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BIOL1782 human phys > Cardiovascular Physiology > Flashcards

Cardiovascular Physiology Flashcards

1
Q

Myocardium

A

muscle tissue of the heart

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2
Q

Cardiac myocytes

A

individual cardiac cells

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3
Q

Endocardium

A

inner tissue layer of the heart

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4
Q

epicardium

A

outer tissue layers of the heart

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5
Q

pericardium

A

fibrous sacs that surround the heart

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6
Q

heart chambers

A

right atrium; right ventricle; left atrium; left ventricle

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7
Q

systole

A

contraction of the heart; ejection of blood from the chamber, can have atrial systole and ventrical systole

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8
Q

diastole

A

relaxation of the heart, chamber filling

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9
Q

systolic pressure

A

pressure within the aorta during systole when blood volumes within the vessel are at their highest

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10
Q

diastolic pressure

A

pressure within the aorta during diastole when blood volumes are at their lowest

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11
Q

cardiac cycle

A

1 heart beat

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12
Q

atria

A

reservoirs for blood; low pressure chambers

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13
Q

ventricles

A

high pressure pumps for the ejection of blood from the heart to the pulmonaries OR the systemic circulation

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14
Q

myocardial blood supply

A
  • 2 major arteries which branch from the root of the aorta
    (i) right corornary artery: supplies right atrium, right ventricle, part of left ventricle
    (ii) left coronary artery; supplies left atrium left ventricle
  • blood returns from the myocardium to the right atrium via;
    (i) great cardiav vein drains into the coronary sinus and then into right atrium
    (ii) middle cardiac vein
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15
Q

Coronary blood supply to the left side of the heart

A
  • during ventricular systole, extravascular compression of the coronary circulation occurs
  • blood flow to the left coronary artery (LCA) is briefly reversed during early systole
  • left ventricular myocardial pressure is greatest near the endocardium and lowest near epicardium
  • maximal left coronary inflow occurs in early diastole when ventricles relax
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16
Q

coronary blood supply to the right side of heart

A
  • lower pressures during systole
  • blood flow reversal does not occure, more coronary inflow during systole than for the left side of the heart, maximum coronary inflow occurs during diastole
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17
Q

AV valves

A

tricuspid valves= between right atrium and right ventricle

mitral valve= between left atrium (also known as bicuspid valve)

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18
Q

Semilunar valve

A

-outflow valves= more blood from a ventricle chamber to a vascular structure
aortic valve= between left ventricle and aorta
pulmonic valve= between right ventricle and pulmonary artery

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19
Q

heart sound

A 
S1= closure of the AV valves; should hear this at the end of diastole and start of systole 
S2= closure of semilunar valves- should hear this at end of systole
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20
Q

Basic cardiac cycle

A

Right atria + right ventricle = transport of blood to the lungs (deoxygenated blood)
left atria + left ventricle= transport of blood to the rest of the body

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21
Q

electrical activity of the heart

A
  • contraction of the heart = shortening of the cardiac muscle fibres
  • contraction is triggered by action potentials
  • transmission of the action potentials from cell to cell is via passage of ions through gap junctions
  • action potential= brief reversal of membrane potential= a brief reversal in the overall charge inside the cell vs. the overall charge outside the cell
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22
Q

SA node

A

-sino-atrial node which is the primary pacemaker of the heart

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23
Q

AV node

A

atrioventricular node, pacemakers for the heart activity

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24
Q

SA and AV nodes

A
  • electrical signals travel from SA node to the AV node down the bundle of His and is split between the left and right bundle branches to the purkinje fibres (these small fibres will send the electrical signals to all the cells of the ventricular myocardium
  • if no normal signals travel down from the SA node to the AV node or from the AV node to the ventricles
  • some cells in the bundle of His or in the purkinje network can become the pacemaker for the ventricles (ectopic beats)
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25
Q

slow response/pacemaker action potentials

A

-occurs mainly in the pacemaker cells
-pacemaker potential= slow depolarization with no true resting potential, although a brief period of negative membrane potential (~-50mV) occurs at the start of the depolarization event
-depolarization is initiated by the negative potential resulting in the closure of any K+ ion channels and opening of T-type Ca2+ channels and F-type Na+ ion channels
phase 0= upstroke mediated mainly by the opening of L-type Ca2+ channels
phase 3= rapid repolarization Ca2+ channels close and K+ channels open
phase 4= negative voltage causes the closure of the K=t ion channels, opening the f-type Na+

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26
Q

Fast response/non-pacemaker action potentials

A

-this occurs in the atrial, ventricular cells and purkinje fibers
-resting membrane potential
is ~-90mV
phase 0= Na+ channels open through relay of signal from the pacemaker cells and adjacent cells resulting in rapid upstroke, as rapid influx of Na+ occurs (as well as leaky K+ channels that tend to be open at the more negative membrane potentials close)
phase 1= as voltages reach 0mV, the voltage gated Na+ channels close and transient outward K+ channels open= partial repolarization
phase 2/plateau phase- L-type Ca2+ channels close and K+ channels open, K+ efflux
phase 4- diastole, resting potential
*for full resting potential to be reached, Na+, K+ and Ca2+ must be restored to their resting concentrations whin and without the cell, accomplished through ATP pumps

