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

Fick principle for calculating CO

A

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

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7
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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8
Q

What is pulse pressure (PP)

A

PP = systolic pressure - diastolic pressure

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9
Q

Method for calculating stroke volume (SV)

A

SV = EDV - ESV

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10
Q

Variables that affect SV

A

Contractility, Afterload, Preload

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11
Q

Effect of increased contractility on SV

A

Increased SV

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12
Q

Effect of increased afterload on SV

A

Decreased SV

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13
Q

Effect of increased preload on SV

A

Increased SV

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14
Q

Effect of decreased contractility on SV

A

Decreased SV

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15
Q

Effect of decreased afterload on SV

A

Increased SV

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16
Q

Effect of decreased preload on SV

A

Decreased SV

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17
Q

Effect of catecholamine binding on contractility and SV

A

Both increased

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18
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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19
Q

Variable that approximates preload

A

EDV

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20
Q

Effect vasodilation has on EDV

A

Decreases EDV due to decreased venous return

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21
Q

Variable that approximates MAP

A

Afterload

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22
Q

Formula for calculating Ejection Fraction (EF)

A

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

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23
Q

Blood vessels that account for most TPR

A

Arterioles

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24
Q

Blood vessels that provide the most storage capacity

A

Veins

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25
What does viscosity depend on most
Hematocrit
26
Condition that decreases blood viscosity
Anemia
27
Condition that increases blood viscosity
Polycythemia and hyperproteinemic (multiple myeloma)
28
Formula for calculating total parallel resistance
R = 1/(1/R1 + 1/R2 + 1/R3)
29
Effect of Vasopressors on TPR and CO for a given RA pressure or EDV
Increase TPR and decrease CO
30
Effect of increased contractility on pressure volume loop
Increased SV and Ejection fraction | Decreased ESV
31
Period between mitral valve closing and aortic valve opening
Isovolumetric contraction
32
Period between aortic valve opening and closing
Systolic ejection
33
Period between aortic valve closing and mitral valve opening
Isovolumetric relaxation
34
Period just after mitral valve opening
Rapid filling
35
Period just before mitral valve closing
Reduced filling
36
Sound made by mitral and tricuspid valve closure
S1
37
Sound made by aortic and pulmonary valve closure
S2
38
Area S1 loudest
Mitral area
39
Area S2 loudest
Left upper sternal border
40
Heart sound associated with increased filling pressures
S3
41
Heart sound made by left atrium pushing against stiff LV wall
S4
42
Heart sound that can be normal in children and young adults
S3
43
Heart sound considered abnormal at any age
S4
44
S4 heart sound is best heard at apex in what position
Left lateral decubitus position
45
JVP associated with atrial contraction
a wave
46
JVP associated with RV contraction
c wave
47
JVP associated with downward displacement of closed tricuspid valve during rapid ventricular ejection phase
x descent
48
JVP associated with increased right atrial pressure due to filling against closed tricuspid valve
v wave
49
JVP associated with RA emptying into RV
y descent
50
Cause of normal splitting between A2 and P2
Inspiration
51
Cause of wide splitting between A2 and P2
Conditions that delay RV emptying (pulmonic stenosis and RBBB) - splitting exaggerated during inspiration
52
Cause of fixed splitting
