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Cardiovascular-First Aid 2017 > Physiology > Flashcards

Physiology Flashcards

1
Q

Heart vessel that supplies anterior 2/3 of interventricular septum, anterolateral papillary muscle and anterior surface of left ventricle

A

Left anterior descending artery (LAD)

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2
Q

What variables maintain cardiac output during the early stages of exercise

A

Increased HR and SV

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3
Q

What variables maintain cardiac output during the late stages of exercise

A

HR only (SV plateaus)

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4
Q

What heart function is shortened by increased HR

A

Diastole

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5
Q

Effect of decreased diastole

A

Less filling time causing decreased cardiac output

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6
Q

Calculating CO

A

CO = HR x SV

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7
Q

Fick principle for calculating CO

A

CO = rate of O2 consumption/(arteriole O2 content - venous O2 content)

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8
Q

Method for calculating mean arterial pressure (MAP)

A 
MAP =  CO x TPR or
MAP = 2/3 diastole + 1/3 systole
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9
Q

What is pulse pressure (PP)

A

PP = systolic pressure - diastolic pressure

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10
Q

Method for calculating stroke volume (SV)

A

SV = EDV - ESV

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11
Q

Variables that affect SV

A

Contractility, Afterload, Preload

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12
Q

Effect of increased contractility on SV

A

Increased SV

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13
Q

Effect of increased afterload on SV

A

Decreased SV

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14
Q

Effect of increased preload on SV

A

Increased SV

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15
Q

Effect of decreased contractility on SV

A

Decreased SV

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16
Q

Effect of decreased afterload on SV

A

Increased SV

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17
Q

Effect of decreased preload on SV

A

Decreased SV

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18
Q

Effect of catecholamine binding on contractility and SV

A

Both increased

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19
Q

Catecholamine MOA on increasing contractility and SV

A

Bind B-1 receptors leading to two outcomes:
1. Phosphorylate Ca channels
2. Phosphorylate phospholamban
Both increase Ca in SR through different mechanisms

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20
Q

Mechanisms that increase contractility and SV

A
  1. Catecholamine binding to B-1 receptors
  2. Increasing intracellular calcium
  3. Decreasing extracellular Na
  4. Digitalis or Digoxin
    All methods increase intracellular calcium
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21
Q

Mechanisms that decrease contractility and SV

A
  1. B-1 blockade decreases cAMP
  2. HF with systolic dysfunction
  3. Acidosis
  4. Hypoxia/hypercapnia
  5. Non-dihydropyridine Ca channel blockers
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22
Q

Variables that increase myocardial O2 demand

A

Increased:

  1. Contractility
  2. Afterload
  3. HR
  4. Diameter of ventricle (increased wall tension)
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23
Q

Variable that approximates preload

A

EDV

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24
Q

Variables that affect EDV

A

Venous tone and circulating blood volume

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25
Q

Effect vasodilation has on EDV

A

Decreases EDV due to decreased venous return

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26
Q

Variable that approximates MAP

A

Afterload

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27
Q

Formula for calculating Ejection Fraction (EF)

A

EF = SV/EDV = (EDV - ESV)/EDV

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28
Q

Heart failure decreases what variable

A

Ejection fraction

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29
Q

Blood vessels with flow velocity

A

Capillaries (highest cross-sectional area)

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30
Q

Blood vessels that account for most TPR

A

Arterioles

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31
Q

Blood vessels that provide the most storage capacity

A

Veins

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32
Q

What does viscosity depend on most

A

Hematocrit

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33
Q

Condition that decreases blood viscosity

A

Anemia

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34
Q

Condition that increases blood viscosity

A

Polycythemia and hyperproteinemic (multiple myeloma)

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35
Q

In Starling forces, force of contraction is proportional to what?

A

End-diastolic length of cardiac muscle fiber

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36
Q

End-diastolic length of cardiac muscle fiber determines what?

