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Step 1 > Cardiac Physiology > Flashcards

Cardiac Physiology Flashcards

1
Q

What does it mean to have Right-dominant circulation

A

PDA comes from the RCA

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2
Q

What percent is R-dom., L-dom., and Co-dom. circulation

A

RCA: 85%
LCX: 8%
Both: 7%

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3
Q

Most commonly occluded artery

A

LAD

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4
Q

When does coronary blood flow peak?

A

Early diastole

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5
Q

What is most post. part of heart

A

L atrium

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6
Q

L atrium can effect GI tract how

A

Enlargement can produce dysphagia, or hoarseness compressing on recurrent laryngeal nerve (branch of the vagus)

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7
Q

What supplies SA and AV nodes

A

RCA

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8
Q

LCX supplies

A

Lateral and post. walls of LV

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9
Q

LAD supplies

A

Anterior 2/3 of interventricular septum, anterior papillary muscle, and anterior surface of left ventricle.

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10
Q

What supplies R ventricle

A

Acute marginal artery

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11
Q

What does the PDA/interventricular artery do

A

Supplies posterior 1/3 of interventricular septum and posterior walls of ventricles.

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12
Q

What happens to CO with increasing HR

A

Less diastolic filling time leads to decreased CO

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13
Q

Increased pulse pressure in what diseases

A

Hyperthyroid, aortic regurgitation, ateriosclerosis, obstructive sleep apnea (inc. sympathetic tone), exercise (transiently)

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14
Q

Decreased pulse pressure in what diseases

A

Aortic stenosis, cardiogenic shock, cardiac tamponade, advanced HF

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15
Q

How to calculate MAP

A

MAP=COxTPR

2/3 diastolic pressure + 1/3 systolic pressure.

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16
Q

What is the point of MAP

A

The heart is in diastole longer than systole so it is counted more.

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17
Q

MAP stands for

A

mean arterial pressure

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18
Q

CO formula

A

=Stroke Volume (SV) x HR (HR)

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19
Q

What is the Fick principle

A

Calculating CO = Rate of O2 consumption/(arterial O2 content-venous O2 content)

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20
Q

How do catecholamines increase contracility

A

Increase activity of Ca2+ pump in SR

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21
Q

Are skeletal muscles the one that can contract several times in calcium free solution?

A

Yes. Cardiac cells get most calcium from ECF, not SR. Without

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22
Q

How to increase contracility

A

Catecholamines, inc. ICF Ca2+, dec. ECF Na+, digitalis (blocks Na/K ATPase)

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23
Q

how does digitalis increase contracility

A

Inhibits Na/K ATPase, increasing ICF Na+, which prevents Ca+ from leaving

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24
Q

How does Na-Ca2+ exchanger work

A

ICF Ca+ is exchanged for ECF Na+. Uses sodium gradient. 3 sodiums in for one calcium out.

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25
Q

how to decrease contracility

A

Beta1-blockade, HF with systolic dysfunction, acidosis, hypoxia/hypercapnea (dec. PO2/Inc. PCO2), non-dihydropyridine Ca2+ blocks

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26
Q

How does beta-1 blockade decrease contracility

A

Decreases cAMP

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27
Q

What are the non-dihydropyridine CCBs

A

Verapamil, diltiazem

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28
Q

What are the dihydropyridine CCBs

A

Nifepidime, amlodipine

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29
Q

How is preload approximated

A

LVEDV

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30
Q

What is afterload approximated by

A

MAP

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31
Q

What do vasodilators do and example

A

Dec. afterload (hydralazine)

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32
Q

What to ACEIs and ARBs do

A

Decrease preload and afterload

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33
Q

What is Laplace’s law

A

Wall tension=(pressure x radius)/(2*wall thickness)

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34
Q

Why does LV hypertrophy to increasing afterload

A

To decrase wall tension (thickening directly decreases wall tension (indirectly proportional))

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35
Q

How to calculate EF

A

SV/EDV

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36
Q

Normal EF?