ASD - increased RA and RV volumes causes increased flow through pulmonic valve delaying closure regardless of breath
53
Cause of paradoxical splitting
Conditions that delay aortic valve closure (aortic stenosis and LBBB) - P2 closes before A2 - on inspiration P2 closer to A2 paradoxically eliminating split
54
Murmurs heard best in Mitral area
Mitral regurgitation Mitral valve prolapse Mitral stenosis
55
Murmurs heard best in Tricuspid area
Tricuspid regurgitation Tricuspid stenosis VSD ASD
56
Murmurs heard best in Pulmonic area
Pulmonic stenosis
57
Murmurs heart best in LUSB
Pulmonic regurgitation HCM Aortic regurgitation
58
Murmurs heard best in Aortic area
Aortic stenosis
59
Maneuver that increases intensity of right heart sounds
Inspiration (increases venous return to RA)
60
Increases intensity of AR and VSD murmurs
Hand grip and rapid squatting
61
Maneuver that decreases intensity of most murmurs including AS
Valsalva and standing up
62
Maneuver that decreases intensity of hypertrophic cardiomyopathy murmurs
Hand grip and rapid squatting
63
Increases intensity of AS
Rapid squatting
64
Maneuver that increases intensity of hypertrophic cardiomyopathy murmurs
Valsalva and standing up
65
Maneuver that causes later onset of click/murmur in MVP
Hand grip and rapid squatting
66
Mnemonic for Systolic murmurs
``` MR VP TRAPS: Mitral Regurgitation VSD Pulmonic stenosis Tricuspid Regurgitation Aortic and Pulmonic Stenosis ```
67
Mnemonic for Diastolic murmurs
MS PAID: Mitral Stenosis Pulmonic and Aortic Insufficiency D - just for diastolic
68
Continuous murmurs
Patent ductus arteriosus
69
Crescendo-decrescendo systolic ejection murmur, radiates to carotids with "pulsus parvus et tardus", heard loudest at heart base
Aortic stenosis
70
Cause of AS in older patients > 60 years
Age-related calcification
71
Cause of AS in younger patients
Early-onset calcification of bicuspid aorta
72
Symptoms of AS
Syncope, Angina, Dyspnea on exertion (SAD)
73
Holosystolic, high-pitched "blowing murmur", loudest at apex and radiates toward axilla
Mitral regurgitation
74
Common cause of MR
Ischemic heart disease, MVP, LV dilatation
75
Holosystolic, high-pitched "blowing murmur", loudest at tricuspid area and increased with inspiration
Tricuspid regurgitation
76
Valvular pathology caused by rheumatic fever and infective endocarditis
Mitral or Tricuspid regurgitation
77
Late systolic crescendo murmur with midsystolic click best heard over apex and loudest just before S2
Mitral Valve Prolapse (MVP)
78
Valvular pathology seen in Marfan and Ehlers-Danlos syndrome, can be caused by rheumatic fever or chordae rupture and predisposes to infective endocarditis
Mitral Valve Prolapse
79
Holosystolic, harsh-sounding murmur, loudest at tricuspid area with hyperdynamic RV impulse and no change in arterial pulse pressure
Ventral Septal Defect (VSD)
80
High-pitched "blowing" early diastolic decrescendo murmur with head bobbing, wide pulse pressure, bounding femoral and carotid pulses
Aortic regurgitation
81
Cause of midsystolic click in MVP
Sudden tensing of chordae tendineae
82
Follows opening snap with delayed rumbling mid-to-late diastolic murmur
Mitral stenosis (low-pitched murmur throughout diastole)
83
Cause of opening snap in MS
Due to abrupt halt in leaflet motion in diastole after rapid opening due to fusion of leaflets
84
Causes of aortic regurgitation
Aortic root dilatation, bicuspid aortic valve, endocarditis, rheumatic fever
85
Consequence of aortic regurgitation
Can progress to left heart failure
86
What correlates with increased severity of mitral stenosis
Decreased interval between S2 and opening snap
87
In mitral stenosis, when is LA pressure >> than LV pressure
During diastole
88
Valvular pathology considered a late sequela of rheumatic fever
Mitral stenosis
89
Consequence of mitral stenosis
Left atrial dilatation
90
Continuous machine-like murmur best heard at left infraclavicular area
Patent ductus arteriosus (PDA)
91
During what phase of cardiac cycle is PDA loudest
S2
92
Common cause of PDA
Congenital rubella or prematurity
93
Ion responsible for rapid upstroke and depolarization in myocardial action potential
Influx of Na ions
94
Ion responsible for plateau phase in myocardial action potential
Influx of Ca ions and efflux of K ions
95
Ion responsible for rapid repolarization in myocardial action potential
Efflux of K ions
96
Responsible for resting membrane potential in myocardial action potential
