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CAPS 301 T1 > Heart Facts > Flashcards

Heart Facts Flashcards

1
Q

Two types of valves in heart

A

Atrio-ventricular and semilunar

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2
Q

Location of Mitral valve

A

Between left atrium and left ventricle

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3
Q

Name the two semilunar valves

A

Aortic, Pulmonary

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4
Q

Location of Tricuspid valve

A

From right atrium to right ventricle

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5
Q

Which type of heart valve is attached by chordae tendinae to the papillary muscles?

A

Atrio-ventricular (Tricuspid - right, Mitral - left)

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6
Q

Location of semi-lunar valves

A

Leading out of heart (ventricles), to aorta and pulmonary artery

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7
Q

Name the two atrio-ventricular valves

A

Tricuspid (right), Mitral (left)

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8
Q

Pressure difference required to open tricuspid valve

A

Right atrium > right ventricle

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9
Q

Pressure difference required to open pulmonary valve

A

right ventricle > pulmonary artery

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10
Q

Pressure difference required to open aortic valve

A

left ventricle > aorta

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11
Q

Pressure difference required to open mitral valve

A

Left atrium > left ventricle

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12
Q

Valve that opens when:

right atrial pressure > right ventricular pressure

A

Tricuspid valve (atrio-ventricular)

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13
Q

Valve that opens when:

right ventricular pressure > pulmonary arterial pressure

A

Pulmonary valve (semilunar)

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14
Q

Valve that opens when:

left ventricular pressure > aortic pressure

A

Aortic valve (semilunar)

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15
Q

Valve that opens when:

left atrial pressure > left ventricular pressure

A

Mitral valve (atrio-ventricular)

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16
Q

Effect of noradrenaline on nodal cells

A

Incr. Phase 4 (slow depol.) slope -> Incr HR

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17
Q

Dominant ion in pacemaker cell AP repolarization

A

K+ out (slow)

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18
Q

Receptors on smooth muscle cells for adrenaline

A

ß2

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19
Q

Result of isovolumetric relaxation

A

Sharp decrease in ventricular pressure

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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

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21
Q

Effect of noradrenaline on vascular smooth muscle cells

A

Incr. intracellular [Ca++] -> Vasoconstriction

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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)

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23
Q

Frank-Starling Law

A

Increase muscle stretch -> Increase contraction strength (within reason)

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24
Q

Mechanism of hormones causing vasodilation

A
  • Activate G protein (GI)
  • Convert GTP -> cGMP
  • Phosphorylate (inhibit) MLCK
  • –> VASODILATION
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25
Q

Effect/mechanism of vasopressin on BP

A
  • Incr SVR
  • Incr. kidney water retention -> Incr blood volume
  • –> Incr BP
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26
Q

Effect of noradrenaline on ventricular muscle cells

A

Incr intracellular [Ca++] -> Incr Stroke Volume

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27
Q

What causes the sounds in the cardiac cycle?

A

Closing of valves:
S1 - atrio-ventricular
S2 - semilunar

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28
Q

Cause of heart attack

A

Plaque (cholesterol core, fibrous exterior) narrows artery
During exertion, coronary artery blood flow does not meed tissue oxygen demands
PAIN

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29
Q

Effect of adrenaline on nodal cells

A

Incr. Phase 4 (slow depol) slope -> Incr HR

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30
Q

Dominant ion in cardiac contractile cell AP downstroke

A

K+ out (fast)

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31
Q

Relation of Frank-Starling law to Cardiac Output

A

Muscle stretch = End-diastolic volume (pre-load)
Contraction = Stroke Volume
-> Incr. EDV, Incr SV (and CO)

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32
Q

When in the cardiac cycle does S1 occur?

A

Early ventricular systole

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33
Q

ECG pen deflection from repolarization, from + to - end of lead

A

Up (T wave)

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34
Q

Direction of depolarization across heart

A

Top to bottom

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35
Q

Mechanism to correct high blood pressure (nervous system)

A
  • Incr baroreceptor stretch
  • Incr AP firing
  • Incr stimulation of PSNS, incr inhibition of SNS
  • Decr HR, SV, SVR
  • Restore BP
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36
Q

Role of chordae tendinae & papillary muscles

A

hold atrio-ventricular valves closed during ventricular contraction

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37
Q

Primary regulatory method for coronary arteries

A

Metabolic regulation

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38
Q

Where are renin & angiotensin II released from?