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27
Q

Circulation path for electrical signals through the heart

A
  • action potentials generated by SA node spread throughout the atria through cell-to-cell conduction
  • myocytes are joined together by low-resistance gap junctions and ionic currents can flow through these adjoining cells spreading the action potential
  • SA node generates initial action potential which spreads throughout the right and left atria
  • action potentials usually only have one pathway available to enter the ventricles through the AV node
  • AV node slows conduction velocity from to allow for time for depolarization and emptying of blood into ventricles
28
Q

12 lead ECG

A

12 different views of the heart that use 6 limb leads and 6 chest/ precordial leads

29
Q

single lead/rhythm or test strip ECG

A

a 12 lead ECG that looks at the elctrical activity of the heart in a cross-sectional plans

a) frontal plane: vertical cut through middle of heart, anterior to posterior view, 6 limb leads
b) horizontal plane: transverse cut, through middle of heart, inferior view of electrical activity, 6 precordial leads (V leads)

30
Q

P wave

A
  • represents atrial depolarization, start of atrial contraction, atrial systole
  • conduction of an electrical impulse through the atria, normal duration 0.06-0.12 seconds
31
Q

PR interval

A
  • beginning of the P wave to the beginng of the QRS complex and represents the time from atrial to ventricular activation
  • 0.12-0.20 seconds
  • time to spread electrical activation from SA note to ventricles
32
Q

QRS complex

A
  • intraventricular conduction time
  • spread of electrical signals through the ventricles, intiates ventricular contraction
  • normally takes 1/2 the time of the PR interval
33
Q

ST segment

A
  • represents full ventricular repolarization

- ventricular recovery/repolarization, initiation of ventricular muscle relaxation

34
Q

QT interval

A
  • measures timing of entire ventricular depolarization and repolarization events
  • length varies according to HR
35
Q

U wave

A
  • not seen on all ECG readings
  • should always follow the T wave and have an upright deflection with a rounded shape
  • represents the recovery period of the purkinje/ventricular conduction fibres
36
Q

Cardiac output

A
  • the amount of blood ejected by the heart in one minute
  • CO=HR X SV
  • at rest, HR 70beats/min
  • at rest, SV 80mL/beat
  • CO at rest 5.6 L/min
37
Q

Stroke volume

A

volume of blood ejected by the heart in one beat

38
Q

Factors that impact CO

A 
Heart rate
Stroke volume 
Venous return and pre load 
afterload (TPR) 
Contractility
39
Q

Heart rate (affecting CO)

A
  • an increase in HR (with no change to SV) will increase CO to a point
  • HR mainly controlled by ANS, with resting rates controlled by parasympathetic
  • acetylcholine released by vagus nerve decreased HR
  • norepinephrine released by sympathetic neruons increases HR
40
Q

Stroke volume (affecting CO)

A
  • (end diastolic volume)-(end systolic volume= EDV-ESV
  • average output of blood per heart beat
  • changing contractility, pre load and afterload will change SV
41
Q

ANS control of HR

A
  • with sympathetic control, epinephrine and norepinephrine bind to specific andrenic receptors on the SA node, changes the time to depolarization and decreases the time between subsequent depolarization
  • with parasympathetic control acetylcholine binds to acetlycholine receptors on the SA node, longer time to depolarization and increased time between subsequent dopolarizations
42
Q

Venous return and preload (affecting CO)

A
  • preload= chamber end-diastolic volume (EDV) and can be considered equal to chamber end-diastolic pressure (EDP)
  • greater the venous return, the greater the preload since there is an increase in blood volume and increased pressure within the chamber
  • preload increases with increased venous return
  • reflects how much the heart is stretched before contraction
  • increased preload results in increased SV and increased SV results in increased CO
43
Q

Afterload (TPR) (affecting CO)

A
  • pressure against which the heart must pump to eject blood
  • a function of the total peripheral resistance and pressure within aorta
  • afterload increases with increased BP and decreased aorta compliance
  • increased afterload results in decreased SV and decreased SV results in decreased CO
44
Q

Contractility (affecting CO)

A
  • the force the heart is capable of developing as it contracts
  • increased contractility results in increased SV
  • positive inotropic factors= increased contractility (ex. beta-sympathetic stimulation
  • negative intropic factors= beta blockers, heart failure, acidosis, hypoxia
45
Q

