First Aid - Cardiology (369) Flashcards
1
Q
what vessel supplies the SA and AV nodes?
A
Right Coronary Artery (80% of the time)
2
Q
what vessel supplies the posterior left ventricle?
A
circumflex artery
3
Q
what vessel supplies the apex and anterior interventricular septum?
A
the left anterior descending
4
Q
what vessel supplies the the posterior septum?
A
posterior descending/interventricular artery
5
Q
what vessel supplies the right ventricle?
A
the acute marginal artery
6
Q
what is the most common site of coronary artery occlusion?
A
the LAD (left anterior descending), which supplies the anterior interventricular septum
7
Q
when do the coronary arteries fill?
A
diastole
8
Q
enlargement of the left atrium can result in?
A
dysphagia (due to compression of the esophageal nerve) or hoarseness (due to compression of the recurrent laryngeal nerve
9
Q
what is the equation for cardiac output?
A
stroke volume x heart rate
10
Q
what is the fick principle?
A
cardiac output = (rate of O2 consumption)/(arterial O2 content - venous O2 content)
11
Q
what arethe equations for mean arterial pressure?
A
(cardiac output) x (total peripheral resistance) OR 2/3 diastolic + 1/3 systolic pressure
12
Q
what is the equation for pulse pressure?
A
systolic pressure - diastolic pressure
13
Q
pulse pressure is a rough correlate for?
A
stroke volume
14
Q
what are the equations for determining stroke volume?
A
CO/HR or EDV-ESV
15
Q
what variables affect stroke volume?
A
contractility, afterload, preload
16
Q
what factors can increase contractility (and therefore stroke volume)?
A
- catecholamines (increase the activity of Ca++ pump) in SR)
17
Q
what factors can decrease contractility (and therefore stroke volume)?
A
- beta blockade (decreased cAMP)
18
Q
the preload is equal to the?
A
ventricular end diastolic volume
19
Q
the afterload is equal to the?
A
mean arterial pressure (proportional to peripheral resistance)
20
Q
venodilators (like nitroglycerine) have what effect on preload?
A
decrease preload
21
Q
vasodilators (like hydralazine) have what affect on afterload?
A
decrease afterload
22
Q
what factors increase preload?
A
exercise, increased blood volume (overtransfusion) and excitement (sympathetics)
23
Q
what is starling’s curve?
A
force of contraction is equal to the initial length of cardiac muscle fiber (preload)
24
Q
what is the equation for ejection fraction?
A
EF=SV/EDV=(EDV-ESV)/EDV
25
the ejection fraction is an index of?
ventricular contractility
26
what is an approximate normal ejection fraction?
> 55%. Decreases in heart failure
27
ohms law states?
change in pressure = the flow times the resistance
28
what are factors can cause increased viscosity?
polycythemia, hyperproteinemic states (multiple myeloma) and hereditary spherocytosis
29
what vessels account for most of the peripheral resistance?
arterioles
30
what is happening during isovolumetric contraction?
mitral valve closes, pressure is increasing in ventricle until aortic valve opens
31
define systole?
aortic valve is open, blood is leaving heart
32
what is isovolumetric relaxation?
period between aortic valve closing and mitral valve opening
33
what is happening during S1:
mitral and tricuspid valved close
34
what is happening during S2?
aortic and pulmonary valve closure
35
what is happening in S3?
in early diastole during rapid ventricular filling phase. Associated with increased filling pressure and more common in dilated ventricles (normal for pg women and kids)
36
S4 is associated with
ventricular hyprtrophy. Left atrium may push against stiff LV wall
37
jugular venous pulse a wave:
atrial contraction
38
jugular venous pulse c wave?
RV contraction (closed tricuspid bulging into atrium
39
jugular venous pulse v wave?
increased right atrial pressure due to filling against closed tricuspid valve
40
what normal physiologic process can cause S2 splitting?
aortic closes before pulmonic. Inspiration increases this difference
41
what is associated with wide splitting?
pulmonic stenosis or right bundle branch block
42
what is associated with fixed splitting?
ASD
43
what is associated with paradoxical splitting?
aortic stenosis and left bundle branch block
44
what is the mechanism of normal S2 splitting
inspiration leads to drop in intrathoracic pressure, which increases the capacity of the pulmonary circulation. The pulmonic valve closes later to accommodate the more blood entering the lungs. Aortic valve closes earlier because of decreased blood return to heart
45
right sternal border sounds:
during systole: aortic stenosis, flow murmur and aortic valve stenosis
46
left sternal border sounds:
during systole: hypertrophic cardiomyopathy. During diastole: aortic regurg, pulmonic regurg
47
where would you listen for an ASD?
pulmonic area (upper right sternal border) during systole
48
where would you listen for mitral valve issues?
5th rib, halfway to axilla (the only non-peristernal location)
49
what happens to the quality of right sided heart sounds with inspiration?
they increase
50
What are the pathologic systolic heart sounds?
Aortic/pulmonic stenosis
51
What are the pathologic diastolic heart sounds?