A

> 55%

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37
Q

Viscosity depends mostly on what?

A

Hematocrit

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38
Q

What diseases increase viscosity

A

Polycythemia, Hyperproteinemic states (e.g. multiple myeloma), Hereditary spherocytosis??

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39
Q

What decreases viscosity?

A

Anemia

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40
Q

Resistance is related to….

A

Directly proprotional to viscosity and vessel length and inversely proportional to the radius to the 4th power.

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41
Q

resistance of vessels in series

A

R1+R2+R3

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42
Q

resistance of vessels in parallel

A

1/R1 + 1/R2 + 1/R3

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43
Q

Resistance formulas

A

=Driving Pressure (deltaP)/ Flow (Q) = 8n(viscosity)xLength / (piR^4)

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44
Q

pg. 269 gist?

A

Effects on contractility, preload, and afterload effect the CO vs. venous return.

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45
Q

Do CO and venous return have to be equal?

A

No.

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46
Q

What are the steps of heart contraction

A
  1. Isovolumetric contraction: ventricles contract, MV and AV closed. Most O2 consumption.
  2. Systolic ejection: AV opens
  3. Isovolumetric relaxation: Between AV closing and MV opening.
  4. Diastolic filling: Rapid
  5. Diastolic filling: Slow
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47
Q

How does inc. afterload and inc. preload and inc. contracility affect pressure-volume loop

A

Inc. afterload increases the End-systolic volume so you have decreased ejection.
Inc. afterload increases EDV so you have increased ejection. Inc. contracticility dec. ESV so more ejection.

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48
Q

Does pressure increase after Aortic valve opens?

A

yes it keeps increasing then decreases. The T wave occurs when it peaks.

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49
Q

What causes the dicrotic notch

A

Occurs when the aortic valve closes, the brief reversal of flow when the LV relaxes closes the aortic valve and this is what increases the pressure

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50
Q

Where is S2 loudest

A

L sternal border

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51
Q

Where is S1 loudest

A

Mitral area

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52
Q

When do you get S3

A

MR, CHF, dilated ventricles, NORMAL in children and pregnant women. Associated with elevated filling pressures.

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53
Q

When do you get S4

A

Late diastole, high atrial pressure, ventricular hypertrophy

54
Q

Name the steps of the JVP

A

a wave: atrial contraction
c wave: RV contraction pushing against closed TV
x descent: Closed TV moves downwards during contraction
v wave: right atrial filling during systole
y decent: blood flow from RA to RV

55
Q

What causes wide splitting

A

Anything that increases the length of RV contraction time. Pulmonic stenosis, RBBB.

56
Q

What causes fixed splitting.

A

ASD makes pulmonic closure delayed in expiration or inspiration.

57
Q

What causes paradoxical splitting

A

Anything that increases the length of LV contraction time. Aortic stenosis, LBBB

58
Q

What can you hear in aortic area

A

Aortic stenosis/sclerosis, flow murmur

59
Q

What can you hear in pulmonic area

A

Pulmonic stenosis, flow murmur

60
Q

What can you hear in tricuspid area

A

Pansystolic: Tricuspid regurg., VSD
Diastolic: Tricuspid stenosis, ASD

61
Q

What can you hear in Mitral area

A

MR, mtiral stenosis

62
Q

What can you hear at L sternal border

A

AR, PR, HOCM

63
Q

What does late ASD sound like

A

Pulmonic diastolic murmur from dilation of pulm. artery

64
Q

What does inspiration increase the sound of

A

Increased intensity of R heart sounds.

65
Q

What does hand grip affect

A

Increased SVR:
MR, AR, and VSD louder
AS, HOCM softer: stents them open
MVP: Incr. murmur intensity, later onset of click/murmur???????????

