becoming more common as a palliative measure for end-stage heart failure

1. S89: know this slide - INCREDIBLY important for understanding why we can't just give these 2 patient populations (in red) unrestricted PO or IV fluids and ways to assess for hypervolemia (KNOW that detail about weights...comes up on the NCLEX as the best way to assess for hypervolemia)

Careful with your CHF and Renal Failure Patients...We HAVE to monitor their I/O because... •Congestive Heart Failure — structural heart disease and the pump that is the heart is not moving blood effectively à hypoperfusion to organs à kidneys respond by retaining more sodium and water...VICIOUS CYCLE because retaining more fluid (hypervolemia) makes the problem of the failing heart even worse •Renal Failure or Chronic Kidney Disease - as urine output declines, patient cannot eliminate excess fluid à HYPERVOLEMIA •Best way to assess for hypervolemia is to trend weights (daily weights)...other s/s of fluid overload: pitting or dependent edema, AMS, seizures, hyponatremia (dilutional), pulmonary edema, increased BP, jugular vein distension

1. S96: know lifestyle modifications for people with HTN (intervention and comments columns of table); Also know the recommendation about smoking and stress at the bottom; what is the DASH diet?

DASH DIET includes: more fruits, vegetables, whole grains, and low-fat dairy. Also recommends reducing intake of added sugars, avoiding saturated fats, refined grains, and sodium weight loss, excerize, low salt, less alch, stop smoking

1. S20: what is ectopy (simply) - images are cardiac monitor devices (cardiologist might have patient wear this for a few weeks or a month and it is continuous recording of cardiac rhythm to assess for rhythm abnormalities). On S21, know common causes of ectopy in red.

Ectopy... abnormal beats in an otherwise sinus rhythm •PVC happens when the beat is initiated by the Purkinje fibers of the ventricles instead of the sinoatrial node. Big, exaggerated QRS complex •PAC happens when a different region of the atria (before the SA node) depolarizes - p-wave comes early Factors that can cause/contribute to PACs and PVCs: •Stress •Acute Illness •Fever •Exercise-induce •HTN and underlying heart disease •Alcohol consumption •Tobacco use •Caffeine •Illicit Drugs •Males > Females •Electrolyte imbalances •Hypercalcemia •Hypomagnesemia •Hypokalemia

1. S30: When someone experiences a cardiac arrest (no heartbeat), while we are performing interventions (we consider the "H's and T's" - a list of possible causes. From tables, know the first column labeled "causes"

T of ACLS causes: cardiac tamponad, toxins, tension pneomothorax, pulmonary thrombosis, coronary thrombosis H of ACLS causes: hypovolemia, hypoxia/ hypoxemia, aciodsis (exess hydrogen ions), hypoklemia/hyperkalmeia, hypothermia

1. S86: I don't need you to have these EXACT number memorized, BUT know which chambers and major vessels have higher and lower pressures in the heart.

High: RV, LV, Pa, aorta low: RA, LA

slide 43 treating MI in hospitial

In-hospital interventions can consist of: •Thrombolytics, such as tissue plasminogen activator (tPA): Medical means of busting up the coronary artery blockage •Need to establish the exact time of onset of chest pain to be able to give thrombolytic therapy because the medicine is ideally given within 6 hours of a coronary event. Concurrent use of anticoagulants such as warfarin is a relative contraindication for thrombolytic therapy. •Heparin infusion: Preventing clot from getting larger...REMEMBER from HEMATOLOGY, there is some fibrin in an arterial clot so you CAN use Heparin in arterial clots, which disrupts fibrin formation •Morphine sulfate to alleviate CP unrelieved by Nitro •The initial dose of morphine of 2 to 4 mg as an IV push can be given, with increments of 2 to 4 mg repeated every 5 to 10 minutes until the pain is relieved - STOP giving if patient is no longer tolerating - hypotension or depressed respiration •Try to prevent patient from straining the heart - anti-emetics to avoid vomiting and stool softeners •If patient is experiencing a STEMI (ST-elevation MI) you want to minimize time to reperfusion (percutaneous coronary intervention [PCI]). Ideally, reperfusion occurs 20-30 minutes after patient arrives at the hospital (known as "time to balloon") •Patients receiving contrast dye and on METFORMIN (medication that lowers blood sugar): Don't give Metformin 24 hrs prior to and for 48hrs after a patient received contrast dye - risk for lactic acidosis

1. S127: know drugs used treat CHF in blue. Also know the red font under "diuretics"

Increase cardiac output by lowering BP and decreasing fluid volume: •ACE-I: demonstrated to slow progression of CHF and reduce mortality •Unless specifically contraindicated, all patients with CHF and many of those at high risk should be on an ACE-I •ARBs Increase cardiac output by reducing fluid volume and decreasing blood pressure •Diuretics •Not prescribed alone for CHF treatment - usually combined with ACE-I or ARB •Helps to reduce peripheral edema and pulmonary congestion •Only prescribed when there is evidence of fluid retention •Patient teaching - Call your doctor right away (or go to urgent care) if any of the following occur: •A shortness of breath that doesn't go away with rest or is becoming progressively worse •Weight gain of 2 to 3 pounds in a day or 5 pounds in 1 week •Swelling of ankles or feet becomes worse, even after elevation and rest

1. S16: two images on right show you what each box of EKG grid represents (number of seconds) and the normal ranges for the different intervals/complexes. Know PR, QRS, and QT lengths

PR: .12-.20 sec QRS: under .10 sec QT: under .40

1. S46: know that if there is multi-vessel disease of MANY coronary arteries, PCI might not be possible and we may need CABG instead (PCI = percutaneous coronary intervention). See S46 so you know basics of CABG

Multi-vessel disease may require more extreme interventions than Cardiac Catheterization - Coronary Artery Bypass Graft (CABG)

1. S37: know how to recognize STEMI vs NSTEMI on EKG; S38 and S39 shows the type of EKG/ECG we get if trying to assess a dysrhythmia, STEMI, NSTEMI - 12-lead EKG/ECG - shows us electrical activity of the heart from multiple views and injury to certain views (aka leads) corresponds to locations on the heart. Don't have to know 12-lead interpretation in this detail for the test, but just take a look on S39

NSTEMI: T waves depression, or looks like no Q wave STEMI: ST segment elevated, "Q wave myocardialinfaction" We use 12-lead EKG to be able to make statements about what part of the heart is being damaged in a STEMI or NSTEMI look at 39

1. S12: what does a P-wave represent (what is happening in heart?), QRS complex? T-wave?

P: artrial depolorization initaited by SA node, causes p wave depolorization delay AV node QRS: ventricular depoloraization begins at apex causes the QRS, artiral repolorization occurs ventricular depolorization is complete T: ventricular repolorization begins at the apex causing t wave ventricular repolorization is complete