A

kidney; stimulated by SNS

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39
Q

Location of pacemaker cells

A

Sinoatrial (SA) node: where superior vena cava meets right atrium
Atrioventricular (AV) node: where right atrium meets right ventricle

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40
Q

Cause of low coronary artery blood flow

A 
Coronary artery spasm (drugs/alcohol)
Artery narrowing (plaques)
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41
Q

Receptors on nodal cells for acetylcholine

A

muscarinic

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42
Q

Hormones causing vasodilation in vascular smooth muscle

A

Atrial Natriuretic Peptide (ANP) -> from heart

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43
Q

Result of isovolumetric contraction

A

Large increase in ventricular pressure

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44
Q

Cause of athletic bradycardia

A

Left ventricular hypertrophy increases SV

Vagal tone increases to lower HR, maintaining CO

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45
Q

ECG pen deflection from depolarization, from + to - end of lead

A

Down

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46
Q

Describe coronary blood flow

A

Always high, but lower during systole, particularly in the left ventricle

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47
Q

Dominant ion in cardiac contractile cell AP plateau

A

Ca++ in (slow) counteracts K+ out (fast)

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48
Q

Physiological response to heart attack

A

Diaphoresis & dyspneia - from exertion or anxiety

Tachycardia - to compensate for narrowed artery

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49
Q

Cause of T wave in ECG

A

Ventricular repolarization, from bottom to top (upward deflection)

50
Q

Path of AP across heart

A 
SA node
AV node
Bundle of His
Right & Left bundle branch
Purkinje fibers
51
Q

2 main locations of baroreceptors for blood pressure & connected sensory nerve

A 
Carotid sinus (Glossopharyngeal nerve)
Aortic arch (Vagus nerve)
52
Q

Receptors on vascular smooth muscle cells for noradrenaline

A

alpha 1

53
Q

When in the cardiac cycle does S2 occur?

A

Early ventricular diastole

54
Q

Result of low coronary artery blood flow

A

Chest pain (angina)

55
Q

Where is vasopressin released from?

A

Brain

56
Q

Result of cardiomyopathy

A

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
Q

Why is training-induced athletic bradycardia considered passive?

A

Has no noticeable effect at rest, other than low HR, because CO is the same

58
Q

General cause of heart murmurs

A

Turbulent blood flow in heart

59
Q

Treatments for heart attack (caused by blocked/narrowed coronary artery)

A

Angioplasty

Coronary Artery Bypass Graft (CABG)

60
Q

ECG pen deflection from repolarization, from - to + end of lead

A

down

61
Q

Mechanism to correct low blood pressure (nervous system)

A
  • Decr baroreceptor stretch
  • Decr AP firing
  • Decr stimulation of PSNS, decr inhibition of SNS
  • Incr HR, SV, SVR
  • Restore BP
62
Q

Dominant ion flux during cardiac contractile cell AP upstroke

A

Na+ influx (fast), then helped by Ca++ influx (slow)

63
Q

Which nervous system usually controls blood pressure?

A

PSNS; SNS is under chronic inhibition

64
Q

Describe general blood pressure control mechanism

A

PNS baroreceptors (afferents) -> signal to medulla -> SNS/PSNS adjust vasoconstriction/dilation

65
Q

Cause of QRS complex on ECG

A

Ventricular depolarization, spreading across ventricles in several directions (down-up-down pen deflection profile)

66
Q

Effect of adrenaline on ventricular muscle cells

A

Incr. intracellular [Ca++] -> Incr Stroke Volume

67
Q

Primary regulatory method for cerebral arteries

A

Metabolic regulation (don’t want sympathetic nervous response to shut down brain function)

68
Q

Result of training-induced athletic bradycardia (4)

A

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
Q

Extrinsic control pathway for SV and CO

A

SNS: NA/Adrenaline secreted

  • Bind ß1 receptors
  • Incr Ca++ levels
  • Incr SV
  • Incr CO
70
Q

Physiological mechanism of splitting S2 during inspiration

A

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
Q

Formula to calculate CO

A

CO = HR x SV ([CO] = mL/min)

72
Q

Effect/mechanism of renin & angiotensin II on BP

A

Renin promotes conversion of zymogen to angiotensin II

  • Incr SVR
  • Stimulate aldosterone release -> Incr kidney Na+ retention -> Incr blood volume
  • –> Incr BP
73
Q

Hormones used to control blood pressure

A

Vasopressin (incr. BP)

Renin, Angiotensin II (incr BP via aldosterone)

74
Q

Dominant ion in pacemaker cell AP depolarization

A

Ca++ in (slow)

75
Q

Treatment for heart failure

A

Heart transplant

76
Q

Formula for BP

A

BP = CO x SVR = HR x SV x SVR

Blood pressure, Cardiac Output, Systemic Vascular Resistance, Heart Rate, Stroke Volume

77
Q

Role of Ca++ in cardiac contractile cell AP

A

Increase rate of depolarization, prolong AP (w/plateau), promote muscular contraction

78
Q

ECG profile of paroxysmal atrial fibrillation

A

Rhythm: irregular, no pattern
P waves: not present
Rate: variable, 80-120 bpm (tachycardia)

79
Q

How is CO regulated?

