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Cardiovascular > Physiology > Flashcards

Physiology Flashcards

1
Q

Cardiac Output =

A

Stroke Volume * Heart Rate

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2
Q

Fick Principle

A

Cardiac Output = rate of O2 consumption/(arterial O2 content - venous O2 content)

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3
Q

Mean arterial pressure (MAP)

A

Cardiac Output * Total Peripheral Resistance
OR
2/3 diastolic pressure + 1/3 systolic pressure

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4
Q

Pulse pressure

A

systolic pressure - diastolic pressure

Pulse pressure is proportionate to stroke volume

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5
Q

Stroke volume

A

CO/HR
or
EDV - ESV

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6
Q

In exercise how is CO maintained
Early
Late
What if HR gets too high?

A

Early: Increased HR and increase SV
Late: Increased HR only (SV plateaus)
If HR is too high, diastolic filling is incomplete and CO decreased (VT)

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7
Q

What effects stroke volume?

Increased stroke volume when…

A

Contractility, Afterload, Preload (SV CAP)

Increased stroke volume when increased preload, decreased afterload, or increased contractility

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8
Q

Contractility increased with

A
  1. Catecholamines (Increased activity of Ca2+ pump in sarcoplasmic reticulum)
  2. Increased intracellular Ca2+
  3. Decreased extracellular Na+ (decreased Na+/Ca+ exchanger)
  4. Digitalis (blocks Na+/K+ pump -> increased intracellular Na+ -> decreased Na+/Ca+)
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9
Q

Contractility decreased with

A
  1. Beta-blockade (decreased cAMP)
  2. Heart failure (systolic dysfunction)
  3. Acidosis
  4. Hypoxia/hypercapnea (decrease PO2/increased PCO2)
  5. Non-dihydropyridine Ca2+ channel blockers
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10
Q

Stroke volume increased in these conditions

A

anxiety, exercise, pregnancy

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11
Q

Stroke volume decreases in this condition

A

Heart failure

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12
Q

Myocardial O2 demand is increased by

A

Increase afterload
Increase contractility
Increase HR
Increased heart size (increase wall tension)

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13
Q

Preload =

A

ventricular EDV

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14
Q

Afterload =

A

mean arterial pressure (proportional to peripheral resistance)

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15
Q

Venodilators do what to preload

A

Decrease preload (nitroglycerin)

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16
Q

Vasodilators do what to afterload

A

Decreased afterload (hydralazine)

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17
Q

Preload increases with

A

Exercise (slightly)
Increased blood volume (overtransfusion)
Excitement (increased SNS)

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18
Q

Force of contraction is proportional to what

A

End diastolic length of cardiac muscle fiber (preload)

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19
Q

Starling curve axis

Slope of curve decreases with

A

X axis = ventricular EDV (preload)
Y axis = CO or Stroke Volume
Slope decreases with CHF + digoxin, CHF
Slope increases with exercise (sympathetic nerve impulses)

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20
Q

Ejection fraction =
What is it an index for?
Normal percent?

A 
Stroke Volume/End Diastolic Volume 
or
EDV - ESV/EDV
Index for ventricular contractility
Normally greater/equal to 55% (decreases in systolic HF)
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21
Q

Driving pressure =

A

Flow * Resistance (Q*R) (similar to Ohm’s of change in V = IR)

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22
Q

Resistance =

A

driving pressure/flow (deltaP/Q)
or
8n (viscosity) * length/ pi*r^4

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23
Q

Total resistance in vessels in series =

A

R1 + R2 + R3….

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24
Q

Total resistance in vessels in parallel =

A

1/R1 + 1/R2 + 1/R3…

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25
Q

Viscosity depends on…
Viscosity increases in…
Viscosity decreases in…

A

Depends on hematocrit
Increases polycythemia, hyperproteinemic states (multiple myeloma), hereditary spherocytosis
Decreases in anemia

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26
Q

Pressure gradient drives flow to what direction?

