cardio Flashcards
what is a normal resting heart rate?
60 - 100 BPM
< 60 = bradycardia
> 100 = tachycardia
what does the AV node delay allow to occur?
allows atrial systole (contraction) to precede ventricular systole
describe the parasympathetic supply to the heart
vagal tone dominates under normal resting conditions - continuously slows from 100bpm to produce normal (70bpm)
vagus nerve supplies SA node and AV mode
vagal stimulation slows rate of firing from SA node and increases AV nodal delay
== negative chronotropic effect
neurotransmitter = acetyl choline via muscarinic M2 receptors
what do cardiac sympathetic nerves supply? what is the neurotransmitter?
SA node, AV node and MYOCARDIUM (increases firing and contraction, decreases delay)
neurotransmitter = noradrenaline via beta1 adrenoceptors
what are the different waves seen in an ECG and what do they represent?
P wave = atrial depolarisation
QRS complex = ventricular depolarisation (masks atrial repolarisation)
T wave = ventricular repolarisation
what are the main intervals/segments seen on an ECG and what happens there?
PR interval = largely AV node delay
ST segment = ventricular systole occurs here
TP interval = diastole occurs here
where is the only point of electrical contact between atria and ventricles?
AV node
what is the refractory period?
a period following an AP in which it is not possible to produce another action potential
how is muscle tension produced?
sliding of actin filaments on myocin filaments - requires ATP
desmosomes provide mechanical adhesion between adjacent cardiac cells and ensure the tension is transmitted from one to the next
what is stroke volume? how is it calculated? what is it affected by?
the volume of blood ejected by each ventricle per HEART BEAT
SV = end diastolic volume (EDV) - end systolic volume (ESV)
affected by:
- cardiac preload
- myocardial contractility
- cardiac afterload
what effect does sympathetic nerve stimulation have on ventricular contraction + frank starling curve?
peak ventricular pressure rises - contractility of heart at given EDV rises
= frank-starling curve shifts to left
what effect does an increased afterload have on the heart?
unable to eject fully = decreased SV
–> leads to increase EDV –> increase force of contraction
eventually, ventricular hypertrophy to overcome resistance
what is a normal arterial blood pressure?
120/80 - 90/60
pulse pressure = 30 - 50 mmHg
hypertension = 140/90 mmHg (daytime average 135/85 or higher
what determines the cardiac preload?
cardiac preload = diastolic length/diastolic stretch of myocardial fibres
determined by EDV -> EDV determined by venous return
what is MAP? how is it estimated?
mean arterial blood pressure = average arterial blood pressure during a single cardiac cycle
MAP = ((2xdiastolic) + systolic) / 3
–> ((2x80) + 120) / 3 = 93.3 mmHg
normal = 70 - 105mmHg
at least 60 needed to perfuse vital organs
how do you calculate MAP? how can MAP be regulated?
MAP = cardiac output (CO) x systemic vascular resistance (SVR)
heart rate, stroke volume, systemic vascular resistance
what is cardiac output? how is it calculated?
the volume of blood pumped by each ventricle of the heart PER MINUTE
CO = SV x HR
how do baroreceptors respond to an increase in BP?
increase baroreceptor discharge –> CV integrating centre (medulla)
- increase vagal activity - decrease HR hence decrease CO
- decrease cardiac sympathetic activity - decrease SV + HR, hence CO
- decrease sympathetic constrictor tone - venodilation+vasodilation, reduced SVR+SV
what hormones regulate extracellular fluid volume?
- the Renin-Angiotensin-Aldosterone System (RAAS)
- Natriuretic Peptides (NPs)
- Antidiuretic Hormone (ADH)
What is shock?
an abnormality of the circulatory system resulting in inadequate tissue perfusion and oxygenation
what are the 4 types of shock and how are they caused?
- hypovolaemic shock - caused by loss of blood volume
- cardiogenic shock - caused by sudden severe impairment of cardiac function
- obstructive shock - caused by physical obstruction to circulation in/out of heart
- distributive shock - caused by excessive vasodilation and abnormal distribution of blood flow
what is meant by cardiac tamponade?
increased pressure in pericardial cavity which prevents cardiac contraction
what is mean by pericardiocentesis?
drainage of fluid from pericardial cavity
needle inserted via infrasternal angle and directed superoposteriorly, aspirating continuously
where would you palpate the apex (beat of the heart)?
