Heart Failure

Question 1

Definition of circulatory failure

Answer 1

Inability of cardiovascular system to nourish the body’s cells, supply oxygen and remove metabolic products.

Question 2

Causes of circulatory failure

Answer 2

Heart failure, Low cardiac output, High Output Cardiac Failure

Question 3

Defintion/diagnosis of heart failure

Answer 3

1. Symptoms of HF (dyspnea-SOB, fatigue, ankle swelling). 2. Signs of HF (tachycardia, tachypnea, increased venous pressure, edema, hepatomegaly, murmurs). 3. Objective evidence of a structural or functional heart abnormality at rest (cardiomegaly, S3, murmur, abnormal echo, increased BNP).

Question 4

Types of heart failure

Answer 4

1. Systolic/Diastolic (main distinction relevant for prognosis and treatment, the rest semantic), 2. Forward/backward, 3. Left/Right, 4. Low output/high output

Question 5

What are the elements of systolic HF that distinguish it from diastolic HF?

Answer 5

Damage to/reduction of contractile function. Usually will also have diastolic dysfunction.

Question 6

Diastolic HF as distinguished from systolic HF

Answer 6

Problem occurs during diastolic phase/relaxation/filling impairment to ventricle. No actual problem with contractile function of the heart. Implication that systolic fxn is normal.

Question 7

Forward HF as distinguished from backwards HF

Answer 7

Underperfusion of systemic tissues. Patient presents with weakness/tiredness with even mild exertion. Reduction in perfusion of skeletal muscle.

Question 8

Backwards HF as distinguished from forward HF

Answer 8

Increased in LVEDP. Reflected backwards into the lungs. Pulmonary pressure goes up, SOB.

Question 9

Left HF as compared to right HF

Answer 9

Complains of SOB and weakness upon exertion. Crepitations and fluid in lungs on examination.

Question 10

Right HF as compared to left HF

Answer 10

RV not working. Peripheral edema. High jugular venous pressure. If only right with no left: due to severe lung disease.

Question 11

Low output vs high output

Answer 11

Reduced cardiac output, sign of severe LV damage and systolic dysfunction severe HF patients.

Question 12

High output vs low output

Answer 12

Rare and unusual. Heart has to pump an abnormally large amount of blood through the body to supply oxygen. Heart functions normally or above normal

Question 13

When does high output heart failure occur?

Answer 13

1. Increased blood volume (or fluid)/excess salt and water accumulation. No intrinsic circulatory problem. 2. Abnormally high venous return and/or decreased peripheral vascular resistance.

Question 14

What is the definition of oliguria?

Question 15

What are causes of increased blood volume/fluid?

Answer 15

IV fluids, blood transfusion, steriods (or NSAIDs, a lot over a long period of time), oliguria/anuria.

Question 16

What are the causes of abnormally high venous return or high PVR?

Answer 16

Pregnancy (rare), hyperthyroidism, Severe anemia (most common, developed over a long period when compensation fails), AV fistulae/shunts, Beri-beri. Eventually chronic pressure/volume overload–>pump failure.

Question 17

What is an AV fistula?

Answer 17

AV fistula: patients on hemodialysis from chronic renal failure. In dialysis doctors fashion a huge BV but joining radial or brachial artery and vein-looks like a snake under the skin. Sometimes BV are so big that get a huge venous return back to heart and can unusually put patients into HF from huge preload they can’t deal with.

Question 18

What are the 3 basic categories of heart failure?

Answer 18

1. Mechanical abnormalities, 2. Loss of myocyte function, 3. Alteration of cardiac rhythm

Question 19

What are the mechanical abnormalities that can lead to HF?

Answer 19

1. Increased worload, 2. Increase pressure load/afterload (Central: aortic stenosis, or peripheral: HTN). 3. Volume overload/increased preload (mitral regurgitation), 4. Pericardial constriction/tamponade (rare)

Question 20

How does mitral regurgitation lead to heart failure?

