CONGESTIVE HEART FAILURE

2CARDIOLOGY

CARDIOLOGY1

XE "Congestive Heart Failure" CONGESTIVE HEART FAILURECauses of Heart Failure

Predominant systolic failure

1.Coronary artery disease

2.Hypertension

3.Dilated Cardiomyopathy (idiopathic, toxic, infectious)

Predominant diastolic failure

1.Hypertension

2.Hypertrophic cardiomyopathy

3.Restrictive cardiomyopathy (amyloidosis, sarcoid)

4.Constrictive pericarditis

5.High output failure

Ventricular Function

Heart failure (HF) is often associated with impaired ventricular function. Muscle removed from patients and animals with HF shows a in the active length tension relationship and icular function curve. In the presence of a disturbance in myocardial contraction or an excessive Lamic burden placed on the ventricle or both, the heart depends upon :

1.Frank-Starling mechanism: preload (i.e., lengthening of sarcomeres provides an optimal overlap between thick and thin myofilaments) acts to sustain cardiac performance

2. release of catecholamines by adrenergic nerves and the adrenal medulla myocardial contractility

3.Myocardial hypertrophy: w/or w/out chamber dilatation in which the mass of contractile tissue is augmented.

Initially these 3 compensatory mechanisms may be adequate to maintain the overall pumping ability of the heart. However, these compensatory mechanisms have a limited potential, and if the disturbance in myocardial contraction and / or the excessive hemodynamic burden persists, the heart ultimately fails.

Alterations in the function of the Neurohumoral system

Adrenergic nervous system:

Positive inotropic effect mediated by its interaction with the cardiac sarcolemmal -receptor which with the help of G proteins stimulate production of adenlylate cyclase formation of cAMP. intracellular cAMP activates cAMP-dependent protein kinases catalyze transfer of phosphate groups to specific sites on other intracellular proteins transcellular Ca influx through slow channels in response to depolarization, as well as release, faster reaccumulation and storage of Ca in the sarcoplasmic reticulum.

While circulating catecholamines may help to maintain ventricular function for variable periods of time, there is a price to be paid worsened survival. Decompensation may be due to the ability of catecholamines to:

1.cause necrosis and/or apoptosis

2. regulate the -receptor-G protein-adenlylate cyclase complex

3.cause arrhythmia.

Renin-angiotensin-aldosterone system:

In low-output states activation of the renin-angiotensin-aldosterone axis. While there are several signals for renin release, renin conversion of angiotensin 1. Angiotensin II is then formed by ACE.

Angiotensin II: potent vasoconstrictor. Contributes to extreme of systemic vascular resistance. Interruption of the renin angiotensin-aldosterone axis by means of an ACE inhibitor SVR, afterload cardiac output in HF.

ADH: released because the kidneys are now seeing an effective in blood flow. Thus H2O and salt retention occurs.

Endothelin: also released in HF marked vasoconstriction.

Atrial natiuretic peptide: counter regulatory protein that assist in combating the vasoconstriction.

Forms of HF

XE "Heart failure:Backward" Backward heart failure

Inability of cardiac muscle to shorten against a load alters the relationship between ventricular end-systolic pressure and volume. The following adaptations take place:

1. ventricular end-systolic volume ventricular end-systolic pressure

2. volume and pressure in the atrium behind the failing ventricle.

3.atrium contracts more vigorously

4.pressure in the venous and capillary beds behind (and upstream) to the failing ventricle .

5.transudation of fluid from the capillary bed into the interstitial space leading to pulmonary congestion and/or peripheral edema and ascites.

Although an in LVEDP is associated with ventricular function, pressure is not specific for HF and there is no upper limit value specific for LV failure. LVDP may by other factors such as compliance, severe volume overloading (mitral regurgitation), or cardiac tamponade.

Forward Failure Hypothesis.

Clinical manifestations of HF inadequate delivery of blood into the arterial system manifestations due to CO perfusion of vital organs, including:

1.brain mental obtundation

2.skeletal muscles weakness

3.kidneys Na and H2O retention

Although CO is frequently in HF, failure cannot be defined by a minimum value of CO. For instance, CO at rest may be normal even when the heart is failing.

