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Chest Pain Flashcards

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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
Dromotropic effects
Positive dromotropic effect - increases AP conduction, SNS Negative dromotropic effect - decreases AP conduction, PNS
26
P-wave
atrial depolarization, speed of propagation throughout the atria
27
PR-segment
movement of the AP through the AV node
28
QRS-complex
ventricular depolarization
29
Q-wave
left side of the septum depolarizes before the right, resulting in small downward deflection
30
R-wave
depolarization spread from endo to epicardium, large muscle mass involved, large amplitude
31
S-wave
last part of ventricle depolarization is near the atrium, gives brief negative deflection
32
Bundle-branch block
widening of QRS
33
ST-segment
interval between ventricular depolarization and repolarization
34
T-wave
ventricular repolarization
35
Interval between P-waves
'sinus rhythm', HR, tachycardia, bradycardia
36
Lead I, II, aVf, III, aVr, aVL
0, +60, +90, +120, -150, -30
37
Right and left axis deviations
Right - MEA moves right, clockwise, pulmonary HTN Left - MEA moves left, counterclockwise, systemic HTN
38
Normal MEA
between +100 and -30
39
First degree heart block
P-waves are all followed by QRS, but PR-interval is increased
40
Second degree heart block
PR interval lengthened so much that not every P-wave is followed by QRS
41
Third degree heart block
P-wave and QRS depolarize independently with ventricle depol driven by latent pacemaker
42
Atrial flutter
P waves are too fast, driven by atrial pacemaker, but QRS is normal
43
Atrial fibrillation
atria are not driven by SA node, but instead by local currents, result in uncoordinated atrial firing and no P waves are detected
44
Ventricular tachycardia/flutter
ventricular rate is greater than atrial rate, due to ectopic pacemaker
45
Ventricular fibrillation
electrical activity is completely uncoordinated, lethal condition that must be corrected within minutes
46
Spontaneous AP in ventricular cells
abnormal QRS complex
47
ST segment depression/elevation
MI occurred recently
48
S4
Atrial gallop usually due to ventricular hypertrophy, occurs in late diastole, never normal to hear
49
S3
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
Compliance
volume changes with pressure
51
SV
CO = SV x HR
52
Normal EF
\>55%
53
Increasing Preload of the heart?
increases EDV, SV, CO no affect on aortic pressure
54
Heart Failure
decreased CO triggers increased BV, PL, EDV, SV and CO, but this is only a short term compensatory mechanism, decreases starling curve/inotropy
55
Law of LaPlace
wall stress (sigma) = [P x r]/2h Pressure, chamber radius, wall thickness
56
Increasing Afterload of the heart?
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
Aortic stenosis
left ventricular emptying is impaired because of narrowing of the aortic valve, flow through aortic valve generates additional sounds between S1 and S2
58
Increasing Inotropy of the heart?
Shifts ESPVR curve to the left and increases line slope, increases velocity of shortening, decreases ESV, increasing SV and CO
59
Blood flow (Q) =
Q = V x a = P/R
60
Poiseulle's equation
Q = [P(Pi)r^4]/8Ln(viscosity)
61
Changes to viscosity
1. life at high altitudes, increased viscosity 2. polycythemia vera, increased viscosity 3. severe dehydration, increased viscosity 4. sickle-cell anemia, increased viscosity
62
Parallel arrangement has the highest resistance
FALSE - LOWEST
63
Normal MAP
95mmHg
64
TPR =
[MAP-CVP]/CO
65
Normal TPR
15-18mmHg/l/min or 15-18 HRUs or Wood units
66
PP
Pulse pressure = SBP - DBP
67
MAP =
DBP + [PP/3]
68
Septic shock is associated with?
Large drop in TPR, only form of shock that is associated with decrease, rather than increased TPR
69
Factors that affect Poiseuille's law
1. turbulent flow 2. viscosity of blood changes with velocity 3. compliance of blood vessels
70
Reynold's Number
Nr = vdp/n velocity, diameter, density, viscosity Nr\>2000 = turbulent flow
71
Korotkoff sounds
partial occlusion of brachial artery with pressure cuff that reflects blood spurting at high velocity through the constriction
72
compliance =
[^V] / [^P]
73
capacitance vessels
thin walled vessels with minimal resistance to stretching by filling pressures
74
Hydrostatic pressure
pushing fluid out
75
Osmotic pressure
sucking fluid in
76
Starling's Law of the Capillary
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
Hydrostatic v Osmotic pressure for: renal system, pulmonary circulation, CHF, Nutritional Edema
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
Local control
independent of CNS, metabolic waste build-up (adenosine, lactate, CO2, H+, K+) and myogenic (autoregulation) to keep blood flow consistent
79
Central control
CNS makes final decision, humoral mechanisms (ANP, AngII, Epi, NO, ET-1) or neural mechanisms (targeted to certain organs)
80
Phases Wiggers diagram
1. Atrial systole 2. Isovolumetric contraction 3. Rapid Ejection 4. Reduced Ejection 5. Isovolumetric relaxation 6. Rapid Filling 7. Reduced Filling
81
When and what time is S1 heard?
Isovolumetric contraction at 0.1sec
82
When and what time is S2 heard?
Isovolumetric relaxation at 0.4sec
83
Changes in inotropy are dependent on sarcomere length
FALSE - INDEPENDENT
84
Ventricular hypertrophy increases or decreases compliance?
Decreases
85
typical EF?
60%
86
HR equation
=60/R-R interval (#blocks x 0.04sec)
87
Cardiac impulse through AV node plus bundle
0.13sec (0.09 AV, 0.03 His)
88
SA node to epicardium
0.22sec
89
Normal Q-T interval
0.35-0.40sec
90
Normal QRS
0.12sec
91
Right bundle branch block cause
Pulmonary hypertension
92
Left bundle branch block cause
Systemic hypertension, aortic valve stenosis and regurgitation
93
Normal PR interval
0.12-0.20sec
94

Physio (3 decks)

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