1. S42: For treating the MI, Know font in green, red, and blue

Priority Interventions prior to heart surgery or cardiac catheterization: •Intravenous access (2 large bore IVs, 18 gauge), supplemental oxygen if one of the following conditions is present: •indicated only for patients who are breathless, hypoxic (oxygen saturation <90%), who present with heart failure •Immediate administration of Aspirin in ambulance (at least 162-325 mg) •Antiplatelet - trying to prevent clot from getting bigger •Nitroglycerin for active chest pain, given sublingually or by spray •Potent venous vasodilator that reduces cardiac preload and therefore cardiac workload •We give 0.4mg sublingually or spray. Should work in 1 -5 minutes. Can give up to 3 doses, 5 minutes part, so if CP is not relieved after one, given another tablet (continue monitoring BP). Extended-release tablets are used daily to prevent angina. Must store in light-proof containers (light degrades medication) •If CP persists, once patient is in-hospital, then we can start an infusion of nitroglycerin: 5 to 10 mcg/min and gradually increased until relief of chest pain is achieved (maximum dose of 200 mcg/min) •IF Chest Pain is UNRELIEVED by Nitroglycerin, we try Morphine •Main side effects with Nitroglycerin are hemodynamic - hypotension most commonly....SO, KEEP CHECKING BP FREQUENTLY BECAUSE YOU DON'T WANT TO CONTINUE GIVING IF SBP < 90 mm Hg •Patient may c/o headache with Nitroglycerin administration r/t dilation of vessels in the brain •Telemetry and pre-hospital electrocardiography (ECG), if available... In hospital, this is a PRIORITY - if patient experiencing chest pain, then get ECG STAT...EMS will have done an ECG in the field if patient reported CP

1. S10: look at this slide so you know where the electrical structures from S7 and S9 are located

SAN top of right atrium AVN bottom of right atrium bundle branch in the septum PF apex

1. Know treatment on S76 (know drugs in blue and font in red).

Treatment: •Medication is ineffective for curing atherosclerosis, since the damage has already been done •Antiplatelet drugs (e.g., clopidogrel, aspirin) have been used to try to minimize risk of complete occlusion of artery and/or embolus formation •Vasodilator drugs (e.g., Nitroglycerin) are helpful in providing symptom relief for chest pain, but are of no curative value •Balloon angioplasty can open up narrowed vessels and promote improved blood supply •The blood supply to the heart can also be restored by coronary artery bypass surgery

1. S133: know this slide that is a good summary of CHF management goals and tests/diagnostics to assess

Ways to help relieve symptoms and complications associated with CHF...act FAST Fluids - decrease Afterload/Preload - decrease Sodium - decrease Tests to diagnose/assess - echocardiogram ("echo"), EKG, BNP, CXR, Potassium level (if receiving diuretics you need to especially monitor K+ and other electrolytes because these patients are losing electrolytes as they diurese) ØEchocardiogram (ultrasound of the heart, shows us size, wall movement, ejection fraction [% of end diastolic blood volume that the heart pumps out with each beat...50-65% is normal, anything less could be CHF) ØCXR - Chest X-Ray to look for enlarged/hypertrophied heart (aka cardiomegaly) and pulmonary edema ØBNP (B-type natriuretic peptide: is a hormone secreted by cardiac cells in the heart ventricles in response to stretching caused by increased ventricular blood volume). BNP normally less than 100; 100-500 = CHF may be present; >500 then CHF is likely ØEKG/ECG, you already know what this is from dysrhythmias...we should evaluate CHF patients because they are prone to dysrhythmias like A fib

S75: know what can be the end result of plaque formation in artery ("clinical phase" section in red

annurysum/ ruptur occulsion stenosis

S123: know s/s of CHF à when you look at this table, recall that the pulmonary congestion signs and symptoms are going to be seen more so in LEFT-SIDED HF and the venous congestion in RIGHT-SIDED HF...this should make total sense to you sense the blood will be backing up into whatever location it JUST CAME FROM (right ventricle à blood was draining from the head, upper and lower body, including organs

impaired heart contractablity: tachycardia, pale/cool, weak pulse, decrease b/p, weakness, decrease urin output, loss of appetite pulmonary congerstion: dyspeneea, tachycardia, orthopnea systmic venos congestion: heptomegly, edema, jvd, gain weight, ascites

S82: shows common aneurysm locations referred to on S81. Know these locations and be able to identify if you had a picture. (Circle of Willis is the area of cerebral blood vessels on S82, upper left). Abdominal aortic aneurysm is BELOW the renal arteries/below kidneys

look

1. S22: be able to identify these rhythms on the test - Melissa will label each in class

look at it

1. S29: Additional rhythms for you to know for Exam (be able to recognize/label/name)

look at it

1. S136: when you heart releases BNP in response to elevated pressures in the heart (often from hypervolemia), what does BNP do in the body to help decrease the pressure and fluid overload (in image in upper right)

pressure vol overload ------->BNP: vasodialtes, inhibits SAS (in brain), kidney (inhibits RAAS and )diureses,

1. S13: QT prolongation (first saw with macrolides) but this comes up A LOT in pharmacotherapy because lots of drugs cause QT prolongation - VERY concerning when we have the same patient take multiple QT-prolonging medications (can cause Torsades; discussed later in ppt). Be able to identify QT prolongation.

the t hump is long

1. S107: know the ACE-inhibitor prototype and the red font about it

•ACE Inhibitors block the formation of Angiotensin II and decreases blood pressure by decreasing peripheral vascular resistance and blood volume •ACE Inhibitor adverse effects can include: •Persistent dry cough (related to bradykinin accumulation)... LET MD KNOW BECAUSE Bradykinin buildup could start with a cough and progress to angioedema •Angioedema (swelling in face, eyes, throat, lips, tongue - related to bradykinin). Can be serious and cause a compromised airway. Usually occurs within hours of receiving the first dose, but has been reported months or even years after being on the medication •First-dose hypotension ... gets better with repeated doses •Neutropenia (decrease in white blood cells with increased risk of infection) •Rash and metallic taste in mouth •Hyperkalemia •Contraindicated for pregnant women (fetal renal damage) and people with renal artery stenosis •Prototype is Enalapril (Vasotec)

1. S112: You know Clonidine and Doxazosin and Prazosin from Exam 3 (the Adrenergic section) à remember these drugs classes and that we can use to treat HTN and the fact that Clonidine can have a sedating effect

•Alpha 1 receptors in the arterioles are responsible for vasoconstriction, so blocking these receptors results in vasodilation •Alpha-1 adrenergic antagonists are not a first-line therapy for HTN because, unlike diuretics, shown to be less effective at reducing the risk of serious cardiovascular events than diuretics •Doxazosin (Cardura) is prototype drug •Alpha-2 adrenergic agonists are concentrated in the CNS and activating these receptors reduces sympathetic outflow to the rest of the body (reduces release of Norepinephrine), so reduces HR, contractility, BP (dilates arterioles) •Can have CNS adverse effects such as sedation, depression, headache, dizziness, dry mouth. Less commonly anemia, leukopenia, and thrombocytopenia •Clonidine (Catapres) is prototype

1. S93: know what angiotensin II does in the body to increase blood pressure, AND if we block angiotensin II receptors or prevent its formation with DRUGS, we can get BP to go DOWN in those with HTN

•Angiotensin II has a variety of effects on the body: •Throughout the body, it is a vasoconstrictor of arterioles •Angiotensin II also stimulates the secretion of the hormone Aldosterone from the Adrenal Cortex (Adrenals are glands that sit on top of kidneys). Aldosterone causes cells in the kidneys to increase their reabsorption of sodium back into the blood, while at the same time causing these cells to excrete potassium ions that leave the body dissolved into urine •Stimulates release of Antidiuretic Hormone (ADH), also called vasopressin (came up in Sepsis and Hematology). ADH is made in the hypothalamus and released from the posterior pituitary gland in the brain. As its name suggests, it causes vasoconstriction, but it also stimulates reabsorption of water in the kidneys. •ADH also acts on the central nervous system to increase an individual's appetite for salt, and to stimulate the sensation of thirst

1. S108: know the ARB prototype drug and the red font - there is some overlap with ACE-I (angioedema less of a risk but still a risk, hyperkalemia, not for pregnant people)

