Collated Notes Flashcards

(107 cards)

1
Q

what causes an irregularly irregular pulse?

A

atrial fibrillation

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2
Q

what causes a raised JVP?

A

RS heart failure

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3
Q

what causes pericarditis 4-6 weeks post MI?

A

dressler’s syndrome

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4
Q

how does an AF appear on ECG?

A

absence of P waves

presence of F waves

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5
Q

how does pericarditis appear on an ECG?

A

PR depression

saddle shaped ST elevation

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6
Q

what are F waves?

A

pattern of irregular undulations of base line

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7
Q

how does atrial flutter appear on an ECG?

A

saw tooth

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8
Q

how do ventricular related issues appear on an ECG?

A

broad QRS

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9
Q

where do inferior MIs appear on an ECG?

A

II, III, aVF

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10
Q

where do anteroseptal MIs appear on an ECG?

A

V1-V4

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11
Q

where do anterolateral MIs appear on an ECG?

A

I, aVL, V1-V6

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12
Q

MONA-T/C

A
morphine 
oxygen 
nitrates
aspirin
ticagrelor/clopidogrel
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13
Q

SANAB

A
statin 
ACEi/ ARBs
nitrates
aspirin
B blockers
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14
Q

all prostitutes take money

A

aortic
pulmonary
tricuspid
mitral

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15
Q

MRS ASS

A

mitral regurgitation
systolic

aortic stenosis
systolic

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16
Q

DARMS

A

diastolic
aortic regurgitations
mitral stenosis

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17
Q

sartans

A

ARBs

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18
Q

prils

A

ACEi

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19
Q

olol

A

B blockers

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20
Q

thiazide

A

thiazide diuretics

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21
Q

dipine

A

calcium channel blockers

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22
Q

what does bat wings and cardiomegaly on a CXR mean?

A

pulmonary oedema

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23
Q

what does rib notching on a CXR mean?

A

aortic stenosis

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24
Q

what does a straight left heart border on a CXR mean?