A

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
Q

ECG pen deflection from depolarization, from - to + end of lead

A

Up (P wave)

81
Q

Receptors on nodal cells for noradrenaline

A

ß1

82
Q

Effect of adrenaline on vascular smooth muscle cells

A

Decr intracellular [Ca++] -> Vasodilation

83
Q

Tunica primarily responsible for constriction/dilation of arteries & arterioles

A

Tunica media (middle, smooth muscle & elastic tissue)

84
Q

3 causes of heart murmur

A
  1. Aortic stenosis (narrowed artery, normal flow)
  2. Mitral regurgitation (backflow to LA)
  3. Ventricular septal defect (flow between ventricles)
85
Q

Typical ECG paper speed in mm/s and squares/min

A

25 mm/s, 300 squares/min

86
Q

Intrinsic rate of SA node

A

60-100 bpm

87
Q

RMP In cardiac contractile cells

A

-90 mV

88
Q

Starling force difference required for filtration

A

CHP > COP (arterial end of capillary bed)

89
Q

Position/polarity of leads in Einthoven’s triangle (for ECG)

A

I: RA (-) -> LA (+)
II: RA (-) -> LL (+)
III: LA (-) -> LL (+)
A = arm, L = leg

90
Q

Result of paroxysmal atrial fibrillation

A

High HR -> decreased CO (not enough blood flows into heart during diastole) -> hypotension
Atrial blood stagnation -> coagulation -> embolisms (clots) -> break off & block artery

91
Q

Three control mechanisms of Vascular Smooth Muscle

A

Hormones
Sympathetic Nervous System
Metabolic Regulation (tissue metabolites)

92
Q

Dominant ion in pacemaker cell slow depolarization

A

Na+, not through usual channels

93
Q

Effect of parasympathetic nervous system on vascular smooth muscle

A

Little direct effect

94
Q

Receptors on nodal cells for adrenaline

A

ß1

95
Q

What does “resistance vessels” refer to?

A

Arterioles

96
Q

Mechanism to correct high blood pressure (hormonal)

A

Brain increases inhibition of SNS and vasopressin release, restoring BP

97
Q

Cause of P wave on ECG

A

Atrial depolarization, moving down across heart

98
Q

Intrinsic pathway for SV/CO control

A

SNS & epinephrine incr venous return to heart, incr end-diastolic volume, incr SV, incr CO

99
Q

Effect of Acetylcholine on nodal cells

A

Decr Phase 4 (slow depol) slope -> Decr HR

100
Q

Mechanism of Ventricular septal defect causing heart murmur

A

Blood flow: LV -> RV
Unnecessarily through lungs instead of to body
Incr. HR, LV hypertrophy result
Similar to constant exercise -> sweat, fatigue

101
Q

How is heart rate modulated?

A

By changing slope of slow depolarization:
SNS (Noradrenaline, Adrenaline): ß1 receptors -> incr. slope -> incr. HR
PSNS (ACh): Muscarinic receptors -> decr. slope -> decr. HR

102
Q

Cause of paroxysmal atrial fibrillation

A

Severe intoxication

103
Q

Mechanism for SNS control of vascular smooth muscle with adrenaline

A
  • 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
Q

Vasoconstricting hormones for vascular smooth muscle

A 
Angiotensin II (AII) -> from kidney
Vasopressin (AVP) -> from brain
105
Q

Describe shape of contractile cardiac cell action potential

A 
Stable RMP
Sharp upstroke
Plateau
Sharp downstroke
Return to RMP (no hyperpolarization)
106
Q

State of arteriole smooth muscle at rest

A

Not fully constricted or dilated; can be opened or closed further by hormones & nervous system

107
Q

Starling force difference required to cause reabsorption

A

COP > CHP (venous end of capillary bed)

108
Q

Effect of Acetylcholine on ventricular muscle cells

A

No direct action

109
Q

Receptors on ventricular muscle cells for noradrenaline

A

ß1

110
Q

When does the Na+ absolute refractory period occur in cardiac contractile cells?

A

During the rest of the AP (plateau & repolarization) - prevents tetanus

111
Q

Mechanism to correct low blood pressure

A

Brain decreases inhibition of SNS & vasopressin release, restoring BP

112
Q

Why are arterioles called “resistance vessels”?

A

Primary role in blood pressure modulation, based on resistance to blood flow

113
Q

Treatment for Ventricular Septal Defect

A

Surgery or transplant

114
Q

Which 2 factors contribute to SVR?

A

(Systemic Vascular Resistance)
Blood volume in arterioles
Contraction/dilation of arterioles

115
Q

Effect of Acetylcholine on vascular smooth muscle cells

A

Limited direct action

116
Q

Direction of repolarization across heart

A

Bottom to top

117
Q

Mechanism for vasoconstricting hormones on vascular smooth muscle

A

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
Q

Describe pacemaker cell AP

A

No stable RMP, instead slow depolarization
Self-induced AP once threshold reached
Sharper depolarization rate
Smooth transition to repolarization

119
Q

Mechanism for SNS control of vascular smooth muscle with noradrenaline

A
  • 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
Q

Normal relation between filtration & reabsorption rates in capillaries

A

Filtration rate = Reabsorption rate (no fluid build-up/loss, overall)

121
Q

Intrinsic rate of AV node

A

40-50 bpm (forced to beat faster by SA node)

122
Q

Receptors on ventricular muscle cells for adrenaline

A

ß1

CAPS 301 T1 (10 decks)

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