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)
2
Q
What variables maintain cardiac output during the early stages of exercise
A
Increased HR and SV
3
Q
What variables maintain cardiac output during the late stages of exercise
A
HR only (SV plateaus)
4
Q
What heart function is shortened by increased HR
A
Diastole
5
Q
Effect of decreased diastole
A
Less filling time causing decreased cardiac output
6
Q
Calculating CO
A
CO = HR x SV
7
Q
Fick principle for calculating CO
A
CO = rate of O2 consumption/(arteriole O2 content - venous O2 content)
8
Q
Method for calculating mean arterial pressure (MAP)
A
MAP = CO x TPR or MAP = 2/3 diastole + 1/3 systole
9
Q
What is pulse pressure (PP)
A
PP = systolic pressure - diastolic pressure
10
Q
Method for calculating stroke volume (SV)
A
SV = EDV - ESV
11
Q
Variables that affect SV
A
Contractility, Afterload, Preload
12
Q
Effect of increased contractility on SV
A
Increased SV
13
Q
Effect of increased afterload on SV
A
Decreased SV
14
Q
Effect of increased preload on SV
A
Increased SV
15
Q
Effect of decreased contractility on SV
A
Decreased SV
16
Q
Effect of decreased afterload on SV
A
Increased SV
17
Q
Effect of decreased preload on SV
A
Decreased SV
18
Q
Effect of catecholamine binding on contractility and SV
A
Both increased
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
20
Q
Mechanisms that increase contractility and SV
A
- Catecholamine binding to B-1 receptors
- Increasing intracellular calcium
- Decreasing extracellular Na
- Digitalis or Digoxin
All methods increase intracellular calcium
21
Q
Mechanisms that decrease contractility and SV
A
- B-1 blockade decreases cAMP
- HF with systolic dysfunction
- Acidosis
- Hypoxia/hypercapnia
- Non-dihydropyridine Ca channel blockers
22
Q
Variables that increase myocardial O2 demand
A
Increased:
- Contractility
- Afterload
- HR
- Diameter of ventricle (increased wall tension)
23
Q
Variable that approximates preload
A
EDV
24
Q
Variables that affect EDV
A
Venous tone and circulating blood volume
25
Effect vasodilation has on EDV
Decreases EDV due to decreased venous return
26
Variable that approximates MAP
Afterload
27
Formula for calculating Ejection Fraction (EF)
EF = SV/EDV = (EDV - ESV)/EDV
28
Heart failure decreases what variable
Ejection fraction
29
Blood vessels with flow velocity
Capillaries (highest cross-sectional area)
30
Blood vessels that account for most TPR
Arterioles
31
Blood vessels that provide the most storage capacity
Veins
32
What does viscosity depend on most
Hematocrit
33
Condition that decreases blood viscosity
Anemia
34
Condition that increases blood viscosity
Polycythemia and hyperproteinemic (multiple myeloma)
35
In Starling forces, force of contraction is proportional to what?
End-diastolic length of cardiac muscle fiber
36
End-diastolic length of cardiac muscle fiber determines what?
Force of contraction
37
Formula for calculating change in pressure
P = Q x R
38
Formula for calculating Resistance
R= P/Q
39
Formula for calculating total parallel resistance
R = 1/(1/R1 + 1/R2 + 1/R3)
40
Formula for calculating total series resistance
R = R1 + R2 + R3
41
Effect of Vasopressors on TPR and CO for a given RA pressure or EDV
Increase TPR and decrease CO
42
Effect of exercise or AV shunt on TPR and CO for a given RA pressure or EDV
Decrease TPR and increase CO
43
Effects of increased afterload on pressure volume loop
Increased aortic pressure and ESV
| Decreased SV
44
Effect of increased preload on pressure volume loop
Increased SV
45
Effect of increased contractility on pressure volume loop
Increased SV and Ejection fraction
| Decreased ESV
46
Period between mitral valve closing and aortic valve opening
Isovolumetric contraction
47
Period of highest O2 contraction
Isovolumetric contraction
48
Period between aortic valve opening and closing
Systolic ejection
49
Period between aortic valve closing and mitral valve opening
Isovolumetric relaxation
50
Period just after mitral valve opening
Rapid filling
51
Period just before mitral valve closing
Reduced filling
52
Sound made by mitral and tricuspid valve closure
S1
53
Sound made by aortic and pulmonary valve closure
S2
54
Area S1 loudest
Mitral area
55
Area S2 loudest
Left upper sternal border
56
Heart sound associated with increased filling pressures
S3
57
Heart sound made by left atrium pushing against stiff LV wall
S4
58
Heart sound that can be normal in children and young adults
S3
59
Heart sound considered abnormal at any age