A

High pressure to low pressure

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27
Q

Resistance is proportional and inversely proportional to

A

Directly proportional to viscosity and vessel length

Inversely proportional to radius to the 4th power

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28
Q

Most peripheral resistance comes from these vessels…

A

arterioles (regulate capillary flow)

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29
Q

Phases of cardiac cycle in LV: isovolumetric contraction

A

period between mitral valve closure and aortic valve opening; period of highest O2 consumption

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30
Q

Phases of cardiac cycle in LV: systolic ejection

A

period between aortic valve opening and closing

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31
Q

Phases of cardiac cycle in LV: isovolumetric relaxation

A

period between aortic valve closing and mitral valve opening

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32
Q

Phases of cardiac cycle in LV: rapid filling

A

Period just after mitral valve opening

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33
Q

Phases of cardiac cycle in LV: reduced filling

A

Period just before mitral valve closure

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34
Q

S1

A

Mitral and tricuspid valve closure. Loudest at mitral area.

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35
Q

S2

A

Aortic and pulmonary valve closure. Loudest at left sternal border

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36
Q

S3

A

In early diastole during rapid ventricular filling phase. Associated with increased filling pressures (MR, CHF) and more common in dilated ventricles (but normal in pregnant and children)

To hear: https://www.youtube.com/watch?v=xbLMC0kPQ-E&list=UUkiESbCo0zbmPwovRiXC8VQ&index=14

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37
Q

S4

A

Atrial kick - in late diastole. High atrial pressure. Associated with ventricular hypertroph. Left atrium must push against stiff LV wall.

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38
Q

Systole includes

A

Isovolumetric contraction
Rapid ejection
Reduced ejection

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39
Q

Jugular venous pulse

A

a wave - atrial contraction
c wave - RV contraction (closed tricuspid bulging into atrium)
x descent - atrial relaxation and downward displacement of closed tricuspid valve during ventricular contraction
v wave - increased R atrial pressure due to filling against closed tricuspid valve
y descent - blood flow from RA to RV

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40
Q

Normal splitting

A

Inspiration –> drop in intrathoracic pressure –> increase venous return to the RV –> increased RV stroke volume –> increased RV ejection time –> delayed closure of pulmonic valve (also due to decreased pulmonary impedance during inspiration)

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41
Q

Wide splitting

A

Conditions that delay RV emptying (pulm stenosis, right bundle branch block)
Delay in RV emptying causes delayed pulmonic sound (regardless of breath) –> exaggeration of normal splitting

to hear: https://www.youtube.com/watch?v=5tBk1XuEyuM&list=UUkiESbCo0zbmPwovRiXC8VQ

42
Q

Fixed splitting

A

Seen in ASD. ASD –> left-to-right shunt –> increased right atrial and right ventricular volumes –> increased flow through pulmonic valve such that (regardless of breath) pulmonic closure is greatly delayed

to hear: https://www.youtube.com/watch?v=5tBk1XuEyuM&list=UUkiESbCo0zbmPwovRiXC8VQ

43
Q

Paradoxical splitting

A

Seen in conditions that delay LV emptying (aortic stenosis, left BBB)
Normal order of valve closure is reversed so that P2 sounds occur before delayed A2 sound so on inspiration P2 closes later and moves closer to A2 (paradoxically eliminating the split)

to hear: https://www.youtube.com/watch?v=5tBk1XuEyuM&list=UUkiESbCo0zbmPwovRiXC8VQ

44
Q

Aortic ascultation

A

Right sternal border
Systolic murmur = aortic stenosis, flow murmur, aortic valve sclerosis

MR SAS (Mitral regur, Systolic, Aortic Stenosis)

45
Q

Left sternal border ascultation

A

Left sternal border
Diastolic murmur = aortic regurgitation, pulmonic regurgitation
Systolic murmur = hypertrophic cardiomyopathy

MS DAR (mitral sten, diastolic, aortic regur)

46
Q

Pulmonic ascultation

A

Systolic ejection murmur

Pulmonic stenosis, flow murmur (ASD, PDA)

47
Q

Tricuspid ascultation

A

Pansystolic murmur =Tricuspid regurgitation, VSD

Diastolic murmur = tricuspid stenosis, ASD

48
Q

Mitral ascultation

A

Systolic murmur = mitral regrug

Diastolic murmur = mitral stenosis

49
Q

Machine-like murmur of PDA is best appreciated in this location

A

Left infraclavicular region

50
Q

ASD presents with this kind of murmur - early and late

A

pulmonary flow murmur (increase flow through pulmonary valve) and a diastolic rumble (increased flow across tricuspid)
later progresses to louder diastolic murmur of pulmonic regurg from dilatation of pulmonary artery

