Cardiac Physiology Flashcards

1
Q

What does it mean to have Right-dominant circulation

A

PDA comes from the RCA

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2
Q

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

A

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

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3
Q

Most commonly occluded artery

A

LAD

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4
Q

When does coronary blood flow peak?

A

Early diastole

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5
Q

What is most post. part of heart

A

L atrium

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6
Q

L atrium can effect GI tract how

A

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

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7
Q

What supplies SA and AV nodes

A

RCA

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8
Q

LCX supplies

A

Lateral and post. walls of LV

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9
Q

LAD supplies

A

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

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10
Q

What supplies R ventricle

A

Acute marginal artery

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11
Q

What does the PDA/interventricular artery do

A

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

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12
Q

What happens to CO with increasing HR

A

Less diastolic filling time leads to decreased CO

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13
Q

Increased pulse pressure in what diseases

A

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

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14
Q

Decreased pulse pressure in what diseases

A

Aortic stenosis, cardiogenic shock, cardiac tamponade, advanced HF

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15
Q

How to calculate MAP

A

MAP=COxTPR

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

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16
Q

What is the point of MAP

A

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

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17
Q

MAP stands for

A

mean arterial pressure

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18
Q

CO formula

A

=Stroke Volume (SV) x HR (HR)

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19
Q

What is the Fick principle

A

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

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20
Q

How do catecholamines increase contracility

A

Increase activity of Ca2+ pump in SR

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21
Q

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

A

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

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22
Q

How to increase contracility

A

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

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23
Q

how does digitalis increase contracility

A

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

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24
Q

How does Na-Ca2+ exchanger work

A

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

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25
how to decrease contracility
Beta1-blockade, HF with systolic dysfunction, acidosis, hypoxia/hypercapnea (dec. PO2/Inc. PCO2), non-dihydropyridine Ca2+ blocks
26
How does beta-1 blockade decrease contracility
Decreases cAMP
27
What are the non-dihydropyridine CCBs
Verapamil, diltiazem
28
What are the dihydropyridine CCBs
Nifepidime, amlodipine
29
How is preload approximated
LVEDV
30
What is afterload approximated by
MAP
31
What do vasodilators do and example
Dec. afterload (hydralazine)
32
What to ACEIs and ARBs do
Decrease preload and afterload
33
What is Laplace's law
Wall tension=(pressure x radius)/(2*wall thickness)
34
Why does LV hypertrophy to increasing afterload
To decrase wall tension (thickening directly decreases wall tension (indirectly proportional))
35
How to calculate EF
SV/EDV
36
Normal EF?
>55%
37
Viscosity depends mostly on what?
Hematocrit
38
What diseases increase viscosity
Polycythemia, Hyperproteinemic states (e.g. multiple myeloma), Hereditary spherocytosis??
39
What decreases viscosity?
Anemia
40
Resistance is related to....
Directly proprotional to viscosity and vessel length and inversely proportional to the radius to the 4th power.
41
resistance of vessels in series
R1+R2+R3
42
resistance of vessels in parallel
1/R1 + 1/R2 + 1/R3
43
Resistance formulas
