Chapter 14 Flashcards
(41 cards)
Cardiac output
Volume of blood pumped per minute by each ventricle
CO equation
Stroke volume x heart rate
Average: 5,500 ml/minute
Sympathetic effects on HR
Norepenephrine and adrenal epinephrine keep HCN channels open (which allows na+ in) increasing heart rate
Parasympathetic effects on HR
Acetylcholine opens K+ channels slowing heart rate
Regulation of cardiac rate
Cardiac control center of medulla regulates this
3 variables regulating stroke volume
EDV, TPR, and contractility
EDV
Volume of blood in the ventricles at the end of diastole aka preload
When this increases stroke volume increases
Total peripheral resistance
Frictional resistance to blood flow in the arteries aka afterload
Inversely related to stroke volume
Contractility
Strength of ventricular contraction
When this increases stroke volume increases
Ejection fraction
Normally about 60% of the EDV is ejected
Frank-Starling law
Increased EDV results in increased contractility and thus increased stroke volume, this is an intrinsic property of heart muscle
How does increased EDV result in increased contractility
The increased EDV stretches the myocardium increasing contraction strength via increased actin and myosin overlap (sarcomere length) + increased sensitivity to Ca2+
Sympathetic contractility regulation
Norepinephrine and adrenal epinephrine make more Ca2+ available to sarcomeres increasing contraction strength
Extrinsic control contractility
Parasympathetic acetylcholine decreases heart rate which will increase EDV which then increases contraction strength and thus stroke volume but not enough to overcome the slowed heart rate so cardiac output decreases overall
Blood flow proportion
Proportional to differences in pressure and inversely proportional to resistance
Most important factors in blood flow
Mean arterial pressure and vascular resistance to flow
Extrinsic regulation of blood flow
Control by the autonomic nervous system and endocrine system
Sympathetic extrinsic control of blood flow
Release norepinephrine onto smooth muscles of arterioles stimulating vasoconstriction increasing cardiac output and total peripheral resistance (alpha)
Release ACh and epinephrine to vasodilator skeletal muscles (beta adrenergic)
Parasympathetic extrinsic control of blood flow
Release of ACh leading to vasodilation in limited tissues
Myogenic (intrinsic) control of blood flow
Decrease in arterial pressure causes cerebral vessels to dilate to maintain adequate blood flow
High blood pressure causes cerebral vessels to constrict to protect the vessels
Metabolic control of blood flow
Decreased oxygens increased CO2, decreased tissue pH, and release k+ promotes vasodilation
Circulatory changes during exercise
Sympathoadrenal activity increases and parasympathetic activity decreases causing increased heart rate, stroke volume, and cardiac output
Blood flow to skeletal and cardiac muscles increases
Cerebral circulation
Constant at about 750 ml/min, almost exclusively regulated by local intrinsic control or autoregulation
Blood pressure falls cerebral vessels dilate, rises vessels automatically constrict
Hypoventilation (increased CO2) causes dilation, hyper causes constriction