•Angiotensin II receptor blockers (ARBs) - these drugs involve blocking the action of angiotensin II after it has formed. Blocks receptors on the arteriole smooth muscles and in the adrenal gland (where aldosterone is made), ultimately causing blood pressure to fall •Potential adverse effects: Angioedema (occurs less than with ACE inhibitors, but still a potential risk); Headache, dizziness, hypotension, insomnia, hyperkalemia •Not to be taken if pregnant •Prototype is Losartan (Cozaar) •Direct Renin Inhibitors prevent the formation of Angiotensin I •Aliskiren (Tekturna) is prototype •Common adverse effect hyperkalemia, cough, angioedema, abdominal pain, diarrhea, cough, flulike symptoms, and rash •Not to be used in combination with ACE-I or with patients who have chronic kidney disease; not to be taken if pregnant (fetal harm)

1. S55: know last 3 BPs about antidysrhythmic problems

•Antidysrhythmic drugs have the potential to correct dysrhythmias but also to worsen or even create new dysrhythmias •Also, many Antidysrhythmics cause hypotension and bradycardia as adverse effects, which can present as dizziness, faintness, fatigue •Prodysrhythmic effects have resulted in less use of drugs in class I and increased use of drugs in classes II and III (specifically, use of amiodarone has increased)

1. S94: know potential consequences of HTN in red

•Asymptomatic for many people •However, four target areas most often affected by prolonged or improperly controlled HTN: heart, brain, kidneys, retina •One of the most serious consequences is that the heart must work harder to pump blood to organs and tissues. Excessive cardiac workload can cause the heart to fail, and the lungs to fill with fluid (left-sided heart failure) and for fluid to accumulate in tissues and organs (right-sided heart failure) •High pressure in the system also damages blood vessels that supply blood and oxygen to the brain, which can result in cerebral vascular accidents (stroke) •Chronic HTN damages the arteries in the kidneys, leading to progressive loss of renal function •Vessels in the retina can rupture or become blocked, resulting in impaired vision and/or blindness

1. Read S50-S54. Talks about the ions involved in generating cardiac action potentials (aka electrical impulses = depolarization). While I have ALWAYS stressed K+ in cardiac function - Na+ and Ca+ also play a role.

•Because most antidysrhythmic drugs act by interfering with myocardial action potentials, we will consider action potential before we move on to the specific drugs •Action potentials occur in both neurons and cardiac muscle cells due to differences in concentrations of certain ions found inside and outside of the cell •Under resting conditions, sodium (Na+) and calcium (Ca2+) are found in higher concentrations outside myocardial cells, and potassium ions (K+) are found in higher concentration inside these cells •These imbalances are responsible for the slight negative charge inside a myocardial cell membrane relative to the outside of the membrane •A cell having this negative membrane potential is called polarized •An action potential begins when sodium ion channels located in the plasma membrane open and Na+ rushes into the cell, producing a rapid depolarization, or loss of membrane potential (inside of cell suddenly become more positive relative to outside of cell) •During this period, Ca2+ also enters the cell through calcium ion channels, although the influx is slower than that of sodium •The entry of calcium into the cell also signals the release of additional intracellular calcium that is held in storage inside the sarcoplasmic reticulum - it is this large increase in intracellular Ca2+ that is responsible for the contraction of cardiac muscle •Trace amounts of K+ moving out of the cell during depolarization antidyrythmic drug •Blocking potassium, sodium, and calcium ion channels is the primary pharmacologic strategy used to prevent or terminate dysrhythmias •Pumping action of heart requires alternating periods of contraction and relaxation. There is a brief period following depolarization, and most of repolarization, during which the cell cannot initiate another action potential. This time is called the refractory period, and it ensures that myocardial cells finishing contracting before a second action potential begins •Some antidysrhythmic drugs produce there effects by prolonging the refractory period

1. S56: know last 3 BPs about Lidocaine

•Because the action potential in the heart is dependent on the opening of sodium ion channels, a blockade of these channels will prevent depolarization - the spread of the action potential across the myocardium will slow, and dysrhythmias will be suppressed •The reduced heart rate caused by these drugs can cause hypotension, dizziness, and syncope. Some class I drugs also have significant anticholinergic effects such as dry mouth, constipation, and urinary retention •Prototype: Lidocaine (Class IB Antidysrhythmic: Sodium Channel Blocker) - used in ventricular dysrhythmias. Monitor blood pressure and cardiac monitor during therapy with lidocaine. Assess neurological and respiratory status frequently for signs of toxicity. (early toxicity s/s) agitation, confusion (late toxicity s/s) seizures, coma, respiratory arrest

1. S58: know the 2nd and 4th BP about Amiodarone = We LOVE giving this for dysrhythmias because works on BOTH ventricular and atrial dysrhythmias

•Beta Blockers are used as antidysrhythmics to treat atrial dysrhythmias associated with CHF. In post-MI patients, Beta Blockers decrease the likelihood of sudden death due to their antidysrhythmic effects •Prototype: Metoprolol (Class II Antidysrhythmic: Beta Blockers) •NOTE: Beta Blockers also lower heart rate (working on Beta 1 receptors in the heart) and treat hypertension •Avoid giving to people with airway diseases such as COPD and asthma because these drugs cause bronchoconstriction; assess for bradycardia and hypotension; assess for hypoglycemia in patients with DM because BBs mask s/s of hypoglycemia

1. S5: what are the differences in brady vs tachydysrhythmias and potential consequences (in red)

•Bradydysrhythmias occur when the HR is less than 60 bpm. The patient may tolerate this dysrhythmia if the blood pressure is adequate. If not, the bradydysrhythmia may lead to myocardial ischemia or infarction, hypotension, or heart failure. •Tachydysrhythmias occur when the HR is greater than 100 bpm. The major concerns are: •The fast rhythm shortens diastolic time and therefore coronary perfusion time (the amount of time available for blood to flow through the coronary arteries to the myocardium) •A continued rise in HR decreases ventricular filling time because of shortened diastole, decreasing stroke volume, cardiac output, and eventually blood pressure. •As with bradydysrhythmias, heart failure can also occur

1. S59: know CCB (Calcium Channel Blockers) slide - know all the drugs in blue on the slide and what they do in the body (also in blue), and the last 3 BPs on the slide (don't have to know the images, just more S/A/Es...focus on list on slide).

•By slowing conduction velocity, CCBs are able to stabilize certain dysrhythmias •About ten CCBs are approved for treating cardiovascular disease, but only a limited number are approved for treating dysrhythmias •A few CCBs, such as Diltiazem (Cardizem) [myocardium depressant and vasodilator] and Verapamil (Calan) [myocardium depressant mostly with minimal vasodilation effect] block calcium ion channels in both the heart and arterioles; the remaining CCBs are specific to calcium channels in the vascular smooth muscle and result in vasodilation (Amlodipine [Norvasc]), Nicardipine [Cardene], Nifedipine [Procardia])... see a trend? They end in "-dipine" •For CCBs, watch out for shortness of breath, hypotension, bradycardia, unexplained weight gain, peripheral edema (swelling of hands and feet) - PATIENT should be instructed to LET MD KNOW if any of these s/s appear! Diltiazem an Verapamil can worsen heart failure because the reduce heart contractility. •Grapefruit juice interacts with calcium channel blockers and should be avoided. •Because the cardiac effects of CCBs are almost identical with those of BBs, patients concurrently taking drugs from both classes are especially at risk for bradycardia...so, avoid giving patients BOTH a CCB and a BB