S4
60
S4 heart sound is best heard at apex in what position
Left lateral decubitus position
61
JVP associated with atrial contraction
a wave
62
JVP associated with RV contraction
c wave
63
JVP associated with downward displacement of closed tricuspid valve during rapid ventricular ejection phase
x descent
64
JVP associated with increased right atrial pressure due to filling against closed tricuspid valve
v wave
65
JVP associated with RA emptying into RV
y descent
66
Cause of normal splitting between A2 and P2
Inspiration
67
Cause of wide splitting between A2 and P2
Conditions that delay RV emptying (pulmonic stenosis and RBBB) - splitting exaggerated during inspiration
68
Cause of fixed splitting
ASD - increased RA and RV volumes causes increased flow through pulmonic valve delaying closure regardless of breath
69
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
70
Murmurs heard best in Mitral area
Mitral regurgitation
Mitral valve prolapse
Mitral stenosis
71
Murmurs heard best in Tricuspid area
Tricuspid regurgitation
Tricuspid stenosis
VSD
ASD
72
Murmurs heard best in Pulmonic area
Pulmonic stenosis
73
Murmurs heart best in LUSB
Pulmonic regurgitation
HCM
Aortic regurgitation
74
Murmurs heard best in Aortic area
Aortic stenosis
75
Maneuver that increases intensity of right heart sounds
Inspiration (increases venous return to RA)
76
Increases intensity of AR and VSD murmurs
Hand grip and rapid squatting
77
Maneuver that decreases intensity of most murmurs including AS
Valsalva and standing up
78
Maneuver that decreases intensity of hypertrophic cardiomyopathy murmurs
Hand grip and rapid squatting
79
Increases intensity of AS
Rapid squatting
80
Maneuver that increases intensity of hypertrophic cardiomyopathy murmurs
Valsalva and standing up
81
Maneuver that causes later onset of click/murmur in MVP
Hand grip and rapid squatting
82
Mnemonic for Systolic murmurs
```
MR VP TRAPS:
Mitral Regurgitation
VSD
Pulmonic stenosis
Tricuspid Regurgitation
Aortic and Pulmonic Stenosis
```
83
Mnemonic for Diastolic murmurs
MS PAID:
Mitral Stenosis
Pulmonic and Aortic Insufficiency
D - just for diastolic
84
Continuous murmurs
Patent ductus arteriosus
85
Crescendo-decrescendo systolic ejection murmur, radiates to carotids with "pulsus parvus et tardus", heard loudest at heart base
Aortic stenosis
86
Cause of AS in older patients > 60 years
Age-related calcification
87
Cause of AS in younger patients
Early-onset calcification of bicuspid aorta
88
Symptoms of AS
Syncope, Angina, Dyspnea on exertion (SAD)
89
Holosystolic, high-pitched "blowing murmur", loudest at apex and radiates toward axilla
Mitral regurgitation
90
Common cause of MR
Ischemic heart disease, MVP, LV dilatation
91
Holosystolic, high-pitched "blowing murmur", loudest at tricuspid area and increased with inspiration
Tricuspid regurgitation
92
Valvular pathology caused by rheumatic fever and infective endocarditis
Mitral or Tricuspid regurgitation
93
Late systolic crescendo murmur with midsystolic click best heard over apex and loudest just before S2
Mitral Valve Prolapse (MVP)
94
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
95
Holosystolic, harsh-sounding murmur, loudest at tricuspid area with hyperdynamic RV impulse and no change in arterial pulse pressure
Ventral Septal Defect (VSD)
96
High-pitched "blowing" early diastolic decrescendo murmur with head bobbing, wide pulse pressure, bounding femoral and carotid pulses
Aortic regurgitation
97
Cause of midsystolic click in MVP
Sudden tensing of chordae tendineae
98
Follows opening snap with delayed rumbling mid-to-late diastolic murmur
Mitral stenosis (low-pitched murmur throughout diastole)
99
Cause of opening snap in MS
Due to abrupt halt in leaflet motion in diastole after rapid opening due to fusion of leaflets
100
Causes of aortic regurgitation
Aortic root dilatation, bicuspid aortic valve, endocarditis, rheumatic fever
101
Consequence of aortic regurgitation
Can progress to left heart failure
102
What correlates with increased severity of mitral stenosis
Decreased interval between S2 and opening snap
103
In mitral stenosis, when is LA pressure >> than LV pressure
During diastole
104
Valvular pathology considered a late sequela of rheumatic fever
Mitral stenosis
105
Consequence of mitral stenosis
Left atrial dilatation
106
Continuous machine-like murmur best heard at left infraclavicular area
Patent ductus arteriosus (PDA)
107
During what phase of cardiac cycle is PDA loudest