A

Force of contraction

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37
Q

Formula for calculating change in pressure

A

P = Q x R

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38
Q

Formula for calculating Resistance

A

R= P/Q

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39
Q

Formula for calculating total parallel resistance

A

R = 1/(1/R1 + 1/R2 + 1/R3)

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40
Q

Formula for calculating total series resistance

A

R = R1 + R2 + R3

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41
Q

Effect of Vasopressors on TPR and CO for a given RA pressure or EDV

A

Increase TPR and decrease CO

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42
Q

Effect of exercise or AV shunt on TPR and CO for a given RA pressure or EDV

A

Decrease TPR and increase CO

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43
Q

Effects of increased afterload on pressure volume loop

A

Increased aortic pressure and ESV

Decreased SV

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44
Q

Effect of increased preload on pressure volume loop

A

Increased SV

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45
Q

Effect of increased contractility on pressure volume loop

A

Increased SV and Ejection fraction

Decreased ESV

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46
Q

Period between mitral valve closing and aortic valve opening

A

Isovolumetric contraction

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47
Q

Period of highest O2 contraction

A

Isovolumetric contraction

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48
Q

Period between aortic valve opening and closing

A

Systolic ejection

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49
Q

Period between aortic valve closing and mitral valve opening

A

Isovolumetric relaxation

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50
Q

Period just after mitral valve opening

A

Rapid filling

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51
Q

Period just before mitral valve closing

A

Reduced filling

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52
Q

Sound made by mitral and tricuspid valve closure

A

S1

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53
Q

Sound made by aortic and pulmonary valve closure

A

S2

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54
Q

Area S1 loudest

A

Mitral area

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55
Q

Area S2 loudest

A

Left upper sternal border

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56
Q

Heart sound associated with increased filling pressures

A

S3

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57
Q

Heart sound made by left atrium pushing against stiff LV wall

A

S4

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58
Q

Heart sound that can be normal in children and young adults

A

S3

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59
Q

Heart sound considered abnormal at any age

A

S4

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60
Q

S4 heart sound is best heard at apex in what position

A

Left lateral decubitus position

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61
Q

JVP associated with atrial contraction

A

a wave

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62
Q

JVP associated with RV contraction

A

c wave

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63
Q

JVP associated with downward displacement of closed tricuspid valve during rapid ventricular ejection phase

A

x descent

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64
Q

JVP associated with increased right atrial pressure due to filling against closed tricuspid valve

A

v wave

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65
Q

JVP associated with RA emptying into RV

A

y descent

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66
Q

Cause of normal splitting between A2 and P2

A

Inspiration

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67
Q

Cause of wide splitting between A2 and P2

A

Conditions that delay RV emptying (pulmonic stenosis and RBBB) - splitting exaggerated during inspiration

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68
Q

Cause of fixed splitting

A

ASD - increased RA and RV volumes causes increased flow through pulmonic valve delaying closure regardless of breath

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69
Q

Cause of paradoxical splitting

A

Conditions that delay aortic valve closure (aortic stenosis and LBBB) - P2 closes before A2 - on inspiration P2 closer to A2 paradoxically eliminating split

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70
Q

Murmurs heard best in Mitral area

A

Mitral regurgitation
Mitral valve prolapse
Mitral stenosis

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71
Q

Murmurs heard best in Tricuspid area

A

Tricuspid regurgitation
Tricuspid stenosis
VSD
ASD

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72
Q

Murmurs heard best in Pulmonic area

A

Pulmonic stenosis

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73
Q

Murmurs heart best in LUSB

A

Pulmonic regurgitation
HCM
Aortic regurgitation

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74
Q

Murmurs heard best in Aortic area

A

Aortic stenosis

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75
Q

Maneuver that increases intensity of right heart sounds

A

Inspiration (increases venous return to RA)

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76
Q

Increases intensity of AR and VSD murmurs

A

Hand grip and rapid squatting

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77
Q

Maneuver that decreases intensity of most murmurs including AS

A

Valsalva and standing up

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78
Q

Maneuver that decreases intensity of hypertrophic cardiomyopathy murmurs

A

Hand grip and rapid squatting

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79
Q

Increases intensity of AS

A

Rapid squatting

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80
Q

Maneuver that increases intensity of hypertrophic cardiomyopathy murmurs

A

Valsalva and standing up

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81
Q

Maneuver that causes later onset of click/murmur in MVP

A

Hand grip and rapid squatting

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82
Q

Mnemonic for Systolic murmurs

A 
MR VP TRAPS:
Mitral Regurgitation
VSD
Pulmonic stenosis
Tricuspid Regurgitation
Aortic and Pulmonic Stenosis
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83
Q

Mnemonic for Diastolic murmurs

A

MS PAID:
Mitral Stenosis
Pulmonic and Aortic Insufficiency
D - just for diastolic

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84
Q

Continuous murmurs

A

Patent ductus arteriosus

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85
Q

Crescendo-decrescendo systolic ejection murmur, radiates to carotids with “pulsus parvus et tardus”, heard loudest at heart base