1. S109: CCB for treat dysrhythmias - they are also used in HTN treatment so be aware of their use in HTN

•CCBs used to treat angina pectoris, dysrhythmias, and HTN - work on the heart and the blood vessels by blocking calcium ion channels •Contraction of the heart muscle is regulated by the amount of calcium inside the cell. Muscular contraction occurs when calcium enters the cell through channels in the plasma membrane. CCB block these channels, inhibit calcium ions from entering the cell, and limit muscular contraction in both the heart and blood vessels (mostly arteries and arterioles since these are more muscular than veins) These are also used as antidysrhythmics

1. S106: know the nursing implications of diuretic therapy

•Carbonic anhydrase inhibitor: Acetazolamide (Diamox) •Carbonic anhydrase is an enzyme that works in the kidneys to move sodium and bicarbonate from the urine back into the blood •A carbonic anhydrase INHIBITOR prevents these ions from moving so sodium stays in the urine (pulling water with it) as do bicarbonate ions (bicarbonate is an acid buffer) •End result is carbonic anhydrase inhibitors produce diuresis but it's not that impressive (not a lot of volume) AND makes the urine more alkaline (helps reduce uric acid kidney stone formation) •Used in CHF but also for patients with seizure disorders and increased intraocular pressure from glaucoma •Avoid in patients with renal failure and liver failure (hepato- and nephrotoxic); ALSO this is a sulfa-based drug so tell MD if you have a sulfa allergy (contraindicated) •Nursing Considerations for Diuretics: •What is it doing to the patient's BP? Check BP before you give...daily weights as well to trend fluid balance •What about urine output? •What about electrolytes? What about kidney function labs (BUN, Creatinine)? •Any other adverse effects (Ringing in the ear? Dizziness? Be careful when getting them out of bed r/t orthostatic hypotension and dizziness from volume loss) •How much fluid are they drinking? •When are the doses timed? Is it a good idea to give this medication at HS?

1. S78: lifestyle modifications always part of CAD management; know drug CAD patients are on. Know what to watch out for with statins - last bullet point. What do you measure/assess prior to starting these meds?

•DASH diet, exercise, quit smoking, healthy weight, manage chronic conditions (diabetes, HTN) •Prior to starting therapy with statin medications (e.g., rosuvastatin [Crestor], simvastatin, pravastatin, atorvastatin [Lipitor]), the client's liver function tests should be assessed. The drug is metabolized by the hepatic enzyme system and could cause drug-induced hepatitis and increased liver enzymes. •Statins can also cause muscle aches and, rarely, severe muscle injury (rhabdomyolysis). CALL MD if patient experiencing muscle aches/pain/swelling!!!

1. S81: know red font (aneurysm slide) and text box about management in the upper right-hand corner

•Definition: Out-pouching of vessel wall that occurs in an area of marked weakening of an arterial wall •Most non-intracranial aneurysms (95%) arise distal to the origin of the renal arteries - called an abdominal aortic aneurysm, a condition mostly caused by atherosclerosis...if this aneurysm ruptures completely, the chances of mortality are extremely high (up to 85%); s/s: abdominal or back pain, pulsating abdominal mass, s/s of blood loss, bruit - MEDICAL EMERGENCY!! Patient will need to go to OR to repair the aneurysm and will probably needs unit of blood •Berry aneurysms of the anterior communicating artery of the circle of Willis •Aortic Dissection (this is the THORACIC aorta, coming off the heart) occurs when blood separates arterial wall layers to form a blood-filled channel within the aortic wall (s/s sudden-onset severe, tearing chest pain radiating into the back; dyspnea, hoarseness, cough - ANOTHER MEDICAL EMERGECNY!!) •Risk factors: Diabetes, obesity, high blood pressure (CONTROL THAT BLOOD PRESSURE!!), tobacco smoking, alcoholism, and insomnia Management for abdominal and thoracic aneurysms: we monitor until > 5cm in size, then rate of rupture increases so surgery may be required. Pre-op goal is to keep SBP 100-120 to prevent rupture. Also tight BP control after to prevent sutures from breaking. Monitor circulation after surgery. Low BP post-op??? Could be HEMORRHAGE...Notify surgeon

1. S73: Atherosclerosis know red font...re-read the risk factors a few times so you have some familiarity; Know total cholesterol, triglycerides, HDL, and LDL from the "Lab Values to Know for Exam 2" doc

•Definition: a disease of arteries characterized by the hardening of the arteries due to plaque deposition. •It is the leading cause of mortality in the United States •Major risk factors: •Hyperlipidemia: •↑ cholesterol, ↑ TG and ↓ HDL (<45 mg/dl) •Smoking •Hypertension Diabetes mellitus •Atheromatous plaque: Slow build-up as fatty substances, cholesterol, and other blood components (platelets, macrophages) in the inner lay of the arterial vessel wall. Fibrin and calcium also get deposited on the outer edge of the plaque Labs: cholestrol- high risk over 240 trigylcerids: over 200 high risk HDL- under 35 high risk LDL: over 160

1. S88: in Pain unit too - know what orthostatic hypotension is...know symptoms, causes, management

•Definition: a sudden fall in blood pressure, typically 20 mm Hg (for SBP) and/or 10 mm Hg (for DBP) WITH a rise in heart rate, that occurs when a person assumes a standing position from supine position. •Also known as postural hypotension... CAME UP w/ Morphine/Opioids...people getting these analgesics are at risk for orthostatic hypotension, ESPECIALLY if they are dehydrated •Symptoms: •dizziness, lightheadedness, headache, blurred or dimmed vision and syncope (temporary loss of consciousness) •Causes: •Hypovolemia from different diseases or states: dehydration, sepsis, blood loss •Medications: antihypertensives in particular - including diuretics, vasodilators, ACE-I •Treatment and management: •Caused by hypovolemia: treat THE CAUSE of the hypovolemia...give IVF, give PRBCs •Caused by medication: adjusting the dosage or by changing the medication to one that produces the same outcome but is less likely to cause orthostatic hypotension. STAY HYDRATED while on medication, if not contraindicated

1. S40: know definition of an MI (red font at top of slide); Know the 2 BPs under "Mechanism"; Know s/s of MI, including the atypical ones. For image, just read names of the coronary arteries so you have familiarity.

•Definition: localized area of cardiac muscle damage due to blocked blood flow •Mechanisms: •Coronary artery atherosclerosis with plaque, platelets aggregate over plaque and thrombus forms, completely occluding artery over time •Coronary artery spasm causes coronary arteries to constrict, restricting blood flow •Typical Clinical presentation of acute MI •Sudden onset of severe substernal chest pain •Often radiates to the left arm, jaw, and neck •Chest heaviness, tightness, and shortness of breath •Jugular venous distension •Anxiety and often have a "feeling of impending doom" •Atypical Clinical presentation of acute MI •Female, elderly, and diabetic clients tend to present with atypical symptoms of myocardial infarction (MI), such as diaphoresis, nausea, fatigue, or dyspnea, but may not always experience chest discomfort. Pain may be absent or atypical or may radiate to unusual locations (e.g., jaw, back). Some clients may report pain as "indigestion" (epigastric burning or gas).