High K ion permeability through K channels
97
Phase of myocardial action potential characterized by opening of voltage-gated Na channels
Phase 0
98
Responsible for activating fast voltage-gated Na channels in myocardial action potential
Low negative resting membrane potential
99
Phase of myocardial action potential characterized by inactivation of voltage-gated Na channels and opening of voltage-gated K channels
Phase 1
100
Ion responsible for initial repolarization in myocardial action potential
Decreased Na influx
101
Phase of myocardial action potential characterized influx of Ca through voltage-gated Ca channels balancing K efflux
Phase 2
102
Phase of myocardial action potential characterized by massive K efflux due to opening of voltage-gated slow K channels
Phase 3
103
Phase of myocardial action potential characterized by high K permeability via K channels
Phase 4
104
Upstroke of pacemaker action potential is caused by what
Influx of Ca via opening of voltage gated Ca channels
105
Upstroke is what phase of pacemaker action potential
Phase 0
106
Phase of pacemaker action potential characterized by inactivation of Ca channels and activation of K channels
Phase 3
107
Ion responsible for depolarization in phase 3 of pacemaker action potential
K efflux
108
Ion responsible for slow spontaneous diastolic repolarization in phase 4 of pacemaker action potential
Na/K influx via I-funny channels
109
What determines HR
Slope of phase 4 in SA node
110
What accounts for automaticity of SA and AV node
I-funny current
111
Effect of ACh and adenosine on heart function
Decrease rate of diastolic depolarization and HR
112
Effect of catecholamines on heart function
Increase depolarization and HR
113
Effect of sympathetic stimulation on heart function
Increase chance I-funny channels open and HR
114
Conduction pathway
SA node - AV node - R and L bundle branches - Purkinje fibers - ventricles (left anterior and posterior fascicles)
115
Pacemaker of the heart
SA node
116
Blood supply for AV node
Right coronary artery
117
Structure in heart located in posteroinferior part of interatrial septum
AV node
118
Allows time for ventricular filling
AV nodal delay
119
Average time of AV nodal delay
100 msec
120
Pacemaker rates
SA > AV > bundle of His/Purkinje/ventricles
121
Speed of conduction
Purkinje > atria > ventricles > AV node
122
Fibers in heart that can travel greater distances in less time
Purkinje fibers
123
Indicates atrial depolarization on ECG
P-wave
124
Indicates time from start of atrial depolarization to start of ventricular depolarization on ECG
PR interval
125
Average length of time of PR interval
< 200 msec
126
Indicates ventricular depolarization on ECG
QRS complex
127
Average length of time of QRS complex
< 120 msec
128
Indicates depolarization, mechanical contraction and repolarization of ventricles on ECG
QT interval
129
Indicates ventricular repolarization on ECG
T-wave
130
Indicates ischemia or recent MI on ECG
T-wave inversion
131
Indicates junction between QRS complex and start of ST segment on ECG
J point
132
Indicates isoelectric point, ventricles depolarized on ECG
ST segment
133
Indicates hypokalemia or bradycardia on ECG
U-wave
134
ECG tracing characterized by shifting sinusoidal waveforms or "twisting of the points"
Torsades de pointes
135
Cardiac condition that predisposes to torsades de pointes
Long QT interval
136
Drugs that cause torsades de pointes
``` ABCDE: anti-Arrhythmics (class IA, III) anti-Biotics (macrolides) anti-C(ychotics) - (haloperidol) anti-Depressants (TCAs) anti-Emetics (ondansetron) ```
137
Decrease of what ions causes torsades de pointes
Hypokalemia and Hypomagnesemia
138
Treatment for torsades de pointes
Magnesium sulfate
139
Congenital long QT syndrome characterized by a pure cardiac phenotype and NO deafness
Romano-Ward syndrome
140
Congenital long QT syndrome characterized by sensorineural deafness
Jervell and Lange-Nielsen syndrome
141
Inheritance pattern in Romano-Ward syndrome
Autosomal dominant
142
Inheritance pattern in Jervell and Lange-Nielsen syndrome
Autosomal recessive
143
Autosomal dominant disorder characterized by pseudo-right BBB and ST elevations in V1-V3 leads seen in Asian males
Brugada syndrome
144
Complications of Brugada syndrome
Ventricular tachyarrhythmias and sudden cardiac death
145
Treatment for Brugada syndrome
ICD to prevent SCD
