PSL 431 Exam 3 Questions and
Answers
pericardium - ANSWER-encases the heart in a fibrous sac
AV valves - ANSWER-one-way valves between the atrium and ventricle
semilunar valve - ANSWER-separates ventricles from downstream arteries,
preventing reflux of blood back into the heart chambers during diastole
coronary arteries - ANSWER-blood supply to the heart muscle from first branches of
the aortic arch
angina - ANSWER-cardiac chest pain
atherosclerosis - ANSWER-blockage of arteries caused by lipid plaques
embolus - ANSWER-dislodged blood clot
ischemia - ANSWER-inadequate blood supply to an organ or tissue, esp heart mm
myocardial infarction - ANSWER-local death of cardiac tissue due to sustained
blockage within one of the coronary arteries
right artery dominant - ANSWER-posterior part of the heart is served by the right
marginal (coronary) artery
systole - ANSWER-active, contraction of heart, decreased blood flow to tissue
diastole - ANSWER-passive, relaxation of heart, increased blood flow to tissue
striated - ANSWER-due to regular arrangement of myosin thick filaments and actin
thin filaments
intercalated discs - ANSWER-adjacent cells in cardiac mm joined end to end
autorhythmic cells - ANSWER-initiate cardiac AP and conduct electrical activity
contractile cardiac myocytes - ANSWER-bundled and spiral around ventricles
atrial natriuretic peptide - ANSWER-hormone released by myocytes in atrium in
response to atrial wall stretch and enhances Na+ excretion by kidneys
desmosomes - ANSWER-promote structural integrity
, gap junctions - ANSWER-provide electrical connectivity between cells
primary active transporter - ANSWER-use ATP hydrolysis to transport vs
concentration gradient
secondary active transporter - ANSWER-use pre-existing concentration gradient to
drive ion transport, no ATP hydrolysis
cardiac conduction system - ANSWER-specialized cardiac myocytes that accelerate
and direct wave of depolarization through the heart
autorhythmicity - ANSWER-capacity for spontaneous, rhythmic self-excitation
intrinsic rate - ANSWER-natural firing rate of SA node at 100 depol/min
leaky Kir channels - ANSWER-open in resting state, driving resting membrane
potential near -90 mV
rapid voltage gated Na+ channels - ANSWER-open with AP, triggering rapid
membrane depolarization
Kto channels - ANSWER-opening causes partial membrane repolarization
L-type Ca2+ channels - ANSWER-opening of these channels causes membrane pot
to be held near 0 mV for an extended period of time due to counter-balance by
continued leakage of K+ channels; maintain depolarization
Kv channels - ANSWER-opening causes repolarization, re-establishing resting state
calcium channel blockers - ANSWER-inhibit L-type Ca++ channels and decrease
Ca++ conductance, shortening length of plateau phase and reducing cardiac
contractility
Treat HTN, angina pectoris
cardiac glycosides - ANSWER-inhibit Na/K ATPase, lowering intracellular K+ and
raising intracellular Ca++, strengthened force of contraction
Treat CHF, cardiac arrhythmias
potassium channel blockers - ANSWER-prolong cardiac AP by slowing K+
conductance during Phase 3 repolarization, helping to restore NSR
Class III anti-arrhythmic drugs
ECG - ANSWER-a surface recording of electrical activity of the heart
Lead I - ANSWER-right arm and left arm
Lead III - ANSWER-left arm and left leg
Lead III - ANSWER-left arm and left leg
Answers
pericardium - ANSWER-encases the heart in a fibrous sac
AV valves - ANSWER-one-way valves between the atrium and ventricle
semilunar valve - ANSWER-separates ventricles from downstream arteries,
preventing reflux of blood back into the heart chambers during diastole
coronary arteries - ANSWER-blood supply to the heart muscle from first branches of
the aortic arch
angina - ANSWER-cardiac chest pain
atherosclerosis - ANSWER-blockage of arteries caused by lipid plaques
embolus - ANSWER-dislodged blood clot
ischemia - ANSWER-inadequate blood supply to an organ or tissue, esp heart mm
myocardial infarction - ANSWER-local death of cardiac tissue due to sustained
blockage within one of the coronary arteries
right artery dominant - ANSWER-posterior part of the heart is served by the right
marginal (coronary) artery
systole - ANSWER-active, contraction of heart, decreased blood flow to tissue
diastole - ANSWER-passive, relaxation of heart, increased blood flow to tissue
striated - ANSWER-due to regular arrangement of myosin thick filaments and actin
thin filaments
intercalated discs - ANSWER-adjacent cells in cardiac mm joined end to end
autorhythmic cells - ANSWER-initiate cardiac AP and conduct electrical activity
contractile cardiac myocytes - ANSWER-bundled and spiral around ventricles
atrial natriuretic peptide - ANSWER-hormone released by myocytes in atrium in
response to atrial wall stretch and enhances Na+ excretion by kidneys
desmosomes - ANSWER-promote structural integrity
, gap junctions - ANSWER-provide electrical connectivity between cells
primary active transporter - ANSWER-use ATP hydrolysis to transport vs
concentration gradient
secondary active transporter - ANSWER-use pre-existing concentration gradient to
drive ion transport, no ATP hydrolysis
cardiac conduction system - ANSWER-specialized cardiac myocytes that accelerate
and direct wave of depolarization through the heart
autorhythmicity - ANSWER-capacity for spontaneous, rhythmic self-excitation
intrinsic rate - ANSWER-natural firing rate of SA node at 100 depol/min
leaky Kir channels - ANSWER-open in resting state, driving resting membrane
potential near -90 mV
rapid voltage gated Na+ channels - ANSWER-open with AP, triggering rapid
membrane depolarization
Kto channels - ANSWER-opening causes partial membrane repolarization
L-type Ca2+ channels - ANSWER-opening of these channels causes membrane pot
to be held near 0 mV for an extended period of time due to counter-balance by
continued leakage of K+ channels; maintain depolarization
Kv channels - ANSWER-opening causes repolarization, re-establishing resting state
calcium channel blockers - ANSWER-inhibit L-type Ca++ channels and decrease
Ca++ conductance, shortening length of plateau phase and reducing cardiac
contractility
Treat HTN, angina pectoris
cardiac glycosides - ANSWER-inhibit Na/K ATPase, lowering intracellular K+ and
raising intracellular Ca++, strengthened force of contraction
Treat CHF, cardiac arrhythmias
potassium channel blockers - ANSWER-prolong cardiac AP by slowing K+
conductance during Phase 3 repolarization, helping to restore NSR
Class III anti-arrhythmic drugs
ECG - ANSWER-a surface recording of electrical activity of the heart
Lead I - ANSWER-right arm and left arm
Lead III - ANSWER-left arm and left leg
Lead III - ANSWER-left arm and left leg
