Cardiovascular Flashcards
In terms of action potentials, in what type of muscle are slow Ca++ channels found?
Slow Ca++ channels are found in cardiac muscle, not skeletal muscle. These open during a cardiac action potential to allow Ca++ from the extracellular fluid, not just the sarcoplasmic reticulum, as is the case with skeletal muscle. The slow Ca++ channels are responsible for the “plateau” phase in the action potential. They take much longer to open than Na+ channels & they stay open much longer. They are contrasted against the “fast Na+ channels” in cardiac muscle, open & close very quickly.
In the context of a cardiac action potential, when does a heart-muscle contraction reach its peak strength?
In the late plateau phase, as the calcium concentrations are just starting to drop inside the cell (repolarisation beginning). Contractile strength decreases during the repolarisation phase of each action potential.
The mitral valve is the valve between the X and Y and its closure marks the Z of the ventricular systole.
X = left atrium Y = left ventricle Z = beginning The mitral valve is the valve between the left atrium and left ventricle and its closure marks the end of the ventricular systole.
The two heart sounds, lub-dub, are associated with the closure of the AV valves, the X & the Y. The sounds is not actually due to the closure of the leaflets of the valves, but the sound of momentary backflow of blood from the A to the B at the C of ventricular systole.
X= mitral - left Y= tricuspid - right A = ventricles B = atria C = beginning
Cardiac Output is equal to:
Stroke Volume X Heart Rate CO = SV x HR
The second heart sound is associated with closure of the aortic valve on the left side of the heart and the pulmonic valve on the right side of the heart. Is it longer or shorter, louder or quieter than the first heart sound? Why?
It is shorter, sharper & higher-pitched than the first heart sound because it is the reverberation caused when the momentary backflow into the ventricles is suddenly stopped by the closure of the valves.
What exactly is Stroke Volume, besides SV = Cardiac Output / Heart Rate
Stroke volume is end-diastolic volume minus end-systolic volume ie., the total amount of blood that fills the ventricles during diastole minus the total that’s left over at the end of systole.
Does greater end-diastolic ventricular volume increase or decrease the force of contraction, all else being equal? What is the effect on stroke volume?
Increases. This is because the muscle fibres are placed in a “more favourable geometry for the ejection of blood during the next systole”, and stretching the ventricular muscle fibres during diastole causes a greater amount of calcium to be released from the SR during subsequent systolic contraction (like a rubber band). Increases or decreases from normal ventricular end-diastolic volume result in approximately proportional increases or decreases in stroke volume.
What do you call the pressure within a ventricle during diastolic filling?
Ventricular pre-load.
End-diastolic ventricular volume is determined by pre-load, but also by x and y.
x = Ventricular COMPLIANCE - a measure of the ease with which the ventricular walls stretch to accommodate incoming blood during diastole. Also, compliance = change in volume/change in pressure. y = Diastolic filling time
An increase in contractility brings about an increase in stroke volume without requiring an increase in end-diastolic volume. True or False?
True. More contractility means there’s more complete emptying of the ventricles, so end-diastolic volume decreases.
How can contractility be increased?
Sympathetic nerve activity: neurotransmitter norepinephrine binds beta receptors on ventricular muscle, causing increased influx of extracellular Ca++ during action potential, resulting in stronger contractions that are faster and shorter. Epinephrine & norepinephrine produced in adrenal medulla, beta-receptor agonists such as epinephrine & isoproterenol, & cardiac glycosides such as digitalis can all increase cardiac contractility - ie., inotropic.
What are beta-receptor antagonists used most often to DECREASE heart contractility?
Beta blockers propranolol & atenolol. There are also Ca++ channel blockers.
What is another name for arterial pressure?
Cardiac afterload.
If CO = SV x HR, why is it that doubling the heart rate doesn’t double the cardiac output?
When HR increase, diastolic-filling time decreases, so end-diastolic volume is reduced, and this reduces SV, because SV is: SV = end-diastolic volume - end-systolic volume In fact, when heart rates increase so much eg., beyond 160 bpm, SV decreases so much that CO actually DECLINES! However, there usually is some increase in CO, especially when heart rate increases due to exercise, but this is because SV also increases.