A

Aortic stenosis

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86
Q

Cause of AS in older patients > 60 years

A

Age-related calcification

87
Q

Cause of AS in younger patients

A

Early-onset calcification of bicuspid aorta

88
Q

Symptoms of AS

A

Syncope, Angina, Dyspnea on exertion (SAD)

89
Q

Holosystolic, high-pitched “blowing murmur”, loudest at apex and radiates toward axilla

A

Mitral regurgitation

90
Q

Common cause of MR

A

Ischemic heart disease, MVP, LV dilatation

91
Q

Holosystolic, high-pitched “blowing murmur”, loudest at tricuspid area and increased with inspiration

A

Tricuspid regurgitation

92
Q

Valvular pathology caused by rheumatic fever and infective endocarditis

A

Mitral or Tricuspid regurgitation

93
Q

Late systolic crescendo murmur with midsystolic click best heard over apex and loudest just before S2

A

Mitral Valve Prolapse (MVP)

94
Q

Valvular pathology seen in Marfan and Ehlers-Danlos syndrome, can be caused by rheumatic fever or chordae rupture and predisposes to infective endocarditis

A

Mitral Valve Prolapse

95
Q

Holosystolic, harsh-sounding murmur, loudest at tricuspid area with hyperdynamic RV impulse and no change in arterial pulse pressure

A

Ventral Septal Defect (VSD)

96
Q

High-pitched “blowing” early diastolic decrescendo murmur with head bobbing, wide pulse pressure, bounding femoral and carotid pulses

A

Aortic regurgitation

97
Q

Cause of midsystolic click in MVP

A

Sudden tensing of chordae tendineae

98
Q

Follows opening snap with delayed rumbling mid-to-late diastolic murmur

A

Mitral stenosis (low-pitched murmur throughout diastole)

99
Q

Cause of opening snap in MS

A

Due to abrupt halt in leaflet motion in diastole after rapid opening due to fusion of leaflets

100
Q

Causes of aortic regurgitation

A

Aortic root dilatation, bicuspid aortic valve, endocarditis, rheumatic fever

101
Q

Consequence of aortic regurgitation

A

Can progress to left heart failure

102
Q

What correlates with increased severity of mitral stenosis

A

Decreased interval between S2 and opening snap

103
Q

In mitral stenosis, when is LA pressure&raquo_space; than LV pressure

A

During diastole

104
Q

Valvular pathology considered a late sequela of rheumatic fever

A

Mitral stenosis

105
Q

Consequence of mitral stenosis

A

Left atrial dilatation

106
Q

Continuous machine-like murmur best heard at left infraclavicular area

A

Patent ductus arteriosus (PDA)

107
Q

During what phase of cardiac cycle is PDA loudest

A

S2

108
Q

Common cause of PDA

A

Congenital rubella or prematurity

109
Q

Ion responsible for rapid upstroke and depolarization in myocardial action potential

A

Influx of Na ions

110
Q

Ion responsible for plateau phase in myocardial action potential

A

Influx of Ca ions and efflux of K ions

111
Q

Ion responsible for rapid repolarization in myocardial action potential

A

Efflux of K ions

112
Q

Responsible for resting membrane potential in myocardial action potential

A

High K ion permeability through K channels

113
Q

Phase of myocardial action potential characterized by opening of voltage-gated Na channels

A

Phase 0

114
Q

Responsible for activating fast voltage-gated Na channels in myocardial action potential

A

Low negative resting membrane potential

115
Q

Phase of myocardial action potential characterized by inactivation of voltage-gated Na channels and opening of voltage-gated K channels

A

Phase 1

116
Q

Ion responsible for initial repolarization in myocardial action potential

A

Decreased Na influx

117
Q

Phase of myocardial action potential characterized influx of Ca through voltage-gated Ca channels balancing K efflux

A

Phase 2

118
Q

Phase of myocardial action potential characterized by massive K efflux due to opening of voltage-gated slow K channels

A

Phase 3

119
Q

Phase of myocardial action potential characterized by high K permeability via K channels

A

Phase 4

120
Q

Upstroke of pacemaker action potential is caused by what

A

Influx of Ca via opening of voltage gated Ca channels

121
Q

Upstroke is what phase of pacemaker action potential

A

Phase 0

122
Q

Phase of pacemaker action potential characterized by inactivation of Ca channels and activation of K channels

A

Phase 3

123
Q

Ion responsible for depolarization in phase 3 of pacemaker action potential

A

K efflux

124
Q

Ion responsible for slow spontaneous diastolic repolarization in phase 4 of pacemaker action potential

