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145 Cards in this Set

  • Front
  • Back
In simple terms, what is heart failure?
In simple terms, heart failure is the inability of the heart to meet the demands of the body.
What is the most common cause of heart failure?
Left Ventricular Dysfunction
What is preload? What factors determine preload?
Preload is the pressure stretching the ventricles at the end of diastole, which is a marker for the volume of fluid in the ventricle at the end of diastole. In other words, it is the amount of fluid with which the ventricle is filled - "preloaded" - just prior to contraction. Preload is determined by venous return and atrial contraction.
What is afterload? What factors determine afterload?
Resistance to ventricular ejection. Afterload is determined by ejection impedance, wall tension, and regional wall geometry.
What is systolic dysfunction?
A problem with the ejection of blood from the heart during systole (EF < 40%).
What is diastolic dysfunction?
Diastolic dysfunction is a problem with the heart during diastole, i.e. the heart is stiff, unable to relax and completely fill with blood.
What is HFrEF?
Heart failure with reduced ejection fraction (EF < 40%)
What is HFpEF?
Heart failure with preserved ejection fraction (EF > 40%)
What is the most common etiology of heart failure?
Ischemia (from CAD, MI, etc.)
What are some of the nonischemic causes of heart failure? (7)
Prolonged HTN, valvular disorders (regurgitation and stenosis), endocrine disorders (thyroid), pregnancy, viral illness, chemotherapy, alcohol or illicit drug use
How does the renin-angiotensin-aldosterone system (RAAS) get activated in cases of HF?
Decreased cardiac contractility and output leads to decreased renal perfusion, which activates RAAS.
What effect does aldosterone have on the kidneys?
Aldosterone causes sodium and water retention.
Describe the Frank-Starling Mechanism. [Why does it not apply in cases of HF?]
Increased preload of a normal, healthy heart, leads to stretch of sarcomeres, which increases cross-bridge formation between actin and myosin, resulting in an increased force of contraction. [A diseased heart is incapable of adapting to this increase in preload to increase cardiac output.]
What are the compensatory mechanisms for reduced cardiac output?
Activation of renin-angiotension-aldosterone system (RAAS) and activation of the sympathetic nervous system (SNS).
Describe what happens upon activation of the sympathetic nervous system (SNS).
Increased heart rate, through activation of cardiac beta receptors, and vasoconstriction of peripheral arteries to shunt blood away from peripheral organs and thereby facilitate perfusion of the heart and brain instead.
What is the most frequent clinical symptom of HF? How does it relate to the severity of HF?
Acute onset of dyspnea (SOB). The severity of HF is inversely proportional to the amount of activity required to produce dyspnea.
What is orthopnea?
Pulmonary congestion and dyspnea in a supine position. It is measured by the # of pillows / angle required for comfortable rest.
What is paroxysmal nocturnal dyspnea (PND)? What causes it, what is the typical time course of its onset, and how does it differ from orthopnea?
Sudden awakening from sleep due to cough / wheezing (“cardiac asthma”). PND is the result of increased venous return and it typically occurs within 1 to 4 hrs of sleep. Unlike orthopnea, it may persist in an upright position.
What is Cheyne-Stokes respiration?
A pattern of irregular breathing in which breathing goes back and forth from breathing deeply and rapidly to breathing slowly and shallowly, or even to apnea, where the individual stops breathing altogether for a period of time.
What are the signs and symptoms of pulmonary edema?
The patient may produce a pink, frothy sputum and feel extremely breathless.
What causes peripheral edema in HF?
Right ventricular failure leads to peripheral edema.
What are the gastrointestinal effects of HF? What causes them?
Abdominal fullness, nausea, bloating, and early satiety result from edema of the gut wall and congestion of the liver / portal venous system.
What causes fatigue in HF?
Hypoperfusion of skeletal muscles
What are the symptoms of decreased perfusion of the CNS?
Confusion, hallucinations, insomnia, & lethargy
What are the signs of decreased perfusion of the periphery?