146
Most common type of ventricular pre-excitation syndrome
Wolff-Parkinson-White syndrome
147
ECG finding in Wolff-Parkinson-White syndrome
Delta wave with widened QRS complex and shortened PR interval
148
Complication of Wolff-Parkinson-White syndrome
Re-entry circuit causing supraventricular tachycardia
149
Bypasses AV node in Wolff-Parkinson-White syndrome
Bundle of Kent
150
Abnormal fast accessory conduction pathway from atria to ventricle in Wolff-Parkinson-White syndrome
Bundle of Kent
151
Type of rhythm with absent P-waves, irregularly irregular R-R waves and narrow QRS complex with HR 90-170 bpm
Atrial fibrillation
152
Most common risk factors in atrial fibrillation
HTN and coronary artery disease
153
Complications of atrial fibrillation
Thromboembolic events like stroke
154
Treatment for atrial fibrillation
Anticoagulation, rate and rhythm control, cardioversion
155
Condition with ECG findings of identical, back-to-back atrial depolarizations with "sawtooth" appearance
Atrial flutter
156
Definitive treatment for atrial flutter
Catheter ablation
157
Completely erratic rhythm with no identifiable waves
Ventricular fibrillation
158
Consequence of ventricular fibrillation
Fatal arrhythmia
159
Treatment for atrial fibrillation
Immediate CPR and defibrillation
160
Type of AV block with prolonged PR interval > 200 msec that is usually benign
First degree AV block
161
Treatment for first degree AV block
No treatment required since usually benign and asymptomatic
162
AV block with progressive lengthening of PR interval with dropped beat afterward and regularly irregular RR interval, usually asymptomatic
Second degree Mobitz type I (Wenckebach)
163
AV block with dropped beats not preceded by a change in length of PR interval
Second degree Mobitz type II
164
Consequence of Second degree Mobitz type II
May progress to 3rd-degree block
165
Treatment for Second degree Mobitz type II
Pacemaker
166
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
3rd degree AV block (complete)
167
Treatment for 3rd degree AV block
Pacemaker
168
Action of ANP on renal arterioles
Dilates afferent arteriole, Constricts efferent arteriole
169
Mechanism for release of ANP
Increased blood volume and atrial pressure
170
Recombinant form of BNP used for treatment of HF
Nesiritide
171
Carotid sinus location
Dilated region at carotid bifurcation
172
Transmits via glossopharyngeal nerve to solitary nucleus of medulla
Carotid sinus
173
Respond to changes in blood pressure
Carotid sinus and Aortic arch
174
Transmits via vagus nerve to solitary nucleus of medulla
Aortic arch
175
Effect of hypotension on ANS
Increased efferent sympathetic and decreased efferent parasympathetic causing increased vasoconstriction, HR, BP, and contractility
176
Effect of carotid massage on HR
Decreased HR via increased afferent baroreceptor firing increasing AV node refractory period
177
Chemoreceptors that do not respond to PO2
Central chemoreceptors
178
PO2 pressure that stimulates peripheral chemoreceptors
< 60 mmHg
179
Chemoreceptors that respond to decreased PO2, increased PCO2 and decreased pH
Peripheral chemoreceptors
180
Chemoreceptors that respond to changes in pH and PCO2 of brain interstitial fluid
Central chemoreceptors
181
Measure that approximates left atrial pressure
Pulmonary capillary wedge pressure (PCWP)
182
Condition in which PCWP > LV end diastolic pressure
Mitral stenosis
183
Device used to measure PCWP
Swan-Ganz catheter
184
Normal RA pressure
< 5 mmHg
185
Normal RV pressure
25/5 mmHg
186
Normal pulmonary trunk pressure
25/10 mmHg
187
Normal PCWP
4-12 mmHg
188
Normal LA pressure
< 12 mmHg
189
Normal LV pressure
130/10
190
Normal aortic arch pressure
130/90
191
Function that permits constant blood flow to an organ over wide range of perfusion pressures
Autoregulation
192
Metabolites that cause vasodilation of heart
Adenosine, NO, CO2, decreased O2
193
Metabolites that cause vasodilation of brain vasculature
CO2 (pH)
194
Causes vasoconstriction of lung vasculature
Hypoxia
195
Metabolites that cause vasodilation of skeletal muscle during exercise
Lactate, adenosine, K, H+, CO2
196
Metabolites that cause vasodilation of skeletal muscle at rest
Sympathetic tone
197
Mechanism that causes vasodilation of vessels in skin
Sympathetic tone for temperature control
198
Mechanism that causes renal vasodilation
Myogenic and tubuloglomerular feedback