Congestive Heart Disease

Question 2

What is CHF?

Answer 2

Congestive Heart Failure CHF is endpoint of serious heart disease which is evidenced by cardiac, pulmonary, and systemic congestion.

Question 3

When refering to Congestive Heart Failure, what does the word congestion mean?

Answer 3

Congestion in relation to CHF refers to pooling of blood in different places. Typically in caridac, pulmonary, and systemically.

Question 4

What does predispose mean?

Answer 4

To make someone inclined to a specific condition.

Question 5

What are some of the main risk factors of CHF?

Answer 5

HTN, Ischemic heart disease, Hyperlipidemia, Smoking, Obesity, Age, Ethnicity, Physical inactivity.

Question 6

What are the most important risk factor to target when trying to prevent CHF?

Answer 6

HTN, Ischemic heart disease, hyperlipidemia, smoking, low ejection fraction.

Question 7

What is the etiology of Congestive Heart Failure?

Answer 7

Risk Factors. MI Cardiomyopathy Increased Cardiac Workload Hypervolemia Uncontrolled HTN

Question 8

What is residual volume? (In respect to the heart’s ventricles)

Answer 8

Residual volume is the amount of blood that fails to be ejected from one of the heart’s ventricles. Example- If LV is suppose to push 200mL but only expells 125, there is a residual volume of 75 mL of blood.

Question 9

If the LV becomes congested, what is the result?

Answer 9

If the LV becomes congested, the residual volume will back up into the pulmonary vessels (not the lungs) This will result in the RV having to work harder to push back against the residual volume and ultimately it will fail.

Question 10

Left-ventricule failure leads to _________ failure.

Answer 10

Right-ventricular

Question 11

Left sided heart failure leads to..?

Answer 11

Pulmonary congestion & Pulmonary Edema Left equals Lung

Question 12

Right sided heart failure leads to…?

Answer 12

Peripherial Edema, Abdominal Organ Distention, and Systemic Congestion

Question 13

What is the pathophysiology of Left-sided failure?

Answer 13

1. Left-Ventricle does not eject sufficient volume, leaving residual volume in the LV. 2. The Left-Artium pumps harder to empty blood nto the LV, but fails to fully empty 3. As a result of not being able to fully empty, the LA cannot receive full pulmonary return of oxygenated blood. 4. Pulmonary congestion and pulmonary edema results as the blood flow is inhibited. 5. The Right-Ventricle workload increases as it tries to force blood into the pulmonary vessels. 6. Right-Ventricle hypertrophy occurs as its workload increases. RV failure usually follows LV failure.

Question 14

What are the manifestation of Right-heart Failure?

Answer 14

Congestion of peripheral tissues (peripheral edema and ascites) Abdominal organ distention (liver congestion, GI tract congestion)

Question 15

What are the manifestations of Left-sided Heart Failure?

Answer 15

Decreased Cardiac Output Pulmonary Congestion (Impaired gas exchange, pulmonary edema)

Question 16

Here, check out this picture of L and R sided heart failure manifestations!

Fig. 26-2

Answer 16

Question 17

What is compensated heart failure?

Answer 17

The body attempts to maintain the cardiac reserve through compensatory or adaptive responses. Because of this heart failure may initially be asymptomatic because of compensatory mechanisims which are maintaining the proper funtion of the heart.

Question 18

Check out this graphic! Cool, eh?

It’s of compensatory mechanisms in heart failure!

The Frank-Stirling mechanism, sympathetic reflexes, RAAS, and Myocardial hypertrophy function.

So cool!

Answer 18

Question 19

What are the 6 mechanisims of Compensated Heart Failure?

Answer 19

1. Frank-Starling mechanism. 2. Sympathetic Nervous System (SNS) 3. Renin-Angiotensin-Aldosterone 4. Natriuretic Peptides (ANP and BNP) 5. Endothelins 6. Cardiac Hypertrophy and Remodelling

Question 20

Explain the Frank-Starling Mechanism (Law)

Answer 20

The Frank-Starling Mechanisim is also known as Ventricle Dilation. In heart failure, deceased CO and renal blood flow leads to increased sodium and water retention, which increases vascular volume and venous return to the heart, and increases end-diastolic volume. The increase results in the stretching of the heart muscle, increasing pre-load and resulting in an increase in Cardia Output. However, due to the increased muscle stretching, and corresponding ventricular wall tension, the heart muscle required a higher level of oxygen. Thus, the long-term ramifications of the Frank-Starling mechanism is an overstretch of the ventricular walls and increased oxygen requirment for the heart. Elastic Example: Stretch, stretch, stretch… loss of elasticity.