Aortic/pulmonic regurgitation
52
Heart Murmurs: MItral/Tricuspid Regurgitation (MR/TR)
Holosystolic, high pitched blowing murmur
53
What increases a mitral regurgitation murmur?
Maneuvers that increase TPR (squatting, hand grip) or LA return (exhalation)
54
What are the common causes of mitral regurgitation?
Ischemic heart disease, mitral valve prolapse, LV dilation, rheumatic fever
55
What are the common causes of tricuspid regurgitation?
RV dilation, endocarditis, rheumatic fever
56
Heart Murmurs: Aortic Stenosis
Crescendo-decresendo systolic ejection murmur following ejection click (due to abrupt halting of valve leaflets)
57
What is the cause of an ejection click in aortic stenosis?
Abrupt halting of valve leaflets
58
What are the common causes of aortic stenosis?
Age-related calcific aortic stenosis or bicuspid aortic valve
59
Heart Murmurs: Ventricular Septal Defect
Holosystolic, harsh sounding murmur
60
Heart Murmurs: MItral Prolapse
Late systolic crescendo murmur with midsystolic click (due to sudden tension of chordae tendineae)
61
What is the most common cause of midsystolic click in mitral prolapse?
Sudden tensing of the chordae tendineae
62
What are the common causes of mitrial prolapse?
Myxomatous degeneration, rheumatic fever, or chordae rupture.
63
Heart Murmurs: Aortic Regurgitation
Immediate, high pitched blowing diastolic murmur with wide pulse pressure, bounding pulses and head bobbing
64
What are the common causes of aortic regurgitation?
Aortic root dilation, bicuspid aortic valve or rheumatic fever.
65
What medications can decrease the intensity of the aortic regurgitation murmur?
Sasodilators
66
Heart Murmur: Mitral Stenosis
Following opening snap (due to tensing of chordae tendineae)
67
What are the common causes of mitral stenosis?
rheumatic fever
68
Heart Murmur: Patent Ductus Arteriosus
Continuous machine like mumur
69
What are the common causes of PDA?
Congenital rubella or prematurity
70
describe the role of calcium in cardiac muscle contraction:
cardiac muscle contraction depends on extracellular calcium, which enters during the plateau of action potential and stimulates calcium release from SR.
71
compare cardiac muscle to skeletal muscle
cardiac has a plateau (due to calcium influx), cardiac nodal cells spontaneously depolarize during diastole, cardiac myocytes are electrically coupled to each other by gap junctions
72
what is happening in phase 0 of the ventricular action potential?
rapid upstroke. Opening of voltage gated Na+ channels
73
what is happening in phase 1 of the ventricular action potential?
initial repolarization. Inactivation of voltage-gated Na+ channels. Voltage gated K+ channels begin to open
74
what is happening in phase 2 of the ventricular action potential?
plateau. Ca++ influx through voltage gated Ca++ channels balances K+efflux. Ca++ influx triggers Ca++ release from SR and myocyte contraction
75
what is happening during phase 3 of the ventricular action potential?
rapid reploarization. Massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca++ channels
76
what is happening during phase 4 of the ventricular action potential?
resting potential. High K+ permeability through K+ channels
77
where does the pacemaker action potential take place?
the SA and AV nodes
78
phase 0 of the pacemaker action potential?
upstroke. Opening of voltage gated Ca++ channels. These cells lack fast voltage-gated Na+ channels, results in slow conduction velocity that is used by AV node to prolong transmission from the atria to ventricles
79
describe phase 2 of the pacemaker action potential?
no plateau
80
describe phase 3 of the pacemaker action potential?
inactivation of the Ca++ channels and increased activation of K+ channels, increasing K+ efflux
81
describe phase 4 of the pacemaker action potential?
slow diastolic depolarization, membranse potential spontaneously depolarizes as Na+ conductance increases. . This accounts for the automacity of the SA and AV nodes.
82
what phase of the of the pacemaker action potential determines heart rate?
phase 4
83
what does administration of Ach or adenosine do to diastolic depolarization and heart rate?
decreases heart rate
84
the P wave represents?
atrial depolarization
85
what is a normal PR interval?
less than 200 ms
86
what does the QRS complex represent?
ventricular depolarization (normally less than 120 ms)
87
what is happening during the QT interval?
mechanical contraction of the ventricles
88
what does the T wave represent?
ventricular repolarization
89
what does T -wave inversion indicate?
a recent MI
90
what might cause a U wave on ekg?
hypokalemia or bradycardia
91
what is torsades de pointes?
ventricular tachycardia characterized by sinusoidal waveforms on ECG. Can progress to v-fib
92
what is Jervell and Lange-Nielsen syndrome?
congenital long QT syndrome due to defects in cardiac sodium and potassium channels. Presents with severe congenital sensorineural deafness
93
what is wolff-parkinson-white syndrome?
ventricular preexcitation syndrome. Accessory conduction pathway from atria to ventricle (bindle of kent) bypassing AV node. Ventricles partially depolarize early, making a delta wave on EKG. May lead to recurrent entry and supraventricular tachycardia
94
describe the trace of A fib:
chaotic and erratic baseline (irregularly regular) with no discrete P waves. Irregularly spaced ORS complexes.
