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FACEM Primary Physiology > Heart and Circulation > Flashcards

Heart and Circulation Flashcards

1
Q

Describe the phases of the cardiac AP in muscle cells

A

0 - upshoot;rapid Na influx
1 - early repolarisation; cesation of Na influx
2 - plateau - Ca influx
3 - repolarisation - K+ efflux
4 - back to RMP, Balance of ongoing K+ efflux vs Na influx - close to Em for K of -90mV

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2
Q

The rate of rise of the AP in SA and AV node is slower than in myocytes because….

A

It is due to Ca current only

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3
Q

Speed of conduction in SA and AV nodes

A

0.05m/s

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4
Q

Normal axis is between

A

+110 and -30

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5
Q

The chest ECG leads are located…

A 
V1 R 4th ICS, sternal boarder
V2 L 4th ICS, sternal boarder
V3 L 4th ICS, mid clav line
V4 apex - 5th ICS
V5 5th rib lateral
V6 ?ant ax line
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6
Q

How does vagal stimulation slow the heart rate

A

Opens K+ channels (M2, Ach, G protein, cAMP) - antagonises the funny current - slows rate of rise of pacemaker potential

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7
Q

How does sympathetic stimulation increase the heart rate

A

NA - B1 receptors, - cAMP - opening of L type calcium channels increases the rate of rise of the pacemaker potential

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8
Q

PR interval duration

A

0.12 - 0.2

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9
Q

Does the PR interval change with heart rate?

A

yes - at rest 0.18 - at 130/min - 0.14

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10
Q

QRS duration

A

< 0.1s

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11
Q

QT interval

A

<0.43s

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12
Q

Long PR interval is called

A

first degree heart block

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13
Q

LAFB ecg findings?

A

Left axis deviation, widened qrs

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14
Q

LPFB ecg findings?

A

Right axis deviation, widened qrs

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15
Q

dropped QRS complexes, PR interval constant

A

Second Degree Heart Block Type 2. Dangerous - block almost always occuring in the distal his-perkionje system and may progress to 3rd degree block - if it does, it is likely no escape rhythm will generate

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16
Q

dropped QRS complexes, PR lengthens until dropped beat

A

Second Degree Heart Block Type 1 (WenckeBack), usually medically benign - unlikely to progress to complete HB. Almost always a disease of the AV node

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17
Q

Bundle of Kent

A

An extra abnormal bundle of conducting fibres between the atria and ventricles

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18
Q

HR in atrial tachycardia

A

up to 220/min

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19
Q

HR in Atrial Flutter

A

200-350/min - due to large counter-clockwise movement in the R atrium - produces the saw tooth pattern on ECG

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20
Q

What is the max conduction rate of the AV node?

A

230/min

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21
Q

Atrial rate in AF?

A

300-500 beats/min. The AV node discharges at irregular intervals producing a ventricular rate usually 80-160/min

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22
Q

why do fast heart rates cause 1) heart failure and 2) angina

A

1) HF due to insufficient time for ventricular filling - cardiac output decreases
2) The coronary arteries are perfused only during diastole - with fast rates, diastole is shortened more than systole.

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23
Q

Vagal stimulation has what effects on the AV node?

A

Increases the degree of AV block - lowers the ventricular rate in tachyarrythmias

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24
Q

Why is the t wave a dangerous time to give a shock

A

Some of the ventricular muscle is depolarised, some repolarised, some is incompletely repolarised - perfect conditions for setting up a circus movement - VF

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25
Q

peak pressure in L andSV R ventricles

A

120mmHg and 25mmHg

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26
Q

SV at rest is _____

EDV at rest is ______

A

SV 70-90mL, EDV is about 130ml

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27
Q

a wave

A

due to atrial systole - some backflow of blood from atria into VC

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28
Q

c wave

A

due to bulging of the tricuspid valve during ventricular systole

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29
Q

v wave

A

mirrors atrial filling pressure

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30
Q

phase 1 of cardiac cycle

A

atrial systole, 0.1s, p wave

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31
Q

Phase 2 of cardiac cycle

A

isovolumetric ventricular contraction, 0.05s, RS segment on ecg

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32
Q

Phase 3 of cardiac cycle

A

Ventricular ejection, 0.3s, until end of t wave on ecq

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33
Q

Phase 4 of cardiac cycle

A

Isovolumetric ventricular relaxation,

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34
Q

Phase 5 of cardiac cycle

A

Ventricular filling

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35
Q

When the heart rate increases which shortens more out of systole and diastole

A

Systole; 0.27 -> 0.16
Diastole; 0.62 -> 0.14

at HR 65:200

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36
Q

why is cardiac muslce unable to undergo tetany

A

Becuase of the prolonged Action Potential. It cannot respond to a second stimulus until near the end of the initial contraction.