Cool extremities and cyanosis (hypoxemia, blue-tinged tongue, lips, & nail beds)
What might lead to polyuria in a case of HF?
Increased release of natriuretic pepetides due to volume overload may lead to more frequent urination.
What might lead to nocturia in a case of HF?
Increased renal perfusion at night due to reduced SNS activity.
What is the description of NYHA Class I HF?
No symptoms w/ ordinary activity.
What is the description of NYHA Class II HF?
SOB / fatigue w/ > ordinary activity.
What is the description of NYHA Class III HF?
SOB / fatigue w/ ordinary activity.
What is the description of NYHA Class IV HF?
SOB / fatigue at rest during the day
What is Stage A HF?
High risk for structural heart disease.
What is Stage B HF?
Asymptomatic HF (has structural heart disease, but no symptoms yet)
What is Stage C HF?
Symptomatic HF (current or prior symptoms and structural heart disease)
What is Stage D HF?
Refractory end stage HF (no longer successfully managed w/ meds).
What signs, i.e. physical findings, are commonly seen in HF?
Cyanosis, Tachycardia, Jugular Venous Distention (JVD), & Hepato-Jugular Reflux (HJR), S3 Gallop, Pulmonary Rales, Edema, Hepatomegaly, Cardiac Cachexia
Describe jugular venous distention (JVD).
Right internal jugular neck vein distension, at > 4 cm above the sternal angle, is noted when the patient is seated and reclined at a 45 degree angle.
What is hepato-jugular reflux (HJR).
HJR is a distention of the jugular vein induced by applying firm pressure over the liver.
What do the heart sound S3 and S4 indicate, respectively?
S3 relates to increased preload in the left ventricle. S4 relates to stiffening of the ventricle.
What are pulmonary rales?
Inspiratory crackles due to fluid in the alveolar space.
What is hepatomegaly?
An enlarged liver (due to excess fluid in HF cases).
What is cardiac cachexia?
Unexplained weight loss of >10% of their total body weight in a person having HF. [Thought to be due to excess cytokines. The prognosis of such cases is poor.]
What is the role of magnesium in cardiac cells?
Magnesium is a cofactor that helps potassium get into cardiac cells.
How does one distinguish between dyspnea from HF versus asthma/COPD?
B-Type Natriuretic Peptide will be elevated in HF.
What is Takotsubo cardiomyopathy?
A stress-induced cardiomyopathy, also referred to as “broken heart syndrome.”
Describe three types of medications that can exacerbate HF?
Medications that have negative inotropic effects, medications that cause sodium/water retention, and cardiotoxic agents.
List four types of negative inotropic agents.
1) Antiarrhymics (IA & IC), 2) Beta Blockers, 3) Non-DHP CCBs (verapamil & diltiazem), 4) Certain Antifungals (Itraconazole, Terbinafine)
List six types of medications that can cause sodium/water retention.
Steroids, NSAIDs (including COX-2 inhibitors & high dose ASA), Thiazolidinediones, Androgens, Estrogen, & Sodium-Containing Drugs, i.e. anionic drugs having sodium as the counterion.
What are the goals of therapy in HF? (5)
1) Improved quality of life, 2) Reduced symptoms, 3) Reduced hospitalizations, 4) Slow progression of disease process, & 5) Prolong survival.
Describe the aims in the management of heart failure. (3)
1) Removal of the underlying causes of HF, 2) Removal of the precipitating cause, & 3) Control of HF state (improved cardiac performance, reduced cardiac workload, & control of sodium/water overload).
What is the goal for minimizing salt intake?
Less than 2 g NaCl per day.
If a HF patient is placed on fluid restriction, what is the target?
Limit to 2 L per day.
What is the weight reduction goal in HF?
Goal of weight loss to within 15% of IBW.
What recommendation is given to HF patients with respect to heavy lifting?
Recommend not lifting over 30 lbs.
For a HF patient, weighing him or herself at home each day, at what rate of weight gain should the doctor be called?
Call the doc if wt. gain > 3 lbs per day or > 5 lbs over 5 days.
