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95 Cards in this Set

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Chronic right-sided heart failure:
Chronic right-sided heart failure: jugular venous distension, peripheral edema, ascites, GI symptoms, bowel edema, and hepatic edema.
Chronic left-sided heart failure:
Chronic left-sided heart failure: dyspnea (usually with activity, sometimes at rest); in severe cases, pulmonary edema, rales, and sometimes pleural effusions; inadequate cardiac output causing exertional muscle fatigue, decreased renal function andsalt excretion, or depressed mental condition.
Subacute heart failure:
Subacute heart failure: progressive dyspnea plus systemic fluid retention develop over a period of days to a few weeks
Acute heart failure:
Acute heart failure: maximum shortness of breath develops even within minutes (e.g., severe myocardial infarction, bacterial endocarditis, aortic dissection, rapidly progressive myocarditis, aortic dissection, rapidly progressive myocarditis or toxic damage, and valvular regurgitation from ruptured chordae tendineae) .
The most common cause of right ventricular pressure overload (important):
The most common cause of right ventricular pressure overload (important): left-sided heart dysfunction resulting in
pulmonary hypertension.
Right-sided heart failure: due to either chronic right ventricular pressure overload (e.g., pulmonary hypertension due to cor
pulmonale or pulmonary vascular disease) or to intrinsic dysfunction of right ventricle or its valves
Heart failure and ejection fraction
Heart failure and ejection fraction:please remember, 20 to 40 % of heart failure patients have normal EF
Most common primary cause of heart failure in elderly patients (65 and older):
Most common primary cause of heart failure in elderly patients (65 and older): diastolic dysfunction. They have normal or mildly impaired systolic function. Diastolic dysfunction is a diagnosis of exclusion. The test most commonly used to measure diastolic dysfunction: Doppler echocardiography which is neither sensitive nor specific.
Flash pulmonary edema:
Flash pulmonary edema: espisodic heart failure due to intermittent ischemia. Revascularization may be indicated.
Heart failure with preserved systolic function (important):
Heart failure with preserved systolic function (important):
(i)
Hypertension causes left ventricular hypertrophy and increased fibrosis causing chamber stiffness.
(ii)
Ischemic heart disease causes subendocardial fibrosis or acute, intermittent ischemic dysfunction.
(iii) Diabetes mellitus causes loss of myocytes (apoptosis), increased fibrosis with shifts to more rigid collagen, and loss of vascular compliance.
The most important cause of dyspnea in heart failure:
The most important cause of dyspnea in heart failure: pulmonary congestion with increased interstitial or intra-alveolar fluid which activates juxtacapillary J receptors, which stimulates a rapid and shallow breathing. Cheyne-Stokes respiration or periodic breathing can occur in advanced heart failure and is usually associated with the low output state
A patient appears with H/O of an attack of acute, severe shortness of breath 1 to 3 hours after the patient retires. The symptoms improve 10 to 30 minutes after the patient arises (very important). Most likely diagnosis:
A patient appears with H/O of an attack of acute, severe shortness of breath 1 to 3 hours after the patient retires. The symptoms improve 10 to 30 minutes after the patient arises (very important). Most likely diagnosis: paroxysmal nocturnal dyspnea (PND).