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37
Q

1st heart sound

A

closure of the AV valves

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38
Q

2nd heart sound

A

closure of the semilunar valves

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39
Q

C.O. at rest

A

about 70 mL x 72 beats/min = 5.0L/min

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40
Q

anxiety and excitement on CO

A

50-100% increase

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41
Q

Eating on CO

A

30% increase

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42
Q

Exercise on CO

A

up to 700%

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43
Q

Pregnancy

A

increase

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44
Q

hot temperature

A

increase

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45
Q

Sitting or standing from lying

A

DECREASE by about 20-30%

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46
Q

catecholamines exert they action on the heart through….

A

Beta1 receptors, Gs, cAMP

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47
Q

How do xanthenes such as cafiene and theophylline exert their effects on the heart

A

They inhibit the breakdown of cAMP

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48
Q

How does digitalis affect the heart

A

Inhibits NaKATPase in the myocardium which in turn causes a decrease in calcium removal from the cytosol by Na/Ca exchange

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49
Q

Depressants of myocardial contractility

A 
Hypercapnia
hypoxia
acidosis
quinidine
procainamide
barbiturates
Heart Failure
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50
Q

oxygen consumption by myocardial tissue (not beating)

A

2ml/100g/min

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51
Q

O2 consumption by beating heart at rest

A

9ml/100g/min

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52
Q

Compare arterial pressure and stroke work for the right and left side of the heart

A

7x higher pressure in the aorta than pulmonary artery = 7x stroke work

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53
Q

Does an increase in afterload or preload cause a greater increase in oxygen consumption

A

Afterload - pressure work requires more oxygen than volume work for unknown reasons. This is why angina is more common in aortic stenosis than regurg

54
Q

Endothelial Vasoconstrictors

A

Endothelin-1
Local platelet serotonin
Thromboxane A2

55
Q

Endothelial Vasodilators

A

Nitric Oxide
Kinins
Prostacyclin

56
Q

Circulating neurohormonal vasoconstrictors

A 
Epinephrine (except in skeletal muscle and liver)
Norepinephrine
Arginine vasopressin
Angiotensin II
Endogenous-digitalis-like substance
Neuropeptide Y
57
Q

Circulating neurohormonal vasodilators

A 
Epinephrine in skeletal muscle and liver
Calcitonin G related protein
Substance P
Histamine
ANP
Vasoactive Intestinal peptide
58
Q

Stimulation of atrial stretch receptors

A

Hypotension, tachycardia

59
Q

Raised ICP causes

A

Hypertension and bradycardia

60
Q

Baroreceptors are found…

A

aortic arch, carotid sinus,right and left atria, superior and inferior vena caval entrances, pulmonary veins and circullation. They are located in the ADVENTITIA of the vessels.

61
Q

The vasomotor area is located…

A

Rostral Ventrolateral Medulla (RVLM)

62
Q

The carotid sinus is connected to the RVLM by the…..

A

carotis sinus n which is a branch of the glossophrangeal n.

63
Q

The aortic arch baroreceptors are connecte to the RVLM by the….

A

aortic depressor n, a branch of the vagus n

64
Q

BEFORE affecting the RVLM the fibres from the aortic depressor n and the carotid sinus n

A

terminate in the Nucleus of the tractus solitarius

65
Q

excitatory projections from the NTS also extend to….

A

Nucleus ambiguus and dorsal motor nucleus - activate vagal outflow in response to baroreceptor activation

66
Q

NTS action on the RVLM is _____

A

inhibitory - inhibits sympathetic outflow

67
Q

Direct stimulation of the RVLM is by

A

CO2 and hypoxia

68
Q

Excitatory inputs to the RVLM….

