Integration of Cardiac Function Flashcards
what receptors are used for sympathetic and parasympathetic effects upon the heart and what are their second messengers?
SNS- beta1 adrenergic receptors (increase cAMP)
PNS- M 2 muscarinic receptors (decrease cAMP)
what are the two intrinsic mechanisms or regulating cardiac output?
starlings law- increased volume=increased contractility
membrane potentials and therefore ionic concentrations
what are the extrinsic mechanisms of regulation of cardiac output?
neuronal and hormonal signaling
why is the cardiac output the same into the aorta and into the pulmonary artery?
because the two circuits are in series
graphically what is the difference between cardiac output and oxygen consumption?
linear
what eight factors increase cardiac output?
fever, exercise, anxiety, body weight, pregnancy, hyperthyroidism, chronic anemia and hypoxia
what five factors decrease cardiac output?
sleep, aging, severe anoxia, acute hemorrhage and heart disease
what is histotoxic hypoxia?
tissue poisoning that causes the tissues to be less able to use oxygen
why does cardiac output have varying responses to hypoxia and severe anoxia?
because severe anoxial causes oxygen deprivation in the heart and decreases cardiac output
what is the effect of hypertension on cardiac output?
it is unaltered
what are the only two ways to produce a different steady state match of CO?
changing the cardiac function curve or the vascular function curve
during exercise what happens to the body’s vasculature and what is the overall effect?
there is arteriolar and venous vasoconstriction. the overall effect is functionally increasing venous return by the venous constriction
how does muscle contraction promote venous return?
by pumping venous blood past valves towards the heart
why is there an overall decrease in peripheral resistance to blood flow during exercise?
because local hypoxia, hypercapnea and acidemia promote vasodilation and prevent MAP from increasing too much
what happens to the mean systemic filling pressure during an increase and a decrease in sympathetic stimulation?
increase- increase in MSFP and decrease with a decrease in sympathetic stimulation
what happens to cardiac output and venous return during exercise? does a difference in central venous pressure cause this?
both increase, however here is not an increase in CVP
what does depolarization and repolarization look like on an EKG?
depolarization is a bump on the graph in the positive y axis while repolarization is a bump in the negative region of the graph
what does the P wave of the electrocardiogram correspond to?
atrial depolarization
what does the QRS complex correspond to in the EKG?
ventricular depolarization
what does the T wave in the EKG correspond to?
ventricular repolarization
why is the T wave of the EKG inverted?
because the ventricles repolarize from the epicardium towards the endocardium (opposite of depolarization)
why can’t atrial repolarization be seen in EKG?
because it is obscured by ventricular depolarization
what depolarizations occur during the PR interval?
the SA node, atria, AV node, the His bundle, the bundle branches and the purkinji fibers
why do the depolarization of the AV node, AV bundle, bundle branches and Purkinje fibers not appear on the EKG?
because they do not generate voltages large enough to be detected
what does the ST segment correspond to in the action potential of the ventricular myocardium?
the plateau phase
what is produced by the upstroke of all of the ventricular action potentials?
the QRS complex
what segments are contained in ventricular diastole?
the TP segment and the PR interval
when does most ventricular filling occur? how does this correspond to atrial contraction?
ventricular filling occurs mostly in early diastole and atrial contraction occurs at the end of ventricular diastole
what does atrial contraction contribute to preload?
produces only a small rise in ventricular volume and pressure (both sides of the heart)
when does atrial diastole occur and what happens to the atrial pressure during this time?
it occurs during ventricular diastole and the atrial pressure increases
why is there a fall in ventricular pressure even after the mitral and tricuspid valves open?
because the forward momentum of blood into the ventricle expands them and drops the pressure simultaneously
how does blood flow into the aorta continue during systole even though there are times when aortic pressure is greater than ventricular pressure?
because the forward momentum continues the flow even though there is a deceleration of flow until it stops and closes the aortic valve
what is the relationship of the P wave and atrial contraction?
the P wave precedes atrial contraction
what happens to flow at the dichrotic notch?
the decrease of the pressure gradient causes the reversal of flow
what does the R wave coincide with?
the onset of ventricular contraction
how many sounds are produced by the heart? which ones can be heard with a stethoscope?
4
closure of the AV valves and closure of the semilunar valves
when does the T wave occur with respect to blood flow?
during the second half of the ejection phase
what six factors affect stroke volume?
atrial filling pressure, ventricular filling time, ventricular compliance, heart rate (increase causes a decrease in diastole time), preload and afterload
what is the timing of the right and left atria? the ventricles?
the right atrium contracts prior to the left atrium
the left ventricle contracts prior to the right
how does the amount of time that the pulmonary valve is open compare to the aortic valve?
the aortic valve is open for less time even though the left ventricle contracts earlier because there is an increased time of isovolumetric contraction because aortic pressure is higher
what two sounds are not normally heard in adults?
ventricular diastolic filling and atrial contraction
