Heart Facts Flashcards
1
Q
Two types of valves in heart
A
Atrio-ventricular and semilunar
2
Q
Location of Mitral valve
A
Between left atrium and left ventricle
3
Q
Name the two semilunar valves
A
Aortic, Pulmonary
4
Q
Location of Tricuspid valve
A
From right atrium to right ventricle
5
Q
Which type of heart valve is attached by chordae tendinae to the papillary muscles?
A
Atrio-ventricular (Tricuspid - right, Mitral - left)
6
Q
Location of semi-lunar valves
A
Leading out of heart (ventricles), to aorta and pulmonary artery
7
Q
Name the two atrio-ventricular valves
A
Tricuspid (right), Mitral (left)
8
Q
Pressure difference required to open tricuspid valve
A
Right atrium > right ventricle
9
Q
Pressure difference required to open pulmonary valve
A
right ventricle > pulmonary artery
10
Q
Pressure difference required to open aortic valve
A
left ventricle > aorta
11
Q
Pressure difference required to open mitral valve
A
Left atrium > left ventricle
12
Q
Valve that opens when:
right atrial pressure > right ventricular pressure
A
Tricuspid valve (atrio-ventricular)
13
Q
Valve that opens when:
right ventricular pressure > pulmonary arterial pressure
A
Pulmonary valve (semilunar)
14
Q
Valve that opens when:
left ventricular pressure > aortic pressure
A
Aortic valve (semilunar)
15
Q
Valve that opens when:
left atrial pressure > left ventricular pressure
A
Mitral valve (atrio-ventricular)
16
Q
Effect of noradrenaline on nodal cells
A
Incr. Phase 4 (slow depol.) slope -> Incr HR
17
Q
Dominant ion in pacemaker cell AP repolarization
A
K+ out (slow)
18
Q
Receptors on smooth muscle cells for adrenaline
A
ß2
19
Q
Result of isovolumetric relaxation
A
Sharp decrease in ventricular pressure
20
Q
Signal path of low coronary artery blood flow
A
Low O2 (ischemia)
Afferent nerve ending signal to brain
“Pain” signal, localized in chest
21
Q
Effect of noradrenaline on vascular smooth muscle cells
A
Incr. intracellular [Ca++] -> Vasoconstriction
22
Q
Mechanism of blood flow from atrium to ventricle
A
First: passive flow based on pressure difference
Second: atrial contraction (‘bump’ in atrial & ventricular pressure, increase in ventricular blood volume)
23
Q
Frank-Starling Law
A
Increase muscle stretch -> Increase contraction strength (within reason)
24
Q
Mechanism of hormones causing vasodilation
A
- Activate G protein (GI)
- Convert GTP -> cGMP
- Phosphorylate (inhibit) MLCK
- –> VASODILATION
25
Effect/mechanism of vasopressin on BP
- Incr SVR
- Incr. kidney water retention -> Incr blood volume
- --> Incr BP
26
Effect of noradrenaline on ventricular muscle cells
Incr intracellular [Ca++] -> Incr Stroke Volume
27
What causes the sounds in the cardiac cycle?
Closing of valves:
S1 - atrio-ventricular
S2 - semilunar
28
Cause of heart attack
Plaque (cholesterol core, fibrous exterior) narrows artery
During exertion, coronary artery blood flow does not meed tissue oxygen demands
PAIN
29
Effect of adrenaline on nodal cells
Incr. Phase 4 (slow depol) slope -> Incr HR
30
Dominant ion in cardiac contractile cell AP downstroke
K+ out (fast)
31
Relation of Frank-Starling law to Cardiac Output
Muscle stretch = End-diastolic volume (pre-load)
Contraction = Stroke Volume
-> Incr. EDV, Incr SV (and CO)
32
When in the cardiac cycle does S1 occur?
