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Cardio Week 1 Flashcards

1
Q

where is SA node (location of excitation)

A

right atrium

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2
Q

what is phase 4 of SA node excitation

A

slow depolarisation and upstroke due to slow Na+

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3
Q

what is phase 0 of SA node excitation

A

upstroke due to Ca2+ channels

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4
Q

what are Ib and If and when are they activated

A

funny currents - at end of repolarisation by negative potentialsas threshold approached, transient Ca2+ activated

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5
Q

through what junctions is excitation spread

A

gap junctions

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6
Q

where is AV node located

A

base of atrium

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7
Q

why is conduction delayed in AV node

A

allows atrial systole to precede ventricle systole

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8
Q

what is the role of bundle of his and purkinje fibres

A

rapid spread of action potential to ventricles

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9
Q

what is phase 0 of ventricular muscle action potential

A

INa

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10
Q

what is phase 1 of ventricular muscle action potential

A

closure of Na+ channels and transient K+ efflux

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11
Q

what is phase 2 of ventricular muscle action potential

A

mainly Ca++ influx

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12
Q

what is phase 3 of ventricular muscle action potential

A

closure of Ca++ channels and K+ efflux

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13
Q

what is phase 4 of ventricular muscle action potential

A

resting membrane potential

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14
Q

what causes the plateau phase

A

opening of voltage gated Ca2+ channels whilst Na+ channels still activated - resultant Ca2+ current is sufficient to slow repolarisation

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15
Q

what is a competitive inhibitor of acetyl choline acting on M2 receptors

A

atropine - used in extreme bradycardia to speed up heart

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16
Q

what does adrenaline acting on a1 receptors cause

A

vasoconstriction of the blood vessels of splanchnic, renal, cutaneous and skeletal muscle vascular beds

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17
Q

what does adrenaline acting on B2 receptors cause

A

vasodilation of cardiac and skeletal muscle arterioles - dilates vessels and increases HR

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18
Q

sympathetic coupling through G protein activates what

A

adenylyl cyclase to increase cAMP and cause increased HR

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19
Q

what causes increased contractility (positive inotropic) as a sympathetic response

A

increase in phase 2 of cardiac MUSCLE action potential and sensitisation of contractile proteins to Ca2+

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20
Q

what causes increased conduction (positive dromotropic) as sympathetic response

A

enhancement of If an Ica in SA node potential

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21
Q

what causes decreased duration of systole (positive lusitropic action) as sympathetic response

A

increased uptake of Ca2+ into SR

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22
Q

parasympathetic coupling through G protein channels does what

A

reduced adenylate cyclase and thus cAMP opens potassium channels (GIRK) to cause hyperpolarisation of SA node mediated by Gi BY subunits

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23
Q

what causes decreased conduction in AV node (negative dromotropic)

A

decreased activity of Ca2+ channels and hyperpolariation (dip) via opening of K+ channels

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24
Q

how is pacemaker potential modulated

A

depolarising the funny current (If) mediated by channels activated by hyper polarisation and cyclic AMP gated (HCN) channels

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25
Q

what is a selective blocker of HCN channels

A

ivabradine - slows HR and reduces O2 consumption

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26
Q

what is a summary of the mechanism causing contraction in cardiac MUSCLE cells

A

opening of Ca2+ channels, Ca2+ influx, Ca2+ release from SR caused by Ca2+ activating RyR2, Ca2+ binds to troponin C and shifts tropomyosin out of actin cleft resulting in cross bridge (contraction via sliding filaments)

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27
Q

what is a summary of the mechanism causing relaxation in cardiac MUSCLE cells

A

repolarisation in phase 3/4, Ca2+ channel close, Ca2+ efflux occurs by NCX1, Ca2+ release from SR ceases and sequestration via Ca2+ ATPase (SECRA) takes place - Ca2+ dissociates from troponin C and cross bridge break

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28
Q

give examples of b-adrenoceptor agonists on the heart

A

dobutamine, adrenaline and noradrenaline

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29
Q

what do b-adrenoceptor agonists do to heart

A

increase rate, force (B1), constricts vessels in skin, mucosa etc to redistribute blood flow (a1) and dilation of coronary arteries (b2)also increases O2 consumption

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30
Q

give examples of b-adrenoceptor antagonists on heart

A

propranolol (non selective), atenolol, bisoprolol, metoprolol - act only on B1 in heart

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31
Q

what are b-adrenoceptor antagonists used to treat

A

angina, cardiac arrhythmias, MI (carvediol also causes vasodilation) and chronic heart failure no longer hypertension unless co-morbidities present