5th left intercostal space in the midclavicular line
where is the coronary sinus? what does it do?
atrioventricular groove posteriorly - separates base from diaphragmatic surface
receives deoxygenated blood from most cardiac veins and drains into right atrium
- main venous drainage for myocardium
name the branches of the right coronary artery
1 - right marginal artery - long bottom one along margin
2 - posterior interventricular artery - in interventricular groove
name the branches of the left coronary artery
(main stem is short)
1 - left anterior descending (LAD)
2 - lateral (diagonal) branch - branches from LAD
3 - left marginal artery
4 - circumflex artery - anastomoses with branches of right coronary artery
how many openings are there into the right atrium? what are they?
3 - SVC, coronary sinus, IVC
which of the heart valves are leaflet valves?
tricuspid (RA-RV) + mitral (LA-LV)
consist of:
- valve leaflets
- tendinous cords - close + prevent prolapse of leaflets (+ regurgitation of blood)
- papillary muscles - cardiac muscle attached to chamber wall
pulmonary + aortic = semilunar
where do you auscultate the aortic valve?
2nd right ICS sternal angle
what valve can be auscultated at the 5th left ICS in midclavicular line?
mitral valve
where do you auscultate the tricuspid valve?
4th left ICS sternal edge
where do you auscultate the pulmonary valve?
2nd left ICS sternal edge
what is the first branch of the aorta?
coronary arteries from coronary sinuses just above aortic valve
coronary arteries = blood supply to epicardium + myocardium
what are the 5 dilations of the initial heart tube and what is their fate?
most caudal
1. sinus venosus (inflow area, 2 horns) contributes to smooth part of RA (right horn) + coronary sinus (left horn)
- atrium - forms trabeculated (muscular part) of both atria
- ventricle - forms trabeculated part of LEFT ventricle
- bulbus cordis - forms trabeculated part of right ventricle + outflow part of both ventricle
- truncus arterious - forms aorta and pulmonary trunk (most proximal part)
most cranial
when does looping and folding of the heart begin?
approx. day 21-23
how do the different dilations of the heart fold?
atrium = dorsal and cranially
ventricle = displaced left
bulbus cordis = inferiorly, ventrally to the right
what are the 2 atrial septums?
septum primum - flexible, forms valve for foramen ovale
septum secundum - more rigid, right of septum primum and grows over it but never divides atria
what is the foramen ovale?
opening that continues until birth that allows communication between right and left atria (avoids lungs as not in use)
describe the process of ventricular septation
muscular portion (growing upwards from wall of expanding ventricle) and membranous protein (growth of tissue from endocardial tissue - cranial) fuse to form ventricular septum
what is the fate of the 6 pairs of the aortic arches
never all present at one time, develop cranial-caudal sequence
1 + 2 - mostly obliterated, contribute to maxilllary and stapedial aa.
3 - common carotid + first part of internal carotid
4 - right subclavian a. + part of aortic arch
5 - absent / rudimentary
6 - sprout branches that form pulmonary aa. + ductus arteriosus on left
why do the 2 atrial septums fuse at birth?
at birth, pressure becomes greater in left side, causes septum primum to push against septum secundum and eventually fuse
leaves “thumb print” in right atrium = fossa ovalis
what is the recommended weekly exercise duration for adults?
150 mins of moderate
what are some clinical signs of hypertension?
- loud aortic second sound
- fourth heat sound
- prominent left ventricular impulse
- hypertensive retinopathy
what are secondary causes of hypertension?
- renal disease
- renal stenosis
- endocrine disease
- Conn’s syndrome = excess aldosterone
- Cushing’s syndrome = excess corticosteriod
- Phaeochromocytoma = excess noradrenaline
- aortic disease
- coarctation of aorta (congenital narrowing of
segments of the aorta
- coarctation of aorta (congenital narrowing of
- drug therapy
what are the stages of hypertension?
Stage 1: >=140/90 AND daytime >=135/85
stage 2: >= 160/100 AND daytime 150/95
severe: systolic >= 180 OR diastolic >= 110
how does a atheromatous plaque progress?
- fatty streak (flat)
- fibrofatty plaque (raised)
- complicated plaque (overlying thrombus)
- superadded thrombus
what are complications of atheroma?