A 
Cortex via hypothalamus
mesencephalic periaqueductal gray
Brain stem reticular formation
pain pathways
somatic afferents
carotid and aortic chemoreceptors
69
Q

Inhibitors inputs to the RVLM…..

A 
Cortex via hypothalamus
Caudal ventrolateral medulla
Caudal medullary raphe nuclei
Lung inflation afferents
Carotid, aortic and cardiopulmonary baroreceptors.
70
Q

why does raised ICP cause bradycardia and hypertension

A

Raised ICP threatens the blood supply to the RVLM - the neurons respond by increasing the BP to preserve their blood supply. The raise in BP causes decreased carotid baroceptor firing which acts to decrease the heart rate.

71
Q

Hypercapnia does what to the peripheral circulation

A

Locally acts as a vasodilator. It actually stimulates the RVLM to vasoconstrict but its peripheral local action is stronger.

72
Q

myogenic theory of autoregulation

A

stretch due to increased BP causes smooth muscle in the vessel wall to contract, reducing the radius to offset the effect of increased pressure…. in order to maintain flow

73
Q

metabolic theory of autoregulation

A

vasodilatory substances accumulate in active tissues, Accumulation is increased in states on low flow… these metabolites then act locally to dilate vessels, increase flow, and instigate their own removal.

74
Q

how do injured vessels cause constriction?

A

Local liberation of serotonin from platelets.

75
Q

Thromboxine A2 vs Prostacyclin

A

Thromboxine A2

  • produced by platelets
  • causes platelet aggregation and vasoconstriction

Prostacyclin

  • produced by endothelial cells
  • causes vasodilation and prevents platelet aggregation
76
Q

How does Aspirin alter the thromboxine A2 / Prostacyclin balance

A

Aspirin produces irreversible inhibition of cyclooxygenase - reduces production of BOTH… but endothelial cells produce new cyclooxygenase in a few hours, platelets can not. half-life of a platelet is about 4 days

77
Q

NO causes ______ by activation of ______

A

Vascular SM dilation through activation of guanylyl cyclase and elevated cyclic GMP

78
Q

NO release is stimulated by

A 
ACh
Bradykinin
Histamine on H1 receptors
VIP
Substance P

It is produced in the endothelium and diffuses into vascular SM cells

79
Q

Endothelin 1

A

Most potent vascoconstrictor
Produced by upregulation of gene transcription
Is released locally and into blood
Not stored in secretory granules

80
Q

Stimulators of endothelin 1 transcription

A 
Angiotensin II
Catecholamines
Growth Factors
Hypoxia
Insulin
Oxidised LDL
HDL
Shear Stresss
Thrombin
81
Q

Inhibitors of endothelin 1 transcription

A

NO
ANP
PGE2
Prostacyclin

82
Q

Cerebral circulation flow and o2 consumption

A

750ml/min and 3.3ml/100g/min

83
Q

Volume and rate of turnover of the CSF

A

150ml, produced at 550ml/day so turned over about 3.7x/day

84
Q

Route of flow of the CSF

A

Choroid plexus -> ventricles -> through foramens of magendie and Luschka -> subarachnoid space -> arachnoid villli -> veins/sinuses

85
Q

Lumbar CSF pressure is

A

70-180mmHg

86
Q

What substances are passive rapidly transported across BBB

A

CO2, H20, O2

87
Q

What substances are transcellular regulated across BBB

A

H+, HCO3-

88
Q

What substances are actively atransported across BBB

A

Glucose, AAs, Choline

89
Q

The four regions of the brain OUTSIDE the BBB are:

A

1) Posterior Pituitary
2) Area Posterna
3) Organm vasculosum of lamina termialis (OVLT)
4) Subfornical organ (SFO)

90
Q

Area Posterna does….

A

chemoreceptor trigger zone -> vomitting in respose to chemical changes in plasma

91
Q

OVLT does….

A

Angiotensin II action to increase thirst.
Osoreceptor for vasopressin secretion.
Interleukin -1 acts here to produce fever.

92
Q

SFO does…

A

Angiotensin II also acts here to cause thirst

93
Q

Brain energy metabolism; % of O2 consumption is ____, RQ is_______. % reliant on glucose for enery is _____

A

20% of body O2 consumption
90% reliant on glucose for energy
brain RQ is 0.95 - 0.99

94
Q

Coronary circulation flow is ____

A

250ml/min, 5% of C.O.