95
what are the risks and treatments of A fib?
atrial stasis leading to stroke. Tx with beta blockers/calcium-channel blockers, and warfarin (prophylaxis against thromboembolism)
96
describe the trace of atrial flutter:
a rapid succession of identical, back to back atrial depolarization waves. "sawtooth"
97
tx for atrial flutter?
Class IA, IC or III antiarrhythmics
98
describe first degree AV block:
the PR interval is prolonged (>200) asymptomatic
99
describe second degree heart block, Mobitz type I, wenkebach:
progressive lengthening of PR interval until a beat is 'dropped' (P wave not followed by a QRS complex) usually asymptomatic
100
describe second degree heart block, Mobitz type II
dropped beats are not preceded by a change in PR interval. Abrupt, non-conducted P waves result in a pathologic condition.
101
describe a third degree heart block:
the atria and ventricles beat independently of each other. Both P waves and QRS complex are present, but the P waves bear no relation to the QRS complex.
102
tx for third degree heart block?
a pacemaker
103
infectious cause of third degree heart block?
lyme disease
104
describe V fib:
a completely erratic rhythm with no identifiable waves. Fatal without immidiate CPR and defribillation
105
what does decreased MAP do to the JGA?
JGA senses decreased MAP, stimulates the renin-angiotensin system, angiotensin II causes vasoconstriction and increased TPR, aldosterone increases blood volume, increasing cardiac output.
106
what does decreased MAP do to the baroreceptors?
decreases firing rate, increasing sympathetic activity
107
what does increased sympathetic activity do to cardiac output and TPR?
stimulation of beta 1's increase heart rate and contractility, increase CO. Stimulation of alpha 1's cause venoconstriction, increasing venous return and cardiac output, and alpha stimulation also causes arteriolar vasoconstriction increasing TPR
108
what causes the release of ANP?
ANP is released from the atrial in response to increased blood volume and atrial pressure.
109
what does increased ANP cause?
relaxation of vasculature. Constricts efferent renal arterioles and dilates afferent arterioles, promoting diuresis.
110
by what nerve does the aortic arch receptor transmit information?
vagus
111
by what nerve does the carotid sinus receptor transmit information?
glossopharyngeal to solitary nucleus of medulla.
112
what affect does hypotension have on the baroreceptors?
hypotension causes a decrease in arterial pressure, decreasing stretch, decreasing afferent baroreceptor firing, increasing efferent sympathetic firing and decreasing efferent parasympathetic stimulation, leading to vasoconstriction, increased heart rate and BP.
113
what happens when you massage the carotid?
increase pressure on carotid artery, increasing streth, increasing the afferent baroreceptor firing rate and decreasing heart rate
114
to what stimuli do the peripheral chemoreceptors respond?
decreased PO2 (
115
what stimuli do the central chemoreceptors respond?
changes in pH and PCO2 in brain interstitial fluid. Does not respond to P02.
116
what vessel supplies the SA and AV nodes?
the RCA (80% of the time)
117
what vessel supplies the posterior left ventricle?
circumflex artery
118
what vessel supplies the apex and anterior interventricular septum?
the left anterior descending
119
what vessel supplies the the posterior septum?
posterior descending/interventricular artery
120
what vessel supplies the right ventricle?
the acute marginal artery
121
what is the most common site of coronary artery occlusion?
the LAD, which supplies the anterior interventricular septum
122
when do the coronary arteries fill?
diastole
123
enlargement of the left atrium can result in?
dysphagia (due to compression of the esophageal nerve) or hoarseness (due to compression of the recurrent laryngeal nerve
124
what is the equation for cardiac output?
stroke volume x heart rate
125
what is the fick principle?
cardiac output = (rate of O2 consumption)/(arterial O2 content - venous O2 content)
126
what arethe equations for mean arterial pressure?
(cardiac output) x (total peripheral resistance) OR 2/3 diastolic + 1/3 systolic pressure
127
what is the equation for pulse pressure?
systolic pressure - diastolic pressure
128
pulse pressure is a rough correlate for?
stroke volume
129
what are the equations for determining stroke volume?
CO/HR or EDV-ESV
130
what variables affect stroke volume?
contractility, afterload, preload
131
what factors can increase contractility (and therefore stroke volume)?
catecholamines (increase the activity of Ca++ pump) in SR), increased intracellular calcium, decreased extracellular sodium (decreased activity of the Na+/Ca++ exchanger), digitalis (increased intracellular Na+, resulting in increased Ca++)
132
what factors can decrease contractility (and therefore stroke volume)?
beta blockade (decreased cAMP), heart failure (systolic dysfunction) acidosis, hypoxia/hypercapnea, and non-dihydropyridine Ca++ channel blockers
133
the preload is equal to the?
end diastolic volume
134
the afterload is equal to the?
mean arterial pressure (proportional to peripheral resistance)
135
venodilators (like nitroglycerine) have what effect on preload?
they decrease it
136
vasodilators (like hydralazine) have what affect on afterload?
they decrease it
137
what factors increase preload?
exercise, increased blood volume and excitement (sympathetics)
138
what is starling's law?
force of contraction is equal to the initial length of cardiac muscle fiber (preload)
139
what is the equation for ejection fraction?