- stenosis
- thrombosis
- aneurysm - persistent dilation
- dissection - flowing blood splitting media
- embolism
name a potent vasoconstrictor/dilator
constrictor = angiotensin II
dilator = nitric oxide
list the 3 types of syncope
- reflex syncope - vasovagal, situational, carotid sinus
- orthostatic (postural) hypotension
- cardiac syncope
what is a positive result for orthostatic hypotension indicated by?
a drop within 3 minutes of standing from lying position of at least 20 mmHg in systolic bp (with or without symptoms)
or
drop in diastolic by 10mmHg WITH symptoms
(symptoms = lightheaded, dizziness)
name side effects of ACE inhibitors
dry cough
angioneuretic oedema
name side effects of diuretics
hypokalaemia (low potassium)
hyperglycaemia (high blood glucose)
name a side effect of CCBs
ankle oedema
what is a sign of hyperlipidaemia?
xanthelasma - plasma/lipids round eyes, weird backs of ankles and ringed eyes
what are the 4 main causes of oedema?
- raised capillary hydrostatic pressure - arteriolar dilatation, raised venous pressure (ankle swelling)
- reduced plasma osmotic pressure - <30g/l, malnutrition, hepatic failure
- lymphatic insufficiency - lymph node damage, filariasis
- changes in capillary permeability - inflammation, histamine increases leakage of protein
what is oedema?
accumulation of fluid in interstitial space
what regulates blood flow to the capillary bed? how fast is this blood flow?
terminal arterioles (mostly), precapillary sphincters in a few
blood flow throw capillary bed is slow - allows time for exchanges
where do hydrophilic and lipophilic molecules cross the capillary wall?
hydrophilic - go through water-filled pores
lipophilic - go through endothelial cells
what are the major forces involved in systemic transcapillary flow?
- capillary hydrostatic pressure -> favouring filtration
- capillary osmotic (oncotic) pressure -> opposing filtration
capillary hydrostatic pressure falls from 35mmHg at arteriole end to 17mmHg at venule end
capillary osmotic (oncotic) pressure remains constant at 25mmHG due to plasma proteins staying in capillaries (too big to diffuse)
what do starling forces favour in transcapillary flow?
what happens to the excess fluid?
favour filtrations at arteriolar end + reabsorption at venule end
filtration exceeds absorption so excess fluid is returned to circulation via lymphatics as lymph
-> able to reabsorb due to osmotic pressure
what is ERBs point and where is it?
best area for listening to S1 + S2
3rd intercostal space on sternal edge
where does an aortic stenosis murmur radiate to?
carotid arteries
where does a mitral regurgitation murmur radiate to?
axilla
what manoeuvre could you do to a patient to better hear mitral stenosis?
turn patient on left hand side
what manoeuvre could you do to a patient to better hear aortic regurgitation?
sit patient up and leaning forward, exhale and hold
which valves are heard loudest on inspiration?
tricuspid + pulmonary
which valves are heard loudest on expiration?
Mitral + aortic
what murmurs are heard during systole?
- aortic + pulmonary stenosis
- mitral + tricuspid regurgitation
- mitral valve prolapse causes systolic murmur with opening click
what are the inferior leads of an ECG?
II, III, aVF
what are the lateral leads of an ECG?
aVL, I, V5, V6
what causes a 4th heart sound?
atrial contraction causing rapid blood flow into a less compliant (STIFF) VENTRICLE
common causes of decreased LV compliance -
- myocardial ischaemia
- hypertension
- aortic stenosis
** always pathological + should be referred for echocardiography
what causes an innocent murmur?
turbulence of blood in the right ventricular outflow tract
- normal in child/young adult
- soft mid systolic (diastolic always pathological)
- usually heard in pulmonary area
- localised
- no other cardiac abnormalities
what happens in each of the phases of ventricular muscle excitation?
phase 0 = depolarisation due to Na influx
phase 1 = closure of Na channels and transient K efflux
phase 2 = Ca2+ influx through L-type Ca2+ channels
phase 3 = closure of Ca channels and K efflux
phase 4 = resting potential due to K efflux
what is a tall, tented T wave on an ECG a sign of?
hyperkalaemia
what is T wave inversion a sign of?
myocardial ischaemia
PE
what are features of first degree heart block?
PR interval longer than 0.12s-0.2s
no treatment, monitor for progression
what are the different types of second degree heart block?
mobitz type 1 = PR interval progressively gets longer and eventually drops a beat
mobitz type 2 = P:QRS ratio
requires ventricular pacemaker
what are features of 3rd degree heart block?
complete heart block - no electrical current getting through AV node
no correlation between P waves and QRS
requires ventricular pacemaker
what should pregnant woman be given instead of ACE or ARB?