1. S134: Know blue and red font. Know that the Unstable angina is REAL BAD - high risk for MI

•Definition: transient cardiac ischemia without cell death resulting in substernal chest pain •Types of Angina: •Stable angina •Most common type of angina; chronic •Caused by coronary artery atherosclerosis with luminal narrowing > 75% •Chest pain is caused by ↑ cardiac demand (exertional or emotional) •Relieved by rest or nitroglycerin (cause venous vasodilation à reduces blood flow back to the heart à decreases workload of heart; at high doses, nitroglycerin dilates the coronary arteries which improves blood flow to the myocardium) •Prinzmetal variant angina •Caused by coronary artery vasospasm; longer in duration than stable angina episodes •Episodic chest pain often occurring at rest and early in the day •treated with calcium channel blockers. Beta blockers are contraindicated because they may actually worsen the spasm •Unstable or crescendo angina •Caused by formation of a non-occlusive thrombus in an area of coronary atherosclerosis •Increasing, frequency, intensity and duration of episodes over time •May occur at night or at rest or with activity High risk for myocardial infarction

1. S3: know the TYPICAL s/s of dysrhythmias - SEE THE OVERLAP with s/s of hypoperfusion. One of the problems with dysrhythmias is that many of them cause the heart to beat in an abnormal way which causes CARDIAC OUTPUT to drop which then leads to POOR TISSUE PERFUSION

•Dysrhythmias are abnormalities in electrical conduction of the heart that may result in alteration in heart rate or rhythm •Whereas some dysrhythmias produce no symptoms and have negligible effects on cardiac functioning, others can be life-threatening and require immediate treatment •Typical symptoms include palpitations (feeling your heartbeat: often irregular or abnormal contraction occurring; may be fast), dizziness, weakness, activity intolerance, fainting/syncope, chest pain, dyspnea •Persistent dysrhythmias are associated with increased risk for stroke and heart failure. Severe dysrhythmias may result in sudden death

1. Know the blue and red font on S4 about s/s of dysrhythmias

•Dysrhythmias that originate in the atria are sometimes referred to as supraventricular (above the level of the ventricles) - Atrial fibrillation is the most common type of dysrhythmia (and the most common cause of ischemic stroke), and it is an example of a supraventricular dysrhythmia •Dysrhythmias that originate in the ventricles are generally considered more serious because they are more likely to interfere with the normal functioning of the heart (the ventricles, after all, are responsible for pumping blood to the entire body, including the heart's coronary arteries) •For example, ventricular fibrillation is a total disorganization of cardiac electrical activity - life-threatening and requires immediate reversal with the use of an electrical current (we call this device a defibrillator)

1. S87: VERY SIMPLY, know the difference between essential and secondary hypertension

•Essential (Primary) Hypertension •Essential hypertension indicates that no specific medical cause can be found to explain a patient's condition...a number of factors likely contribute to primary HTN (genetics, salt intake, obesity, ETOH intake, sleep apnea) •Over 90% of all individuals with high BP have essential HTN •Secondary Hypertension •This means high blood pressure is a result of (i.e. secondary to) another condition •Less than 10% of all individuals with high blood pressure •Most often result of chronic kidney disease and adrenal gland abnormalities (e.g., Pheochromocytoma [PCC] is a neuroendocrine disorder of the adrenal glands, that secrete high amounts of norepinephrine and epinephrine).

1. S121: know the common causes/etiology of right-sided vs left-sided HF (lots of overlap between the two)

•Etiology of Right HF: •Left-sided heart failure (most common):Right heart failure usually is the consequence of left-sided heart failure, since any pressure increase in the pulmonary circulation inevitably produces an increased burden on the right side of the heart •Pulmonary or tricuspid valve disease •Pulmonary hypertension (often caused by chronic respiratory disease) •Myocardial infarction •Essential hypertension Etiology of Left HF: •Myocardial infarction •Essential hypertension •Aortic or mitral valve disease

1. S98: know the first line therapies for treating HTN (don't have to know them in this order BUT, good to know that ACE-I are REALLY popular for treating HTN as a first-line therapy)

•First-line drugs: •Angiotensin converting enzyme inhibitors (ACE-I) •Angiotensin receptor blockers (ARB) •Calcium channel blockers (CCB) •Thiazide diuretics •Beta-adrenergic blockers ("Beta Blockers") à NOT FIRST-LINE THERAPY FOR ADULTS > 60 years old •Second-line drugs: •Alpha-2 adrenergic agonists •Alpha-1 adrenergic antagonists •Centrally acting beta and alpha blockers •Direct renin inhibitors

1. Know S28 on PEA and Asystole - know entire slide as it include management of both which are identical

•In PEA, the monitor will show electrical activity in the heart, but the patient will have no palpable pulse (in other words, patient is dead). PEA and Asystole are managed the same way: CPR, Epinephrine, Figure out the cause and treat THAT [MI, cardiac tamponade, pneumothorax, hypovolemia, hypoxemia, abnormal labs]) •Neither asystole nor PEA are shockable rhythms - In PEA, the electrical system in the heart is actually working properly (shocking the patient is done to 'reset' the heart's rhythm, but the problem in PEA isn't in the conduction of electrical stimuli in the heart) •We do not shock Asystole because defibrillation involves us trying to shock a patient from one rhythm into another - patients in Asystole HAVE NO ELECTRICAL ACTIVITY TO shock. •A patient in PEA or Asystole will be completely unconscious •In PEA, when the cardiac monitor is attached, you will see a rhythm on the monitor - Normal sinus rhythm, sinus bradycardia, and sinus tachycardia are possible •Despite having a rhythm on the monitor, the patient will not have a palpable pulse or blood pressure

1. S74: read patho of atherosclerosis - expectation that you have a basic understanding on how this occurs

•Lipids circulating in the blood (especially LDL) get into the vessel wall lining •Monocytes adhere to vessel walls, enter tissue, and become macrophages •Macrophages are transformed into foam cells after engulfing LDL •Foam cells accumulate in the intima •Foam cells release factors causing the aggregation of platelets, growth factors are released from vascular endothelium •Growth factors promote plaque formation •After formation of plaque, calcification occurs (plaque is made of fat, cholesterol, calcium and other blood elements) •The central core of the plaque consists mainly of cholesterol •Plaques block the arteries

1. S91: Know what the RAA system is in terms of the cascade of enzymes and proteins (equation in the middle of the S92 in blue is a good summary AND you need to know where these substances come from - ACE comes from kidneys and lungs, renin from kidneys, etc.). SECOND to LAST BP on S92 is critical to read and re-read so it sinks in that many of the anti-hypertensives we give, work by blocking SOME pathway in the RAA system to prevent blood pressure and/or HR from rising.

•Liver is always making this protein Angiotensinogen that floats around in our bloodstream, inactive •When the kidneys detect low blood volume in the body or when there is a decrease in sodium ions flowing through the kidneys, they release Renin, a hormone that converts Angiotensinogen into Angiotensin I •Then, the capillaries in the lungs produce Angiotensin Converting Enzyme (ACE), which converts Angiotensin I to Angiotensin II •To summarize: •Angiotensinogen (+ Renin) à Angiotensin I (+ ACE) à Angiotensin II •This RAA system is where numerous ANTI-hypertensive medications have their effect. They work by blocking a particular point in this cascade, with the end result being lowering a person's blood pressure •This idea of "blocking" part of the RAA cascade is similar to Hematology and the clotting cascade...how anticoagulants work usually involves blocking some part of the clotting cascade to prevent clot formation... Anti-hypertensives that lower blood pressure do so by blocking some component of the RAA system

1. S104: How do Loop diuretics work? Are they potassium-wasting? What does this mean? Do they produce a lot of diuresis? Are they used in long-term management of HTN? What are the side effects. Are thiazide diuretics as effective as Loop diuretics? Are they potassium-wasting?