S2
108
Common cause of PDA
Congenital rubella or prematurity
109
Ion responsible for rapid upstroke and depolarization in myocardial action potential
Influx of Na ions
110
Ion responsible for plateau phase in myocardial action potential
Influx of Ca ions and efflux of K ions
111
Ion responsible for rapid repolarization in myocardial action potential
Efflux of K ions
112
Responsible for resting membrane potential in myocardial action potential
High K ion permeability through K channels
113
Phase of myocardial action potential characterized by opening of voltage-gated Na channels
Phase 0
114
Responsible for activating fast voltage-gated Na channels in myocardial action potential
Low negative resting membrane potential
115
Phase of myocardial action potential characterized by inactivation of voltage-gated Na channels and opening of voltage-gated K channels
Phase 1
116
Ion responsible for initial repolarization in myocardial action potential
Decreased Na influx
117
Phase of myocardial action potential characterized influx of Ca through voltage-gated Ca channels balancing K efflux
Phase 2
118
Phase of myocardial action potential characterized by massive K efflux due to opening of voltage-gated slow K channels
Phase 3
119
Phase of myocardial action potential characterized by high K permeability via K channels
Phase 4
120
Upstroke of pacemaker action potential is caused by what
Influx of Ca via opening of voltage gated Ca channels
121
Upstroke is what phase of pacemaker action potential
Phase 0
122
Phase of pacemaker action potential characterized by inactivation of Ca channels and activation of K channels
Phase 3
123
Ion responsible for depolarization in phase 3 of pacemaker action potential
K efflux
124
Ion responsible for slow spontaneous diastolic repolarization in phase 4 of pacemaker action potential
Na/K influx via I-funny channels
125
What determines HR
Slope of phase 4 in SA node
126
What accounts for automaticity of SA and AV node
I-funny current
127
Effect of ACh and adenosine on heart function
Decrease rate of diastolic depolarization and HR
128
Effect of catecholamines on heart function
Increase depolarization and HR
129
Effect of sympathetic stimulation on heart function
Increase chance I-funny channels open and HR
130
Conduction pathway
SA node - AV node - R and L bundle branches - Purkinje fibers - ventricles (left anterior and posterior fascicles)
131
Pacemaker of the heart
SA node
132
Blood supply for AV node
Right coronary artery
133
Structure in heart located in posteroinferior part of interatrial septum
AV node
134
Allows time for ventricular filling
AV nodal delay
135
Average time of AV nodal delay
100 msec
136
Pacemaker rates
SA > AV > bundle of His/Purkinje/ventricles
137
Speed of conduction
Purkinje > atria > ventricles > AV node
138
Fibers in heart that can travel greater distances in less time
Purkinje fibers
139
Indicates atrial depolarization on ECG
P-wave
140
Indicates time from start of atrial depolarization to start of ventricular depolarization on ECG
PR interval
141
Average length of time of PR interval
< 200 msec
142
Indicates ventricular depolarization on ECG
QRS complex
143
Average length of time of QRS complex
< 120 msec
144
Indicates depolarization, mechanical contraction and repolarization of ventricles on ECG
QT interval
145
Indicates ventricular repolarization on ECG
T-wave
146
Indicates ischemia or recent MI on ECG
T-wave inversion
147
Indicates junction between QRS complex and start of ST segment on ECG
J point
148
Indicates isoelectric point, ventricles depolarized on ECG
ST segment
149
Indicates hypokalemia or bradycardia on ECG
U-wave
150
ECG tracing characterized by shifting sinusoidal waveforms or "twisting of the points"
Torsades de pointes
151
Cardiac condition that predisposes to torsades de pointes
Long QT interval
152
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)
```
153
Decrease of what ions causes torsades de pointes
Hypokalemia and Hypomagnesemia
154
Treatment for torsades de pointes
Magnesium sulfate
155
Congenital long QT syndrome characterized by a pure cardiac phenotype and NO deafness
Romano-Ward syndrome
156
Congenital long QT syndrome characterized by sensorineural deafness
Jervell and Lange-Nielsen syndrome
157
Inheritance pattern in Romano-Ward syndrome
Autosomal dominant
158
Inheritance pattern in Jervell and Lange-Nielsen syndrome
Autosomal recessive
159