Etiology of PND and orthopnea: increased venous return from the extremities and splanchnic circulation, and mobilization of interstitial fluid from the extremities and elsewhere resulting in alveolar edema.
PND is a rare clinical manifestation. PND usually represents cardiac failure
Acute pulmonary edema in heart failure
Acute pulmonary edema in heart failure:due to transudation of fluid into the alveolar spaces as a result of acute rises in capillary hydrostatic pressure which is due to acute decompression of cardia function or to an acute elevation of intravascular volume.
Exercise intolerance in heart failure is due to:
Exercise intolerance in heart failure is due to:
(i)
Increased pulmonary venous pressure and pulmonary congestion.
(ii)
Reduced blood flow to exercising muscles as a result of decreased cardiac output reserve, impaired peripheral vasodilatation, and reduced oxygen delivery.
(iii) Biochemical changes and alterations in fiber types of skeletal muscles.
(iv) Reduced respiratory muscle function and ventilatory control.
Edema in heart failure
Edema in heart failure:transudation of fluid occurs due to increased capillary hydrostatic pressure in the systemic circulation as a result of elevated right atrial pressure. Ascites occurs due to elevated pressure in the hepatic, portal, and
systemic veins draining from the peritoneum.
Ascites is uncommon in heart failure.The lives damage is most commonly, due to tricuspid regurgitation
Etiology of cardiac cachexia:
Etiology of cardiac cachexia: unknown; may be due to elevated levels of proinflammatory cytokines (e.g., tumor necrosis I ~factor),
loss of appetite, malabsorption, andelevated metabolic rates.
Brain function in heart failure:
Brain function in heart failure: not affected except in advanced cases in which cerebral hyoperlusion may result in loss of memory, altered mentation, limited attention span, and irritability
Physical examination findings in heart failure (important):
Physical examination findings in heart failure (important): due to elevated left ventricular filling pressures and to a
lesser extent, reduced cardiac output.
Please remember,in chronic heart failure many of these findings are absent
Physical examination findings in heart failure (important
Appearance: of patients in the cardiac failure
Appearance:
(a)
Severe symptoms:restless,dyspneic,and diaphoretic or pale.
(b)
Compensated patients: comfortable.
Physical examination findings in heart failure (important
Vital signs:
Vital signs:
(a)
Heart rate: above 80 beats/minute (high end of normal range); lower in chronic stable patients; premature beats or arrythmias are present. Please remember, pulsus alternans (alternating amplitude of successive beats) indicates advanced heart failure or a large pericardial effusion.
(b)
Blood pressure (BP): normal or high;usually low end of normal or below in advanced heart failure.
Physical examination findings in heart failure (important)
Jugular veins and neck examinations
(a)
Examination of jugular veins: please remember, one of the most important aspect of the evaluation; an elevated jugular venous pressure (normal 8 em of water or less) by estimating the level of pulsations above the sternal angle and adding 5 cm in any posture or abnormal abdominal-jugular reflex (rise in the jugular pressure of at least 1 cm) by putting pressure on the right upper quadrant of the abdomen for 30 seconds and avoiding an induced Valsalva maneuver is found in 80% cases of advanced heart failure.
(b)
Tricuspid regurgitation (TI): a large CV wave is noted in patients with high jugular venous pressure. TI is confirmed by hepatic pulsation during the abdominal-jugular reflex determination.
(c)
Carotid pulsation is examined to rule out aortic stenosis.
(d)
Thyroid abnormalities should be ruled out.
Physical examination findings in heart failure (important)
Pulmonary examination:
Pulmonary examination: the most common symptom is dyspnea. The presence of rales (alveolar fluid) indicate heart failure.

Please remember, rales are usually absent in chronic heart failure even when the pulmonary capillary wedge pressure above 20 rom Hg (normal, less than 12 mm Hg).

Please remember, left ventricular failure cannot be ruled out by the absence of rales. In rare cases, pleural effusions occur which indicates bilateral heart failure.
Physical examination findings in heart failure (important)
Cardiac examination:
Cardiac examination:
to identify the associated cardiac abnormalities than the assessment of the severity.
(a)
Parasternal lift: indicates pulmonary hypertension Pulmonic component of the second heart sound (P') may be accentuated.
(b)
Point of maximal impulse displaced below the fifth intercostals space or lateral to the mid-clavicular line: indicates cardiac en1argement.
(c)
Additional precordial pulsation: indicates left ventricular aneurysm.
(d)
Apical third heart sound (S3 indicates left ventricular dysfunction. The first heartsound (S) may be diminished.
(e)
An S3 at the lower left or right sternal border or below the xiphoid process: indicates right ventricular disfunction.
(f)
The presence of murmurs: indicates valvular disease causing the heart failure, however, MR (mitral regurgitation) and TR (tricuspid regurgitation) can occur due to severe ventricular dilation and dysfunction
Physical examination findings in heart failure (important)
Examination of the abdomen:
Examination of the abdomen: determines the size, tenderness, and pulsality of the liver due to passive congestion and TR (tricuspid regurgitation), and degree of ascitis.
Physical examination findings in heart failure (important)