EF=SV/EDV=(EDV-ESV)/EDV
140
the ejection fraction is an index of?
ventricular contractility
141
what is an approximate normal ejection fraction?
55%. Decreases in heart failure
142
ohms law states?
change in pressure = the flow times the resistance
143
what are factors can cause increased viscosity?
polycythemia, hyperproteinemic states (multiple myeloma) and hereditary spherocytosis
144
what vessels account for most of the peripheral resistance?
arterioles
145
what is happening during isovolumetric contraction?
mitral valve closes, pressure is increasing in ventricle until aortic valve opens
146
define systole?
aortic valve is open, blood is leaving heart
147
what is isovolumetric relaxation?
period between aortic valve closing and mitral valve opening
148
what is happening during S1:
mitral and tricuspid valved close
149
what is happening during S2?
aortic and pulmonary valve closure
150
what is happening in S3?
in early diastole during rapid ventricular filling phase. Associated with increased filling pressure and more common in dilated ventricles (normal for pg women and kids)
151
S4 is associated with
ventricular hyprtrophy. Left atrium may push against stiff LV wall
152
jugular venous pulse a wave:
atrial contraction
153
jugular venous pulse c wave?
RV contraction (closed tricuspid bulging into atrium
154
jugular venous pulse v wave?
increased right atrial pressure due to filling against closed tricuspid valve
155
what normal physiologic process can cause S2 splitting?
aortic closes before pulmonic. Inspiration increases this difference
156
what is associated with wide splitting?
pulmonic stenosis or right bundle branch block
157
what is associated with fixed splitting?
ASD
158
what is associated with paradoxical splitting?
aortic stenosis and left bundle branch block
159
what is the mechanism of normal S2 splitting
inspiration leads to drop in intrathoracic pressure, which increases the capacity of the pulmonary circulation. The pulmonic valve closes later to accommodate the more blood entering the lungs. Aortic valve closes earlier because of decreased blood return to heart
160
right sternal border sounds:
during systole: aortic stenosis, flow murmur and aortic valve stenosis
161
left sternal border sounds:
during systole: hypertrophic cardiomyopathy. During diastole: aortic regurg, pulmonic regurg
162
where would you listen for an ASD?
pulmonic area (upper right sternal border) during systole
163
where would you listen for mitral valve issues?
5th rib, halfway to axilla (the only non-peristernal location)
164
what happens to the quality of right sided heart sounds with inspiration?
they increase
165
what are the pathologic systolic heart sounds:
aortic/pulmonic stenosis, mitral/tricuspid regurg
166
what are the pathologic diastolic heart sounds:
aortic/pulmonic regurg, mitral/tricuspid stenosis
167
holosystolic, high pitched 'blowing' murmur?
mitral/tricuspid regurg
168
what can increase a mitral regurg murmur?
maneuvers that increase TPR (squatting, hand grip) or LA return (exhalation)
169
common causes of mitral regurg?
ischemic heart disease, mitral valve prolapse or LV dilation
170
common causes of tricuspid regurg?
RV dilation or endocarditis. Also rheumatic fever
171
crescendo-decresendo systolic ejection murmur following ejection click, radiating to carotids:
aortic stenosis
172
what is the cause of an ejection click?
abrupt halting of valce leaflets
173
common causes of aortic stenosis?
age-related calcific aortic stenosis or bicuspid aortic valve
174
pulses weak compare to heart sounds?
aortic stenosis
175
holosystolic, harsh sounding murmur loudest at tricuspid area?
VSD
176
late systolic crescendo murmur with midsystolic click?
mitral prolapse
177
what is the most common cause of midsystolic click?
sudden tensing of the chordae tendineae
178
mitral proplase can predispose to what?
endocarditis
179
causes of mitrial prolapse:
myxomatous degeneration, rheumatic fever, or chordae rupture.
180
immediate, high pitched blowing diastolic murmur with wide pulse pressure, bounding pulses and head bobbing:
aortic regurg
181
causes of aortic regurg:
aortic root dilation, bicuspid aortic valve or rheumatic fever.
182
what medications can decrease the intensity of the aortic regurg murmur?
vasodilators
183
opening snap, followed by delayed rumbling late in diastole:
mitral stenosis
184
common cause of mitral stenosis:
rheumatic fever
185
continuous machine-like murmur:
PDA
186
common causes of PDA
congenital rubella or prematurity
187
describe the role of calcium in cardiac muscle contraction:
cardiac muscle contraction depends on extracellular calcium, which enters during the plateau of action potential and stimulates calcium release from SR.