•Loop diuretics: blocks the sodium-potassium-chloride transporter in the ascending loop of Henle part of nephrons - this is normally where about 25% of the filtered sodium is reabsorbed back into the bloodstream so blocking this transporter has a huge impact on the amount of diuresis produced. potassium-wasting meaning "patient losses K+ via urine" •LOOP Diuretics produce the most profound diuresis of any diuretics available •NOT IDEAL for long-term HTN therapy because the risk of adverse effects is great (extreme dehydration [hypernatremia r/t dehydration], hypokalemia, ototoxicity, tinnitus, dizziness, and nephrotoxicity in the critically ill) •Works very quickly if given IV (starts working within 5 minutes; PO tablets start working in 30-60 minutes) •Thiazide diuretics: inhibit the sodium-chloride transporter in the distal tubule of the nephron. Because this transporter normally only reabsorbs about 5% of filtered sodium, these diuretics are less effective than loop diuretics in producing diuresis. ALSO Potassium-wasting

1. S113: know the prototype direct vasodilator and that it can cause reflex tachycardia (read the third bullet point) and potential sodium/water retention (4th BP)

•Many of the anti-hypertensives we have discussed so far lower blood pressure by indirect means, such as affecting enzymes (ACE-I), changing fluid volume (diuretics), influencing autonomic nerves (alpha and beta drugs) •There are drugs that directly impact vascular smooth muscle and are highly effective at lowering blood pressure •These drugs run the risk of producing reflex tachycardia, a compensatory response to the sudden decrease in blood pressure. Reflex tachycardia causes the heart to have to work harder and blood pressure increases, counteracting the effect of the drug •A second potential serious complication of direct vasodilator therapy is sodium and water retention. As BP drops, the blood flow to the kidneys is reduced and the RAA system is activated stimulating Aldosterone release, which results in sodium and water retention •Hydralazine (Apresoline) is prototype

1. S44: Know post-MI discharge meds and instructions regarding caffeine

•Memory Aid for Interventions: Asp feeds ON MoTH (Aspirin, Oxygen, Nitro, Morphine, Thrombolytics, Heparin)...NOT always done in this exact order BUT Aspirin we try to get in as soon as possible, so it is often FIRST Prior to Discharge - patient who was admitted with an MI will go home on the following: •Beta Blocker: work by reduction of oxygen consumption of the myocardium by lowering the heart rate, blood pressure, and myocardial contractility. They also play an important role in reduction of re-infarction •Antiplatelet medication such as Clopidogrel (Plavix) or aspirin - cardiologist needs to advise patient since conflicting evidence on which treatment is ideal •Cholesterol lowering medication ("statins" are HMG-CoA reductase inhibitors and reduce the production of cholesterol in the liver; examples include atorvastatin [Lipitor], simvastatin [Zocor]...They all end in "-statin" and are therefore called the "statins." •Caffeine should be avoided - has a vasoconstrictive effect on arteries so avoid soda, tea, coffee unless decaffeinated

1. S45: know what we do in cardiac catheterization lab? What are the possible interventions?

•NPO for 6 hours prior to procedure •Mark pedal pulses to get a baseline •Explain that during procedure may have a metallic taste in mouth, may feel heart pounding during the procedure, may feel flush during the procedure or like they are urinating (contrast dye injected into veins) •Verify no dye allergy and no shellfish allergy After Catheterization (femoral approach): •No flexion at the hips/keep affected leg straight for 4-6 hrs post-procedure. Maintain bedrest during this time •Monitor for s/s of bleeding, hematoma at catheter site, retroperitoneal bleed •Frequent BP and apical pulse monitoring (pt should be wearing continuous cardiac monitor); These VS are usually taken Q15mins for 2 hrs post-procedure •Neurovascular checks Q15mins for first 2 hours, then 30 mins until patient able to site up (includes pedal pulses and checking skin temperature and sensation/motor strength in legs/feet) •Encourage fluids to flush dye through kidneys (pt may receive some IVF after procedure to help with this) •Assess for chest pain and dysrhythmias

slide 34- know dicharge intrustion of pt with pacemaker

•Patient Discharge Instructions: •For the first week after placement of pacemaker or AICD, take your temperature and check your incision for signs of infection (redness, swelling, drainage, or warmth). WATCH OUT FOR S/S of INFECTION!! •Before you receive any treatment, tell all healthcare providers (including your dentist) that you have a pacemaker. •You will be given an ID card that contains information about your pacemaker. Always carry this card with you. You can show this card if your pacemaker sets off a metal detector. You should also show it to avoid screening with a hand-held security wand. •Keep your cell phone away from your pacemaker. Don't carry the phone in your shirt pocket overlying the pacemaker, even when it's turned off. •Avoid strong magnets. Examples are those used in MRIs or in hand-held security wands. Some pacemakers are now safe to use with MRI scanners. Ask your doctor if you have such a pacemaker. Avoid strong electrical fields. Examples are those made by radio transmitting towers, "ham" radios, and heavy-duty electrical equipment •Do not lean over running engines (they generate an electrical field) •Most household and yard appliances will not cause any problems. If you use any large power tools, such as an industrial arc welder, talk with your doctor.

1. S105: know the red and orange font about potassium-sparing diuretics and the prototype drugs in blue

•Potassium-sparing diuretics: blocks the aldosterone receptors in the collecting duct of the nephron. This causes a decrease in sodium and water reabsorption into the bloodstream and decreases potassium loss in urine (therefore, potassium-sparing diuretic). Especially useful for patients who are chronically hypokalemic, but you have to watch out for them retaining too much potassium. •Taking potassium supplements in addition to a potassium-sparing diuretic is not advised because this may lead to hyperkalemia which could cause cardiac arrhythmias; AVOID with RENAL FAILURE and LIVER FAILURE PATIENTS •Taking with a ACE-I or an ARB with a potassium-sparing diuretic can also significantly increase the potential for developing hyperkalemia and should be avoided •Potassium-sparing diuretics (e.g., spironolactone, amiloride, triamterene eplerenone) are generally very weak diuretics and antihypertensives. However, they are useful when combined with thiazide diuretics to reduce potassium (K+) loss. Thiazide diuretics can cause hypokalemia when used as monotherapy. Prototypes to Know for Exam: •Loop Diuretics: Furosemide (Lasix)...others: Bumetanide, Torsemide, Ethacrynic acid - ending "-ide" for some but non-loop drugs have that ending too •Thiazide Diuretic: Hydrochlorothiazide, abbreviated "HCTZ" (Microzide) • Potassium-sparing diuretic: Spironolactone (Aldactone)

1. Know Goals of MI Treatment (S41), including primary goal

•Primary goal is restoration of the balance between oxygen supply and demand to prevent further ischemia (e.g., re-perfusion therapy à Cardiac Cath Lab for Percutaneous Coronary Intervention/Balloon Angioplasty) •Pain relief •Prevention and treatment of complications

1. S126: know the 3 aims of the CHF drugs (what are they trying to do)

•Reduce preload (reduce blood volume by removing water) •Reduce afterload (reduce BP; vascular resistance) •Inhibit the RAA system and the vasoconstrictor mechanisms of the sympathetic nervous system that will activate when cardiac output is reduced because of CHF (these systems will only make the CHF worse) •MANY of THESE DRUG CLASSES/DRUGS used for CHF are familiar to you because we see them in treatment of HTN

S68: be able to recognize SVT if you see it (bottom image on this slide). S69: look at an example of giving adenosine and what you see on cardiac monitor

•Synchronized cardioversion is indicated for ventricular tachycardia with a pulse, supraventricular tachycardia, and unstable atrial fibrillation •The synchronizer switch must be turned on when cardioversion is planned. The synchronize circuit in the defibrillator is programmed to deliver a shock on the R wave of the QRS complex on the electrocardiogram (ECG). This allows the unit to sense this client's rhythm and time the shock to avoid having it occur during the T wave. A shock delivered during the T wave could cause this client to go into a more lethal rhythm (e.g., ventricular tachycardia, ventricular fibrillation). If this client becomes pulseless, the synchronize function should be turned off and the nurse should proceed with defibrillation.