Examination of the extremities:
Examination of the extremities: determines the peripheral edema
The most useful procedure to make the diagnosis of heart failure (important)
The most useful procedure to make the diagnosis of heart failure (important): transthoracic echocardiogram which has replaced the plain chest x-ray. A cardiothoracic ratio above 0.50 in chest x-ray indicates heart failure, however, nearly 50% of heart failure patients do not have a high cardiothoraic ratio. EKG is to evaluate cardiac rhythm, identify prior MI, and diagnose left ventricular hypertrophy
How to diagnose heart failure (important):Acute heart failure
Acute heart failure: diagnosis is simple when a patient appears with classic clinical manifestations. The most frequent symptoms are dyspnea and fatigue, which are nonspecific findings. The most specific symptoms are orthopnea, paroxysmal nocturnal dyspnea, and edema which are uncommon manifestations
How to diagnose heart failure (important):Chronic heart failure
Chronic heart failure: to make the diagnosis is difficult because no single sign or symptom is diagnostic. The most important is to maintain a high degree of suspicion, especially in high risk patients (e.g., coronary artery disease, chronic high BP, diabetes, advanced age, and h/o heavy alcohol use).
How to diagnose heart failure (important)
Investigations:
Investigations: transthoracic echocardiography is the preferred diagnostic test.
Please remember, chest x-ray is not very useful
How to diagnose heart failure (important)
Echocardiographic findings
Echocardiographic findings: quantitative assessment of left ventricular function which is abnormal in heart failure; also detects both ventricuIar sizes, regional wall motion (as an indicator of prior MI), left ventricular hypertrophy, and determination of abnormality of the heart valves
How to diagnose heart failure
How to differentiate from pulmonary diseases
How to differentiate from pulmonary diseases: abnormaI lung function test and additional tests to determine the lung pathology.
A patient appears with heart failure and evidence of ongoing cardiac ischemia. How to evaluate coronary artery disease (important):
coronary angiography should be performed.
A patient appears with heart failure without angina and prior RIO MI. How to evaluate coronary artery disease (important):
noninvasive
stress testing in conjunction with nuclear myocardial perfusion imaging or echocardiography.
A patient appears with heart failure with or without underlying coronary artery disease, How to evaluate coronary artery disease:
does not need any evaluation for coronary artery disease.
Myocardial biopsy in a patient with heart failure:
routine myocardial biopsy is not indicated except in patients with acute fulminant myocarditis, especially eosinophilic and giant cell myocarditis which require immunosuppressive therapy; the patient being evaluated for heart transplantati
A patient appears with asymptomatic arrhythmia. What is the next step in management?
Further evaluation is not indicated. However, a patient with symptomatic (syncope or hemodynamic compromise) ventricular arrythmia should be evaluated and treated
immediately.
Different mechanism in heart failure:
(i)
Early phase:
(ii)
Terminal phase:
Early phase: neurohormonal mechanisms
(ii)
TerminaI phase: hemodynamic mechanisms
Drugs that slow the progression of heart failure and reduce the risk of major cardiac problems in patients with asymptomatic left ventricular dysfunction or established symptoms of heart failure (important):
ACE (angiotensin-converting enzyme) inhibitors (e.g., captorpril, enalapril, llsinopril, quinapril, fosinopril)
and beta-adrenergic receptor blockers (e.g., carvedilol, bisoprolol, metoprolol)
Prevention of heart failure (important):
1. Decreases the risk of the initial cardiac injury:
(a) Lipid lowering drugs are used in patients with hyperlipidemia.

(b) Antihypertensive drugs are used inpatients with hypertension.

2. Decreases heart failure after cardiac injury:
(a) Aggressive therapy in patients with acute MI.
Percutaneous transluminal coronary angioplasty and thrombolytic agents are useful.
The use of beta-blocker and ACE inhibitor reduce the risk of heart failure, reinfarction, and death;
this combined neurohormonal blockade produces synergistic benefits.