Early ventricular systole
33
ECG pen deflection from repolarization, from + to - end of lead
Up (T wave)
34
Direction of depolarization across heart
Top to bottom
35
Mechanism to correct high blood pressure (nervous system)
- Incr baroreceptor stretch
- Incr AP firing
- Incr stimulation of PSNS, incr inhibition of SNS
- Decr HR, SV, SVR
- Restore BP
36
Role of chordae tendinae & papillary muscles
hold atrio-ventricular valves closed during ventricular contraction
37
Primary regulatory method for coronary arteries
Metabolic regulation
38
Where are renin & angiotensin II released from?
kidney; stimulated by SNS
39
Location of pacemaker cells
Sinoatrial (SA) node: where superior vena cava meets right atrium
Atrioventricular (AV) node: where right atrium meets right ventricle
40
Cause of low coronary artery blood flow
```
Coronary artery spasm (drugs/alcohol)
Artery narrowing (plaques)
```
41
Receptors on nodal cells for acetylcholine
muscarinic
42
Hormones causing vasodilation in vascular smooth muscle
Atrial Natriuretic Peptide (ANP) -> from heart
43
Result of isovolumetric contraction
Large increase in ventricular pressure
44
Cause of athletic bradycardia
Left ventricular hypertrophy increases SV
| Vagal tone increases to lower HR, maintaining CO
45
ECG pen deflection from depolarization, from + to - end of lead
Down
46
Describe coronary blood flow
Always high, but lower during systole, particularly in the left ventricle
47
Dominant ion in cardiac contractile cell AP plateau
Ca++ in (slow) counteracts K+ out (fast)
48
Physiological response to heart attack
Diaphoresis & dyspneia - from exertion or anxiety
| Tachycardia - to compensate for narrowed artery
49
Cause of T wave in ECG
Ventricular repolarization, from bottom to top (upward deflection)
50
Path of AP across heart
```
SA node
AV node
Bundle of His
Right & Left bundle branch
Purkinje fibers
```
51
2 main locations of baroreceptors for blood pressure & connected sensory nerve
```
Carotid sinus (Glossopharyngeal nerve)
Aortic arch (Vagus nerve)
```
52
Receptors on vascular smooth muscle cells for noradrenaline
alpha 1
53
When in the cardiac cycle does S2 occur?
Early ventricular diastole
54
Result of low coronary artery blood flow
Chest pain (angina)
55
Where is vasopressin released from?
Brain
56
Result of cardiomyopathy
Insufficient CO
High diastolic pressure in LA, LV
High pressure in pulmonary vein (no valve to LA)
High pulmonary CHP at venous end (CHP > COP)
Filtration at venous end
Fluid moves into lungs (pulmonary edema)
Fluid leaks into alveoli & is coughed up
57
Why is training-induced athletic bradycardia considered passive?
Has no noticeable effect at rest, other than low HR, because CO is the same
58
General cause of heart murmurs
Turbulent blood flow in heart
59
Treatments for heart attack (caused by blocked/narrowed coronary artery)
Angioplasty
| Coronary Artery Bypass Graft (CABG)
60
ECG pen deflection from repolarization, from - to + end of lead
down
61
Mechanism to correct low blood pressure (nervous system)
- Decr baroreceptor stretch
- Decr AP firing
- Decr stimulation of PSNS, decr inhibition of SNS
- Incr HR, SV, SVR
- Restore BP
62
Dominant ion flux during cardiac contractile cell AP upstroke
Na+ influx (fast), then helped by Ca++ influx (slow)
63
Which nervous system usually controls blood pressure?