What is the limit below which low blood pressure becomes a concern due to hypoperfusion of the organs (brain and kidneys)?
< 80/50 mmHg
Beyond what time limit of resolution for orthostatic hypertension should the doctor be called?
3 min
Which vaccinations are recommended for HF patients?
Annual Influenza Vaccine & Pneumonoccal Booster (if received initial vaccination under age of 65)
What is the only class of medications that is effective in controlling fluid retention in heart failure?
Diuretics
Which class of diuretic, loop or thiazide, is most potent for fluid reduction?
Loop Diuretics
Which thiazide diuretic is the only one that retains its efficacy at low GFR, i.e. CrCl < 30 mL/min?
Metolazone
What is the goal for weight loss when using diuretics for fluid reduction in HF cases?
0.5 to 1 kg / day (1 to 2 lbs / day)
What are the adverse effects of loop diuretics?
Hypotension, Electrolyte Imbalances (hypokalemia & hypomagnesemia), Alkalosis, Dehydration, Gout, Ototoxicity
What are the electrolyte targets for serum potassium and magnesium levels in HF?
> 4 mEq/L potassium & > 2 mg/dL magnesium
Describe the decision to give potassium supplements when initiating a loop diuretic. If used, how is it dosed?
If serum potassium < 4 mEq/L, initiate at half the dose of the loop diuretic as a starting point, e.g. furosemide 20 mg BID coupled w/ KCl 10 mEq BID. If also initiating an ACE-I and the serum potassium is almost 4 mEq/L, wait until follow up to decide.
Describe the mechanism for the development of refractory edema. How is it managed?
Chronic loop diuretic therapy can lead to resistance due to hypertrophy of the distal convoluted tubule, creating more surface area for absorption of sodium. This leads to gut wall edema that decreases oral loop diuretic absorption by up to 50%. Switching to IV loop diuretic, increasing the oral loop diuretic dose, or adding a thiazide diuretic to the loop diuretic are each strategies utilized to overcome such refractory edema.
By how much, relative to placebo, do ACE-Is reduce mortality from HF?
~25%
Among HF patients, who should receive an ACE-I?
All patients, symptomatic or asymptomatic, who have an EF < 40%, should receive an ACE-I. For post-MI patients, wait until they are hemodynamically stable.
What ADRs are associated with ACE-Is?
Hypotension, HA, Fatigue, Cough, Hyperkalemia, Agranulocytosis (dose related), Neutropenia (dose related), Anemia, Acute Renal Failure, & Angioedema
How common is cough experienced as an ADR of an ACE-I?
5 to 20% of Europeans & up to 50% of Chinese experience cough when taking an ACE-I.
How common is angioedema experienced as an ADR of an ACE-I?
0.3%
What are the three true contraindications to ACE-Is?
1) Pregnancy, 2) Bilateral Renal Artery Stenosis, & 3) Angioedema
Under what three conditions should an ACE-I be utilized with extra caution?
1) SBP < 90 mmHg, 2) SCr > 3 mg/dL, & 3) Serum K+ > 5 mmol/L
In a case of HF, how does one distinguish low blood pressure caused by vasoconstriction vs. too much of an ACE-I?
If the low blood pressure is coupled with a lack of perfusion, vasoconstriction is the likely culprit. If the person is well perfused and have low blood pressure, then the problem may be that the dose of ACE-I is too high.
In which conditions is hypotension most likely with an ACE-I? (3)
1) Hypovolemia, 2) Recent marked diuresis, & 3) Severe hyponatremia (Na < 130 mmol/L)
How might one approach management of hypotension as a concern upon initiation of an ACE-I?
Start with a shorter acting agent (captopril) and switch to twice or once daily agent once stable.
What is the target dose for enalapril in HF?
10 to 20 mg BID
What is the target dose for captopril in HF?
50 mg TID
What is the target dose for lisinopril in HF?
20 to 40 mg Qday
What is the target dose of quinapril in HF?
20 mg BID
What is the target dose of ramipril in HF?