51
Q

Increase intensity of right heart sounds by

A

inspiration

52
Q

Increase intensity of left heard sound by

A

expiration

53
Q

Increase intensity of MR, AR, VSD, MVP murmurs

Decrease intensity of AS, hypertrophic cardiomyopathy murmur

A

Hand grip (increase systemic vascular resistance)

54
Q

Decrease intensity of most murmur

Increase intensity of MVP, hypertrophic cardiomyopathy murmur

A

Valsalva (decrease venous return)

55
Q

Decrease intensity of MPV, hypertrophic cardiomyopathy murmur

A

Rapid squatting (increase venous return, increase preload, increase afterload with prolonged squatting)

56
Q

Systolic heart sounds

A

aortic/pulmonic stenosis, mitral/tricuspid regurg, VSD

To hear normal: https://www.youtube.com/watch?v=xS3jX1FYG-M&list=UUkiESbCo0zbmPwovRiXC8VQ

57
Q

Diastolic heart sound

A

aortic/pulmonic regurg, mitral/tricuspid stenosis

To hear normal: https://www.youtube.com/watch?v=xS3jX1FYG-M&list=UUkiESbCo0zbmPwovRiXC8VQ

58
Q 
Mitral Regurgitation Murmur
Sounds like
Best heard at
Enhanced with
Due to
A

Holosystolic, high-pitched “blowing murmur”
Mitral - loudest at apex and radiates toward axilla
Enhanced by maneuvers that increase TPR (squatting, hand grip) or LA return (expire)
MR due to ischemic heart disease, MVP, LV dilation; rheumatic fever and infective endocarditis

To hear: https://www.youtube.com/watch?v=MMJBSd5Z_Uc

59
Q 
Tricuspid Regurgitation Murmur
Sounds like
Best heard at
Enhanced with
Due to
A

Holosystolic, high-pitched “blowing murmur”
Tricuspid - loudest at tricuspid area and radiates to right sternal border
Enhanced by maneuvers that increase RA return (inspire)
TR due to RV dilation; rheumatic fever and infective endocarditis

To hear: https://www.youtube.com/watch?v=Jk50shI9vV8

60
Q 
Aortic Stenosis 
Sounds like
Also heard at
Other signs
Due to
Can cause
A

Crescendo-decrescendo systolic ejection murmur following ejection click (due to abrupt halting of valve leaflets)
Radiates to carotids/heart base
Pulsus parvus et tardus - pulses are weak with a delayed peak
LV&raquo_space; aortic pressure during systole; age-related calcific aortic stenosis or bicuspid aortic valve
Can lead to syncope, angina, dyspnea on exertion (SAD)

To hear: https://www.youtube.com/watch?v=Gbk2465HO98&list=UUkiESbCo0zbmPwovRiXC8VQ

61
Q

VSD
Sounds like
Best heard at
Enhanced by

A

Holosystolic, hard sounding murmur
Loudest at tricuspid area
Enhanced by hand grip bc increased afterload

To hear: https://www.youtube.com/watch?v=7oKz6J0Ay_I

62
Q 
MVP
Sounds like
Best heard at
Enhanced by
Due to
A

Late systolic crescendo murmur with midsystolic click (due to sudden tensing of chordae tendineae)
Best heard over apex, loudest at S2
Enhanced by maneuvers that decrease venous return (standing/Valsalva)
Due to valvular lesion but benign usually or myxomatous degeneration, rheumatic fever, chordae rupture; predispose to infective endocarditis

Mid-systolic click: https://www.youtube.com/watch?v=PsmGx2XMxF8&list=UUkiESbCo0zbmPwovRiXC8VQ

63
Q 
Aortic regurgitation 
Sounds like
Enhanced/depressed by
Other sx
Due to
A

Immediate high-pitched “blowing” diastolic decrescendo murmur
Enhanced by hand grip, vasodilators decrease intensity
Wide pulse pressure when chronic - present with bounding pulses and head bobbing
Due to aortic root dilation, bicuspid aortic valve, endocarditis, rheumatic fever