66
Q

What does Valsalva (Phase II) and Standing

A

Dec. venous return. Most murmur decrease in intensity including AS ?????????????????
Inc. HOCM intesntiy
MVP: dec. murmur intensity, earlier click/murmur????????

67
Q

Rapid squatting (inc. venous return, inc. preload, inc. afterload with prolonged squatting) does what

A

Dec. HOCM, inc. AS, MVP: inc. murmur, later onset of click/murmur

68
Q

Pulsus parvus et tardus

A

Aortic Stenosis

69
Q

Aortic stenosis mnemonic

A

SAD: syncope, angina, dyspnea

70
Q

Why does MR/TR and VSD get louder with handgrip

A

Increased SVR makes the blood flow preferentially through the lower pressure exits

71
Q

Most frequent valvular lesion

A

Mitral valve prolapse

72
Q

Why does MVP happen earlier with standing/Valsalva?

A

Because the decreased preload makes the chordae more lax so they prolapse earlier.

73
Q

Why is MVP louder with hand-grip, squatting

A

The inc. afterload and preload mean more flow past murmur so it is more intense, but it doesn’t happen earlier.

74
Q

MR/TR murmur sound

A

high pitched blowing murmur

75
Q

TR radiates to

A

Loudest at tricuspid area and radiates to R sternal border

76
Q

VSD murmur sound

A

Harsh-sounding

77
Q

Causes of MVP (mitral valve prolapse)

A

Myxomatous degeneration, rheumatic fever, or chordae rupture

78
Q

What is the midsystolic click

A

It’s when the chordae tendinae suddenly tense

79
Q

What is a sign of Mitral stenosis worsening

A

Dec. interval between S2 and OS.

80
Q

Common causes of PDA

A

Congenital rubella or prematurity

81
Q

Where to hear PDA best?

A

L infraclavicular area

82
Q

Know ventricular cell Action Potential graph..

A

….

83
Q

Ventricular AP similar to what cells

A

His Purkinje fibers

84
Q

What is the order of calcium channels opening

A

First voltage gated, then the increased ICF Ca2+ leads to the SR release of Ca2+

85
Q

What is the funny current

A

If channels: slow, mixed Na/K inward current

86
Q

membrane potential for ventricles

A

-85 mV

87
Q

membrane potential for SA node

A

around -65 mV

88
Q

Na+ channels in SA node

A

permanently shut off due to high resting membrane potential

89
Q

Know the curve of SA node action potential

A

…..

90
Q

What chemicals decrease and increase HR

A

ACh/adenosine decrease by slowing Phase 4 of SA node. Catecholamines inc. depolarization and HR. Sympathetic stimulation increases the chance that If channels are open.

91
Q

Organize the following in terms of speed of conduction: atria, AV node, Purkinje, ventricles

A

Purkinje>atria>ventricles>AV node

92
Q

How long is AV node delay?

A

100 msec

93
Q

What predisposes to Torsades de pointes

A

Long QT, drugs, dec. K+, dec. Mg, other abnormalities.

94
Q

Torsades causes mnemonic

A 
Some Risky Meds Can Prolong QT
Sotalol
Risperidone (antipsychotic)
Macrolides
Chloroquine
Protease inhibitors (-navir)
Quinidine (class Ia; also class III)
Thiazides
95
Q

What are the important congenital long QT syndromes

A

Romano-Ward syndrome; jervell and Lange-Nielsen syndrome

96
Q

Romano-Ward syndrome

A

cong. long QT; aut. dom.; pure cardiac phenotype (no deafness)

97
Q

Jervell and Lange-Nielsen syndrome

A

Cong. long QT; aut. rec.; sensorineural deafness

98
Q

Wolff-Parkinson-White anatomy

A

Bundle of Kent. Drugs that slow down the AV node increase risk of tachyarrhythmias.

99
Q

How to cardiovert chemically a.flutter

A

Class IA, IC, or III antiarrhythmics.