ACE + ARB effect feotus
give beta blocker instead - atenolol
give an example of an ACE inhibitor and describe it’s mechanism of action
lisinopril
Block angiotensin converting enzyme, i.e. prevent conversion of angiotensin I to angiotensin II; aldosterone is not stimulated, so vasodilation occurs.
first line hypertension
heart failure - lengthens prognosis
give an example of an ARB and describe it’s mechanism of action
losartan
Angiotensin II receptor blocker; angiotensin II is a vasoconstrictor. Antagonising its action leads to vasodilation.
hypertension
heart failure
give an example of a thiazide diuretic and describe it’s mechanism of action
bendrofluazide
Inhibit NaCl reabsorption in distal tubules by blocking NaCl co-transporter
hypertension
give an example of a loop diuretic and describe it’s mechanism of action
furosemide
Inhibit NaCl reabsorption in the thick ascending loop of Henle
heart failure
describe amiodarone’s mechanism of action
block K+ channels
slows repolarisation and prolong AP + refractory period in cardiac tissue
give an example of a statin and describe it’s mechanism of action
simvastatin, atorvastatin
Block HGM-CoA reductase (competitive inhibition)
Reduction of LDL production in liver
Increased clearance of LDL in liver
describe the mechanism of action of glyceryl trinitrate?
arginine is converted into a neurotransmitter that activates guanylate cyclase
what is the primary drug target of atorvastatin?
hepatocytes
atorvastatin = HMG-CoA reductase inhibitor that reduces plasma cholesterol
Main way an increase sympathetic outflow results in increase preload
increases renin secretion
what is the mechanism of action of natriuretic peptides?
promotes excretion of sodium
lowers bp
antagonises actions of angiotensin II, aldosterone
what would an ECG of someone with hypOkalaemia look like?
U waves - deflections immediately after T wave
what criteria is used in infective endocarditis?
Duke criteria
which nerve supplies the pericardium?
phrenic nerve
what are the only 2 shockable rhythms? how would you differentiated between them?
VF
sustained VT
most patients with VT remain conscious
In VF the patient is pulseless and cardioversion is always required. In sustained VT the patient can be cardioverted with amiodarone if they are stable
Dressler syndrome
autoimmune mediated pericarditis 2-6 weeks post MI
Fever and new onset murmur
bacterial endocarditis until proven otherwise
myocardial necrosis
coagulative necrosis due to ischaemia and hypoxia in first 3 days post MI
torsades de pointes treatment
magnesium sulphate
what would be seen in V1 + V6 in LBBB?
V1 - W shape
V6 - M shape
what is the pacemaker potential due to?
decreased K+ efflux
how do cardiac muscles relax + contract?
both require ATP
relax - troponin-tropomyosin complex prevents myosin bridge binding by covering site on actin
contract - calcium displaces troponin-tropomyosin complex, myosin cross bridge binds to binding sites - calcium comes from sarcoplasmic reticulum
–> binding triggers power stroke that pulls filament inward during contraction
rate limiting step of RAAS
renin secretion
how is renin secretion reduced
natriuretic peptides
what effect does adrenaline have on alpha and beta receptors respectively?
alpha1 = vasoconstriction
beta2 = vasodilation
intrinsic chemicals that cause vasoconstriction
serotonin
thromboxane A2
leukotrienes
factors that influence venous return
skeletal muscle pump
venomotor tone
blood volume
respiratory pump
–> increase in any of these increases venous return - increase arterial pressure, EDV + SV
what do cardiac muscle fibrils contain?
myofibrils which contain actin + myocin
actin = thin myocin = thick
these are arranged into sacromeres
what effect does exercise have on the frank starling curve?
shifts to left
exercise causes peal ventricular pressure to rise –> increasing contractility of heart at a given EDV
frank-starling law
stroke volume of LV will increase as the LV volume increases
–> due to myocyte stretch causing more forceful systolic contraction
changes in contractility shifts curve -
increase = left
decrease = right - increase afterload (increase SVR)
phases of pacemaker potential
phase 0 - depolarisation, Ca influx via L-type channels
phase 3 - repolarisation, Ca channels close + K open = K efflux
phase 4(pacemaker potential) = slow depolarisation (funny current) - mixed Na/K –> important to determine HR
** pacemaker potential due to decrease K+ efflux **
give examples of drugs that increase + decrease pacemaker potential respectively
decrease = adenosine
increase = catecholamines