To hear: https://www.youtube.com/watch?v=42IahK-zxj0&list=UUkiESbCo0zbmPwovRiXC8VQ

64
Q

Mitral stenosis
Sounds like
Enhanced by
Due to

A

Follows opening snap (due to abrupt halt in leaflet motion in diastole after rapid opening due to fusion at leaflet tips); delayed rumbling late diastolic murmur
Enhanced by maneuvers that increase LA return (expire)
LA&raquo_space; LV pressure during diastole
Occurs 2ndary to rheuamtic fever, chronic MS can result in LA dilation

To hear: https://www.youtube.com/watch?v=L5DEqvgS_xs
Opening snap: https://www.youtube.com/watch?v=E0fDFsmVQfY&list=UUkiESbCo0zbmPwovRiXC8VQ

65
Q

PDA
Sounds like
Best heard at
Due to

A

Continuous machine-like murmur, loudest at S2
Best heard at left infraclavicular area
Congenital rubella or prematurity

To hear: https://www.youtube.com/watch?v=UOOylGXPsyQ

66
Q

Ventricular action potential (and at bundle of His and Purkinje fibers) - Phase 0

A

Phase 0 = rapid upstroke, voltage gated Na+ channels open

67
Q

Ventricular action potential (and at bundle of His and Purkinje fibers) - Phase 1

A

Phase 1 = initial repolarization - inactivation of voltage-gated Na+ channels. Voltage-gated K+ channels begin to open

68
Q

Ventricular action potential (and at bundle of His and Purkinje fibers) - Phase 2

A

Phase 2 = plateau - Ca2+ influx through voltage-gated Ca2+ channels balances K+ efflus. Ca2+ influx triggers Ca2+ relase from sarcoplasmic reticulum and myocyte contraction

69
Q

Ventricular action potential (and at bundle of His and Purkinje fibers) - Phase 3

A

Phase 3 = rapid repolarization - massive K+ efflus due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca2+ channels

70
Q

Ventricular action potential (and at bundle of His and Purkinje fibers) - Phase 4

A

Phase 4 = resting potential - high K+ permeability through K+ channel

71
Q

Hows is ventricular different than skeletal muscle?

A
  • Cardiac muscle AP has a plateau - due to Ca2+ influx and K+ efflux
  • Myocyte contraction occurs due to Ca2+ induced Ca2+ release from SR
  • Cardiac nodal cells spontaneously depolarize during diastole resulting in automaticity due to I-f channels (slow mixed Na+/K+ inward current)
  • Cardiac myocytes are electrically coupled to each other by gap junctions
72
Q

Pacemaker action potential - Phase 0 (SA and AV nodes)

A

Phase 0 = upstroke - opening of voltage gated Ca2+ channels. Fast voltage gated Na+ channels are permanently inactivated bc of the less negative resting voltage of these cells. Results in a slow conduction velocity that is used by the AV node to prolong transmission from the atria to ventricles

73
Q

Pacemaker action potential - Phase 2 (SA and AV nodes)

A

Phase 2 = plateau is absent

74
Q

Pacemaker action potential - Phase 3 (SA and AV nodes)

A

Phase 3 = inactivation of Ca2+ channels and increase activation of K+ channels leading to K+ efflux

75
Q

Pacemaker action potential - Phase 4 (SA and AV nodes)

A

Phase 4 = slow diastolic depolarization - membrane potential spontaneously depolarizes as Na+ conductance increases. Accounts for automaticity of SA and AV nodes. Slope of phase 4 in SA = HR.
ACh/adenosine decrease rate of diastolic depol and decrease HR
Catechols increase depol and HR
SNS stim increase the chance that I-f channels are open and thus increase HR

76
Q

Pulmonary stenosis

A

to hear: https://www.youtube.com/watch?v=SWW1PTL9Jbw&list=UUkiESbCo0zbmPwovRiXC8VQ

77
Q

Aortic arch receptor
transmits via what?
to what?
responding to what?

A

transmits via vagus nerve to solitary nucleus of medulla

responds only to increased BP

78
Q

Carotid sinus receptor
transmits via what?
to what?
responding to what?

