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Cardio Week 1 Flashcards

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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
what is a selective blocker of HCN channels
ivabradine - slows HR and reduces O2 consumption
26
what is a summary of the mechanism causing contraction in cardiac MUSCLE cells
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)
27
what is a summary of the mechanism causing relaxation in cardiac MUSCLE cells
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
28
give examples of b-adrenoceptor agonists on the heart
dobutamine, adrenaline and noradrenaline
29
what do b-adrenoceptor agonists do to heart
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
30
give examples of b-adrenoceptor antagonists on heart
propranolol (non selective), atenolol, bisoprolol, metoprolol - act only on B1 in heart
31
what are b-adrenoceptor antagonists used to treat
angina, cardiac arrhythmias, MI (carvediol also causes vasodilation) and chronic heart failure no longer hypertension unless co-morbidities present
32
what are the adverse effects of b-adrenoceptor antagonists
bronchospasm, aggravation of cardiac failure, bradycardia, hypoglycaemia, fatigue, cold extremities
33
give example of non-selective muscarinic ACh antagonist
atropine
34
what is the role of non-selective muscarinic ACh antagonist
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
35
what is the role of digoxin
increases contractility by blocking sarcolemma ATPase IV in acute HR or orally in acute HF (particularly HF with AF)
36
how does digoxin work
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
37
what is the unwanted effects of digoxin
excessive depression of AV node (heart block), propensity to cause arrhythmias, nausea, vomiting, diarrhoea and disturbances of colour vision
38
give examples of 3 other inotropic drugs
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
what is the role of desmosomes within the intercalated discs of cardiac myocytes
provide mechanical adhesion between adjacent cells - ensures tension developed by one passed to next
40
what are myofibrils
contractile units of muscle - contain actin and myosin arranged into sacromeres
41
what is the refractory period
a period following an action potential in which it is not possible to produce another action potential
42
how is the long refractory period protective for the heart
prevents generation of tetanic contractions in cardiac muscle
43
what is the stoke volume
volume ejected by each ventricle per heart beat SV=EDV-ESV
44
what effects the SV
preload (Inc=inc), myocardial contractility (inc=inc) and after load (inc=dec)
45
what is end diastolic volume
volume of blood within each ventricle at end of diastole - determined by venous return to heart
46
what is the starling law
If EDP (so EDV) increased, the force of the following contraction (thus SV) increases
47
how is stretch involved in force
increases affinity of troponin for Ca++
48
what is afterload
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
a rise in peak ventricular pressure (contractility of heart at given EDV rises) shifts frank Starling curve in what direction
left
50
what change in pressure (dP/dt) reduces duration of systole
increases
51
what does vagal stimulation influence in heart
the rate - NOT FORCE
52
adrenaline and noradrenaline have what effects
inotropic and chronotropic
53
what is cardiac output
volume of blood pumped by each ventricle per minute CO = SV x HR (5l per min is normal)
54
what is diastole
heart ventricles relaxed and filled with blood (0.5)
55
what is systole
heart ventricles contract and pump blood into aorta (LV) and pulmonary artery (RV) - 0.3 sec
56
what events occur during passive filling
AV valves open and venous return flows into ventricles - ventricles become 80% full (aortic pressure 80mmHg and pulmonary lower)
57
what events occur during atrial contraction
completes end diastolic volume (130ml) - EDP is few mmHgcontracts between p wave and QRS
58
what events occur in isometric ventricular contraction
Pressure rise and when it exceeds atrial pressure the AV valves shut (LUB) - QRS
59
what events occur in ventricular ejection
SL valves open and SV ejected by each ventricle leaving behind ESV - ST segment - then ventricles relax where the SL valves shut (DUB)
60
what events occur in isometric ventricular relaxation
ventricle again a closed box and tension falls around closed volume - when falls below atrial pressure, AV valves open and start again
61
when is s1 (first heart sound) heard
closure of mitral and tricuspid valves - LUB - and heralds beginning of systole
62
when is s2 (second heart sound) heard
closure of aortic and pulmonary valves - DUB - and heralds end of systole and beginning of diastole
63
JVP has own a, c and v waves - what do these stand for
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
what is korotkoff sounds
blood flow though vessel when blood exceeds cuff pressure 1st sound - peak systolic2nd - no sound (record diastolic when sound disappears)
65
what is the equation to calculate pressure gradient between aorta and right atrium that drives blood sound systemic circulation
MAP - CVP (central venous - right atrial pressure)
66
what is SVR
total peripheral resistance - sum of resistance of all vasculature in systemic circulation MAP = CO x SVR
67
what is the pressure sensors, control centre and effector in the regulation of MAP
sensor - baroreceptors control centre - medulla effector - heart (HR and SV) and blood vessels (SVR)
68
how do baroreceptor reflexes correct postural hypotension
fall in MAP -->, decreased baroreceptor discharge, HR increases, SV increases, SVR increases
69
what are the two main components of EXCF what control blood pressure
water and Na+ (retention - increased BP)
70
what converts angiotensin I (formed by renin) to angiotensin II
ACE - produced by vascular endothelium
71
angiotensin II stimulates release of aldosterone - what does this do?
systemic vasoconstriction, increases SVR, thirst and ADH release, steroid hormone which increases Na+ and water
72
RAAS is regulated by mechanisms which stimulates renin releasee from juxtaglomuler apparatus in kidneys: this includes:
renal artery hypotension, stimulation of renal sympathetic nerves, decreased Na+ in renal tubular fluid (sensed by macula dense)
73
what are natriuretic peptides (NPs)
peptide hormone synthesised by heart and released in response to cardiac distension
74
what do NPs cause
excretion of salt and water (reduce blood volume and pressure), decrease renin release, vasodilation, counter regulatory system for RAAS
75
what is the two main types of NPs
Atrial natriuretic peptide (ANP) and brain type natriuretic peptide (BNP_
76
what is antidiuretic hormone (ADH) - vasopressin
peptide hormone derived by hypothalamus and stored in posterior pituitary - stimulated by reduced EXF volume or increased EXF osmolarity
77
what does vasopressin do
vasoconstriction, increases reabsorption of water, increases CO and BP
78
what is the resistance to blood flow and how is it controlled
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
what factors cause relaxation of arteriolar smooth muscle resulting in vasodilation and metabolic hyperaemia
decreased local PO2, increased local PCO2, increased [H+], increased extracellular K+, increased ECF osmolarity, adenosine release (from ATP)
80
what is examples of humoral agents (other chemicals) that cause vasodilation
histamine, bradykinin, nitric oxide
81
how can NO be stimulated and how does it work
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
what are examples of humoral agents that cause vasoconstriction
serotonin, thromboxane A2, leukotrienes, endothelin
83
how can endothelial damage/dysfunction be caused
HBP, high cholesterol and smoking
84
how can temperature control MAP
cold cause vasoconstriction, warmth causes vasodilation
85
what is the myogenic response to stretch
MAP rises - vessels constrict to limit flow MAP falls - vessels dilate to increase flow
86
how does sheer stress influence arterioles
dilation of arterioles cause sheer stress in arteries upstream to make them dilate
87
what increases venous return
increased venomotor tone, increased skeletal pump, increased blood volume, increased atrial pressure (caused by increased EDV and SV) and increased respiratory pump
88
what does increased venomotor tone do
increase venous return, SV and MAP
89
what does increased vasomotor tone do
increase SVR and MAP
90
what is the acute cardiovascular response to exercise
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
what is the chronic CVS response to exercise
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
what does regular aerobic exercise do to blood pressure
reduces it

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