An enlarged heart may produce the same SV with ejection fraction.

A CO may be above normal, as in cardiac failure associated with sever anemia or severe hyperthyroidism (high output failure).

XE "Heart failure:Right vs. Left" Right sided versus left sided failure

Fluid localizes behind the specific cardiac chamber that is initially affected. Thus, symptoms secondary to pulmonary congestion predominate in patients with myocardial infarction, hypertension, aortic and mitral valve disease (left heart failure). With time, fluid accumulation becomes generalized and ankle edema, congestive hepatomegaly, and ascites occurs (right heart failure).

The most common cause of right heart failure is left heart failure.

Systolic versus diastolic

Diastolic failure is impaired capacity to accept blood or fill without a compensatory increase in LAP. It may be the sole cause of HF in 1/3 of pts. Unlike systolic dysfunction, in diastolic dysfunction, LV is usually small and thick, with a good overall ejection fraction. Diastolic dysfunction may be seen in ischemic heart disease, HTN, LVH, and infiltrative diseases. Some patients with systolic dysfunction also have a component of diastolic dysfunction

Precipitating Causes of CHF

1.Inappropriate treatment reductions or additions, (salt, beta blockers, estrogens)

2.Arrhythmias:

(Tachyarrhythmias: time available for ventricular filling, O2 consumption ischemia

(Bradycardia: SV is max and cant further CO

3.Late complications from an MI: papillary muscle dysfunction

4.infections: metabolic rate, fever, tachycardia

Symptoms related to pulmonary congestion

XE "Dyspnea" Dyspnea

1.Pulmonary congestion is associated with dyspnea (difficult or labored breathing) only with exertion in mild heart failure. W/worse HF progressively less exertion and finally even at rest.

2.Orthopnea: When a subject is supine, the fraction of the blood volume contained in the lungs is .

3.PND: In its worst form, it is accompanied by cough, sometimes productive of white frothy sputum which is occasionally blood stained. These attacks are termed pulmonary edema.

4.Cough: 1 a respiratory symptom. However cough, on assuming the supine position or on performing exercise, is an important symptom of cardiac disease and is related to pulmonary congestion.

Other Evidence of Pulmonary Congestion

W/ pulmonary congestion can hear on PE.

Chest X-ray: Redistribution of the blood in the lungs engorgement of the pulmonary veins and to fluid in the interstitial spaces of the lungs or in the alveoli. Normal standing subject:

(upper lung zones are lucent (blood flow is least and the veins are almost collapsed)

(blood lower lung zones flow is greatest.

In HF normal distribution of blood flow from top bottom of the lungs is abolished and eventually even reversed in cardiac failure in appearance of lung fields on X-ray.

Enlarged heart: most forms of HF cardiac enlargement. See an enlarged heart on X-ray. If a patient presents with new onset severe CHF and a normal heart size, think of a recent AMI.

Systemic Congestion

Pulmonary circulation: Normally pressure, capacitance system. 5-10 mmHg suffices to drive blood from the head of the pulmonary circulation (the pulmonary artery ) to its termination (the left atrium).

If LV diastolic pressure pulmonary venous pressure (from 10-30 mmHg), normal mean pulmonary arterial pressure of approximately 11 mmHg will not suffice to perfuse the pulmonary vascular bed. Then obligatory pulmonary arterial HTN accompanies LVD HTN.

systolic RVAP hypertrophy and dilate and failure RVD pressure transmitted throughout diastole through the open tricuspid valve to RA SVC and IVC (not separated by valves from the right atrium) in CVP congestion of systemic tissues and organ:

1.liver becomes congested and eventually its function is grossly impaired

2.subcutaneous fluid appears as edema

3.effusions in the peritoneum (ascites) and in the pleural and pericardial cavities.

Cardiac Manifestations of HF

Heart Enlargement: Manifested by clinical examination, the chest radiograph, the electrocardiogram, and the echocardiogram.

Cardiac Auscultation

S-1 is related to the closure of the mitral valve.

S-2 to the closure of first the aortic. Then the pulmonary valves.