100
Q

A. flutter rate control

A

Beta-blocker, CCBs

101
Q

A. flutter definitive tx

A

Catheter ablation

102
Q

Normal PR interval

A

<200 ms

103
Q

What is Mobitz type I

A

Wenckebach, progressive PR prolongation

104
Q

Which second degree AV block is worse

A

Mobitz type II, randomly drops, can progress to third degree, tx with pacemaker

105
Q

Lyme disease and SA node

A

Third degree heart block

106
Q

atrial natriuretic peptide

A

Atrial myocytes in response to increased blood volume and atrial pressure.

107
Q

Atrial natriuretic peptide actions

A

Vasodilation and dec. Na+ reabsorption in renal collectin tubule. Constricts efferents, dilates afferents via cGMP promoting diuresis and contributing to aldosterone mechanism.

108
Q

Aldosterone escape?

A

Escape from the sodium-retaining effects of excess aldosterone

109
Q

B-type (brain) natriuretic peptide

A

Ventricular myocytes in response to increased tension. Similar to ANP with longer-half life. Diagnosing HF (very good negative predictive value)

110
Q

Recombinant BNP

A

Nesiritide

111
Q

What has greater pressure pulmonary Artery or LA

A

pulm. artery (25/10) compared to LA (<12)

112
Q

Heart autoregulation

A

CO2, adenosine, NO (local metabolites)

113
Q

Brain autoregulation

A

CO2 (pH) (local metabolites)

114
Q

Kidney autoregulation

A

Myogenic and tubuloglomerular feedback

115
Q

Lungs autoregulation

A

Hypoxia causes vasoconstriction

116
Q

Skeletal muscle autoregulation

A

Lactate, adenosine, K+, H+, CO2

117
Q

Skin autoregulation

A

Sympathetic stimulation most important mechanism-temperature control

118
Q

What sites have baroreceptors?

A

Aortic arch and carotid sinus

119
Q

Aortic arch pathway

A

Vagus nerve to solitary nucleus of medulla (only responds to increases in BP)

120
Q

Carotid sinus pathway

A

Glossopharyngeal nerve to solitary nucleus of medulla (responds to both decreases and increases in BP)

121
Q

What is the specific pathway for baroreceptor function

A

Hypotension leads to dec. arterial BP which leads to decreased stretch; decreased afferent baroreceptor firing; increased efferent sympathetic and decreased parasympathetic firing; vasoconstriction; increases HR, contractility, BP

122
Q

How does carotid massage work

A

Pressing increases stretch, so you decrease sympathetics and increase parasympathetics to slow down the heart

123
Q

How does Cushing reaction work?

A

HTN, bradycardia, and hypopnea: elevated ICP constricts arterioles in brain leading to ischemia and reflex sympathetic increase in perfusion pressure leading to inc. stretch and reflex baroreceptor induced-bradycardia

124
Q

Chemoreceptors are found where

A

peripheral and central

125
Q

Peripheral chemoreceptors pathway

A

Carotid and aortic bodies stimulated by low PO2 (<60 mmHg), inc. PCO2, and dec. pH in blood.

126
Q

Central chemoreceptors pathway

A

Stimulated by changes in pH and PCO2 of brain interstitial fluid, which influences arterial CO2. Does not respond directly to PO2.

127
Q

Liver gets how much blood

A

largest share of systemic CO

128
Q

Kidney gets how much blood

A

Highest blood flow per gram of tissue

129
Q

Heart and oxygen consumption

A

O2 extraction is always around 80%, so increased oxygen demand met by increased coronary blood flow, not by extraction of O2.

130
Q

What else besides hydrostatic and oncotic pressure determine capillary fluid exchange

A

Increased capillary permeability (increased filtration constant Kf (capillary permeability)) caused by toxins, infections, burns

131
Q

What increases interstitial fluid colloid osmotic pressure

A

lymphatic blockage

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