A

Na/K influx via I-funny channels

125
Q

What determines HR

A

Slope of phase 4 in SA node

126
Q

What accounts for automaticity of SA and AV node

A

I-funny current

127
Q

Effect of ACh and adenosine on heart function

A

Decrease rate of diastolic depolarization and HR

128
Q

Effect of catecholamines on heart function

A

Increase depolarization and HR

129
Q

Effect of sympathetic stimulation on heart function

A

Increase chance I-funny channels open and HR

130
Q

Conduction pathway

A

SA node - AV node - R and L bundle branches - Purkinje fibers - ventricles (left anterior and posterior fascicles)

131
Q

Pacemaker of the heart

A

SA node

132
Q

Blood supply for AV node

A

Right coronary artery

133
Q

Structure in heart located in posteroinferior part of interatrial septum

A

AV node

134
Q

Allows time for ventricular filling

A

AV nodal delay

135
Q

Average time of AV nodal delay

A

100 msec

136
Q

Pacemaker rates

A

SA > AV > bundle of His/Purkinje/ventricles

137
Q

Speed of conduction

A

Purkinje > atria > ventricles > AV node

138
Q

Fibers in heart that can travel greater distances in less time

A

Purkinje fibers

139
Q

Indicates atrial depolarization on ECG

A

P-wave

140
Q

Indicates time from start of atrial depolarization to start of ventricular depolarization on ECG

A

PR interval

141
Q

Average length of time of PR interval

A

< 200 msec

142
Q

Indicates ventricular depolarization on ECG

A

QRS complex

143
Q

Average length of time of QRS complex

A

< 120 msec

144
Q

Indicates depolarization, mechanical contraction and repolarization of ventricles on ECG

A

QT interval

145
Q

Indicates ventricular repolarization on ECG

A

T-wave

146
Q

Indicates ischemia or recent MI on ECG

A

T-wave inversion

147
Q

Indicates junction between QRS complex and start of ST segment on ECG

A

J point

148
Q

Indicates isoelectric point, ventricles depolarized on ECG

A

ST segment

149
Q

Indicates hypokalemia or bradycardia on ECG

A

U-wave

150
Q

ECG tracing characterized by shifting sinusoidal waveforms or “twisting of the points”

A

Torsades de pointes

151
Q

Cardiac condition that predisposes to torsades de pointes

A

Long QT interval

152
Q

Drugs that cause torsades de pointes

A 
ABCDE:
anti-Arrhythmics (class IA, III)
anti-Biotics (macrolides)
anti-C(ychotics) - (haloperidol)
anti-Depressants (TCAs)
anti-Emetics (ondansetron)
153
Q

Decrease of what ions causes torsades de pointes

A

Hypokalemia and Hypomagnesemia

154
Q

Treatment for torsades de pointes

A

Magnesium sulfate

155
Q

Congenital long QT syndrome characterized by a pure cardiac phenotype and NO deafness

A

Romano-Ward syndrome

156
Q

Congenital long QT syndrome characterized by sensorineural deafness

A

Jervell and Lange-Nielsen syndrome

157
Q

Inheritance pattern in Romano-Ward syndrome

A

Autosomal dominant

158
Q

Inheritance pattern in Jervell and Lange-Nielsen syndrome

A

Autosomal recessive

159
Q

Autosomal dominant disorder characterized by pseudo-right BBB and ST elevations in V1-V3 leads seen in Asian males

A

Brugada syndrome

160
Q

Complications of Brugada syndrome

A

Ventricular tachyarrhythmias and sudden cardiac death

161
Q

Treatment for Brugada syndrome

A

ICD to prevent SCD

162
Q

Most common type of ventricular pre-excitation syndrome

A

Wolff-Parkinson-White syndrome

163
Q

ECG finding in Wolff-Parkinson-White syndrome

A

Delta wave with widened QRS complex and shortened PR interval

164
Q

Complication of Wolff-Parkinson-White syndrome

A

Re-entry circuit causing supraventricular tachycardia

165
Q

Bypasses AV node in Wolff-Parkinson-White syndrome

A

Bundle of Kent

166
Q

Abnormal fast accessory conduction pathway from atria to ventricle in Wolff-Parkinson-White syndrome

A

Bundle of Kent

167
Q

Type of rhythm with absent P-waves, irregularly irregular R-R waves and narrow QRS complex with HR 90-170 bpm