(b) Patients with established Ischemic or non-ischemic left ventricular dysfunction (i,e.,ejection fraction less than 35-40%) with no or minimal symptoms of heart failure: ACE inhibitor is useful.
(c) Patients with a h/o heart failure after an acute MI: ACE inhibitor or beta-blocker reduces the risk of death.
Outpatient treatment for patients with heart failure (important):
general measures
General measures:

Please remember, bed rest should be avoided (bed rest increases disability) except in patients with condition; exercise should be encouraged; heavy labor or exhaustive sports should be avoided.
(b) Please remember, water restriction is not indicated except inpatients with moderate to severe hyponatremia.(

c) Moderate sodium restriction is indicated to allow use of lower dose of diuretic drugs.
(d) Obese patients should lose weight.
(e) Smokers should stop smoking.
(f) Lipid lowering drugs are used for hyperlipidemia.
outpatient tx for patients with heart failure (important):
Specific therapies:
Specific therapies:
(a) Please remember, NSAIDs should not be used because these drugs inhibit the effects of diuretics and ACE inhibitors and may worsen cardiac and renal function.
(b) Calcium channel blockers should not be used because of their cardiodepressant effects.
(c) Antiarrythmic drugs should not be used because of their proarrythmic effects.
(d) Patients with asymptomatic ventricular tachycardia do not require therapy.
(e) Electrophysiologic devices are useful in patients with sustained ventricular tachycardia or ventricular fibrillation or who have been resuscitated from sudden cardiac arrest.
(f) Anticoagulants are used in patients with atrial fibrillation or a history of an embolic episode.
(g) Antihypertensive medications are used in patients with hypertension to improve both systolic and diastolic function
The first step in the treatment of patients with chronic heart failure (important):
diuretic therapy, however, diuretics should be combined with ACE inhibitors to increase effectivity of the therapy.
The preferred diuretic drugs for patients with heart failure:
loop diuretics (e.g., furosemide, torsemide, ad bumetanide).
Site of action of different diuretic drugs:
(i) Loop of Henle: furosemide, torsemide, andbumetanide
(ii) Distal tubule: thiazides and metolazone
(iii) Collecting duct: spironolactone (potassium-sparing diurectic)
Mechanism of action of diuretics:
inhibit the reabsorption of sodium and chloride at specific sites of renal tubules.
Diuretics recommeded in patients with heart failure and impaired renal function and perfusion (important): l
loop diuretics (e.g., furosemide, torsemide, and bumetanide).

Please remember, thiazide diuretics lose their effectiveness in patients with only moderately impaired renal function and perfusion.
The effect of NSAIDs on diuretic therapy (important):
NSAIDs decrease the efficacy of diuretic therapy.

Please remember, NSAIDs should not be used along with diuretics.
Importance of using diuretics in patients with heart failure (important):
(
i) Diuretics are the only drugs, which can control fluid retention inpatients with heart failure.

Please remember, ACE inhibitors can cause pulmonary and peripheral congestion.

(li) Diuretics can relieve pulmonary and peripheral edema within hours or days.
The effects of ACE inhibitors, betablockers, and digoxin take weeks or months to become apparent.

(iii) The response of ACE inhibitors and beta-blockers depends on diuretics (i.e., if the dose of diuretic is less than adequate), intravascular volume increases which decreases the response of ACE inhibitors, and enhances the risks of treatment with beta-blockers.
the dose of furosemide:
the starting dose is low (Le., 20-40 mg once or twice daily); subsequent doses are provided to achieve dry weight up to 400 mg/day.
Indications for using high doses of diuretics: patients with advanced heart failure and decreased renal function.
The effect of simultaneous use of diuretics and digoxin in a patient with heart failure (important):
diuretics can cause hypokalemia and hypomagnesemia, which can cause cardiac arrhythmia, especially in patients receiving digoxin therapy.
Adverse effects of diuretics in patients with hear failure and their managements (very important): .~~
(i) Hypotension: if the patient is asymptomatic and has signs of fluid overload, diuretic therapy should be continued.
(li) Azotemia:it the patient is asymptomatic and has signs of fluid overload, diuretic therapy should be continued.
(iii) Hypokalemia and hypomagnesemia: the patient can develop cardiac arrythmias, especially in the presence of digoxin therapy. ACE inhibitors (e.g., captopril, enalapril) , angiotensin II receptor blockers, or aldosterone antagonist (e.g., spironlactone) should be given concomitantly to prevent the loss of electrolytes.
(iv) Neurohormonal activation: the risk of disease progression can occur in a patient with heart failure. ACE inhibitors or sympathetic antagonists are used concomitantly to avoid neurohormonal
activation.
The drug of choice in patient with heart failure due to left ventricular systolic dysfunction (important):
The drug of choice in patient with heart failure due to left ventricular systolic dysfunction (important): ACE inhibitors
captopril
enalapril
fosinopril
ramipril
are approved to use for tx of P. with heart failure after acute MI

