Physiology Exam 2

anskorczewski12's version from 2016-03-15 03:05


Question Answer
pericardiumthe membrane enclosing the heart, consisting of an outer fibrous layer and an inner double layer of serous membrane.
layers of the heart wall1. endothelium (thin, inner ET) 2. myocardium (cardiac muscle, bulk of walls) 3. Epicardium, thin outer layer
interventricular septummuscular partition that prevents blood mixing from 2 sides of heart
atrioventricular valvesright is tricuspid, left is bicuspid or mitrial valve
chordae tendineae prevent the AV valves from everting, extend to papillary muscles on ventricle walls (that contract when ventricles do)
sinoatrial nodein R. atrial wall near superior vena cava (normal pacemaker of heart-beats at 70 bpm under rest condition)
Bundle of Hisoriginates at AV node, goes between ventricles, curves around each ventricle and goes back towards atria (ensures 1 smooth contraction)--has left and right branches
atrioventricular nodebase of R. atrium near septum, just above atria and ventricles (pacemaker at 50 bpm)
coronary arteryartery supplying blood to heart
intercalated discsstructures that join together cells (have desmosomes and gap junctions)
semilunar valves1. aortic valve 2. pulmonary valve
Purkinje fibersextend from bundle of His and spread through ventricular myocardium (ensure 1 smooth contraction)
ischemialow blood flow; heart is very intolerant of this compared to other muscles
angina pectorislow blood flow (heart pain before heart attack)
ventricular fibrillationAP's aren't synchronized in ventricles
sphygmomanometercuff with pressure gauge to measure arteriol pressure
atherosclerosishardening of arteries (can't hold pressure as well and more pressure to pump against)
arteriosclerosistype of atherosclerosis where there is build up of plaque


Question Answer
parasympathetic influence on heart rate1.decreases SA node frequency (Ach increases K permeability which hyperpolarizes and decreases pacemaker potential; decrease If and T-type Ca permeability) 2.decreases AV node's conduction velocity/excitability (prolong AV nodal delay when increase K permeability) 3.shortens plateau phase of atrial contractile cells (less Ca=weakened atrial contraction) ---leads to decrease in cardiac output
sympathetic effects on heart rate1.increase SA frequency (enhance If and T type channels) 2.increases conduction velocity of all cells (reduces AV nodal delay-enhance L type Ca-inward movement and fast Na) 3. increases contraction strength (increase Ca permeability through L type---increase stroke volume) --double increase in CO
parasympathetic effect on cAMPreduces activity
control of stroke volume1. intrinsic (change EDV) 2. extrinsic control (sympathetic stimulation) 3. MABP (afterload)
intrinsic control of stroke volumevenous return; depends on length-tension relationship (stretch increases tension)--EDV determines stretching
Frank-Starling Lawdistolic filling determines length (more EDV-higher preload, more SV); this is good because it equilizes R.L. pumping (reduces edema), and can increase stroke volume by symp. increasing contraction strength
Implications of Frank-Starling Relationship1.control ESV 2.match LV and RV output 3.prevention of rise in venous pressure (stretching compensates by pumping out more, so vein pressure isn't too high)
extrinsic control of stroke volumesympathetic input (nore-epinephrine enhances contractions-more Ca due to enhanced cAMP activity) enhances venous return and cardiac contraction
Intrinsic/local controls to match blood supply to hyperemia 2.reactive hyperemia 3.myogenic autoregulation 4.local response to injury
local causes of vasodilationincrease CO2, ECF K, Adenosinne; decrease pH (lactic acid), O2-->act on either smooth muscle or endothelium (NO)
receptors affected by sympathetic innervvation of arteriolesa1 (strong bind to Norepinephrine) constriction (a lot in kidneys/stomach); B2 (weak bind to norepinephrine) dilate (more in skeletal-binds to epinephrine in low doses)

Study Guide Questions

Question Answer
What is responsible for long period of contraction of cardiac muscleCa sparks (increased Ca supply with slow Ca removal)- amount of cytosolic Ca varies, so the amount of cross bridges varies
rank velocity of cells(things above threshold) conducting (higher permeability of Na) 2. myocardial 3.SA node (high permeability for L-type Ca) 4. AV
rank frequency of cells(below threshold) 1.SA (high permeability for Na and Ca) 2. AV conducting 4.myocardial
types of turbulent flowstenotic (whistle from not opening completely); insufficient (gurgle from not closing completely); caused by rheumatic fever
laminar flowno sound, healthy
if you got a heart transplant and no pacemaker, what is heart rate100b/m (SA's node rate)
blood pressure depends onvolume and compliance/distensibility (how easily it is stretched)
functions of arterioles1.determine blood flow to individual organs 2.determine mean arteriole pressure (total body pressure) [match flow of local demand, protect MABP by TPR cooperation, temperature regulation of skin]
pathway of myogenic autoregulationdecrease flow to tissue, decrease stretch of arteriolar smooth muscle, myogenic relaxation (vasodilation), increase blood flow to tissue


Question Answer
Flow ratechange in P / Resistance
Resistance8Ln/piR to the fourth
Pulse pressuresystolic pressure - diastolic pressure (fee systolic and not diastolic)
Mean arterial pressurediastolic pressure + 1/3 pulse pressure (or 2/3 diastolic + 1/3 systolic)
Things that determine blood pressure/ MABPCO X TPR (total peripheral resistance)