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32
Q

what are the adverse effects of b-adrenoceptor antagonists

A

bronchospasm, aggravation of cardiac failure, bradycardia, hypoglycaemia, fatigue, cold extremities

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33
Q

give example of non-selective muscarinic ACh antagonist

A

atropine

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34
Q

what is the role of non-selective muscarinic ACh antagonist

A

blocks parasympathetic system, increases HR esp in athletes, no effect on arterial BP/exercise, first line in severe bradycardia (following MI) and in anti cholinesterase poisoning

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35
Q

what is the role of digoxin

A

increases contractility by blocking sarcolemma ATPase IV in acute HR or orally in acute HF (particularly HF with AF)

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36
Q

how does digoxin work

A

inhibits Na+ pump which removes Na+ from cells, thus [Na}i increases so reducing Na+ gradient that drives NCX - less ca2+ removed and peak [Ca2+] force increases

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37
Q

what is the unwanted effects of digoxin

A

excessive depression of AV node (heart block), propensity to cause arrhythmias, nausea, vomiting, diarrhoea and disturbances of colour vision

38
Q

give examples of 3 other inotropic drugs

A

levosimendan - calcium sensitisers (acute decompensated HF - binds to troponin C sensitising it to Ca2+)amrinone and milrinone - indicators (use limited to IV in acute HF - inhibit PDE and increase cAMP)

39
Q

what is the role of desmosomes within the intercalated discs of cardiac myocytes

A

provide mechanical adhesion between adjacent cells - ensures tension developed by one passed to next

40
Q

what are myofibrils

A

contractile units of muscle - contain actin and myosin arranged into sacromeres

41
Q

what is the refractory period

A

a period following an action potential in which it is not possible to produce another action potential

42
Q

how is the long refractory period protective for the heart

A

prevents generation of tetanic contractions in cardiac muscle

43
Q

what is the stoke volume

A

volume ejected by each ventricle per heart beat SV=EDV-ESV

44
Q

what effects the SV

A

preload (Inc=inc), myocardial contractility (inc=inc) and after load (inc=dec)

45
Q

what is end diastolic volume

A

volume of blood within each ventricle at end of diastole - determined by venous return to heart

46
Q

what is the starling law

A

If EDP (so EDV) increased, the force of the following contraction (thus SV) increases

47
Q

how is stretch involved in force

A

increases affinity of troponin for Ca++

48
Q

what is afterload

A

resistance into which heart is pumping -> heart unable to eject full SV so EDV rises but eventually force of contraction rises by frank starling

49
Q

a rise in peak ventricular pressure (contractility of heart at given EDV rises) shifts frank Starling curve in what direction

A

left

50
Q

what change in pressure (dP/dt) reduces duration of systole

A

increases

51
Q

what does vagal stimulation influence in heart

A

the rate - NOT FORCE

52
Q

adrenaline and noradrenaline have what effects

A

inotropic and chronotropic

53
Q

what is cardiac output

A

volume of blood pumped by each ventricle per minute CO = SV x HR (5l per min is normal)

54
Q

what is diastole

A

heart ventricles relaxed and filled with blood (0.5)

55
Q

what is systole

A

heart ventricles contract and pump blood into aorta (LV) and pulmonary artery (RV) - 0.3 sec

56
Q

what events occur during passive filling

A

AV valves open and venous return flows into ventricles - ventricles become 80% full (aortic pressure 80mmHg and pulmonary lower)

57
Q

what events occur during atrial contraction

A

completes end diastolic volume (130ml) - EDP is few mmHgcontracts between p wave and QRS

58
Q

what events occur in isometric ventricular contraction

A

Pressure rise and when it exceeds atrial pressure the AV valves shut (LUB) - QRS

59
Q

what events occur in ventricular ejection

A

SL valves open and SV ejected by each ventricle leaving behind ESV - ST segment - then ventricles relax where the SL valves shut (DUB)

60
Q

what events occur in isometric ventricular relaxation

A

ventricle again a closed box and tension falls around closed volume - when falls below atrial pressure, AV valves open and start again

61
Q

when is s1 (first heart sound) heard

A

closure of mitral and tricuspid valves - LUB - and heralds beginning of systole

62
Q

when is s2 (second heart sound) heard

A

closure of aortic and pulmonary valves - DUB - and heralds end of systole and beginning of diastole

63
Q

JVP has own a, c and v waves - what do these stand for

A

a - atrial contraction c - bulging of tricuspid valve into atrium during ventricular contraction v - rise of atrial pressure during atrial filling: release as AV valves open