ACEi should be used even if P. do not have symptomatic benefits, have low BP
or have impaired renal function
Mechanisms of action of ACE inhibitors: .
1 increase the actions of kinin
and inhibit the degradation of kinins.
these actions are more important than that of inhibition or angiotensin II formation.

2. inhibit the formation of II from angiotensin I.

both action inhibits cardiac hypertrophy and programmed cell death- apoptosis
Doses of ACE inhibitors
initially the patient should receive low dose, followed by gradual increments in does if tolerated.
2. high doses are decreased the hospitalization more than lower doses

clinical effect may take weeks or months from the onset of therapy
Drug should be used along with ACE inhibitor
diuretics, because the fluid retention inhibit the action of ACEi
Drug should not be used along with ACE inhibitor
NSAIDs- they increase the risk and decreased the action of ACEi
the clinical effects of ACE inhibitors (important):
the clinical effects of ACE inhibitors (important):
1. Improve left ventricular ejection fraction.
2. decrease left ventricular chamber size,
3. Relieve dyspnea and reduces the need for emergency care for worsening heart failure.
4 Reduce the risk of death and retard the progression of heart failure in patients with an ischemic (e.g., MI) or non ischemic cardiomyopathy who are receiving digoxin and diuretics.
5. Reduce the need for large dose of diuretics and potassium supplements .
6 Reduce the adverse effects of diuretics (e.g., hypokalemia and hyponatremia
Complications of using ACE inhibitors (important):
1/Angiotensin suppression effects:
Complications of using ACE inhibitors (important):

Angiotensin suppression effects:

(a) Early in therapy, low BP and high BUN in an asymptomatic patient.
Treatment: no therapy is required.

(b) Low BP, dizziness or blurred vision or significant worsening of renal function. Treatment: reduce the dose of diuretic except in case of a fluid retention.

( c) High K in patients who are receiving potassium-sparing diuretics.
Treatment: stop potassium supplement or change those medications.

Please remember, most patients with above conditions can be treated without stopping ACE inhibitors.
(ii)
Kinin potentiation effects:
(a)
Angioedema(lessthan 1%ofpatients): maybelliethreatening. Treatment: ACE inhibitors should not be given for the llietime of the patient Use angiotensin receptor Il antagonists (e.g., losartan, valsartan, irbesartan, eprosartan, and cardesartan.)
(b)
Non-productive cough (5 to 15% of cases): appears within first several months of therapy, disappears within 1to2 weeksofdiscontinuingtherapy, andrecurs within days ofrestarting therapy. Treatment: stop using ACE inhibitors. Use angiotensin receptor Il antagonists. Please remember, if the patient
cantolerate ACEinhibitors, neveruseangiotensin receptor Ilantagonists
Complications of using ACE inhibitors (important)
2 Kinin potentiation effects:
Kinin potentiation effects:


(a) Angioedema(less than 1% of patients): maybe life-threatening. Treatment: ACE inhibitors should not be given for the life time of the patient
Use angiotensin receptor Il antagonists (e.g., losartan, valsartan, irbesartan, eprosartan, and cardesartan.)

(b) Non-productive cough (5 to 15% of cases): appears within first several months of therapy, disappears within 1 to 2 weeks of discontinuing therapy, and recurs within days of restarting therapy.

Treatment: stop using ACE inhibitors. Use angiotensin receptor Il antagonists.
Please remember, if the patient
can tolerate ACE inhibitors, never use angiotensin receptor Il antagonists
Effects of beta-blockers
Effects of beta-blockers (e.g., carvedilol, metoprolol, and bisoprolol) in patients with heart failure: used along with ACE inhibitors.