A

mitral stenosis

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25
what does cardiomegaly on a CXR mean?
aortic regurgitation
26
what does autorhythmicity mean?
ability of the heart to beat in absence of external stimuli
27
where is the SA node?
in upper right atrium, close to SVC
28
where is the AV node?
at the base of the right atrium, just above the junction of the atria and ventricles
29
what creates pacemaker potential?
decrease in K+ efflux Na+ and K+ influx transient Ca2+ influx
30
what causes the rising phase?
activation of L-type Ca2+ channels resulting in Ca2+ influx
31
what causes the falling phase?
inactivation of L-type Ca2+ channels and the activation of K+ channels resulting in K+ efflux
32
describe the spread of electrical impulse
``` SA node AV node bundle of His L and R branches Purkinje fibres ```
33
how can impulse travel?
cell to cell via gap junctions
34
what is special about the AV node?
the only point of electrical contact between atria and ventricles conduction is delayed at the AV node to allow atrial systole to precede ventricular systole
35
describe phase 0
fast Na+ influx
36
describe phase 1
closure of Na+ channels | transient K+ efflux
37
describe phase 2
mainly Ca2+ influx
38
describe phase 3
closure of Ca2+ channels and K+ efflux
39
describe phase 4
resting membrane potential
40
what does sympathetic stimulation do to the HR?
increases it
41
what does parasympathetic stimulation do to the HR?
decreases it
42
what exerts continuous influence at the SA node at rest?
vagus nerve (parasympathetic)
43
what does vagal tone do?
slows intrinsic HR of 100 bpm to 70 bpm
44
what does vagal stimulation do?
slows HR and increases AV nodal delay
45
what is the neurotransmitter involved in parasympathetic control?
acetyl cholin acts through the muscarinic M2 receptors
46
where do cardiac sympathetic nerves supply?
SA node AV node myocardium
47
what does sympathetic stimulation do?
increases HR decreases AV nodal delay increases force of contraction
48
what is the neurotransmitter involved in sympathetic control?
noradrenaline acts through beta-1 adrenoreceptors
49
what does sympathetic stimulation do to the slope of pacemaker potential?
increases it
50
what does parasympathetic stimulation do to the slope of pacemaker potential?
decreases it
51
what does sympathetic stimulation do to the pacemaker cell K+ efflux?
decreases it
52
what does parasympathetic stimulation do to the pacemaker cell K+ efflux?
increases it
53
what does sympathetic stimulation do to the pacemaker cell Na+ and Ca2+ influx?
increases it
54
what does parasympathetic stimulation do to the pacemaker cell Na+ and Ca2+ influx?
decreases it
55
what does sympathetic stimulation do to AV nodal delay?
decreases it
56
what does parasympathetic stimulation do to AV nodal delay?
increases it
57
what creates the striation of cardiac muscle?
regular arrangement of contractile protein
58
how are cardiac myocytes electrically coupled?
gap junctions
59
what are gap junctions?
protein channels which form low resistance communication electrical pathways
60
where are desmosomes found and what do they do?
within intercalated discs and provide mechanical adhesion between adjacent cardiac cells
61
what are myofibrils made up of?
actin and fibrin arranged in sacromeres
62
what is the sliding filaments theory?
force is generated when actin filaments slide on myocin filaments ATP dependant- ATP is required for contraction and relaxation Ca2+ required to switch on cross bridge formation the binding of actin and myosin cross-bridge triggers the power stroke that pulls the filament inwards during contraction
63
what is a refractory period?
a period following an action potential in which it is not possible to produce another action potential
64
why does a refractory period occur?
during the plateau phase of the ventricular action potential as the Na+ channels are in the depolarised state so they are not available for opening during the descending phase of action potential as the K+ channels are open so the membrane cannot be depolarised
65
what is used to calculate SV?
EDV-ESV
66
what is EDV determined by?
venous return to the heart
67
what determines the diastolic length of myocardial fibres?
EDV
68
what are the intrinsic mechanisms which control SV?
diastolic length of myocardial fibres EDV Frank Stirling Mechanism
69
what is the Frank Starling Mechanism?
the more blood in the ventricle during diastole, the greater volume of ejected blood during systolic contraction stretch increases affinity of troponin for Ca2+
70
what are the extrinsic mechanisms which determine SV?
stimulation of sympathetic nerves which has a positive inotropic and a positive chronotropic effect sympathetic stimulation on ventricular contraction vagal stimulation has major influence on rate but not on force of contraction adrenaline from adrenal medulla have inotropic and chronotropic effects
71
what is a positive inotropic effect?
an increase in the force on contraction
72
what is a positive chronotropic effect?
an increase in the rate of contraction
73
describe sympathetic stimulation on ventricular contraction
greater Ca2+ influx, cAMP mediated and force of contraction increased peak ventricular pressure rises rate of pressure change during systole increases, duration of systole decreased rate of ventricular relaxation increases (increased rate of Ca2+ pumping)
74
what are the events on the cardiac cycle?
``` passive filling atrial contraction isovolumetric ventricular contraction ventricular ejection isovolumetric ventricular relaxation ```
75
describe passive filling
``` AV valves open atria and ventricular pressure close to zero aortic valve closed aortic pressure = -80mmHg ventricles fill 80% ```
76
describe atrial contraction
P wave in ECG depolarisation EDV = when atrial contraction is complete
77
describe isovolumetric ventricular contraction
starts after QRS ventricular pressure rises; when ventricular pressure > atrial pressure, AV valves shut AV valve shutting is the first heart sound ventricular pressure rises very steeply because aortic valve is still shut
78
describe ventricular ejection
Ventricular pressure > aortic/pulmonary artery pressure Aortic/pulmonary valves open Each ventricle ejects SV, leaving ESV Ventricles relax, ventricular pressure falls; When ventricular pressure falls below aortic/pulmonary pressure, aortic/pulmonary valves shut Aortic/pulmonary valves shutting is 2nd heart sound