PSNS; SNS is under chronic inhibition
64
Describe general blood pressure control mechanism
PNS baroreceptors (afferents) -> signal to medulla -> SNS/PSNS adjust vasoconstriction/dilation
65
Cause of QRS complex on ECG
Ventricular depolarization, spreading across ventricles in several directions (down-up-down pen deflection profile)
66
Effect of adrenaline on ventricular muscle cells
Incr. intracellular [Ca++] -> Incr Stroke Volume
67
Primary regulatory method for cerebral arteries
Metabolic regulation (don't want sympathetic nervous response to shut down brain function)
68
Result of training-induced athletic bradycardia (4)
Can incr. CO higher than normal by incr. HR during exercise
Usually higher BV b/c of hydration
Save or lower BP
Better CO distribution to active muscles
69
Extrinsic control pathway for SV and CO
SNS: NA/Adrenaline secreted
- Bind ß1 receptors
- Incr Ca++ levels
- Incr SV
- Incr CO
70
Physiological mechanism of splitting S2 during inspiration
WANT MORE BLOOD IN LUNGS:
Increase venous return to right atrium & lungs
More blood needs to get out of right ventricle during systole
Delayed pulmonary valve closure
---------------
Reduced venous return to left atrium
Less blood to eject from left ventricle during systole
Early closing of aortic valve
71
Formula to calculate CO
CO = HR x SV ([CO] = mL/min)
72
Effect/mechanism of renin & angiotensin II on BP
Renin promotes conversion of zymogen to angiotensin II
- Incr SVR
- Stimulate aldosterone release -> Incr kidney Na+ retention -> Incr blood volume
- --> Incr BP
73
Hormones used to control blood pressure
Vasopressin (incr. BP)
| Renin, Angiotensin II (incr BP via aldosterone)
74
Dominant ion in pacemaker cell AP depolarization
Ca++ in (slow)
75
Treatment for heart failure
Heart transplant
76
Formula for BP
BP = CO x SVR = HR x SV x SVR
| Blood pressure, Cardiac Output, Systemic Vascular Resistance, Heart Rate, Stroke Volume
77
Role of Ca++ in cardiac contractile cell AP
Increase rate of depolarization, prolong AP (w/plateau), promote muscular contraction
78
ECG profile of paroxysmal atrial fibrillation
Rhythm: irregular, no pattern
P waves: not present
Rate: variable, 80-120 bpm (tachycardia)
79
How is CO regulated?
By HR:
- down with PSNS
- up with SNS
By SV:
- up with SNS: extrinsic (NA/Adrenaline binds ß1 receptors, incr Ca++, incr SV)
- up with SNS & epinephrine: intrinsic (incr venous return, incr end-diastolic volume, incr SV)
80
ECG pen deflection from depolarization, from - to + end of lead
Up (P wave)
81
Receptors on nodal cells for noradrenaline
ß1
82
Effect of adrenaline on vascular smooth muscle cells
Decr intracellular [Ca++] -> Vasodilation
83
Tunica primarily responsible for constriction/dilation of arteries & arterioles
Tunica media (middle, smooth muscle & elastic tissue)
84
3 causes of heart murmur
1. Aortic stenosis (narrowed artery, normal flow)
2. Mitral regurgitation (backflow to LA)
3. Ventricular septal defect (flow between ventricles)
85
Typical ECG paper speed in mm/s and squares/min
25 mm/s, 300 squares/min
86
Intrinsic rate of SA node
60-100 bpm
87
RMP In cardiac contractile cells
-90 mV
88
Starling force difference required for filtration
CHP > COP (arterial end of capillary bed)
89
Position/polarity of leads in Einthoven's triangle (for ECG)
I: RA (-) -> LA (+)
II: RA (-) -> LL (+)
III: LA (-) -> LL (+)
A = arm, L = leg
90
Result of paroxysmal atrial fibrillation
High HR -> decreased CO (not enough blood flows into heart during diastole) -> hypotension
Atrial blood stagnation -> coagulation -> embolisms (clots) -> break off & block artery
91
Three control mechanisms of Vascular Smooth Muscle
Hormones
Sympathetic Nervous System
Metabolic Regulation (tissue metabolites)
92
Dominant ion in pacemaker cell slow depolarization
Na+, not through usual channels
93
Effect of parasympathetic nervous system on vascular smooth muscle
Little direct effect
94
Receptors on nodal cells for adrenaline
ß1
95
What does "resistance vessels" refer to?