Autosomal dominant disorder characterized by pseudo-right BBB and ST elevations in V1-V3 leads seen in Asian males
Brugada syndrome
160
Complications of Brugada syndrome
Ventricular tachyarrhythmias and sudden cardiac death
161
Treatment for Brugada syndrome
ICD to prevent SCD
162
Most common type of ventricular pre-excitation syndrome
Wolff-Parkinson-White syndrome
163
ECG finding in Wolff-Parkinson-White syndrome
Delta wave with widened QRS complex and shortened PR interval
164
Complication of Wolff-Parkinson-White syndrome
Re-entry circuit causing supraventricular tachycardia
165
Bypasses AV node in Wolff-Parkinson-White syndrome
Bundle of Kent
166
Abnormal fast accessory conduction pathway from atria to ventricle in Wolff-Parkinson-White syndrome
Bundle of Kent
167
Type of rhythm with absent P-waves, irregularly irregular R-R waves and narrow QRS complex with HR 90-170 bpm
Atrial fibrillation
168
Most common risk factors in atrial fibrillation
HTN and coronary artery disease
169
Complications of atrial fibrillation
Thromboembolic events like stroke
170
Treatment for atrial fibrillation
Anticoagulation, rate and rhythm control, cardioversion
171
Condition with ECG findings of identical, back-to-back atrial depolarizations with "sawtooth" appearance
Atrial flutter
172
Definitive treatment for atrial flutter
Catheter ablation
173
Completely erratic rhythm with no identifiable waves
Ventricular fibrillation
174
Consequence of ventricular fibrillation
Fatal arrhythmia
175
Treatment for atrial fibrillation
Immediate CPR and defibrillation
176
Type of AV block with prolonged PR interval > 200 msec that is usually benign
First degree AV block
177
Treatment for first degree AV block
No treatment required since usually benign and asymptomatic
178
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)
179
AV block with dropped beats not preceded by a change in length of PR interval
Second degree Mobitz type II
180
Consequence of Second degree Mobitz type II
May progress to 3rd-degree block
181
Treatment for Second degree Mobitz type II
Pacemaker
182
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)
183
Treatment for 3rd degree AV block
Pacemaker
184
Action of ANP on renal arterioles
Dilates afferent arteriole, Constricts efferent arteriole
185
Mechanism for release of ANP
Increased blood volume and atrial pressure
186
Recombinant form of BNP used for treatment of HF
Nesiritide
187
Carotid sinus location
Dilated region at carotid bifurcation
188
Transmits via glossopharyngeal nerve to solitary nucleus of medulla
Carotid sinus
189
Respond to changes in blood pressure
Carotid sinus and Aortic arch
190
Transmits via vagus nerve to solitary nucleus of medulla
Aortic arch
191
Effect of hypotension on ANS
Increased efferent sympathetic and decreased efferent parasympathetic causing increased vasoconstriction, HR, BP, and contractility
192
Effect of carotid massage on HR
Decreased HR via increased afferent baroreceptor firing increasing AV node refractory period
193
Chemoreceptors that do not respond to PO2
Central chemoreceptors
194
PO2 pressure that stimulates peripheral chemoreceptors
< 60 mmHg
195
Chemoreceptors that respond to decreased PO2, increased PCO2 and decreased pH
Peripheral chemoreceptors
196
Chemoreceptors that respond to changes in pH and PCO2 of brain interstitial fluid
Central chemoreceptors
197
Measure that approximates left atrial pressure
Pulmonary capillary wedge pressure (PCWP)
198
Condition in which PCWP > LV end diastolic pressure
Mitral stenosis
199
Device used to measure PCWP
Swan-Ganz catheter
200
Normal RA pressure
< 5 mmHg
201
Normal RV pressure
25/5 mmHg
202
Normal pulmonary trunk pressure
25/10 mmHg
203
Normal PCWP
4-12 mmHg
204
Normal LA pressure
< 12 mmHg
205
Normal LV pressure
130/10
206
Normal aortic arch pressure
130/90
207
Function that permits constant blood flow to an organ over wide range of perfusion pressures
Autoregulation
208
Metabolites that cause vasodilation of heart
Adenosine, NO, CO2, decreased O2
209
Metabolites that cause vasodilation of brain vasculature
CO2 (pH)
210
Causes vasoconstriction of lung vasculature
Hypoxia
211
Metabolites that cause vasodilation of skeletal muscle during exercise
Lactate, adenosine, K, H+, CO2
212
Metabolites that cause vasodilation of skeletal muscle at rest
Sympathetic tone
213
Mechanism that causes vasodilation of vessels in skin
Sympathetic tone for temperature control
214
Mechanism that causes renal vasodilation
Myogenic and tubuloglomerular feedback