10 mg Qday
Which two ARBs are FDA approved for the treatment of HF?
Valsartan & Candesartan
What is the target dose for candesartan in HF?
32 mg Qday
What is the target dose for valsartan in HF?
160 mg BID
What is the target dose for losartan in HF?
50 to 100 mg Qday [Note that losartan is second line due to limited efficacy evidence.]
What ADRs are associated with ARBs?
Angioedema, Cough, Hepatotoxicity, Hyperkalemia, Hypotension, & Renal Dysfunction
What are the contraindications to ARBs?
Pregnancy, Bilateral Renal Artery Stenosis, & Hx of ACE Inhibitor-Induced Angioedema
In which conditions should an ARB be utilized with extra caution?
Renal or Hepatic Dysfunction
Aside from being an ADR of an ACE-I, why else might a HF patient experience cough?
Cough could be a symptom of HF. The distinguishing feature is that it will be coupled with edema and other signs and symptoms if it is a direct result of HF.
What is the third line therapy for vasodilation if neither an ACE-I nor an ARB can be utilized?
Hydralazine & Isosorbide Dinitrate
What are the targets for hydralazine and isosorbide in HF?
Hydralazine 75 mg TID & Isosorbide 40 mg TID
By how much, relative to placebo, do ACE-Is reduce mortality from HF?
~65%
Among HF patients, who should receive a beta blocker?
All patients, symptomatic or asymptomatic, who have an EF < 40%, should receive a beta blocker. However, do not initiate a beta blocker in a patient in the ICU or who is receiving an IV positive adrenergic inotropic agent. Also, the patient should be stable and euvolemic before initiating a beta blocker.
What are the three evidence-based beta blockers that may be utilized to treat HF?
Metoprolol Succinate, Carvedilol, & Bisopralol
What should be the starting dose for carvedilol?
3.125 mg BID
How should carvedilol be titrated? [How does the advice differ in the young vs. the old.]
Increase every two weeks or as tolerated up to 25 mg BID (or 50 mg BID if > 85 kg). [This may work in younger adults, but the dose may need to be titrated more slowly in older adults.]
By which CYP enzyme is carvedilol metabolized?
CYP2D6
What should be the starting dose for metoprolol succinate? [That is the maximum dose to which it may be titrated?]
12.5 mg QD [Max 200 mg QD]
What ADRs are associated with beta blockers?
Bradycardia, Hypotension (more pronounced w/ carvedilol), Edema, AV-Block, Dizziness, & Sexual Dysfunction
What are the contraindications to beta blockers? (3)
Reactive Airway Disease, Symptomatic Bradycardia, or Advanced Heart Block (unless treated with a pacemaker)
Describe management of fluid retention in a HF patient on a beta blocker.
Manage with diuretics. The beta blocker dose may be reduced (or discontinued altogether in severe cases).
Describe management of bradycardia in a HF patient on a beta blocker.
Discontinue other rate-limiting agents, such as digoxin, first. The beta blocker may be dose reduced (perhaps ultimately discontinued) or a pacemaker may be installed.
Describe management of hypotension in a HF patient on a beta blocker.
Reduce the dose of diuretic or of other vasodilator, or, in a worst case scenario, reduce the dose (or discontinue) the beta blocker.
What is an MRA?
Mineralocorticoid Receptor Antagonist (i.e. an aldosterone antagonist)
Describe the deleterious effects of aldosterone that contribute to HF.
Aldosterone causes sodium and water retention, which contributes to congestion. Aldosterone also causes fibrosis of cardiac cells, leading to continuing remodeling of the myocardium in a manner that increases the propensity for arrhythmias.
What is “aldosterone escape”?
In response to ACE-I or ARB therapy, alternative pathways that elevate aldosterone are activated, leading to high aldosterone levels in spite of ACE-I or ARB therapy.
What did the RALES trial demonstrate?
For patients having severe HF, addition of spironolactone to standard therapy at the time (ACE-I, diuretics, +/- digoxin) led to a 27% decrease in mortality and a 22% decrease in hospitalizations, compared w/ placebo.