79
describe isovolumetric ventricular relaxation
2nd heart sound signals start of isovolumetric ventricular relaxation Ventricular pressure falls; When ventricular pressure < atrial pressure, AV valves open Heart starts a new cycle
80
describe the sympathetic system
noradrenaline (post-ganglionic transmitter) and adrenaline activate B1 adrenoreceptors in nodal cells and myocardial cells coupling through Gs protein activates adenylyl cyclase to increase conc. of cAMP
81
what is the results of the sympathetic system?
``` increased HR increased contractility increased conduction in AV node increased automaticity decreased duration of systole increased activity of Na+/K+ ATPase increased mass of cardiac muscle over long term ```
82
how does the sympathetic system cause an increase in heart rate?
mediated by SA node due to; an increase in phase 4 depolarisation (pacemaker potential) causes by enhanced If and Ica reduction in threshold for AP initiation causes by enhanced Ica reduction in threshold for AP initiation caused by enhanced Ica
83
how does the sympathetic system cause an increase in contractility?
increase in phase 2 of the cardiac potential in atrial and ventricular myocytes and enhanced Ca2+ influx sensitisation of contractile proteins to Ca2+
84
how does the sympathetic system cause a decrease in the duration of systole?
increased uptake of Ca2+ into the sarcoplasmic reticulum
85
describe the parasympathetic system
acetylcholine activates M2 muscarinic cholinoreceptors in nodal cells coupling through Gi protein; decreases activity of adenylate cyclase and reduces cAMP conc. opens potassium channels to cause hyperpolarisation of the SA node
86
describe the results of the parasympathetic system
decreased heart rate decreased contractility (in atria only) decreased conduction in the AV node
87
how does the parasympathetic system cause a decrease in HR?
mediated by SA node due to; reduced If and Ica causing decreased slope of pacemaker potential hyperpolarisation caused by opening of GIRK channels increase in threshold for AP initiation caused by reduced Ica
88
how does the parasympathetic system cause a decrease in contractility in the atria?
decrease in phase 2 of cardiac action potential and decreased Ca2+ entry
89
how does the parasympathetic system cause a decrease in conduction in the AV node?
decreased activity of voltage dependant Ca2+ channels | hyperpolarisation via opening of K+ channels
90
describe contraction in cardiac muscle
the plateau phase opening of the voltage activated Ca2+ channels (mainly L type) during phase 2 of the action potential Ca2+ influx into cytoplasm Ca2+ released from sarcoplasmic reticulum- caused by Ca2+ activating the ryanodine type 2 channel Ca2+ binds to troponin C and shifts tropomyosin out of the actin cleft cross bridge formation between actin and myosin resulting in contraction via the sliding filament mechanism
91
describe relaxation in cardiac muscle
repolarisation in phase 3 to phase 4 voltage activated L type Ca2+ channels close Ca2+ influx ceases, Ca2+ efflux occurs by the Na+/Ca2+ exchanger Ca2+ release from the SR ceases, sequestration via Ca2+ ATPase of Ca2+ from the cytoplasm now dominates Ca2+ dissociates from troponin C cross bridges between actin and myosin break which results in relaxation
92
what is ivabradine?
selective blocker of HCN channels used to slow HR in angina
93
how does ivabradine act?
block of HCN channels decreases the slope of pacemaker potential
94
name beta-adrenoreceptor agonists
dobutamine adrenaline noradrenaline
95
what are the pharmacodynamic effects of beta-adrenoreceptor agonists?
increase force, rate and cardiac output increase oxygen consumption; decreases cardiac efficiency can cause disturbances in cardiac rhythm
96
what are the clinical uses of adrenaline?
``` alpha agonist as well as beta given IM, SC, IV plasma t(1/2)- 2 mins cardiac arrest (IV) anaphylactic shock ```
97
why is adrenaline given in cardiac arrest?
positive inotropic and chronotropic actions redistribution of blood flow to the heart (vasoconstriction in skin, mucosa and abdomen) dilation of coronary arteries
98
what are the clinical uses of dobutamine?
given as IV infusion plasma t(1/2) 2 mins causes less tachycardia than other beta agonists acute but reversible heart failure- eg after cardiac surgery, cardiogenic or septic shock
99
describe the action of beta-adrenoreceptor antagonists and name examples
may block beta-adrenoreceptors non-selectively (beta 1 and beta 2 eg propranolol) or selectively (beta 1 eg atenolol, bisoprolol, metoprolol) alprenolol is non selective and a partial agonist
100
describe the pharmacodynamic effects of beta-adrenoreceptor antagonists
at rest- little effect on rate, force, CO or MABP during exercise/stress- rate, force and CO are significantly depressed results in reduction in maximal exercise tolerance coronary vessel diameter marginally reduced but myocardial oxygen requirement falls therefore better oxygenation of the myocardium
101
what are the clinical uses of beta-adrenoreceptor antagonists?
treatment of arrhythmias atrial fibrillation and supraventricular tachycardia angina (first line alternative to calcium entry blockers) heart failure (compensated) hypertension (no longer first line)
102
why are beta-adrenoreceptor antagonists used to treat arrythmias?
they decrease excessive sympathetic drive and help to restore normal sinus rhythm they can delay conduction through the AV node
103
what are the adverse effects of beta blockers?
bronchospasm- can be severe in asthmatics aggragation of cardiac failure bradycardia hypoglycaemia in poorly controlled diabetes- tachycardia indirect effect due to warning mechanism fatigue cold extremities
104
name non selective muscarinic ACh receptor antagonists
atropine (competitive antagonist) | digoxin
105
what are the pharmacodynamic effects of atropine?
increase in HR no effect upon arterial BP no effect upon response to exercise
106
what are the clinical uses of atropine?
first line in management of severe or symptomatic bradycardia- particularly following an MI used in anticholinesterase poisoning to reduce parasympathetic activity
107
what is digoxin?
a cardiac glycoside that increases the contractility of the heart