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Physio > Chest Pain > Flashcards

Chest Pain Flashcards

1
Q

Flux (J)

A

=KD[^C/^x]

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2
Q

Fick equation

A

VO2 = CO x (arterialO2-venousO2)

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3
Q

Cardiac output equation

A

CO = HR x SV

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4
Q

Left side of the heart

A

systemic circulation

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5
Q

Right side of the heart

A

pulmonary circulation

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6
Q

Pulmonary and systemic circulation systems are in?

A

Series

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7
Q

Organs are in?

A

Parallel, each organ gets freshly, fully oxygenated blood, flow to one organ can be changed without affecting flow to other organs

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8
Q

Hemodynamic Ohm’s Law equivalent

A

Q = ^P/R

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9
Q

Resistance =

A

^P/CO = (MAP-CVP)/CO

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10
Q

MAP normal?

A

95mmHg

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11
Q

CVP normal?

A

2mmHg

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12
Q

CO normal?

A

5-6L/min

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13
Q

Blood flow is proportional to?

A

Pressure difference

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14
Q

Pressures of heart chambers

A

RA = 2mmHg RV = 25/10mmHg LA = 8-9mmHg LV = 130/80mmHg

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15
Q

Responses to drop in pressure?

A
  1. Reduced outflow (increase R) controlled by SNS 2. Increase inflow by increasing HR and contractility 3. Increase volume (short term - venous return, long term - salt and water retention increase BV)
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16
Q

Depolarization of the heart

A

SA, AV, septum (left to right), His/Purkinje system, ventricular muscle (endo to epicardium)

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17
Q

Fast APs vs Slow APs of heart

A

contracting regions (atrial and ventricular muscles), fast conduction (His, Purkinje), Left side pacemaking (SA) and slow conduction (AV) right side

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18
Q

Fast AP Phases

A

0 - rapid depol due to activation of inward Na+ current 1 - initial repol due to inactivation of Na+ channels and activation of transient outward K+ channels (Ito) 2 - plateau phase due to slow activating inward Ca++ currents, triggers CICR 3 - repol due to inactivation of Ca++ currents and activation of several different K+ currents (Iks, Ikr) 4 - resting membrane potential due to inward-rectifying K+ channels (Ik1)

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19
Q

Slow AP Phases

A

0 - slow depol due to activation of slowly-acting Ca++ channels 1 - absent 2 - absent 3 - repol due to Ca++ channel inactivation and activation of K+ channels 4 - slowly depolarizing resting potential (If - nonselective cation channel - HCN)

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20
Q

Absolute refractory period for fast v slow AP

A

Fast - Na inactivation Slow - Ca inactivation

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21
Q

Spontaneous depol of Slow AP

A

imbalance between outward K channels (Ik,ach, or Igirk) and inward current of not selective cation channel (If)

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22
Q

Parasympathetic stimulation on AP

A

PNS releases ACh, binds to muscarinic ACh receptors, increasing Igirk, reducing rate of phase 4 depol, negative chronotropic effect

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23
Q

Sympathetic stimulation on AP

A

SNS release norepi, epi, binds to b1 adrenergic repectors, increase both If and Ica, increasing phase 4 depol, positive chronotropic effect

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24
Q

Intrinsic rate of SA node, AV node, and His/Purkinje systems

A

SA = 100bpm AV = 40-60bpm His/Purkinje = 30-40bpm

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25
Q

Dromotropic effects

A

Positive dromotropic effect - increases AP conduction, SNS Negative dromotropic effect - decreases AP conduction, PNS

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26
Q

P-wave

A

atrial depolarization, speed of propagation throughout the atria

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27
Q

PR-segment

A

movement of the AP through the AV node

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28
Q

QRS-complex

A

ventricular depolarization

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29
Q

Q-wave

A

left side of the septum depolarizes before the right, resulting in small downward deflection

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30
Q

R-wave

A

depolarization spread from endo to epicardium, large muscle mass involved, large amplitude

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31
Q

S-wave

A

last part of ventricle depolarization is near the atrium, gives brief negative deflection

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32
Q

Bundle-branch block

A

widening of QRS

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33
Q

ST-segment

A

interval between ventricular depolarization and repolarization

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34
Q

T-wave

A

ventricular repolarization

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35
Q

Interval between P-waves

A

‘sinus rhythm’, HR, tachycardia, bradycardia

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36
Q

Lead I, II, aVf, III, aVr, aVL

A

0, +60, +90, +120, -150, -30

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37
Q

Right and left axis deviations

A

Right - MEA moves right, clockwise, pulmonary HTN Left - MEA moves left, counterclockwise, systemic HTN

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38
Q

Normal MEA

A

between +100 and -30

39
Q

First degree heart block

A

P-waves are all followed by QRS, but PR-interval is increased

40
Q

Second degree heart block

A

PR interval lengthened so much that not every P-wave is followed by QRS

41
Q

Third degree heart block

A

P-wave and QRS depolarize independently with ventricle depol driven by latent pacemaker

42
Q

Atrial flutter

A

P waves are too fast, driven by atrial pacemaker, but QRS is normal

43
Q

Atrial fibrillation

A

atria are not driven by SA node, but instead by local currents, result in uncoordinated atrial firing and no P waves are detected

44
Q

Ventricular tachycardia/flutter

A

ventricular rate is greater than atrial rate, due to ectopic pacemaker

45
Q

Ventricular fibrillation

A

electrical activity is completely uncoordinated, lethal condition that must be corrected within minutes

46
Q

Spontaneous AP in ventricular cells

A

abnormal QRS complex

47
Q

ST segment depression/elevation

A

MI occurred recently

48
Q

S4

A

Atrial gallop usually due to ventricular hypertrophy, occurs in late diastole, never normal to hear

49
Q

S3

A

Ventricular gallop heard during ventricular filling, common in children and young adults, due to supple ventricle, but sign of dilated cardiomyopathy in an adult

50
Q

Compliance

A

volume changes with pressure

51
Q

SV

A

CO = SV x HR

52
Q

Normal EF

A

>55%

53
Q

Increasing Preload of the heart?