1. S85: for hypertension, use SBP> 140 and/or DBP >90. For hypotension, use SBP < 90 mm Hg or a MAP <65. Know how to calculate MAP (Exam 1). Know what SBP and DBP mean (middle of the slide)

•Systolic blood pressure (the first number) — indicates how much pressure your blood is exerting against your artery walls when the heart beats •Diastolic blood pressure (the second number) — indicates how much pressure your blood is exerting against your artery walls while the heart is resting between beats

1. S117: know cardiac output, preload and afterload are (know the last 5 BPs). When are preload and afterload increased (see S118)?

•The 2 most important factors influencing cardiac output are preload and afterload •Preload is end diastolic volume (EDV) - think of it as the ventricle stretching, and filling with blood right before the big squeeze (systole) •Afterload, also known as the systemic vascular resistance (SVR), is the amount of resistance the heart must overcome to open the aortic valve and push oxygenated blood out to the tissues Preload increase: hypovolemia, regurgitation of caridac valves afterload increase: hypertension, vasoconstriction, afterload, cardiac worklaod

S61: Prolonged QT causes Torsade de Pointes; identify this rhythm strip (S65 on left) AND know treatments on S66 in blue. S62, just take a look, LOTs of meds prolong QT. S63 shows Torsades developing

•The QT interval is the time from the start of the Q wave to the end of the T wave •It represents the time required for ventricular depolarization and repolarization •The QT interval is shorter at faster heart rates, and longer at slower heart rates •An abnormally prolonged QT is associated with an increased risk for developing ventricular dysrhythmias, especially Torsade de Pointes •well, even though it looks weird and is associated with this prolonged QT interval, Torsades is still a dysrhythmia (a type of V-Tach); therefore, I should treat it with an antidysrhythmic always" •You may treat this condition with an antidysrhythmic but NOT from Class IA (example, Procainamide), because this class is actually associated with causing prolonged QT - for someone with Torsades, we want to shorten the QT interval (get it back into a normal range) •Treatments for/Prevention of Torsades have included: •Amiodarone (a Class III antidysrhythmic), •Administration of Magnesium Sulfate (we also supplement any other electrolytes that are below normal ranges and impact heart function such as sodium, potassium, and calcium)

1. S25, what does a defibrillator do? Know "unstable but awake = cardiovert; dead = defibrillate." "unstable" means - abnormal rhythm, low blood pressure, dyspnea, altered mental status = all signs of POOR PERFUSION b/c the dysrhythmias is reducing cardiac output. Unstable patient who is awake, we can cardiovert (what does that mean? simply).

•The electrical shock generated by a defibrillator momentarily stops all electrical impulses in the heart, both normal and abnormal. The temporary cessation of electrical activity allows the SA node to automatically return conduction to a Normal Sinus Rhythm •Electricity is used as an intervention related to how unstable the patient is: "unstable but awake = cardiovert; dead = defibrillate" •For example, if a patient is experiencing Atrial Fibrillation and has a very low blood pressure, but still has a pulse and is talking to us, we could electively cardiovert them before using medications (we still use a defibrillator but we give the patient less electricity and we time the administration of the shock with their current cardiac rhythm - we are trying to shock the heart back into a Normal Sinus Rhythm) •For a patient that has ventricular fibrillation (Vfib) or ventricular tachycardia (V-Tach), you would consider these patients dead (there is a disorganized electrical wave moving through the heart but it is not generating a palpable pulse or any cardiac output) •BUT, there are ALWAYS exceptions...some people in V-Tach DO still have a pulse and are conscious...obviously those people aren't dead, and we might cardiovert or give drugs

S6: read the risk factor list a few times to become familiar

•The following are diseases and conditions associated with dysrhythmias: •HTN •Cardiac valve diseases such as aortic stenosis •Coronary artery disease •Use of certain medications such as Digoxin •Low K+ and/or Mg+ levels in the blood •MI •Stroke •Diabetes •CHF

1. S23: know slide - what are some non-pharm ways we can try to address certain dysrhythmias? See S24 for example of how to perform Valsalva maneuver

•Therapeutic goal is to prevent or terminate dysrhythmias in order to reduce the risk of sudden death, stroke, or other complications •Because the drugs used to accomplish these goals can have serious adverse effects, antidysrhythmia drugs are reserved for patients experiencing symptoms or in life-threatening danger r/t the dysrhythmia •Vagal maneuvers induce vagus nerve stimulation of the cardiac conduction system, specifically the SA and AV nodes. Although not as common today, vagal maneuvers may be attempted to treat tachydysrhythmias (patient must have a pulse and be conscious/able to follow directions). •Valsalva maneuver is a forced expiration against a closed glottis (can be accomplished using the procedure on the next slide) •PROBLEM with Valsalva: frequency only lowers heart rate temporarily (by stimulating the Vagus nerve of the parasympathetic nervous system) and can cause rebound tachycardia •The most serious type of dysrhythmias are corrected through electrical shock to the heart called cardioversion or defibrillation

1. S99: know second and last bullet point on slide = basics of how most diuretics work

•This is because of the kidney's ability to control the retention and elimination of sodium. If sodium is eliminated from the body, water is also eliminated. •Diuretics work primarily by removing sodium and chloride from the body in the urine, and the sodium and chloride in turn draw excess water from the body to be excreted in the urine

1. S18: if you are taking care of a patient with new onset of afib or aflutter, we can give antidysrhythmics like Amiodarone, BUT they are also at risk for what? What meds can we give to treat? What is IV drug and what is the PO drug...you SAW THESE in hematology. Patient develops NEW A-fib, what would you see/assess?

•This rhythm is the #1 RISK FACTOR FOR ISCHEMIC STROKE (blood clot in a vessel in the brain), because of this link, we frequently ANTICOAGULATE these Afib patients (in addition to giving them antidysrhythmics) to PREVENT clot formation •IV ANTICOAGULANT? What can we give them? You know this from treating patient with pulmonary emboli or DVTs? •After they are therapeutically anticoagulated with the drug above, what PO anticoagulant might we transition them to? (Emily have to look it wasent on slide)

1. S111: know this slide including the prototype BB

•Used to treat HTN, CHF, MI, migraines, and as ophthalmic eye drops for patients with glaucoma •At low doses, adverse effects uncommon, but as doses increase, BBs will slow the HR and can cause bronchoconstriction •Patients with CHF and asthma need to be careful taking beta blockers; at higher doses, patients report fatigue and activity intolerance because the BB prevents the heart from responding appropriately to exertion. Less commonly, can cause decreased libido and impotence •Stopping BBs suddenly can cause rebound HTN, angina, and MI, so they should be tapered over several weeks •Check pulse rate daily before taking drug and report to provider for pulse slower than 60 beats/minute (or prearranged parameter) •Report shortness of breath, extremity edema, night cough to provider. Report increase in angina or new onset of chest pain to provider •Metoprolol (Lopressor) is a prototype

1. Know S11 and what an ECG/EKG is, what we use for, what leads are

•Wave of electrical activity across the myocardium can be measured using an electrocardiograph - the graphic recording from this device is called an electrocardiogram (ECG or EKG) •These tracings are extremely useful in diagnosing many types of cardiac conditions, including dysrhythmias •A lead provides one view of the heart's electrical activity - multiple leads can be obtained by placing multiple electrodes