Question 21

What is the compensatory Symapthetic Nervous System (SNS) How many ways does this system respond? What are they?

Answer 21

The SNS responds to a decrease in cardiac output in three different ways. The goal is to increase cardiac output. The three ways it attempts to respond are, 1. Vasoconstriction (except in coronary and brain vasculature) 2. Tachycardia (increases the heart rate) 3. Increases contractility (the force of the heart’s contractions)

Question 22

How does the Renin-Angiotension-Aldosterone System compensate for heart failure?

Answer 22

You should really already know this information. But, if you need to study it more. 1. A decrease in cardiac output triggers the release of Renin by the Juxta Glumerular Cells in the kidney (because of decreased renal blood flow). 2. Renin and Angiotensongen react and form Angiotensin I 3. In the endotheial cells of the lungs, Angiotension I and ACE (Angiotension Converting Enzyme), form Angiotension II 4. Angiotension II triggers 3 main responses: i. vasoconstriction ii. pituitary gland and ADH release iii. adrenal gland and production of aldosterone 5. Aldosterone triggers the kidney to retain sodium and water, increaseing vascular volume (Hypervolemia) 6. Preload is increased due to the increased venous return to the heart.

Question 23

What are Natriuietic Peptides? What two peotides should we know?

Answer 23

Natriuietic peptides are hormones secreted and produced by the heart which induce diuresis and natriuresis. The excreation of fluid (diuresis) and removal of Sodium (natriuresis). They promote an increase in the glomerular filtration rate. Natruietic peptides decrease reabsorption of Na+ and H2O. ANP - Atrial Natriuretic Peptide: released from the atrial cells in response to atrial stretch, pressure or fluid overload. BNP - Brain Natriuretic Peptide: secreted by the ventricles as a response to incrased vantricular pressure or fluid overload. Elevated levels of ANP and BNP are present in those with heart failure, and well correlated with the extent of ventricular dysfunction. Used to clinically diagnose heart failure and the severity.

Question 24

What are Endothelins?

Answer 24

Endothelins are potent vasoconstrictors. They are released from the endothelial cells thoughtout circulation. They facilitate smooth muscle proliferation and cardiac myocyte hypertrophy.

Question 25

What is inotropic?

Answer 25

Inotropic is modifiying the force or speed of muscle contraction. Negative inotropic - weaken the force Positive inotropic - strengthen the force

Question 26

What is cardiac hypertrophy and remodelling?

Answer 26

Cardiac hypertrophy and remodelling are both long term effects of CHF. The increased workload of the heart results in hypertrophy (increase in cell size, not number), improving the performance of the heart. However, the ventricles can hypertrophy incorrectly or unevenly, resulting in structure changes and function. Eventually, the heart will have decreased contractility. It will also require more oxygen which will lead to myocardial disfunction.

Question 27

Uncompensated Heart Failure

Answer 27

Eventually, compensation fails.

Question 28

What are some manifestations of Congestive Heart Failure?

Answer 28

It depends and varies based on the extent and type of dysfunction. Manifestations of heart failure reflect the effects of the impaired pumping abiity of the heart. Respiratory Manifestations - SOB d/t congestion of pulmonary, Cheyne-Stokes Respiration, Acute Pulmonary Edema.Fatigue, Weakness, Mental ConfusionFluid Retention and EdemaCachexia and MalnutritionCyanosisArrhythmias and Sudden Cardiac Death

Question 29

Diagnosis of Congestive Heart Failure?

Answer 29

History and Physical Exam, Risk Factors Lab Values: CBC, anemia, Liver Function Tests, Electrolytes ECG, Echocardiogram

Question 30

Treatment of Congestive Heart Failure?

Answer 30

Treatment is complex and varies from pt. to pt. Typically split into acute and chonic management Acute: stabilize and correct cause of CHF (see MI) Chronic: symptomatic, decrease the risks, increase the heart function If the pt. has systolic HF (an ejection fraction 40%: i) Treat the cause ii) ACE I +/- BetaBlocker iii) Angiotension receptor blocker (if symptomatic with activity) iv) Increase dose or add diuretic if symptomatic at rest Surgery for repairable defect