What did the EPHESUS trial demonstrate?
Reduced mortality in Post-MI patients w/ epleronone, relative to placebo.
Describe dosing for spironolactone?
25 to 50 mg Qday (12.5 mg/day if elevated serum potassium becomes an issue)
What are the adverse effects of spironolactone?
Hyperkalemia, Breast Tenderness (in women), Gynomastia (in men), & Menstrual Changes (in premenopausal women)
Describe monitoring for the initiation of spironolactone.
Monitor serum potassium during the first 10 days, then monthly for 3 months, then quarterly after that.
Describe dosing for eplerenone.
Initial dose: 25 mg Qday, titrate up to 50 mg Qday
What are the advantages of eplerenone vs. spironolactone? What are the disadvantages?
Eplerenone carried a lower risk of gynecomastia and breast tenderness than spironolactone. However, eplerenone was noted for more serious hyperkalemia events.
What did the EMPHASIS trial demonstrate?
For NYHA FC II HF patients, having EF < 30% (or b/w 31% and 35% w/ QRS > 130 msec), who are maximized on ACE-I/ARB and a BB, the addition of eplerenone 25 mg (up to 50 mg) daily significantly reduced hospitalizations and reduced mortality by 24%, relative to placebo.
For which patients should MRAs, such as spironolactone or eplerenone, be considered?
MRAs should be considered for patients following an acute MI, who have clinical signs of HF and symptoms or history of diabetes mellitus that are already on an ACE-I (or ARB) and a BB and still have an ejection fraction of < 40%.
In which patients should digoxin be considered?
Digoxin should be considered for patients who are already on goal doses of standard HF meds and are still symptomatic, digoxin may help them feel better.
What did the DIG study demonstrate?
The DIG study demonstrated that digoxin has no impact on survival for NYHA FC II-IV patients in normal sinus rhythm. It did reduce hospitalizations though.
Describe dosing for digoxin.
If CrCL < 20 mL/min or pt. < 40 kg: 0.125 mg. If CrCl > 20 mL/min or pt > 40 kg: 0.125 to 0.25 mg. [0.125 mg daily is now typically used in almost all patients though.]
What is the target digoxin serum concentration range for the treatment of patients for atrial fibrillation?
1 to 2 ng/mL
What is the target digoxin serum concentration range for the treatment of patients for heart failure?
0.5 to 1 ng/mL [The DIG study established that digoxin serum concentrations above 1 ng/mL offered no additional benefit for HF patients, but increased the risk of adverse events.]
Above what digoxin level are toxicities associated?
> 2.2 ng/mL
What would be the indications for checking a digoxin levels?
Taking a digoxin level is indicated if toxicity is suspected, if compliance (or benefit) is questionable – if no benefit is seen, the drug should be discontinued – or if a drug or disease interaction leads to questions regarding the safety and efficacy of a given digoxin dosage in a patient.
What are the non-cardiac toxicities associated with digoxin? [Which of these is considered the hallmark of digoxin toxicity, i.e. unique to digoxin toxicity.]
GI toxicities, such as anorexia & N/V/D, are the most common, followed by visual disturbances, such as hazy, blurry vision, difficulty reading, and red-green misperception. CNS effects, including fatigue, weakness, agitation, and hallucinations, are also possible. [Visual disturbances are the hallmark of digoxin toxicity.]
What are the cardiac toxicities associated with digoxin?
SA/AV node depression, AV-block, and atrial/ventricular arrhythmias may occur. Electrolyte imbalances, such as low potassium, low magnesium, high calcium, and metabolic alkalosis can predispose a digoxin patient to arrhythmias.
How long does complete distribution of digoxin take? What time is considered ideal for taking a digoxin level in order to monitor toxicity?
Complete distribution of digoxin takes at least 6 hrs. Trough levels are ideal for monitoring. Have the patient come in for a measurement before they take their daily dose in order to measure the trough level.
How is digoxin cleared from the body? How does this effect whether an individual will be predisposed to digoxin toxicity?
