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What are three mechanisms that try to compensate when there is ventricular dysfunction? What happens when they can't completely compensate?

Frank-Starling Mechanism-Increase preload, increase stretch, increase CO

Release of catecholamines (sympath.)

Myocardial hypertrophy and remodeling

Heart failure symptoms occur when they can't quite compensate.


What specific things cause remodeling of the heart in cardiac dilation, pathological hypertrophy, and physiological hypertrophy? What happens regarding myocyte size/condition, fibrosis, and cardiac function in each?

Cardiac dilation can be caused by MI and dilated CM. Myocyte length increases (too much). Myoctyes die. Fibrosis occurs. Cardiac Dysfunction occurs.

In patholog. hypertrophy, it is caused by pressure loading. Myocytes width is increased, but they are increased in a way that makes them contract less effectively. There is fibrosis. There may or may not be cardiac dysfunction depending on compensation.

In physiol. hypertrophy, it is caused by development, exercise, or pregnancy. Myoctye length increases in a way that makes contraction more efficient. No fibrosis. No cardiac dysfunction.


What are 13 causes of predominant systolic dysfunction? 4 causes of diastolic dysfunction?

Predominant systolic dysfunction

1. Myocardial infarction /severe coronary artery disease

2. Hypertension (severe and prolonged exposure)

3. Idiopathic or familial

4. Toxicity[chemotherapy, cocaine, ETOH]

5. Systemic or infiltrative process [amyloidosis, sarcoidosis, hemochromatosis, scleroderma]

6. Myocarditis

7. Catecholamine-induced ‘Takotsubo’

8. Peri-partum

9. Mitochondrial disease, muscular dystrophy, or glycogen storage disease

10. Congenital or LV non-compaction syndrome

11. Infectious [viral, Chagas]

12. Valvular (aortic valve stenosis or insufficiency, mitral valve insufficiency)

13. Nutritional deficiency (thiamine, selenium, carnitine )

Predominant diastolic dysfunction

1. Hypertension

2. Hypertrophic cardiomyopathy

3. Restrictive cardiomyopathy from a systemic or infiltrative process [amyloidosis, sarcoidosis,
hemochromatosis, eosinophilia/Loeffler’s, fibrosis]

4. High output failure (beri-beri, hyperthyroidism, anemia)


Describe how the neuro-humoral system tries to compensate for ventricular dysfunction.

Circulating catecholamines and NE from nerves bind to their receptor on the heart (Beta 1 likely), activating adenylate cyclase, leading to cAMP which activates protein kinases leading to more calcium, more efficient contracting.

While they due help ventricular function for awhile, they lead to worsened survival (decompensation) due to:

Causing necrosis/apoptosis
Regulating the beta receptor g protein adenylate cyclase complex
Causing arrhythmia


How does the RAAS try to compensate for ventricular dysfunction?

Low cardiac output leads to renin release leading to angiotensis I then II.

Angiotensin II is a potent vasoconstrictor. It also causes the released of ADH and aldosterone.

ADH causes water and salt retention to occur

Endothelin is a very marked vasoconstrictor.

Atrial natriuretic peptide assists in combating the vasoconstriction (causing salt and water to be secreted)

ALdosterone leads to myocardial fibrosis, remodeling, activation of symp. system and salt retention.


What things happen to the myocardium that cause ventricular dysfunction? What are some possible causes of these things?

Increased level of programmed cell death (apoptosis) and suicide gene expression. Likely due to excess catecholamines, angiotensin, oxygen free radicals, and inflammatory cytokines.

There is less intracellular calcium in the failing heart (abnormal contractile mechanisms)

Reversion to the fetal genotype with expression of abnormal proteins including myosin heavy chain-beta. This displays slower contraction velocity and weaker contraction strength from dysfunctional excitation-contraction coupling.


What adaptions occur as a result of myocardial dysfunction that lead to congestive symptoms?

VESV and VESP increase.
Volume and pressure in atrium behind ventricle
Atrium contracts more vigorously
Pressure increases in the venous and capillary beds behind (and upstream) to the failing ventricle.
Transudation of fluid from capillary bed into the interstitial space leading to pulmonary congestion and/or peripheral edema and ascites


What are the low output sequelae of cardiac dysfunction?

Brain: Mental obtundation
Skeletal muscle weakness
Kidneys: Sodium and water retention


What are some causes of Right sided heart failure

left-side heart failure (most common), pulmonic valve stenosis, right ventricular infarction

COPD, interstitial lung disease, ARDS, Chronic lung infection or brochiecstasis

Pulmonary Embolism, Primary pulmonary hypertension


What is the difference between systolic and diastolic failure? What causes diastolic failure? How common is it?

Diastolic failure is when the LV can't accept blood as well as it should. It may be the sole cause of HF in 1/3-1/2 pts. LV is usually small and thick with good overall ejection fraction.

May be seen in pts. with ischemic heart disease, HTN, LVH, and infiltrative diseases. Most with systolic dysfunction will have some diastolic dysfunction.


How is CHF diagnosed? What symptoms exist?

Syndromic clinical definition of cardinal symptoms. Dyspnea, pulmonary congestion, systemic congestion, heart enlargement, abnormal ausculation, jugular venous pressure abnormalities, HR and rhythm/BP abnormalities


What are some different aspects of dyspnea that come along with CHF?

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 increased.

3. PND: In its worst form, it is accompanied by cough, sometimes productive of white or pink frothy sputum which is occasionally blood stained.

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.


What other evidence of pulmonary congestion can be found aside from dyspnea?