188
compare cardiac muscle to skeletal muscle
cardiac has a plateau (due to calcium influx), cardiac nodal cells spontaneously depolarize during diastole, cardiac myocytes are electrically coupled to each other by gap junctions
189
what is happening in phase 0 of the ventricular action potential?
rapid upstroke. Opening of voltage gated Na+ channels
190
what is happening in phase 1 of the ventricular action potential?
initial repolarization. Inactivation of voltage-gated Na+ channels. Voltage gated K+ channels begin to open
191
what is happening in phase 2 of the ventricular action potential?
plateau. Ca++ influx through voltage gated Ca++ channels balances K+efflux. Ca++ influx triggers Ca++ release from SR and myocyte contraction
192
what is happening during phase 3 of the ventricular action potential?
rapid reploarization. Massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca++ channels
193
what is happening during phase 4 of the ventricular action potential?
resting potential. High K+ permeability through K+ channels
194
where does the pacemaker action potential take place?
the SA and AV nodes
195
phase 0 of the pacemaker action potential?
upstroke. Opening of voltage gated Ca++ channels. These cells lack fast voltage-gated Na+ channels, results in slow conduction velocity that is used by AV node to prolong transmission from the atria to ventricles
196
describe phase 2 of the pacemaker action potential?
no plateau
197
describe phase 3 of the pacemaker action potential?
inactivation of the Ca++ channels and increased activation of K+ channels, increasing K+ efflux
198
describe phase 4 of the pacemaker action potential?
slow diastolic depolarization, membranse potential spontaneously depolarizes as Na+ conductance increases. . This accounts for the automacity of the SA and AV nodes.
199
what phase of the of the pacemaker action potential determines heart rate?
phase 4
200
what does administration of Ach or adenosine do to diastolic depolarization and heart rate?
decreases heart rate
201
the P wave represents?
atrial depolarization
202
what is a normal PR interval?
less than 200 ms
203
what does the QRS complex represent?
ventricular depolarization (normally less than 120 ms)
204
what is happening during the QT interval?
mechanical contraction of the ventricles
205
what does the T wave represent?
ventricular repolarization
206
what does T -wave inversion indicate?
a recent MI
207
what might cause a U wave on ekg?
hypokalemia or bradycardia
208
what is torsades de pointes?
ventricular tachycardia characterized by sinusoidal waveforms on ECG. Can progress to v-fib
209
what is Jervell and Lange-Nielsen syndrome?
congenital long QT syndrome due to defects in cardiac sodium and potassium channels. Presents with severe congenital sensorineural deafness
210
what is wolff-parkinson-white syndrome?
ventricular preexcitation syndrome. Accessory conduction pathway from atria to ventricle (bindle of kent) bypassing AV node. Ventricles partially depolarize early, making a delta wave on EKG. May lead to recurrent entry and supraventricular tachycardia
211
describe the trace of A fib:
chaotic and erratic baseline (irregularly regular) with no discrete P waves. Irregularly spaced ORS complexes.
212
what are the risks and treatments of A fib?
atrial stasis leading to stroke. Tx with beta blockers/calcium-channel blockers, and warfarin (prophylaxis against thromboembolism)
213
describe the trace of atrial flutter:
a rapid succession of identical, back to back atrial depolarization waves. "sawtooth"
214
tx for atrial flutter?
Class IA, IC or III antiarrhythmics
215
describe first degree AV block:
the PR interval is prolonged (>200) asymptomatic
216
describe second degree heart block, Mobitz type I, wenkebach:
progressive lengthening of PR interval until a beat is 'dropped' (P wave not followed by a QRS complex) usually asymptomatic
217
describe second degree heart block, Mobitz type II
dropped beats are not preceded by a change in PR interval. Abrupt, non-conducted P waves result in a pathologic condition.
218
describe a third degree heart block:
the atria and ventricles beat independently of each other. Both P waves and QRS complex are present, but the P waves bear no relation to the QRS complex.
219
tx for third degree heart block?
a pacemaker
220
infectious cause of third degree heart block?
lyme disease
221
describe V fib:
a completely erratic rhythm with no identifiable waves. Fatal without immidiate CPR and defribillation
222
what does decreased MAP do to the JGA?
JGA senses decreased MAP, stimulates the renin-angiotensin system, angiotensin II causes vasoconstriction and increased TPR, aldosterone increases blood volume, increasing cardiac output.
223
what does decreased MAP do to the baroreceptors?
decreases firing rate, increasing sympathetic activity
224
what does increased sympathetic activity do to cardiac output and TPR?
stimulation of beta 1's increase heart rate and contractility, increase CO. Stimulation of alpha 1's cause venoconstriction, increasing venous return and cardiac output, and alpha stimulation also causes arteriolar vasoconstriction increasing TPR
225
what causes the release of ANP?
ANP is released from the atrial in response to increased blood volume and atrial pressure.
226
what does increased ANP cause?
relaxation of vasculature. Constricts efferent renal arterioles and dilates afferent arterioles, promoting diuresis.
227
by what nerve does the aortic arch receptor transmit information?
vagus
228
by what nerve does the carotid sinus receptor transmit information?
glossopharyngeal to solitary nucleus of medulla.