95
Q

Branches of RCA

A

Marginal branch

Posterior descending branch

96
Q

Branches of LCA

A

Anterior Descending
Circumflex
Marginal branch

97
Q

3 types of anastomotic vessels in the coronary circulation

A

Arteriosinusoidal cessels
Thesbian vessels
arterioluminal vessels

98
Q

Cutaneous circulation flow

A

1-150ml/100g/min

99
Q

Describe tripple response

A

1) red reaction - capillary dilation
2) wheal - capillary permeability
3) Flare - spreading redness due to arteriolar dilation

100
Q

How does blood flow relate to pressure and resistance

A

Flow = Pressure / Resistance

101
Q

How does velocity relate to flow and area

A

Velocity = Flow / Area

102
Q

Compare CSA of capillaries to aorta

A

capillaries have 1000x CSA than aorta

103
Q

How is Flow and Resistance related to radius of a vessel

A

Flow is directly proportion to r^4

Resistance is inversely proportional to r^4

104
Q

How is Flow and Resistance related to Length of vessel

A

Flow is inversely proportional to L

Resistance is directly proportional to L

105
Q

Explain the Law of Laplace

A

Relates wall tension to radius of a vessel of sphere and pressure. E.g. dilated heart has to produce much more tension to cause the same increase in pressure. E.g. small vessels like capillaries have much lower wall tension than large diameter arteries

106
Q

HbA is made up of…

A

2 alpha and 2 beta subunits

107
Q

HbA2 is made up of

A

2 alpha and 2 delta subunits

108
Q

HbF is made up of

A

2 alpha and 2y subunits

109
Q

What is required for the platelet plug to for a definite clot

A

Fibrin.

110
Q

Activation of Fibrin

A

Fibrinogen is activated to Fibrin by Thrombin

111
Q

Extrinisc Pathway

A

7 -> 7a
activates X
X catalyses prothrombin to thrombin

112
Q

Intrinsic Pathway

A

12 -> 11 -> 9
activates X
X catalyses prothrombin to thrombin

113
Q

Antithrombin III and heparin complex to inhibit which factors

A

9,10,11,12

114
Q

Protein C and Protein S inhibit which factors

A

5,8

115
Q

Warfarin depletes which factors

A

2,7,9,10, Protein C and Protein S

116
Q

Which part of the cascade prevents clot formation

A

tPA converts plasminogen to plasmin, this acts to inhibit fibrinogen and fibrin

117
Q

What is the pressure drop from the aorta to the end arterioles

A

120/70, PP 50 -> 30-38mmHg, PP5

118
Q

What is the pressure drop from the arterial to venous end of the capillary

A

32mmHg -> 15mmHg, PP 5 -> PP 0

119
Q

MAP at heart level, at head level and at foot level

A

heart 100 mmHg
Head 62 mmHg
Foot 180 mmHg

120
Q

How does the BP change with age?

A

Systolic increases. Diastolic tends not to increase much. As such the PP increases

121
Q

What percent of blood volume is in the capillaries

A

ONLY 5%

122
Q

Transit time and velocity in capillaries

A

transit time 1-2s

velocity is SLOW - 0.07cm/s

123
Q

Describe Starling forces in the capillary

A

The diference between the hydrostatic pressure gradient and the oncotic pressure gradient. This is positive at the arterial end of the capillary favouring fluid movement out and negative at the venous end favour fluid movement in. The oncotic pressure does not change but the hydrostatic pressure decreases along the capillary as a result of the decreasing blood pressure towards the venous system.

124
Q

Absolute refractory period of the heart in seconds…

A

0.20s

125
Q

Relative refractory period in seconds

A

0.05s

126
Q

duration of the cardiac action potential

A

0.25s

127
Q

duration of cardiac cycle at hr75

A

0.8s

128
Q

glucagon’s effect on contractility

A

positive ionotrope - increases the formation of cAMP

129
Q

Fuel for the heart at basal conditions

A

60% fat, 35% carbohydrate, 5% by ketones and AAs

130
Q

C.O. can increase by ____ % during exercise

A

700%

131
Q

O2 extraction by the heart can increase by ___% during exercise

A

100%

FACEM Primary Physiology (2 decks)

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