Answer 20

Heart pumps blood in systole, some blood goes out through aorta. But because there is a backup, pressure is lower in the LA and blood goes back. In diastole you get blood from venous side of lungs and regurgitated from LV. Each time there is more blood. Gets worse and worse. “MR begets MR.” gradually the LV will start to dilate. Can stretch to a large degree with no loss of systolic function until there is a significant drop–>HF.

Question 21

Types of loss of myocyte function

Answer 21

1. Cardiomyopathy, 2. Toxic (alcoholic), genetic, medical (anthrocyclines), other rare ones. 2. Ischemic heart failure, 3. Negative inotropes

Question 22

What is cardiomyopathy as relating to HF?

Answer 22

roup of heart muscle diseases. Implication that there is a disease of the myocardial tissue, myocytes themselves, of unknown etiology.

Question 23

What are the 3 main groups of cardiomyopathy?

Answer 23

1. Hypertrophic, 2. Dilated, 3. Restrictive.

Question 24

What is hypertrophic cardiomyopathy?

Answer 24

Significant hypertrophy. Genetic condition with mutations of different genes affecting myosin, actin, or other pieces in the heart itself. Massive hypertrophy. Good function but very stiff so diastolic dysfunction.

Question 25

What is dilated cardiomyopathy?

Answer 25

Significant systolic dysfunction, destruction of myocytes.

Question 26

What is restrictive cardiomyopathy?

Answer 26

Smaller and more uncommon. Infiltrate into cardiac muscle. Heart doesn’t actually dilate but reduction in systolic function. Stiff and noncompliant.

Question 27

What is ischemic heart failure?

Answer 27

Problem in blood supply from coronary arteries blocked off. Can be result of one big MI or a bunch of small ones.

Question 28

How do negative inotropes relate to heart failure?

Answer 28

Reduce heart function to some extent. Beta blockers and calcium channel blockers. Paradox: beta blockers treat HF.

Question 29

How does alteration of cardiac rhythm cause heart failure?

Answer 29

Fast heart rates or slow heart rates cause HF because reduce efficacy in HF. Asynchrony: heart block, detachment between atrial and ventricular contraction, ventricles aren’t being properly filled by atria.

Question 30

What are the components in the etiology of heart failure?

Answer 30

Most common in western lifestyle and low rheumatic fever: coronary artery disease and dilated cardiomyopathy. Most common with rheumatic fever: valvular heart disease. Others: hypertension (not direct but will contribute to others) and congenital heart disease (more children survive now so higher prevalence).

Question 31

What are compensatory mechanisms in heart failure?

Answer 31

Reduction of perfusion to peripheral organs. May cuase more damage than good. 1. Autonomic increase in HR and contractility, 2. decrease renal perfusion-more fluid preservation, 3. increased adrenal stimulation, 4. more renin and angiotensin

Question 32

How do ACE inhibitors affect HF?

Answer 32

They are vasodilators but also blocks all these negative effects of HF from angiotensin II. No other vasodilators improve prognosis similarly.

Question 33

Compensatory hormone mechanisms against HF

Answer 33

1. ANP (released in atrial distension: vasodilation, sodium and water excretion, reduced preload), 2. Prostaglandin vasodilation, 3. Peptides: bradykinin, 4. endothelin (raise BP)

Question 34

What are the 2 patterns of left ventricular hypertrophy (LVH)?

Answer 34

1. Concentric (pressure overload): hypertrophy without change in volume (Aortic stenosis), 2. Eccentric (volume overload): hypertrophy with increased volume of LV (aortic regurgitation).

Question 35

When does hypertrophy lead to heart failure?

Answer 35

When it is chronic overload with increased wall stress and depressed contractility. At first compensated but when necrosis leads to overload and wall stress increases further.

Question 36

Law of Laplace equation

Answer 36

Wall stress=Pxr/2*(wall thickness)

Question 37

How much blood to the ventricles is provided by the atrial kick?

Answer 37

15-20% but decreased with tachycardia

Question 38

How is the blood affinity for oxygen altered in HF?

Answer 38

Increased 2,3DPG-reduced affinity of Hb for O2. Rightward shift. Increased oxygen extraction.