229
what affect does hypotension have on the baroreceptors?
hypotension causes a decrease in arterial pressure, decreasing stretch, decreasing afferent baroreceptor firing, increasing efferent sympathetic firing and decreasing efferent parasympathetic stimulation, leading to vasoconstriction, increased heart rate and BP.
230
what happens when you massage the carotid?
increase pressure on carotid artery, increasing streth, increasing the afferent baroreceptor firing rate and decreasing heart rate
231
to what stimuli do the peripheral chemoreceptors respond?
decreased PO2 (
232
what stimuli do the central chemoreceptors respond?
changes in pH and PCO2 in brain interstitial fluid. Does not respond to P02.
233
what is the Cushing reaction?
increased ICP constricts arterioles, causing cerebral ischemia, leading to systemic hypertension and reflex bradycardia.
234
what is cushing triad?
hypertension, bradycardia and respiratory depression
235
what organ gets the largest share of systemic output?
liver
236
what organ gets the highest blood flow per gram of tissue?
kidney
237
how is the O2 demand of the heart met?
O2 extraction is always 100%. Demand is met by increasing coronary blood flow, not by increasing extraction of O2
238
what factors determine regulation of blood flow to the heart?
local metabolites - O2, adenosine and NO
239
what factors determine regulation of blood flow to the brain?
local metabolites - CO2 (pH)
240
what factors determine regulation of blood flow to the kidneys?
myogenic and tubuloglomerular feedback
241
what factors determine regulation of blood flow to the lungs?
hypoxia causes vasoconstriction (this is unique)
242
what factors determine regulation of blood flow to the skeletal muscle?
local metabolites -- lactate, adenosine, K+
243
what factors determine regulation of blood flow to the skin?
sympathetic stimulation is the most important. Temperature control
244
name the 4 starling's forces:
capillary pressure, interstitial pressure, plasma colloid pressure and interstitial fluid colloid osmotic pressure
245
what is the equation for net filtration pressure?
[(Pc-Pi) - (πc-πi)
246
what is edema?
excess fluid flow into interstitium
247
what are the common causes of edema?
increased capillary pressure (heart failure), decreased plasma proteins (liver failure/nephrotic syndrome), increased capillary permeability (toxins, infections, burns), increased interstitial fluid colloid osmotic pressure (lymphatic blockage)
248
right to left shunts cause?
early cyanosis. Blue babies.
249
5 T's of right to left shunts:
tetralogy of Fallot, Transposition of great vessels, truncus arteriosis, tricuspid atresia, and total anomalous pulmonary venous return
250
what is persistant trunctus arteriosus?
failure of truncus arteriosus to divide into pulmonary trunk and aorta
251
what is tricuspid atresia?
characterized by absence of tricuspid valve and hypoplastic right ventricle. Requires both ASD and VSD for viability
252
what is TAPVR?
total anomalous pulmonary venous return. Pulmonary vein drains into right heart circulation (SVC, coronary sinus, etc)
253
name the 3 types of left to right shunts:
VSD, ASD and PDA
254
what is the most common congenital cardiac anomaly?
VSD
255
what medication is given to close a PDA?
indomethacin
256
what is eisenmenger's syndrome?
uncorrected VSD, ASD or PDA causes compensatory vascular hypertrophy, which results in progressive pulmonary hypertension. As pulmonary resistance increases, the shunt reverses from left to right to right to left, which causes late cyanosis (clubbing and polycythemia)
257
what are the 4 issues in tetralogy of fallot?
pulmonary stenosis (most inportant for prognosis), right ventricular hypertrophy, overiding aorta and VSD
258
S/S of tetralogy of fallot?
early cyanosis is caused by r-l shunt across VSD. R-L shunt exists because of the increased pressure caused by stenotic pulmonic valve. X-Ray: boot shaped heart (because of RVH). Pt suffers cyanotic spells. Pt squats to improve symptoms
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embryology of tetralogy of fallot:
anterosuperior displacement of the infundibular septum
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describe the transposition of the great vessels:
aorta leaves RV, pulmonary trunk leaves left ventricle, keeping the pulmonary and systemic circulations separate. Not compatible with life without a PDA, VSD or patent foramen ovale to allow for mixing of blood
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embryology of transposition of the great vessels:
failure of the aorticopulmonary septum to spiral
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infantile coarctation of the aorta s associated with what chromosomal anomaly?
turner
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where is the coarctation in infantile type CotA?
proximal to insertion of ductus arteriosum
264
notched ribs, hypertension in arms, weak pulse in legs:
adult type coarctation of the aorta
265
coarctation of the aorta can cause what type of murmur?
aorti regurg
266
coarctation of the aorta is associated with what valve abnormality?
bicuspid aortic valve
267
what is the ductus arteriosus?
normal fetal R - L shunt. When an infant takes her first breath lung resistance decreases and PDA should close.
268
what is a patent ductus arteriosus?
DA doesn't close and a left to right shunt forms, causing RVH and failure.
269
how do you maintain a patent ductus arteriosus?
PGE
270
continuous machine-like murmur:
PDA
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late cyanosis in lower extremities?