A

transmits via glossopharyngeal nerve to solitary nucleus of medulla
responds to increase and decrease in BP

79
Q

Baroreceptor response to hypotension

A

decrease arterial pressure –> decrease stretch –> decrease afferent baroreceptor firing –> increase efferent sympathetic firing and decrease efferent parasympathetic stimulation –> vasoconstriction, increase HR/contractility/BP.

Important in severe hemorrhage

80
Q

Carotid massage

A

increase pressure on carotid artery –> increase stretch –> increase afferent baroreceptor firing –> decrease HR

81
Q

How do baroreceptors contribute to Cushing reaction?

A

Cushing reaction: HTN, bradycardia, and respiratory depression
Increase intracranial pressure constricts arterioles –> cerebral ischemia and reflex sympathetic increase in perfusion pressure (HTN) –> increase stretch –> reflex baroreceptor induced-bradycardia

82
Q

Peripheral chemoreceptors where?

Stimulated by?

A

Peripheral - carotid and aortic bodies

Stimulated by decrease in PO2 (<60 mmHg), increase PCO2, and decrease pH of blood (acid)

83
Q

Central chemoreceptors

Stimulated by?

A

stimulated by changes in pH and PCO2 of brain interstitial fluid which in turn are influenced by arterial CO2. Do no directly respond to PO2

84
Q

Organ with the largest blood flow

A

Lung = 100% of cardiac output

85
Q

Organ with largest share of SYSTEMIC cardiac output

A

Liver

86
Q

Organ with highest blood flow per gram of tissue

A

Kidney

87
Q

Organ with largest arteriovenous O2 difference because O2 extraction is 80%.

A

Heart - therefore increase O2 demand is met by increase coronary blood flow, not by increase extraction of O2

88
Q

PCWP approximates what
How does mitral stenosis effect it?
How is it measured?

A

Pulmonary capillary wedge pressure is a good approximation of left atrial pressure. In mitral stenosis the PCWP > LV diastolic pressure
Measured with pulmonary artery catheter (Swan-Ganz)

89
Q

Autoregulation

A

How blood flow to an organ remains constant over a wide range of perfusion pressures

90
Q

Factors determining autoregulation of the heart

A

Local metabolites (vasodilatory) - CO2, adenosine, NO

91
Q

Factors determining autoregulation of the brain

A

Local metabolites (vasodilatory) - CO2 (pH)

92
Q

Factors determining autoregulation of the kidneys

A

Myogenic and tubuloglomerular feedback

93
Q

Factors determining autoregulation of the lungs

A

Hypoxia causes vasoconstriction

94
Q

Factors determining autoregulation of the skeletal muscles

A

Local metabolites - lactate, adenosine, K+

95
Q

Factors determining autoregulation of the skin

A

Sympathetic stimulation most important mechanism - temperature control

96
Q

How does hypoxia effect the pulmonary vasculature?

A

Hypoxia causes vasoconstriction so that only well-ventilated areas are perfused. In other organs, hypoxia causes vasodilation.

97
Q

What determines the fluid movement through capillary membranes? Name all four.

A

Starling forces
Pc = capillary pressure - pushes fluid out of capillary
Pi = interstitial fluid pressure - pushes fluid into capillary
(Pi)c = plasma colloid osmotic pressure - pulls fluid into capillary
(Pi)i = interstitial fluid colloid osmotic pressure - pulls fluid out of capillary

98
Q

Net filtration pressure of capillaries?

A

P net = [(Pc - Pi) - ((Pi)c - (Pi)i)]

99
Q

What is the filtration constant and what does it represent?

A

Kf = filtration constant = capillary permeability

100
Q

Net fluid flow?

A

Jv = net fluid flow = (Kf)(P net)

101
Q

Causes of edema

A

Excess fluid outflow into interstitium caused by:
Increase capillary pressure (Pc; heart failure)
Decrease plasma proteins ((Pi)c; nephrotic syndrome, liver failure)
Increase capillary permeability (Kf; toxins, infections, burns)
Increase interstitial fluid colloid osmotic pressure ((Pi)i; lymphatic blockage)

Cardiovascular (8 decks)

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