=Driving Pressure (deltaP)/ Flow (Q) = 8n(viscosity)xLength / (piR^4)
44
pg. 269 gist?
Effects on contractility, preload, and afterload effect the CO vs. venous return.
45
Do CO and venous return have to be equal?
No.
46
What are the steps of heart contraction
1. Isovolumetric contraction: ventricles contract, MV and AV closed. Most O2 consumption. 2. Systolic ejection: AV opens 3. Isovolumetric relaxation: Between AV closing and MV opening. 4. Diastolic filling: Rapid 5. Diastolic filling: Slow
47
How does inc. afterload and inc. preload and inc. contracility affect pressure-volume loop
Inc. afterload increases the End-systolic volume so you have decreased ejection. Inc. afterload increases EDV so you have increased ejection. Inc. contracticility dec. ESV so more ejection.
48
Does pressure increase after Aortic valve opens?
yes it keeps increasing then decreases. The T wave occurs when it peaks.
49
What causes the dicrotic notch
Occurs when the aortic valve closes, the brief reversal of flow when the LV relaxes closes the aortic valve and this is what increases the pressure
50
Where is S2 loudest
L sternal border
51
Where is S1 loudest
Mitral area
52
When do you get S3
MR, CHF, dilated ventricles, NORMAL in children and pregnant women. Associated with elevated filling pressures.
53
When do you get S4
Late diastole, high atrial pressure, ventricular hypertrophy
54
Name the steps of the JVP
a wave: atrial contraction c wave: RV contraction pushing against closed TV x descent: Closed TV moves downwards during contraction v wave: right atrial filling during systole y decent: blood flow from RA to RV
55
What causes wide splitting
Anything that increases the length of RV contraction time. Pulmonic stenosis, RBBB.
56
What causes fixed splitting.
ASD makes pulmonic closure delayed in expiration or inspiration.
57
What causes paradoxical splitting
Anything that increases the length of LV contraction time. Aortic stenosis, LBBB
58
What can you hear in aortic area
Aortic stenosis/sclerosis, flow murmur
59
What can you hear in pulmonic area
Pulmonic stenosis, flow murmur
60
What can you hear in tricuspid area
Pansystolic: Tricuspid regurg., VSD Diastolic: Tricuspid stenosis, ASD
61
What can you hear in Mitral area
MR, mtiral stenosis
62
What can you hear at L sternal border
AR, PR, HOCM
63
What does late ASD sound like
Pulmonic diastolic murmur from dilation of pulm. artery
64
What does inspiration increase the sound of
Increased intensity of R heart sounds.
65
What does hand grip affect
Increased SVR: MR, AR, and VSD louder AS, HOCM softer: stents them open MVP: Incr. murmur intensity, later onset of click/murmur???????????
66
What does Valsalva (Phase II) and Standing
Dec. venous return. Most murmur decrease in intensity including AS ????????????????? Inc. HOCM intesntiy MVP: dec. murmur intensity, earlier click/murmur????????
67
Rapid squatting (inc. venous return, inc. preload, inc. afterload with prolonged squatting) does what
Dec. HOCM, inc. AS, MVP: inc. murmur, later onset of click/murmur
68
Pulsus parvus et tardus
Aortic Stenosis
69
Aortic stenosis mnemonic
SAD: syncope, angina, dyspnea
70
Why does MR/TR and VSD get louder with handgrip
Increased SVR makes the blood flow preferentially through the lower pressure exits
71
Most frequent valvular lesion
Mitral valve prolapse
72
Why does MVP happen earlier with standing/Valsalva?
Because the decreased preload makes the chordae more lax so they prolapse earlier.
73
Why is MVP louder with hand-grip, squatting
The inc. afterload and preload mean more flow past murmur so it is more intense, but it doesn't happen earlier.
74
MR/TR murmur sound
high pitched blowing murmur
75
TR radiates to
Loudest at tricuspid area and radiates to R sternal border
76
VSD murmur sound
Harsh-sounding
77
Causes of MVP (mitral valve prolapse)
Myxomatous degeneration, rheumatic fever, or chordae rupture
78
What is the midsystolic click
It's when the chordae tendinae suddenly tense
79
What is a sign of Mitral stenosis worsening
Dec. interval between S2 and OS.
80
Common causes of PDA
Congenital rubella or prematurity
81
Where to hear PDA best?
L infraclavicular area
82
Know ventricular cell Action Potential graph..
....
83
Ventricular AP similar to what cells
His Purkinje fibers
84
What is the order of calcium channels opening
First voltage gated, then the increased ICF Ca2+ leads to the SR release of Ca2+
85
What is the funny current
If channels: slow, mixed Na/K inward current
86
membrane potential for ventricles
-85 mV
87
membrane potential for SA node
around -65 mV
88
Na+ channels in SA node
permanently shut off due to high resting membrane potential
