Collated Notes Flashcards
what causes an irregularly irregular pulse?
atrial fibrillation
what causes a raised JVP?
RS heart failure
what causes pericarditis 4-6 weeks post MI?
dressler’s syndrome
how does an AF appear on ECG?
absence of P waves
presence of F waves
how does pericarditis appear on an ECG?
PR depression
saddle shaped ST elevation
what are F waves?
pattern of irregular undulations of base line
how does atrial flutter appear on an ECG?
saw tooth
how do ventricular related issues appear on an ECG?
broad QRS
where do inferior MIs appear on an ECG?
II, III, aVF
where do anteroseptal MIs appear on an ECG?
V1-V4
where do anterolateral MIs appear on an ECG?
I, aVL, V1-V6
MONA-T/C
morphine oxygen nitrates aspirin ticagrelor/clopidogrel
SANAB
statin ACEi/ ARBs nitrates aspirin B blockers
all prostitutes take money
aortic
pulmonary
tricuspid
mitral
MRS ASS
mitral regurgitation
systolic
aortic stenosis
systolic
DARMS
diastolic
aortic regurgitations
mitral stenosis
sartans
ARBs
prils
ACEi
olol
B blockers
thiazide
thiazide diuretics
dipine
calcium channel blockers
what does bat wings and cardiomegaly on a CXR mean?
pulmonary oedema
what does rib notching on a CXR mean?
aortic stenosis
what does a straight left heart border on a CXR mean?
mitral stenosis
what does cardiomegaly on a CXR mean?
aortic regurgitation
what does autorhythmicity mean?
ability of the heart to beat in absence of external stimuli
where is the SA node?
in upper right atrium, close to SVC
where is the AV node?
at the base of the right atrium, just above the junction of the atria and ventricles
what creates pacemaker potential?
decrease in K+ efflux
Na+ and K+ influx
transient Ca2+ influx
what causes the rising phase?
activation of L-type Ca2+ channels resulting in Ca2+ influx
what causes the falling phase?
inactivation of L-type Ca2+ channels and the activation of K+ channels resulting in K+ efflux
describe the spread of electrical impulse
SA node AV node bundle of His L and R branches Purkinje fibres
how can impulse travel?
cell to cell via gap junctions
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
describe phase 0
fast Na+ influx
describe phase 1
closure of Na+ channels
transient K+ efflux
describe phase 2
mainly Ca2+ influx
describe phase 3
closure of Ca2+ channels and K+ efflux
describe phase 4
resting membrane potential
what does sympathetic stimulation do to the HR?
increases it
what does parasympathetic stimulation do to the HR?
decreases it
what exerts continuous influence at the SA node at rest?
vagus nerve (parasympathetic)
what does vagal tone do?
slows intrinsic HR of 100 bpm to 70 bpm
what does vagal stimulation do?
slows HR and increases AV nodal delay
what is the neurotransmitter involved in parasympathetic control?
acetyl cholin acts through the muscarinic M2 receptors
where do cardiac sympathetic nerves supply?
SA node
AV node
myocardium
what does sympathetic stimulation do?
increases HR
decreases AV nodal delay
increases force of contraction
what is the neurotransmitter involved in sympathetic control?
noradrenaline acts through beta-1 adrenoreceptors
what does sympathetic stimulation do to the slope of pacemaker potential?
increases it
what does parasympathetic stimulation do to the slope of pacemaker potential?
decreases it
what does sympathetic stimulation do to the pacemaker cell K+ efflux?
decreases it
what does parasympathetic stimulation do to the pacemaker cell K+ efflux?
increases it
what does sympathetic stimulation do to the pacemaker cell Na+ and Ca2+ influx?
increases it
what does parasympathetic stimulation do to the pacemaker cell Na+ and Ca2+ influx?
decreases it
what does sympathetic stimulation do to AV nodal delay?
decreases it
what does parasympathetic stimulation do to AV nodal delay?
increases it
what creates the striation of cardiac muscle?
regular arrangement of contractile protein
how are cardiac myocytes electrically coupled?
gap junctions
what are gap junctions?
protein channels which form low resistance communication electrical pathways
where are desmosomes found and what do they do?
within intercalated discs and provide mechanical adhesion between adjacent cardiac cells
what are myofibrils made up of?
actin and fibrin arranged in sacromeres
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
what is a refractory period?
a period following an action potential in which it is not possible to produce another action potential
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
what is used to calculate SV?
EDV-ESV
what is EDV determined by?
venous return to the heart
what determines the diastolic length of myocardial fibres?
EDV
what are the intrinsic mechanisms which control SV?
diastolic length of myocardial fibres
EDV
Frank Stirling Mechanism
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+
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
what is a positive inotropic effect?
an increase in the force on contraction
what is a positive chronotropic effect?
an increase in the rate of contraction
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)
what are the events on the cardiac cycle?
passive filling atrial contraction isovolumetric ventricular contraction ventricular ejection isovolumetric ventricular relaxation
describe passive filling
AV valves open atria and ventricular pressure close to zero aortic valve closed aortic pressure = -80mmHg ventricles fill 80%
describe atrial contraction
P wave in ECG
depolarisation
EDV = when atrial contraction is complete
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
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
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
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
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
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
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+
how does the sympathetic system cause a decrease in the duration of systole?
increased uptake of Ca2+ into the sarcoplasmic reticulum
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
describe the results of the parasympathetic system
decreased heart rate
decreased contractility (in atria only)
decreased conduction in the AV node
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
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
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
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
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
what is ivabradine?
selective blocker of HCN channels used to slow HR in angina
how does ivabradine act?
block of HCN channels decreases the slope of pacemaker potential
name beta-adrenoreceptor agonists
dobutamine
adrenaline
noradrenaline
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
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
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
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
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
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
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)
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
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
name non selective muscarinic ACh receptor antagonists
atropine (competitive antagonist)
digoxin
what are the pharmacodynamic effects of atropine?
increase in HR
no effect upon arterial BP
no effect upon response to exercise
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
what is digoxin?
a cardiac glycoside that increases the contractility of the heart