Arterioles
96
Mechanism to correct high blood pressure (hormonal)
Brain increases inhibition of SNS and vasopressin release, restoring BP
97
Cause of P wave on ECG
Atrial depolarization, moving down across heart
98
Intrinsic pathway for SV/CO control
SNS & epinephrine incr venous return to heart, incr end-diastolic volume, incr SV, incr CO
99
Effect of Acetylcholine on nodal cells
Decr Phase 4 (slow depol) slope -> Decr HR
100
Mechanism of Ventricular septal defect causing heart murmur
Blood flow: LV -> RV
Unnecessarily through lungs instead of to body
Incr. HR, LV hypertrophy result
Similar to constant exercise -> sweat, fatigue
101
How is heart rate modulated?
By changing slope of slow depolarization:
SNS (Noradrenaline, Adrenaline): ß1 receptors -> incr. slope -> incr. HR
PSNS (ACh): Muscarinic receptors -> decr. slope -> decr. HR
102
Cause of paroxysmal atrial fibrillation
Severe intoxication
103
Mechanism for SNS control of vascular smooth muscle with adrenaline
- Adrenaline binds ß2 adrenergic receptor
- Activate G protein (Gs)
- Stimulate AC (adenylyl cyclase)
- Convert ATP -> cAMP
- Phosphorylate MLCK, inhibiting function
- Decrease myosin phosphorylation
- ---> VASODILATION
104
Vasoconstricting hormones for vascular smooth muscle
```
Angiotensin II (AII) -> from kidney
Vasopressin (AVP) -> from brain
```
105
Describe shape of contractile cardiac cell action potential
```
Stable RMP
Sharp upstroke
Plateau
Sharp downstroke
Return to RMP (no hyperpolarization)
```
106
State of arteriole smooth muscle at rest
Not fully constricted or dilated; can be opened or closed further by hormones & nervous system
107
Starling force difference required to cause reabsorption
COP > CHP (venous end of capillary bed)
108
Effect of Acetylcholine on ventricular muscle cells
No direct action
109
Receptors on ventricular muscle cells for noradrenaline
ß1
110
When does the Na+ absolute refractory period occur in cardiac contractile cells?
During the rest of the AP (plateau & repolarization) - prevents tetanus
111
Mechanism to correct low blood pressure
Brain decreases inhibition of SNS & vasopressin release, restoring BP
112
Why are arterioles called "resistance vessels"?
Primary role in blood pressure modulation, based on resistance to blood flow
113
Treatment for Ventricular Septal Defect
Surgery or transplant
114
Which 2 factors contribute to SVR?
(Systemic Vascular Resistance)
Blood volume in arterioles
Contraction/dilation of arterioles
115
Effect of Acetylcholine on vascular smooth muscle cells
Limited direct action
116
Direction of repolarization across heart
Bottom to top
117
Mechanism for vasoconstricting hormones on vascular smooth muscle
Same as NA, but different receptor:
- Binds receptor
- Activate G protein (Gq)
- Stimulate PL-C (Phospholipase-C)
- Stimulate IP3 (Inositol triphosphate) synthesis
- Bind IP3 receptor on SR
- Ca++ release
- Bind calmodulin... (contraction as for other smooth muscle)
- ---> VASOCONSTRICTION
118
Describe pacemaker cell AP
No stable RMP, instead slow depolarization
Self-induced AP once threshold reached
Sharper depolarization rate
Smooth transition to repolarization
119
Mechanism for SNS control of vascular smooth muscle with noradrenaline
- NA binds alpha adrenergic receptor
- Activate G protein (Gq)
- Stimulate PL-C (Phospholipase-C)
- Stimulate IP3 (Inositol triphosphate) synthesis
- Bind IP3 receptor on SR
- Ca++ release
- Bind calmodulin... (contraction as for other smooth muscle)
- ---> VASOCONSTRICTION
120
Normal relation between filtration & reabsorption rates in capillaries
Filtration rate = Reabsorption rate (no fluid build-up/loss, overall)
121
Intrinsic rate of AV node
40-50 bpm (forced to beat faster by SA node)
122
Receptors on ventricular muscle cells for adrenaline
ß1