PDA
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what vessel supplies the SA and AV nodes?
the RCA (80% of the time)
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what vessel supplies the posterior left ventricle?
circumflex artery
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what vessel supplies the apex and anterior interventricular septum?
the left anterior descending
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what vessel supplies the the posterior septum?
posterior descending/interventricular artery
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what vessel supplies the right ventricle?
the acute marginal artery
277
what is the most common site of coronary artery occlusion?
the LAD, which supplies the anterior interventricular septum
278
when do the coronary arteries fill?
diastole
279
enlargement of the left atrium can result in?
dysphagia (due to compression of the esophageal nerve) or hoarseness (due to compression of the recurrent laryngeal nerve
280
what is the equation for cardiac output?
stroke volume x heart rate
281
what is the fick principle?
cardiac output = (rate of O2 consumption)/(arterial O2 content - venous O2 content)
282
what arethe equations for mean arterial pressure?
(cardiac output) x (total peripheral resistance) OR 2/3 diastolic + 1/3 systolic pressure
283
what is the equation for pulse pressure?
systolic pressure - diastolic pressure
284
pulse pressure is a rough correlate for?
stroke volume
285
what are the equations for determining stroke volume?
CO/HR or EDV-ESV
286
what variables affect stroke volume?
contractility, afterload, preload
287
what factors can increase contractility (and therefore stroke volume)?
catecholamines (increase the activity of Ca++ pump) in SR), increased intracellular calcium, decreased extracellular sodium (decreased activity of the Na+/Ca++ exchanger), digitalis (increased intracellular Na+, resulting in increased Ca++)
288
what factors can decrease contractility (and therefore stroke volume)?
beta blockade (decreased cAMP), heart failure (systolic dysfunction) acidosis, hypoxia/hypercapnea, and non-dihydropyridine Ca++ channel blockers
289
the preload is equal to the?
end diastolic volume
290
the afterload is equal to the?
mean arterial pressure (proportional to peripheral resistance)
291
venodilators (like nitroglycerine) have what effect on preload?
they decrease it
292
vasodilators (like hydralazine) have what affect on afterload?
they decrease it
293
what factors increase preload?
exercise, increased blood volume and excitement (sympathetics)
294
what is starling's law?
force of contraction is equal to the initial length of cardiac muscle fiber (preload)
295
what is the equation for ejection fraction?
EF=SV/EDV=(EDV-ESV)/EDV
296
the ejection fraction is an index of?
ventricular contractility
297
what is an approximate normal ejection fraction?
55%. Decreases in heart failure
298
ohms law states?
change in pressure = the flow times the resistance
299
what are factors can cause increased viscosity?
polycythemia, hyperproteinemic states (multiple myeloma) and hereditary spherocytosis
300
what vessels account for most of the peripheral resistance?
arterioles
301
what is happening during isovolumetric contraction?
mitral valve closes, pressure is increasing in ventricle until aortic valve opens
302
define systole?
aortic valve is open, blood is leaving heart
303
what is isovolumetric relaxation?
period between aortic valve closing and mitral valve opening
304
what is happening during S1:
mitral and tricuspid valved close
305
what is happening during S2?
aortic and pulmonary valve closure
306
what is happening in S3?
in early diastole during rapid ventricular filling phase. Associated with increased filling pressure and more common in dilated ventricles (normal for pg women and kids)
307
S4 is associated with
ventricular hyprtrophy. Left atrium may push against stiff LV wall
308
jugular venous pulse a wave:
atrial contraction
309
jugular venous pulse c wave?
RV contraction (closed tricuspid bulging into atrium
310
jugular venous pulse v wave?
increased right atrial pressure due to filling against closed tricuspid valve
311
what normal physiologic process can cause S2 splitting?
aortic closes before pulmonic. Inspiration increases this difference
312
what is associated with wide splitting?
pulmonic stenosis or right bundle branch block
313
what is associated with fixed splitting?
ASD
314
what is associated with paradoxical splitting?
aortic stenosis and left bundle branch block
315
what is the mechanism of normal S2 splitting
inspiration leads to drop in intrathoracic pressure, which increases the capacity of the pulmonary circulation. The pulmonic valve closes later to accommodate the more blood entering the lungs. Aortic valve closes earlier because of decreased blood return to heart
316
right sternal border sounds:
during systole: aortic stenosis, flow murmur and aortic valve stenosis
317
left sternal border sounds:
during systole: hypertrophic cardiomyopathy. During diastole: aortic regurg, pulmonic regurg
318
where would you listen for an ASD?
pulmonic area (upper right sternal border) during systole
319
where would you listen for mitral valve issues?
5th rib, halfway to axilla (the only non-peristernal location)
320
what happens to the quality of right sided heart sounds with inspiration?
they increase
321
what are the pathologic systolic heart sounds:
aortic/pulmonic stenosis, mitral/tricuspid regurg
322
what are the pathologic diastolic heart sounds:
aortic/pulmonic regurg, mitral/tricuspid stenosis
323
holosystolic, high pitched 'blowing' murmur?
mitral/tricuspid regurg
324
what can increase a mitral regurg murmur?
maneuvers that increase TPR (squatting, hand grip) or LA return (exhalation)
325
common causes of mitral regurg?
ischemic heart disease, mitral valve prolapse or LV dilation
326
common causes of tricuspid regurg?