A

increases EDV, SV, CO no affect on aortic pressure

54
Q

Heart Failure

A

decreased CO triggers increased BV, PL, EDV, SV and CO, but this is only a short term compensatory mechanism, decreases starling curve/inotropy

55
Q

Law of LaPlace

A

wall stress (sigma) = [P x r]/2h Pressure, chamber radius, wall thickness

56
Q

Increasing Afterload of the heart?

A

force that heart has to overcome to force blood into the aorta, afterload is wall stress, very close to aortic pressure increases aortic pressure that ventricle must contract against to open valve, and valve closes at higher pressure, ESV Decreasing fiber shortening velocity, SV, CO

57
Q

Aortic stenosis

A

left ventricular emptying is impaired because of narrowing of the aortic valve, flow through aortic valve generates additional sounds between S1 and S2

58
Q

Increasing Inotropy of the heart?

A

Shifts ESPVR curve to the left and increases line slope, increases velocity of shortening, decreases ESV, increasing SV and CO

59
Q

Blood flow (Q) =

A

Q = V x a = P/R

60
Q

Poiseulle’s equation

A

Q = [P(Pi)r^4]/8Ln(viscosity)

61
Q

Changes to viscosity

A
  1. life at high altitudes, increased viscosity 2. polycythemia vera, increased viscosity 3. severe dehydration, increased viscosity 4. sickle-cell anemia, increased viscosity
62
Q

Parallel arrangement has the highest resistance

A

FALSE - LOWEST

63
Q

Normal MAP

A

95mmHg

64
Q

TPR =

A

[MAP-CVP]/CO

65
Q

Normal TPR

A

15-18mmHg/l/min or 15-18 HRUs or Wood units

66
Q

PP

A

Pulse pressure = SBP - DBP

67
Q

MAP =

A

DBP + [PP/3]

68
Q

Septic shock is associated with?

A

Large drop in TPR, only form of shock that is associated with decrease, rather than increased TPR

69
Q

Factors that affect Poiseuille’s law

A
  1. turbulent flow 2. viscosity of blood changes with velocity 3. compliance of blood vessels
70
Q

Reynold’s Number

A

Nr = vdp/n velocity, diameter, density, viscosity Nr>2000 = turbulent flow

71
Q

Korotkoff sounds

A

partial occlusion of brachial artery with pressure cuff that reflects blood spurting at high velocity through the constriction

72
Q

compliance =

A

[^V] / [^P]

73
Q

capacitance vessels

A

thin walled vessels with minimal resistance to stretching by filling pressures

74
Q

Hydrostatic pressure

A

pushing fluid out

75
Q

Osmotic pressure

A

sucking fluid in

76
Q

Starling’s Law of the Capillary

A

Q = k[(Pc+[Pi]i)-(Pi+[Pi]c)] Q = k [force in - force out] k is dependent on type of capillary, increasing with leakiness

77
Q

Hydrostatic v Osmotic pressure for: renal system, pulmonary circulation, CHF, Nutritional Edema

A

Renal system - H > O, fluid moves out of cap, urine Pulmonary circulation - H < O, fluid moves into cap, dry alveoli CHF - H > O, fluid moves out of cap, edema Nutritional Edema - H > O, fluid moves out of cap, because lower osmotic pressure because no albumin, ascites

78
Q

Local control

A

independent of CNS, metabolic waste build-up (adenosine, lactate, CO2, H+, K+) and myogenic (autoregulation) to keep blood flow consistent

79
Q

Central control

A

CNS makes final decision, humoral mechanisms (ANP, AngII, Epi, NO, ET-1) or neural mechanisms (targeted to certain organs)

80
Q

Phases Wiggers diagram

A
  1. Atrial systole 2. Isovolumetric contraction 3. Rapid Ejection 4. Reduced Ejection 5. Isovolumetric relaxation 6. Rapid Filling 7. Reduced Filling
81
Q

When and what time is S1 heard?

A

Isovolumetric contraction at 0.1sec

82
Q

When and what time is S2 heard?

A

Isovolumetric relaxation at 0.4sec

83
Q

Changes in inotropy are dependent on sarcomere length

A

FALSE - INDEPENDENT

84
Q

Ventricular hypertrophy increases or decreases compliance?

A

Decreases

85
Q

typical EF?

A

60%

86
Q

HR equation

A

=60/R-R interval (#blocks x 0.04sec)

87
Q

Cardiac impulse through AV node plus bundle

A

0.13sec (0.09 AV, 0.03 His)

88
Q

SA node to epicardium

A

0.22sec

89
Q

Normal Q-T interval

A

0.35-0.40sec

90
Q

Normal QRS

A

0.12sec

91
Q

Right bundle branch block cause

A

Pulmonary hypertension

92
Q

Left bundle branch block cause

A

Systemic hypertension, aortic valve stenosis and regurgitation

93
Q

Normal PR interval

A

0.12-0.20sec

94
Q
A

Physio (3 decks)

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