Digoxin is cleared renally. Hence a patient who has renal dysfunction will be predisposed to digoxin toxicity.
Which calcium channel blockers should be avoided in heart failure patients? Which ones are safe?
Non-dihydropyridine CCBs (diltiazem & verapamil) should be avoided in HF patients. Dihydropyridine CCBs (amlodipine & felodipine) are safe to use in HF patients for treatment of comorbid conditions, such as angina or HTN, but themselves are not effective in reducing mortality in heart failure.
Which heart failure patients are treated with anticoagulant therapy, such as warfarin?
Pt.’s who have a Hx of systemic or pulmonary embolism, atrial fibrillation, or mobile left-ventricular thrombi are placed on anticoagulant therapy.
What is the target INR for anticoagulation in cases of atrial fibrillation?
2 to 3 (unless the patient has an artificial valve, in which case the target is 2.5 to 3.5).
Which strategy has greater efficacy in the treatment of atrial fibrillation, rate control or rhythm control?
A study showed that there was no significant difference in the efficacy of rate control vs. rhythm control for atrial fibrillation. Thus since rate control is associated with fewer adverse effects, i t is generally considered preferable.
Which heart failure patients qualify for implantation of an implantable cardioverter defibrillator?
EF < 35%, NYHA FC II or III despite optimal medical therapy, & reasonable expectation of survival w/ good functional status for > 1 yr.
Device therapy can be used for both ischemic or non-ischemic cardiomyopathy. With respect an ischemic etiology, i.e. an acute myocardial infarction, what time constraints are utilized with regards to the implementation of device therapy?
If the etiology is ischemic, device therapy is not initiated within 40 days of an acute myocardial infarction.
What class of medications is most commonly used for heart rate control?
Beta Blockers
What is the indication for amiodarone?
Heart Rhythm Control
What are the two components of fish oils thought to have beneficial cardiac effects?
DHA & EPA
Does vitamin E prevent cardiovascular disease?
No. Many large, randomized clinical trials show that vitamin E does not prevent cardiovascular disease. Two trials actually revealed that vitamin E actually increased cardiovascular risk in heart failure patients.
What is diastolic dysfunction?
The heart is stiff, unable to completely relax and fill with blood, leading to a reduction in cardiac output.
What is the distinction between diastolic dysfunction and diastolic heart failure?
Both involve impaired relaxation of the heart. If the patient is asymptomatic, this is termed diastolic dysfunction. If the patient is symptomatic, it is termed diastolic heart failure or HFpEF (heart failure w/ preserved ejection fraction).
What fraction of patients who have congestive heart failure have normal or near normal ejection fraction?
~1/3
What is the most common cause of diastolic dysfunction?
Hypertension
Aside from hypertension, what else might cause diastolic dysfunction?
Ischemia, Elevated Heart Rate, Atrial Fibrillation, Excess Ventricle Load (Preload), & Aging
What diagnostic tool is required to diagnose diastolic dysfunction?
Echocardiography
What are the goals of treatment of diastolic dysfunction? (6)
1) Relieve symptoms, 2) Treat underlying etiology, 3) Promote regression of left ventricular hypertrophy (LVH), 4) Slow heart rate to increase diastolic filling time, 5) Decrease intracellular calcium overload, & 6) Maintain atrial contraction.
Why is it important to be extra cautious when treating fluid overload with diuretics in patients having diastolic heart failure?
Because a patient who has diastolic dysfunction does not adequately fill the ventricles during diastole, they rely more heavily on adequate blood supply to fill what little they can. Hence aggressive diuresis that reduces preload too much may result in serious hypotension and worsened condition.
Which type of calcium channel blocker is recommended to treat diastolic heart failure? Why?
Non-DHP CCBs (verapamil or diltiazem (diltiazem is preferred)) are recommended. They reduce the calcium load, and they slow the heart rate, preventing tachycardia. [But never uses these in a patient who also has systolic dysfunction, i.e. an ejection fraction of < 40%.]