89
Know the curve of SA node action potential
.....
90
What chemicals decrease and increase HR
ACh/adenosine decrease by slowing Phase 4 of SA node. Catecholamines inc. depolarization and HR. Sympathetic stimulation increases the chance that If channels are open.
91
Organize the following in terms of speed of conduction: atria, AV node, Purkinje, ventricles
Purkinje>atria>ventricles>AV node
92
How long is AV node delay?
100 msec
93
What predisposes to Torsades de pointes
Long QT, drugs, dec. K+, dec. Mg, other abnormalities.
94
Torsades causes mnemonic
``` Some Risky Meds Can Prolong QT Sotalol Risperidone (antipsychotic) Macrolides Chloroquine Protease inhibitors (-navir) Quinidine (class Ia; also class III) Thiazides ```
95
What are the important congenital long QT syndromes
Romano-Ward syndrome; jervell and Lange-Nielsen syndrome
96
Romano-Ward syndrome
cong. long QT; aut. dom.; pure cardiac phenotype (no deafness)
97
Jervell and Lange-Nielsen syndrome
Cong. long QT; aut. rec.; sensorineural deafness
98
Wolff-Parkinson-White anatomy
Bundle of Kent. Drugs that slow down the AV node increase risk of tachyarrhythmias.
99
How to cardiovert chemically a.flutter
Class IA, IC, or III antiarrhythmics.
100
A. flutter rate control
Beta-blocker, CCBs
101
A. flutter definitive tx
Catheter ablation
102
Normal PR interval
<200 ms
103
What is Mobitz type I
Wenckebach, progressive PR prolongation
104
Which second degree AV block is worse
Mobitz type II, randomly drops, can progress to third degree, tx with pacemaker
105
Lyme disease and SA node
Third degree heart block
106
atrial natriuretic peptide
Atrial myocytes in response to increased blood volume and atrial pressure.
107
Atrial natriuretic peptide actions
Vasodilation and dec. Na+ reabsorption in renal collectin tubule. Constricts efferents, dilates afferents via cGMP promoting diuresis and contributing to aldosterone mechanism.
108
Aldosterone escape?
Escape from the sodium-retaining effects of excess aldosterone
109
B-type (brain) natriuretic peptide
Ventricular myocytes in response to increased tension. Similar to ANP with longer-half life. Diagnosing HF (very good negative predictive value)
110
Recombinant BNP
Nesiritide
111
What has greater pressure pulmonary Artery or LA
pulm. artery (25/10) compared to LA (<12)
112
Heart autoregulation
CO2, adenosine, NO (local metabolites)
113
Brain autoregulation
CO2 (pH) (local metabolites)
114
Kidney autoregulation
Myogenic and tubuloglomerular feedback
115
Lungs autoregulation
Hypoxia causes vasoconstriction
116
Skeletal muscle autoregulation
Lactate, adenosine, K+, H+, CO2
117
Skin autoregulation
Sympathetic stimulation most important mechanism-temperature control
118
What sites have baroreceptors?
Aortic arch and carotid sinus
119
Aortic arch pathway
Vagus nerve to solitary nucleus of medulla (only responds to increases in BP)
120
Carotid sinus pathway
Glossopharyngeal nerve to solitary nucleus of medulla (responds to both decreases and increases in BP)
121
What is the specific pathway for baroreceptor function
Hypotension leads to dec. arterial BP which leads to decreased stretch; decreased afferent baroreceptor firing; increased efferent sympathetic and decreased parasympathetic firing; vasoconstriction; increases HR, contractility, BP
122
How does carotid massage work
Pressing increases stretch, so you decrease sympathetics and increase parasympathetics to slow down the heart
123
How does Cushing reaction work?
HTN, bradycardia, and hypopnea: elevated ICP constricts arterioles in brain leading to ischemia and reflex sympathetic increase in perfusion pressure leading to inc. stretch and reflex baroreceptor induced-bradycardia
124
Chemoreceptors are found where
peripheral and central
125
Peripheral chemoreceptors pathway
Carotid and aortic bodies stimulated by low PO2 (<60 mmHg), inc. PCO2, and dec. pH in blood.
126
Central chemoreceptors pathway
Stimulated by changes in pH and PCO2 of brain interstitial fluid, which influences arterial CO2. Does not respond directly to PO2.
127
Liver gets how much blood
largest share of systemic CO
128
Kidney gets how much blood
Highest blood flow per gram of tissue
129
Heart and oxygen consumption
O2 extraction is always around 80%, so increased oxygen demand met by increased coronary blood flow, not by extraction of O2.
130
What else besides hydrostatic and oncotic pressure determine capillary fluid exchange
Increased capillary permeability (increased filtration constant Kf (capillary permeability)) caused by toxins, infections, burns
131
What increases interstitial fluid colloid osmotic pressure
lymphatic blockage