1. S60: know the red font r/t and nursing implications of patients on these antidysrhythmic meds

•across the different antidysrhythmic classes, you can see reduction in heart rate as a common theme; therefore, common risks for all these drugs include bradycardia and consequences of bradycardia: hypotension, dizziness, and syncope •Nurses should consider the following interventions when caring for patients receiving antidysrhythmics: •Connect the patient to a blood pressure and pulse oximetry monitor, and take frequent BP readings, especially during the first hour after your start the medication •Patient should be wearing telemetry monitor (e.g., continuous cardiac monitoring) •Be careful getting the patient out of bed - patient may overestimate what they can do and not realize how dizzy the medication has made them until it is to late (syncope, fall). They may hate it, but a bedpan or a bedside commode might be safest •Labs and Organ Function: some antidysrhythmics are associated with organ toxicity - for example, Amiodarone can produce liver toxicity and thyroid dysfunction; pulmonary toxicity is a rare though serious side effect •Personally, I avoid having patients eat a big meals when they are first admitted with a dysrhythmia, and a lot of times the doctors have them "NPO except meds" in case the patient needs to be cardioverted •Talk with the doctors about the patient's other medications - are they on any other medications that might exacerbate or make them prone to a dysrhythmia?

1. S67: know red and blue font about adenosine and digoxin - DIGOXIN is HUGE ON NCLEX!!!

•and Digoxin are occasionally used to treat specific dysrhythmias, although they do not act by any of the mechanisms described thus far - both drugs slow electrical conduction through AV node (different mechanisms of action but involve ion channels: sodium, potassium, calcium channels) •When Adenosine is given IV push over 1 to 2 seconds it terminates serious atrial tachycardias by slowing conduction through the AV node and decreasing automaticity of the SA node - it's primary indication is a specific dysrhythmia known as supraventricular tachycardia (SVT) •Side Effects: Although dyspnea is common (drugs causes bronchospasm), as are feelings of lightheadedness and general discomfort (feelings of impending doom), side effects are generally self-limiting since the drug has a 10-second half life •Digoxin is primarily used to treat CHF (usually end stage CHF), but it is also prescribed for certain types of atrial dysrhythmias because it can decrease automaticity of the SA node and slow conduction through the AV node •Excessive levels of digoxin can produce serious dysrhythmias and interactions with other medications are common so patients taking Digoxin for dysrhythmias must be carefully monitored (e.g., Digoxin levels checked and home med lists checked for potential drug-drug interactions) •Bradycardia is an adverse effect of digoxin. Expected apical heart rates vary considerably according to age. The nurse should withhold the digoxin dose for heart rate of 60/min or below in an adult, 70/min or below in a child, and 90/min or below in an infant. •S/S of toxicity: vision changes (yellow halo around light, blind spots), confusion, N/V/D - so, patient complaining of any of these s/s should be assessed for digoxin toxicity (medication cause HR to drop, so check VS!!) •Target serum digoxin levels - 0.5 - 1 ng/mL; TOXIC LEVEL! 2.0 ng/mL... give IV digoxin immune Fab (Digibind) - this is a Digoxin-specific antibody developed from antibody fragments •Risk factors for developing Digoxin toxicity... hypokalemia, hypomagnesemia, hypercalcemia, dehydration

1. S7 and S9: be able to talk through normal electrical conduction in heart - what are the electrical nodes/fibers

•dysrhythmias, they all involve a problem in the generation or conduction of electrical impulses across the myocardium •These electrical impulses, or action potentials, carry the signal for cardiac muscle cells to contract and are precisely coordinated for the chambers to beat in a synchronized manner (electrical impulses precede mechanical events in the heart) •For the heart to function properly, the atria must contract simultaneously, and following atrial contraction, the ventricles must contract simultaneously •Control of electrical conduction and synchronization begins in a small area of tissue in the wall of the right atrium known as the sinoatrial (SA) node - also called the "pacemaker of the heart." •The SA node has a property called automaticity, which is the ability of certain cells to spontaneously generate an action potential. The SA node generates a new action potential approximately 75 times per minute under resting conditions, with a range of 60 to 100 beats per minutes. This is referred to as the normal sinus rhythm •The SA node is greatly influenced by the activity of the sympathetic and parasympathetic divisions of the autonomic nervous system •Once the SA node generates an action potential, it travels quickly across both atria to the atrioventricular (AV) node. The AV node also has the property of automaticity, although less so than the SA node. •Should the SA node malfunction, the AV node has the ability to spontaneously generate action potentials and continue the heart's contraction at a rate of 40 to 60 beats per minute. Impulse conduction through the AV node is slow compared to other areas of the heart - this allows the atria enough time to completely empty blood into the ventricles to maximize cardiac output. •As an action potential leaves the AV node, it travels to the atrioventricular bundle, or bundle of His. The impulse is then conducted down the right and left bundle branches to the Purkinje fibers, which carry the action potential to all regions of the ventricles almost simultaneously. •Should the SA and AV nodes become non-functional, the Purkinje fibers can continue to generate myocardial contractions at a rate of about 30 bpm

Know Slide 31 about pacemakers and AICDs; (S32); Know who gets a Pacemaker vs an AICD (S33

•non-pharm treatments for dysrhythmias include identification and destruction of the myocardial cells responsible for the abnormal conduction through a surgical procedure called an ablation (ablation means "inactivation") •Cardiac pacemakers are sometimes implanted to correct types of dysrhythmias that make the heart beat too slowly (Bradyarhythmias) or beat irregularly (Atrial Fibrillation) •Implanted Cardioverter Defibrillators (ICDs) are placed in patient to restore normal rhythm by either pacing the heart or giving it an electrical shock when a dysrhythmia occurs •Pacemaker: electronic pacemaker generator is inserted under the skin under the clavicle. A pacemaker wire is introduced into a vein (usually subclavian) and passed into the right atrium or ventricle until it gets lodged in the wall of the chamber. Then the other end is connected to the implanted pacemaker generator. Pacemaker manages non-emergency cardiac rhythms/dysrhythmias. Indications include: •Symptomatic sinus bradycardia •A-fib •Heart Blocks •Heart Failure impacting rhythm •Automatic Implanted Cardioverter Defibrillator (AICD): life-saving emergency treatment for ventricular tachycardia and ventricular fibrillation. This generator has similar lead placement as the pacemaker, but it's purpose is to shock a patient out of V-Tach or V-Fib •Generally used in patients with hx of cardiac arrest •Hx of V-tach or V-fib

1. S14 and S15: be able to count out a rhythm (using 6-second EKG strip) to know number of beats per minute

•that we treat with antidysrhythmics are abnormal rhythms (in other words, not sinus rhythms) and many have rates that are fast •How do I know if the HR is faster than normal by looking at the EKG? •We said the pacemaker of the heart generates 60-100 bpm (the normal HR range) •Abnormal rhythms are frequently faster than that •I can estimate the rate by counting the number of QRS complexes in an EKG tracing that is 6 seconds long, and multiplying that by 10 (6 seconds x 10 = 1 minute, which will get me an estimate of beats per minute) •We have variations on Normal Sinus Rhythm...Sinus Tachycardia (HR > 100) and Sinus Bradycardia (HR < 60) These rhythms are out of the normal range of 60-100 bpm, but they are still considered "sinus" (the SA node/pacemaker of the heart is still directing the conduction of electrical activity in the heart and the chambers of the heart are depolarizing [being stimulated/contracting] and repolarizing [relaxing] in a synchronized manner