1.4 (PSIO 202)

Heart Mechanics and Cardiac Output

What is diastole?

the period of the chamber relaxation and filling

What is systole?

the period of chamber contraction and blood ejection

What is atrial diastole?

the atria fill passively; both AV valves are open and blood flows into the ventricles

What is ventricular diastole?

starts with ventricular repolarization, and with a drop in ventricular pressure that results in (passive) filling of the ventricle

What is atrial systole?

a very brief synchronous contraction of the atria; active filling of the ventricles

What is ventricular systole?

starts when the AV valves close and the pressure within the ventricles begins to rise as the cardiac muscle fibers are depolarized and then contract

What is happening during atrial contraction?

ventricular diastole; blood flows through tricuspid and mitral AV valves (open)

What is happening during ventricular contractions?

atrial repolarization; blood pushes AV valves slam closed (chordae tendinae prevent blood from coming back up); first heart sound produce (LUBB); blood is pushed through semilunar valves because ventricular pressure is greater than the pressure in the atria

What happens during ventricular relaxation?

the ventricular pressure is less than the arterial pressure which slams the semilunar valves shut and the second heart sound is produced (DUBB)

What happens to pressure during contraction?

pressure increases

What happens to pressure when ventricular volume increases?

pressure decreases

What is cardiac output?

the volume of blood pumped by the ventricles in a given unit of time

What is the equation for CO?

stroke volume x heart rate

What unit is CO measured in?

L/min

What unit is SV measured in?

L/beat

What unit is HR measured in?

beats/min

What are the determinants of stroke volume?

afterload, preload, and contractility

What is afterload?

aortic blood pressure (load that it’s pushing against- RESISTANCE)

What is preload?

end-diastolic volume (stretching; most relaxed moments- STRETCH)

What is contractility?

how strong muscle is contracting to eject blood out of the heart

What needs to happen in order for the ventricles to eject blood through the semilunar valves into the aorta or pulmonary artery?

the pressure in the ventricles needs to exceed the pressure in the artery

When can stroke volume increase?

when the rate of cardiac filling also increases

What is active contractility?

stimulation of the sympathetic nerves to the heart

What is passive contractility?

the result of changing the length of the cardiac muscle fibers (“Frank-Starling mechanism”)

What are the results of active contractility?

increased rate of pacemaker activity and increased force of cardiac muscle contraction (due to actions of epinephrine and norepinephrine)

What relationship is the “Frank-Starling Mechanism” referring to?

the relationship between the rise in stroke volume and the rise in preload

What happens if the preload is increased?

SV increases systematically

What are the positive chronotropic agents of increased HR?

sympathetic nervous system, epinephrine and norepinephrine, thyroid hormone, glucagon, nicotine and caffeine, and hypocalcemia

What are the causes and positive inotropic agents of increased SV?

\-increased preload (stretch)

\-sympathetic nervous system, epinephrine and norepinephrine, glucagon, digitalis, nicotine and caffeine, and hypercalcemia

What are the negative chronotropic agents of reduced heart rate?

parasympathetic nervous system, ACh, hypercalcemia, hypokalemia, beta blockers

What are the causes and negative inotropic agents of decreased SV?

\-reduced preload, reduced contractility, increased afterload

\-hypocalcemia, hyperkalemia