Chest X-ray: Redistribution of the blood in the lungs is noted as 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 the normal distribution of blood flow from top to bottom of the lungs is abolished and
eventually even reversed in cardiac failure appearance of lung fields on X-ray (will view xrays in future lecture).

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


What evidences of systemic congestion usually exist in CHF? What causes them?

Pulmonary circulation: Normally is a low pressure, low resistance 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 have increased LV diastolic pressure as in HF – the normal mean pulmonary arterial pressure of

approximately 11 mmHg will not suffice to perfuse the pulmonary vascular bed. Thus obligatory

pulmonary arterial HTN occurs to compensate.

systolic RV dysfunction, hypertrophy and possibly dilation/failure can occur leading to 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.


How is heart enlargement manifested? What if someone has new onset severe CHF w/o enlarged heart?

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

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


What abnormal findings on auscultation will exist in CHF?

Abnormal Findings:

S-3 in adults w/enlargement and HF: In early diastole, rapid ventricular filling takes place. In adults specific for the diagnosis of HF. Associated with cardiac dilatation and failure.

Loud S-4: Sign of significantly decreased 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 spurtof blood flow from atrium to ventricle. When ventricular diastolic compliance is reduced , 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.


What are the different waves of jugular venous pressure? What happens to JVP and the waves when the RV fails? What happens to the waves in severed tricuspid regurg?

1. A wave: generated by atrial systole
2. C wave: Associated with isovolumetric 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 elevated.

1. large systolic v wave in the JVP with severe tricuspid regurgitation.

2. y wave is classically precipitous in restrictive heart failure


What are the effects on HR, heart rhythm and BP of CHF?

Hypoperfusion elicits sympathetic stimulation thus tachycardia which may partially correct reduced

CO related to poor intrinsic SV.

Sympathetically mediated vasoconstriction leads to mild HTN which can be detrimental to HF. Left

atrial pressure increase and stretching over a long period of time can predispose to atrial fibrillation

or other arrhythmias (SVT). Failing, remodeled ventricles can be prone to ventricular tachycardia.


What are 4 general precipitating causes of CHF with examples?

1. Inappropriate additions (salt, excess fluid) or lack of compliance with HTN meds, etc.

2. Arrhythmias:

 Tachyarrhythmias: less time available for ventricular filling, increased O2 consumption and ischemia

 Bradycardia: SV is max and can’t increase to augment CO

3. Late complications from an MI: papillary muscle dysfunction and mitral regurgitation

4. Infections: metabolic rate, fever, tachycardia


What are 3 treatment goals of CHF

- Improve symptoms

- Prevent deterioration of function

- Increase survival.


What are some non-pharmacological treatments for CHF?

Removal or treatment of precipitating or aggravating causes:

Treating respiratory or other infections
Management of arrhythmias
Treatment of HTN
Treatment of MI.
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:


How do diuretics help with CHF? What are some guidelines for choosing a diuretic? Examples of different kinds of diuretics. What are some side effects? What are some drug interactions to avoid?

 decreases filling pressures of the heart but does not necessarily 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 severe sodium retention--loop diuretics (furosemide (lasix) bumetanide (bumex).
3. Persistent volume and sodium retention--loop diuretics plus thiazides or metolazone.
4. K+ sparing diuretics (spironolactone or eplerenone) 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.

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


What are two types of vasodilators? How do they work? When do they work well? What are their negative aspects?

Most offer venodilation and/or arterial vasodilation.


Afterload reducer and is therefore used for increased SVR and HTN. In combination w/nitrates affords improved survival in African American patients with CHF already
on BB and ACEi. Work well to reduce congestion from mitral regurgitation or aortic insufficiency. More side effects than ACE inhibitors.


Mostly venodilation with some mild afterload reduction at higher doses. Complement diuretics in reducing right and left atrial pressures. Especially useful if coronary artery
disease and resultant angina 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" can be instituted (3x/day vs. 4X/day).


How well do ACE Inhibitors work? What are some of the things they do? When should they not be used? Side effects? What are the benefits of AT-I Receptor antagonists?

Most important advance in therapeutics for HF in the past two decades.
Up to a 40% improvement in 1-year mortality in class IV pts.

1. Slows remodeling (ventricular enlargement, fibrosis, etc.)

2. Improves hemodynamics and survival rates in patients with LV dysfunction of any etiology.

3. Prevent clinical deterioration in asymptomatic patients with reduced ejection fraction.

4. 1st line therapy for all patients with reduced 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 I receptor antagonists: losartan, valsartan, candesartan. In contrast to ACE inhibitors. No cough as side effect – similar efficacy clinically.


What are the two types of calcium channel blockers with examples? What do they do? When should they be used?

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

Amlodipine and felodipine: 2nd generation drugs. Vascular specific and can reduce HTN to alleviate
some symptoms. Only use if other HF specific meds are maxed out and BP still elevated.


What are some inotropic agents that can be used in CHF? What do they do? When are they used? When are they not used? What are their negative effects?


The only approved oral inotropic drug (very weak compared to infused agents).

Most useful with moderate CHF, esp. in the setting of Atiral fibrillation as helps with heart rate control.


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.

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

1. Dobutamine: beta-agonist (also vasodilates). Increases CO, reduces wedge pressure.

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


What are some examples of beta blockers? What do they due? When are they used? When are they not used?


Start with lower doses in decompensated failure patients and titrate slowly.

Carvedilol: Selective beta-blocker with also alpha blocking effects. Helps cardiac function, reduces symptoms, and increases survival in all but class IV patients with CHF.

Metoprolol: (only the long-acting version, succinate, approved for heart failure). Similar effects compared to carvedilol.