Normally silent opening of the aortic and pulmonary valves, and mitral and tricuspid valves is.

Abnormal Findings:

S-3 in adults w/enlargement and HF: In early diastole, rapid ventricular filling takes place. In young adults, this is signaled by an audible S-3. If in adults collaborates the diagnosis of HF. Associated with cardiac dilatation.

Loud S-4: Sign of ventricular diastolic compliance. Normally, blood flows rapidly from the atrium to ventricle in early diastole. Thereafter, occurs the period of diastasis during which time little or no blood flows from the atrium to ventricle. Atrial contraction causes a 2nd spurt of blood flow from atrium to ventricle. When ventricular diastolic compliance is , atrial systole is accompanied by a loud S-4 sound which occurs in pre-systole.

Pansystolic mumur: When the ventricles dilate, the AV valves may become incompetent. This permits blood to regurgitate from the ventricle to the atrium. A pressure gradient from ventricle atrium exists throughout systole pansystolic mumur.

XE "JVP" JVP

The deep jugular veins are not separated from the superior vena cava by valves, so that the level of the central venous pressure may be noted by observing the jugular venous pulsations. Jugular venous pulsations ought not be visible above the level of the angle of Louis in any posture supervened above 30 degrees.1.A wave: generated by atrial systole

2.C wave: Associated with isovolumic systole

3.X descent: accompanies ventricular ejection

4.V wave: passive filling of the atrium from its supplying veins

5.Y descent: opening of the tricuspid valve.

When the RV fails, JVP is . Rt ventricle dilation 1.large systolic v wave in the JVP

2.y wave, is precipitous

HR and Rhythm; BP

Hypoperfusion sympathetic stimulation tachycardia which may partially correct CO related to SV.

Sympathetically mediated vasoconstriction mild HTN. LA HTN and stretching to A. fib. Extensive myocardial dz ventricular extrasystoles and occasionally ventricular tachycardia.

Regional Perfusion

HF CO (esp. during exercise). Major redistribution of regional perfusion occurs.

1. in renal blood flow retention of Na and H2O blood volume dilation of the heart, of ventricular diastolic pressures, and congestion of the lungs and systemic tissues.

2. capillary pressure (pulmonary and systemic) moves fluid from the vascular compartment to the tissues.

Routine tests for heart failure.

ECG: AMI, arrhythmias, heart block.

Chest x-ray: described above

Echo: allows us to see the size of the heart, the function, and the thickness and any vascular abnormalities.

Treatment Goals of Cardiac Failure

Improve symptoms

Prevent deterioration of function

survival.

Non-pharmacologic

1.Removal or treatment of precipitating or aggravating causes:

2.treating respiratory or other infections

3.management of arrhythmias

4.Treatment of HTN

5.Treatment of MI.

6.Control risk factors for myocardial ischemia.

Diet. Restriction of Sodium Intake- a daily sodium intake of 2 to 3 grams can be quite tolerable with food additives to improve palatability. Salt binges are a major reason that patients decompensated.

Physical activities: because restricting exercise causes reconditioning and regular exercise can increase peak exercise capacity, encouraging patients to exercise regularly and as strenuously as their symptoms permit, or to enter into formal rehabilitation programs can enhance their quality of life.

Cardiac transplantation:

1.Candidates should be < 60 y.o.

2.Advanced CHF

3.Strong psychosocial support system,

4.Exhausted all other therapeutic options,

5.Free of irreversible extra cardiac organ dysfunction that would limit functional recovery or predispose to post-transplant complications.

Survival is 90% at 1 year and 70% at Lye years.

Drug Treatment of HF

XE "Diuretics" Diuretics:

filling pressures of the heart but does not bring the patient to a new Starling curve (no increase in cardiac output).

Choice of appropriate diuretic agent:

1.Mild sodium retention-Thiazides.

2.Moderate to sever sodium retention--loop diuretics (furosemide (lasix) bemetarnde (bumex).

3.Persistent sodium retention--loop diuretics plus thiazides or metolazone.

4.K+ sparing diuretics (spironolactone) may also be added.