(i) Improve left ventricular ejection fraction.
(li) Decrease left ventricular chamber siZe.
(ill) Improve cardiac remodelling.
(iv) Reduce the risk of death and retard the progression of heart failure in patients with ischemic or non-ischemic cardiomyopathy who are receiving digoxin, ACE inhibitors ,and diuretics
Beta-blockers should not used in patients with following conditions (important):
Beta-blockers should not used in patients with following conditions (important):
(i) Bronchospastic disease (e.g., asthma)
(ii) Advanced heartblock
(iii) End-stage cardiac disease patients who are receiving intravenous therapy or class IV symptoms.
Complications of using beta-blockers
Complications of using beta-blockers (e.g., carvedilol, metoprolol, and bisoprolol) (important):

(i) Hypotension (24 to 48 hours after the onset of therapy or the change of doses:due to vasodilation.

Treatment usually subside with repeated dosing without any change in the dose of this medication or ACE inhibitor; advice administration of beta-blocker and ACE inhibitor at different times of the day.

(ii) Bradycardia and heart block: patients are usually asymptomatic or may develop hypotension.

Treatment: reduce the dose of beta-blocker if the heart rate is less than 50 beats per minute or second or third degree heart block is noted.
If the use of beta-blocker is necessary, cardiac pacing is indicated in those selected patients.

(iii) Fluid retention (3 to 5 days after the onset of therapy or the change of doses): patients are always asymptomatic.
Body weight should be measured daily. Treatment: increase the dose of diuretic until the patient's weight is reduced to pre-treatment level.
Use of aldosterone antagonist
Use of aldosterone antagonist (e.g., spironolactone) in heart failure: low dose of this medicine can be used in patients with advanced heart failure, however,such use is not approved by FDA.
Mechanisms of action of digoxin in patients with heart failure:
Use of digoxin in patients with heart failure (important):
Contraindications of using digoxin in patients with heart failure (important):
Doses of digoxin
Monitoring serum digoxin level
Monitoring serum digoxin level:
Complications of digoxin therapy (important):
Digoxin foxicity can occur in normal serum digoxin levels
Can you use digoxin in a patient with advanced heart block?
Can low doses of digoxin cause toxicity in the long term use in a patient
tx of heart failure
A female patient appears with heart failure and she cannot tolerate ACE inhibitors because of cough or angioedema. Next drug of choice:
A male patient appears with heart failure and he cannot tolerate ACE inhibitors because of hypotension or renal insufficiency. Next drug of choice:
A patient appears with heart failure and hypertension. Preferred therapy:
A 86-year-old male patient appears with heart failure and angina. He is not in a good health. Medical therapy:
A patient appears with angina after an unsuccessful revascularization procedure. Medical therapy:
A patient appears with heart failure and atrial arrythmias (important): Preferred therapy:
Apatient appears with asymptomatic ventricular arrythmias (important). Management:
A patient appears with heart failure and symptomatic ventricular arrythmias which indicates the severity of underlying cardiac disease (important). Management:
A patient appears with heart failure and symptomatic ventricular arrythmias which indicates the severity of underlying cardiac disease (important). Management:
A patient appears with heart failure without atrial fibrillation. Echocardiogram reveals a large thrombus within the left ventricle (very important). Is anticoagulation therapy indicated?
The following drugs should be avoided in patients with heart failure
Indications for hospital admission in patients with heart failure: three syndromes
The most frequent cause of fluid overload in patients with heart failure (important
Management of patients hospitalized for refractory peripheral edema from heart failure (important): the goal is
Pulmonary edema in patients with heart failure is due to
Pulmonary edema in patients with heart failure is due to:transudation of fluid in to the alveolar space
Transudation of fluid into the alveolar space does not occur:
Management of patients hospitalized for pulmonary edema from heart failure (important):
Management of patients hospitalized for pulmonary edema from heart failure (important):
cont..Phannacologic dilatation of peripheral vessels improves the clinical condition because peripheral vasoconstriction causes pulmonary edema (very important):
Management of patients hospitalized for pulmonary edema from heart failure (important): cont ..
Indications for mechanical ventilation

Indications for phlebotomy
The most serious clinical manifestation of heart failure in the hospitalized patients
Difference between milrinone and dobutamine
Difference between milrinone and dobutamine