RV dilation or endocarditis. Also rheumatic fever
327
crescendo-decresendo systolic ejection murmur following ejection click, radiating to carotids:
aortic stenosis
328
what is the cause of an ejection click?
abrupt halting of valce leaflets
329
common causes of aortic stenosis?
age-related calcific aortic stenosis or bicuspid aortic valve
330
pulses weak compare to heart sounds?
aortic stenosis
331
holosystolic, harsh sounding murmur loudest at tricuspid area?
VSD
332
late systolic crescendo murmur with midsystolic click?
mitral prolapse
333
what is the most common cause of midsystolic click?
sudden tensing of the chordae tendineae
334
mitral proplase can predispose to what?
endocarditis
335
causes of mitrial prolapse:
myxomatous degeneration, rheumatic fever, or chordae rupture.
336
immediate, high pitched blowing diastolic murmur with wide pulse pressure, bounding pulses and head bobbing:
aortic regurg
337
causes of aortic regurg:
aortic root dilation, bicuspid aortic valve or rheumatic fever.
338
what medications can decrease the intensity of the aortic regurg murmur?
vasodilators
339
opening snap, followed by delayed rumbling late in diastole:
mitral stenosis
340
common cause of mitral stenosis:
rheumatic fever
341
continuous machine-like murmur:
PDA
342
common causes of PDA
congenital rubella or prematurity
343
describe the role of calcium in cardiac muscle contraction:
cardiac muscle contraction depends on extracellular calcium, which enters during the plateau of action potential and stimulates calcium release from SR.
344
compare cardiac muscle to skeletal muscle
cardiac has a plateau (due to calcium influx), cardiac nodal cells spontaneously depolarize during diastole, cardiac myocytes are electrically coupled to each other by gap junctions
345
what is happening in phase 0 of the ventricular action potential?
rapid upstroke. Opening of voltage gated Na+ channels
346
what is happening in phase 1 of the ventricular action potential?
initial repolarization. Inactivation of voltage-gated Na+ channels. Voltage gated K+ channels begin to open
347
what is happening in phase 2 of the ventricular action potential?
plateau. Ca++ influx through voltage gated Ca++ channels balances K+efflux. Ca++ influx triggers Ca++ release from SR and myocyte contraction
348
what is happening during phase 3 of the ventricular action potential?
rapid reploarization. Massive K+ efflux due to opening of voltage-gated slow K+ channels and closure of voltage-gated Ca++ channels
349
what is happening during phase 4 of the ventricular action potential?
resting potential. High K+ permeability through K+ channels
350
where does the pacemaker action potential take place?
the SA and AV nodes
351
phase 0 of the pacemaker action potential?
upstroke. Opening of voltage gated Ca++ channels. These cells lack fast voltage-gated Na+ channels, results in slow conduction velocity that is used by AV node to prolong transmission from the atria to ventricles
352
describe phase 2 of the pacemaker action potential?
no plateau
353
describe phase 3 of the pacemaker action potential?
inactivation of the Ca++ channels and increased activation of K+ channels, increasing K+ efflux
354
describe phase 4 of the pacemaker action potential?
slow diastolic depolarization, membranse potential spontaneously depolarizes as Na+ conductance increases. . This accounts for the automacity of the SA and AV nodes.
355
what phase of the of the pacemaker action potential determines heart rate?
phase 4
356
what does administration of Ach or adenosine do to diastolic depolarization and heart rate?
decreases heart rate
357
the P wave represents?
atrial depolarization
358
what is a normal PR interval?
less than 200 ms
359
what does the QRS complex represent?
ventricular depolarization (normally less than 120 ms)
360
what is happening during the QT interval?
mechanical contraction of the ventricles
361
what does the T wave represent?
ventricular repolarization
362
what does T -wave inversion indicate?
a recent MI
363
what might cause a U wave on ekg?
hypokalemia or bradycardia
364
what is torsades de pointes?
ventricular tachycardia characterized by sinusoidal waveforms on ECG. Can progress to v-fib
365
what is Jervell and Lange-Nielsen syndrome?
congenital long QT syndrome due to defects in cardiac sodium and potassium channels. Presents with severe congenital sensorineural deafness
366
what is wolff-parkinson-white syndrome?
ventricular preexcitation syndrome. Accessory conduction pathway from atria to ventricle (bindle of kent) bypassing AV node. Ventricles partially depolarize early, making a delta wave on EKG. May lead to recurrent entry and supraventricular tachycardia
367
describe the trace of A fib:
chaotic and erratic baseline (irregularly regular) with no discrete P waves. Irregularly spaced ORS complexes.
368
What factors increase myocardial O2 demand?
Increased afterload (arterial pressure)
369
Under what circumstances does stroke volume increase?
Anxiety