A

Atrial fibrillation

168
Q

Most common risk factors in atrial fibrillation

A

HTN and coronary artery disease

169
Q

Complications of atrial fibrillation

A

Thromboembolic events like stroke

170
Q

Treatment for atrial fibrillation

A

Anticoagulation, rate and rhythm control, cardioversion

171
Q

Condition with ECG findings of identical, back-to-back atrial depolarizations with “sawtooth” appearance

A

Atrial flutter

172
Q

Definitive treatment for atrial flutter

A

Catheter ablation

173
Q

Completely erratic rhythm with no identifiable waves

A

Ventricular fibrillation

174
Q

Consequence of ventricular fibrillation

A

Fatal arrhythmia

175
Q

Treatment for atrial fibrillation

A

Immediate CPR and defibrillation

176
Q

Type of AV block with prolonged PR interval > 200 msec that is usually benign

A

First degree AV block

177
Q

Treatment for first degree AV block

A

No treatment required since usually benign and asymptomatic

178
Q

AV block with progressive lengthening of PR interval with dropped beat afterward and regularly irregular RR interval, usually asymptomatic

A

Second degree Mobitz type I (Wenckebach)

179
Q

AV block with dropped beats not preceded by a change in length of PR interval

A

Second degree Mobitz type II

180
Q

Consequence of Second degree Mobitz type II

A

May progress to 3rd-degree block

181
Q

Treatment for Second degree Mobitz type II

A

Pacemaker

182
Q

AV block with atria and ventricles beating independently of each other, P waves and QRS complexes not rhythmically associated and can be caused by Lyme disease

A

3rd degree AV block (complete)

183
Q

Treatment for 3rd degree AV block

A

Pacemaker

184
Q

Action of ANP on renal arterioles

A

Dilates afferent arteriole, Constricts efferent arteriole

185
Q

Mechanism for release of ANP

A

Increased blood volume and atrial pressure

186
Q

Recombinant form of BNP used for treatment of HF

A

Nesiritide

187
Q

Carotid sinus location

A

Dilated region at carotid bifurcation

188
Q

Transmits via glossopharyngeal nerve to solitary nucleus of medulla

A

Carotid sinus

189
Q

Respond to changes in blood pressure

A

Carotid sinus and Aortic arch

190
Q

Transmits via vagus nerve to solitary nucleus of medulla

A

Aortic arch

191
Q

Effect of hypotension on ANS

A

Increased efferent sympathetic and decreased efferent parasympathetic causing increased vasoconstriction, HR, BP, and contractility

192
Q

Effect of carotid massage on HR

A

Decreased HR via increased afferent baroreceptor firing increasing AV node refractory period

193
Q

Chemoreceptors that do not respond to PO2

A

Central chemoreceptors

194
Q

PO2 pressure that stimulates peripheral chemoreceptors

A

< 60 mmHg

195
Q

Chemoreceptors that respond to decreased PO2, increased PCO2 and decreased pH

A

Peripheral chemoreceptors

196
Q

Chemoreceptors that respond to changes in pH and PCO2 of brain interstitial fluid

A

Central chemoreceptors

197
Q

Measure that approximates left atrial pressure

A

Pulmonary capillary wedge pressure (PCWP)

198
Q

Condition in which PCWP > LV end diastolic pressure

A

Mitral stenosis

199
Q

Device used to measure PCWP

A

Swan-Ganz catheter

200
Q

Normal RA pressure

A

< 5 mmHg

201
Q

Normal RV pressure

A

25/5 mmHg

202
Q

Normal pulmonary trunk pressure

A

25/10 mmHg

203
Q

Normal PCWP

A

4-12 mmHg

204
Q

Normal LA pressure

A

< 12 mmHg

205
Q

Normal LV pressure

A

130/10

206
Q

Normal aortic arch pressure

A

130/90

207
Q

Function that permits constant blood flow to an organ over wide range of perfusion pressures

A

Autoregulation

208
Q

Metabolites that cause vasodilation of heart

A

Adenosine, NO, CO2, decreased O2

209
Q

Metabolites that cause vasodilation of brain vasculature

A

CO2 (pH)

210
Q

Causes vasoconstriction of lung vasculature

A

Hypoxia

211
Q

Metabolites that cause vasodilation of skeletal muscle during exercise

A

Lactate, adenosine, K, H+, CO2

212
Q

Metabolites that cause vasodilation of skeletal muscle at rest

A

Sympathetic tone

213
Q

Mechanism that causes vasodilation of vessels in skin

A

Sympathetic tone for temperature control

214
Q

Mechanism that causes renal vasodilation

A

Myogenic and tubuloglomerular feedback

Cardiovascular-First Aid 2017 (5 decks)

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