64
Q

what is korotkoff sounds

A

blood flow though vessel when blood exceeds cuff pressure 1st sound - peak systolic2nd - no sound (record diastolic when sound disappears)

65
Q

what is the equation to calculate pressure gradient between aorta and right atrium that drives blood sound systemic circulation

A

MAP - CVP (central venous - right atrial pressure)

66
Q

what is SVR

A

total peripheral resistance - sum of resistance of all vasculature in systemic circulation MAP = CO x SVR

67
Q

what is the pressure sensors, control centre and effector in the regulation of MAP

A

sensor - baroreceptors control centre - medulla effector - heart (HR and SV) and blood vessels (SVR)

68
Q

how do baroreceptor reflexes correct postural hypotension

A

fall in MAP –>, decreased baroreceptor discharge, HR increases, SV increases, SVR increases

69
Q

what are the two main components of EXCF what control blood pressure

A

water and Na+ (retention - increased BP)

70
Q

what converts angiotensin I (formed by renin) to angiotensin II

A

ACE - produced by vascular endothelium

71
Q

angiotensin II stimulates release of aldosterone - what does this do?

A

systemic vasoconstriction, increases SVR, thirst and ADH release, steroid hormone which increases Na+ and water

72
Q

RAAS is regulated by mechanisms which stimulates renin releasee from juxtaglomuler apparatus in kidneys: this includes:

A

renal artery hypotension, stimulation of renal sympathetic nerves, decreased Na+ in renal tubular fluid (sensed by macula dense)

73
Q

what are natriuretic peptides (NPs)

A

peptide hormone synthesised by heart and released in response to cardiac distension

74
Q

what do NPs cause

A

excretion of salt and water (reduce blood volume and pressure), decrease renin release, vasodilation, counter regulatory system for RAAS

75
Q

what is the two main types of NPs

A

Atrial natriuretic peptide (ANP) and brain type natriuretic peptide (BNP_

76
Q

what is antidiuretic hormone (ADH) - vasopressin

A

peptide hormone derived by hypothalamus and stored in posterior pituitary - stimulated by reduced EXF volume or increased EXF osmolarity

77
Q

what does vasopressin do

A

vasoconstriction, increases reabsorption of water, increases CO and BP

78
Q

what is the resistance to blood flow and how is it controlled

A

directly proportional to blood viscosity and length of blood vessel and inversely proportional to radius of blood vessel to power 4controlled by vascular smooth muscles through changes in radius

79
Q

what factors cause relaxation of arteriolar smooth muscle resulting in vasodilation and metabolic hyperaemia

A

decreased local PO2, increased local PCO2, increased [H+], increased extracellular K+, increased ECF osmolarity, adenosine release (from ATP)

80
Q

what is examples of humoral agents (other chemicals) that cause vasodilation

A

histamine, bradykinin, nitric oxide

81
Q

how can NO be stimulated and how does it work

A

stress on endothelium -> calcium release -> activation of NOS, can also be receptor stimulated NO diffuses into adjacent smooth muscle where it forms cGMP (relaxation)

82
Q

what are examples of humoral agents that cause vasoconstriction

A

serotonin, thromboxane A2, leukotrienes, endothelin

83
Q

how can endothelial damage/dysfunction be caused

A

HBP, high cholesterol and smoking

84
Q

how can temperature control MAP

A

cold cause vasoconstriction, warmth causes vasodilation

85
Q

what is the myogenic response to stretch

A

MAP rises - vessels constrict to limit flow MAP falls - vessels dilate to increase flow

86
Q

how does sheer stress influence arterioles

A

dilation of arterioles cause sheer stress in arteries upstream to make them dilate

87
Q

what increases venous return

A

increased venomotor tone, increased skeletal pump, increased blood volume, increased atrial pressure (caused by increased EDV and SV) and increased respiratory pump

88
Q

what does increased venomotor tone do

A

increase venous return, SV and MAP

89
Q

what does increased vasomotor tone do

A

increase SVR and MAP

90
Q

what is the acute cardiovascular response to exercise

A

HR, SV and force increase, vasoconstriction of kidneys and gut, vasodilation of skeletal and cardiac muscle, decrease SVR and DBP (PP increases)rise in peak ventricular pressure (contractility at given EDV) - Stirling curve shifted to left

91
Q

what is the chronic CVS response to exercise

A

reduction in sympathetic tone, increased parasympathetic tone, cardiac remodelling, reduction in plasma renin levels, improved endothelial function (increased dilators, decreased constrictors) and decreased arterial stiffening

92
Q

what does regular aerobic exercise do to blood pressure

A

reduces it

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