Ejection fraction

A
  • measure of CO and contractility
  • (SV)/(left ventricular end-systolic volume)=SV/LVEDV
  • and indicator of left and ventricular function
  • a more forceful contraction propels more blood into the arteries resulting in smaller en d systolic volumes
  • increasing contractility will increase EF
46
Q

CO can also be calculated from…

A
  • CO=MAP/TPR
  • MAP: mean arterial pressure that is continuously changing throughout the cardiac cycle
  • TPR= total peripheral resistance
  • TPR mainly controlled by arterioles where smooth muscle tone is regulated by ANS, blood-borne agents
47
Q

MAP

A
  • at normal resting rates, MAP is not 1/2 between systolic and diastolic pressure (since the time spent in diastole is 2x as long as systole)
  • at high heart rates, MAP can be calculated as the average of the systolic and diasolic pressures
  • MAP= CO XTPR= HR X SV X TPR
  • MAP= DP + 1/3 (SP-DP), DP= diastolic pressure, SP= systolic pressure
48
Q

PP

A
  • pulsation/throb in the arteries of the wrist or neck
  • should not be felt during diastole but during systole, the artery wall is pushed out by the rush of blood entering arterial system
  • magnitude affected by
    (a) increased SV=increased PP
    (b) increrased speed of ejection = Increased PP
    (c) decreased arterial compliance = increased PP
49
Q

Blood pressure and body position

A
  • gravity influences circulating blood volume when standing
  • when standing, blood collects in peripheral leg veins, pooling blood can expand the vein walls without returning blood to the heart
  • increased pressure with pooling blood will increase the capillary pressures, pushing fluid out of the circulation and into tissues (edema)
50
Q

Hemodynamics

A
  • relationship between pressure and flow
  • depends on:
    (a) pressure gradients (P)
    (b) resistance to flow (R)
  • blood flow Q=P/R
  • P(ressure) gradient: blood flows from area of high pressure to an area of low pressure
51
Q

Intropy

A

contractility of the cardiac muscle

52
Q

dromotropy

A

velocity of conduction of the electrical signals

53
Q

chronotropy

A

rate of heart beats

54
Q

lusitropy

A

relaxation of functions of the cardiac muscle and chambers

55
Q

Sympathetic NS

A
  • major transmitter is norepinephrine (NE)
  • release of NE results in: increases HR (SA node stimulation), increased contractility and increased rate of conductance (increased Ca2+, AV nodal and His-purkinje stimulation), increased CO (increased HR and SV)
56
Q

Parasympathetic NS

A
  • via the vagus nerve
  • transmitter is acetylcholine
  • release of acetylcholine cases: decreased HR (SA node), decreased atrial contraction and decreased conduction velocity (AV node), decreased CO
57
Q

CNS

A
  • 2 centres associated with tthe CNS and control of the cardiovascular function
    (i) cardiopulmonary plexus which is part of the sympathetic response
    (ii) the vagus which is part of the parasympathetic response
  • increased arterial pressures will inhibit the cardipulmonary plexus response and excite the vagal response
58
Q

CNS + parasympathetics

A

-increase in parasympathetic activity the vagus nerve will be sitmulated and acetylcholine will be released from fibers resulting in primarily decreased HR and decreased CO

59
Q

CNS + sympathetics

A
  • increase in sympathetic activity, norepinephrine will be secreted and epinephrine will be released be adrenal gland
  • both result in dilation of B2 blood vessels and increased HR and increased Myocardial contractility, increased CO
60
Q

Baroreceptor reflexes

A
  • carotid sinuses act as pressure baroceptors
  • the rate of neural discharge is directly proportional to the mean arterial pressure AND pulse pressure (ensuring the CNS does not receive both)
61
Q

if arterial pressure decreases, the discharge rate from baroreceptors decreases including…

A
  • increased HR due to increased sympathetic activity
  • increased ventricular contractibility due to sympathetic activity
  • arteriolar constriction
  • increased venous constriction
  • all this results in increased CO, peripheral resistance and increased blood pressure
62
Q

Blood borne regulation

A
  • ADH
  • ANP
  • Angiotensis II
  • Kinins
  • Histamine
63
Q

ADH

A
  • increases water retention

- decreased BP, dehydration, increased Na+ intake

64
Q

ANP

A
  • atrial natiuretic peptide
  • released by myocardium in response to atrial pressures
  • stimulation of water loss through the renal system
65
Q

angiotensin II

A
  • increased BP by;
    (1) direct action on vascular smooth moscule
    (2) increases sympathetic activity
    (3) simulates the release of ADH
    (4) stimulates the release of aldosterone
66
Q

Kinins

A
  • example of bradykinin
  • vasodilators-relaxes arterioles
  • decreases BP
  • increases venular permeability
  • induces non-vascular smooth muscle contractions
67
Q

Histamines

A
  • causes arteriolar dilation resulting in decreased BP
  • increases venular permeability
  • induces non-vascular smooth muscle contractions

BIOL1782 human phys (3 decks)

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