Cardiovascular System

Question 1

Main components of the cardiovascular system

Answer 1

heart (pump + endocrine function)
+
vessels (diameter, integrity)
+
blood (volume, viscosity, PCV, Hb)

Question 2

2 backgrounds of circulatory (cardiovascular) insufficiency

Answer 2

1. Heart failure
2. Peripheral circulatory failure (=shock)

Question 3

Peripheral circulatory failure

Answer 3

Causes: decreased blood volume, sudden change in volume of blood vessels

Short acting accommodation possible: adrenergic effect: vasoconstriction in “less important” organs + increase of HR + salt and water retention

Treatment: replacement of blood volume

Question 4

Hemodynamic determinants of cardiac output

Answer 4

• preload
• afterload
• contractility
• heart rate
• distensibility
• synchronization of heart beats (rhythm)

cardiac output = HR x stroke volume

Question 5

Frank-Starling law

Answer 5

The more heart muscle is stretched during filling, the stronger the force of contraction during systole and the greater the stroke volume

(Lengthening of cardiac cells are improving actin-myosin overlap and increasing the myofibrils’ (troponin C) sensitivity to Ca++)

In failing heart, it won’t work as good as in healthy heart (with significant increase of preload, there will be only small increase in stroke volume) -> increase of venous pressure -> if hydrostatic pressure overcomes oncotic pressure -> extravasation (=congestion)

Question 6

Laplace law

Answer 6

Wall tension = internal pressure x radius of the chamber / wall thickness

Bigger radius -> higher wall tension
Higher wall tension -> more energy (ATP) myocardium needs to generate contraction -> increased oxygen demand but weaker performance.

Thicker wall -> lower wall tension
Increasing wall thickness reduces the tension needed to generate a given pressure. That’s why heart develops concentric hypertrophy in chronic pressure overload: thick walls reduce wall stress

Question 7

Heart response to pressure overload vs volume overload

Answer 7

Pressure overload: ventricle must generate very high pressure to eject blood. To tolerate already high pressure, heart will adapt by developing concentric hypertrophy to decrease wall stress due to thick walls. Chamber size stays normal or even decreases.

Volume overload: ventricle filed with excess volume during diastole -> chamber radius increases. Ventricle dilates to accommodate extra volume. Wall stress remains high, leading to eccentric hypertrophy.

Question 8

Chance in contractility in the failing heart

Question 9

Compensation of heart failure. Priorities

Answer 9

1. To sustain systemic arterial blood pressure in the most important organs (brain, heart, kidneys)
2. To sustain systemic arterial blood pressure in other organs
3. To keep systemic venous pressure (preload) on a reasonable level

Question 10

Compensation of heart failure. Neurohormonal compensatory processes

Answer 10

1. Increased HR (but decreased diastolic filing, decreased coronary flow)
2. Increased myocardial activity (but it causes increased oxygen and energy consumption, myocardial hypertrophy)
3. Peripheral vasoconstriction (but causes increased aterload)
4. Increased blood volume: vasoconstriction + RAAS

Question 11

Heart failure. Definition

Answer 11

Cardiac output is not enough to transport the necessary amount of blood to the tissues according to their actual demands.

Always secondary to severe heart disease

Question 12

Contractility in the failing heart

Answer 12

Contractility depends on Ca++ transport.
1. Ca++ channel in membrane of cardiomyocyte
2. Ca++ in SR
3. Binding of Ca++ to troponin C

In failing heart all these will be affected to some degree —> decrease of contractility

Sometimes its primary problem: canine dilated cardiomyopathy

Question 13

Decreased distensibility of the heart

Answer 13

Due to:
- hypertrophy
- fluid in pericardium
- constrictive pericarditis
- cardyomyopathy

Will lead to increase of pressure in ventricles -> in atria -> in venous system -> congestion