Diuretic dose should be titrated to relieve congestive symptoms and signs, normalize CVP, and stabilize weight. Side effects include intravascular volume depletion, hyponatremia, hypokalemia, hyperkalemia, metabolic alkalosis, hyperuricemia

Pearls concerning diuretics:

1.It's generally better to give HCTZ or lasix as a single daily dose. If inadequate, more diuresis will usually be obtained by doubling the dose rather than giving the same dose twice.

2.Avoid excessive diuresis that might prevent titrating ACE inhibitors to full therapeutic levels.

3.Check serum K frequently during initiation and titration (about every 3 days)

4.Beware of combo of ACE inhibitor and K sparing agents.

5.If large doses of diuretics are used, Mg levels should be checked.

6.Pt adjustment of dose: Since the need for diuretics varies depending on the patient's diet and level of activity, having patient adjust the dosage themselves is a useful approach. Pt can be advised to or their diuretic dose to maintain their weight-as measured each morning--titrate to a range in which they have few symptoms of congestion.

XE "Vasodilators" Vasodilators

Always used in patients w/CHF.

Most offer venodilation and/or arterial vasodilation. Most effective when pulmonary congestion is 2 to pulmonary wedge pressure rather than CO.

Hydralazine

Afterload and is therefore used for SVR and HTN.

In combination w/nitrates survival in patients with CHF. Work well to mitral regurgitation or aortic insufficiency. More SE than ACE inhibitors.

Nitrates

Mostly venodilation with some afterload .

Complement diuretics in right and left atrial pressures. Especially useful if coronary artery dz is present. They are available orally or as a patch.

Tolerance to its effects have become an issue and to prevent this, a "nitrate free interval" should be instituted (3x/day vs. 4X/day).

XE "ACE inhibitors" ACE inhibitors

Most important advance in therapeutics for HF in the past two decades.

Up to a 40% in 1-year mortality in class IV pts.

1.Slows remodeling (ventricular enlargement)

2. hemodynamics and survival rates in patients with LV dysfunction due MI.

3.Prevent clinical deterioration in asymptomatic patients with ejection fractions.

4.1st line therapy for all patients with LV function. Even mildly symptomatic patients who used to do fine just on a diuretic should now also receive an ACE inhibitor.

ACE inhibitors should be instituted with caution if there is renal dysfunction or hyperkalemia. While ACE inhibitors can cause a cough, many patients with CHF also have cough.

Angiotensin II receptor antagonists: losarten, valsarten. In contrast to ACE inhibitors. No bradykinin levels cough and angioedema.

XE "Calcium channel blockers" Calcium channel blockers

Verapamil, nifedapine, diltiazem: 1st generation drugs. Vasodilation counterbalanced by negative inotropic effects. Not well tolerated in congestive heart failure.

Amlodipine and felodipine: 2nd generation drugs. Vascular specific. symptoms.

XE "Inotropes" Inotropic agents

Digitalis

The only approved oral inotropic drug.

Most useful with moderate CHF, esp. in the setting of A. fib.

Least useful in cardiogenic shock with pulmonary edema. Up to 25% of hospitalized patients get toxic. Toxicity most often occurs in the setting of old age, renal failure, COPD, hypokalemia, hypocalcemia, hypothyroidism, and some drugs such as quinidine, verapamil and amiodarone.

Other inotropes have been tested, including beta agonists, dopamine like drugs and hospodiesterase inhibitors. While short term improvement has been seen, tachyflaxis and long term side effects (including increased mortality) currently preclude their use.

Parenteral inotropes have been used with much success for decompensated patients. These drugs include:

1.Dobutamine: -agonist. CO, wedge pressure at doses that don't HR and BP.

2.Milrinone: phosphodiesterase inhibitor. Both inotropic and vasodilatory effects.

XE "Beta-blockers" -Blockers:

Some success in moderately severe CHF.

Start with doses and titrate slowly in a compliant patient.

Cavedilol: Newer -blockers may offer even better results. Selective -blocker with -1 blocking effects. Also anti-oxidant effects. function, symptoms, and survival in all but class IV patients with CHF.

Should be instituted (with a cardiologist) at 3.125 mg bid and doubled every 2 weeks up until 25-50 bid.