Cardio Flashcards
What are the risk factors for IHD?
modifiable: smoking, diabetes, hypertension, hypercholesterolaemia
non-modifiable: age, family history
Describe the NYHA heart failure classification
I - No limitation of physical activity
II - Slight limitation of physical activity
III - marked limitation of physical activity
IV - symptoms at rest
When is the third heart sound normal?
children and young adults <30
What are causes of a third heart sound?
heart failure, myocardial infarction, cardiomyopathy, hypertension
what are causes of a 4th heart sound?
always abnormal
heart failure, MI, cardiomyopathy, hypertension
Describe the grading of murmurs
1 - very faint
2 - soft
3 - heard easily
4 - loud, with a palpable thrill
5 - very loud, with thrill, may be heard with stethoscope slightly off chest
6 - very loud, with thrill, may be heard with stethoscope off chest
what are causes of mitral stenosis?
50% have a history of rheumatic fever or chorea, old age and calcification
describe the mitral stenosis murmur?
rumbling mid-diastolic murmur, best heard with he bell of the stethoscope at the apex with the patient lying on their left
what signs might you see in a patient with mitral stenosis?
pulse - AF
face - malar flush
palpation - tapping apex beat
CXR - enlarged left atrium, pulmonary oedema
what are the signs of pulmonary oedema on a CXR?
same as heart failure (idiot) a alveolar oedema b kerley b lines c cardiomegaly d dilated upper lobe vessels e pleural effusion
what are the causes of mitral regurgitation?
prolapsing mitral valve, rheumatic mitral regurge, papillary muscle rupture, cardiomyopathy, CT disorders
Describe the murmur in mitral regurgitation
pansystolic murmur radiating to the axilla
what are signs of mitral regurge
pulse - sinus
face - malar flush
palpation - displaced apex beat and palpable thrill
CXR - caridomegaly
ECG - bifid p, left ventricular hypertrophy
aortic stenosis causes
bicuspid aortic valve
age related calcification (over 65)
rheumatic fever
symptoms of aortic stenosis
exercise induced syncope, angina and dyspnoea
signs of aortic stenosis
pulse - slow rising, low volume with narrow pulse pressure
palpation - forceful apex beat
CXR - relatively small heart with dilated ascending aorta
ECG - left ventricular hypertrophy and left ventricular strain pattern (depressed ST and T inversion)
describe the aortic stenosis murmur
ejection systolic murmur radiating to the carotids
what causes aortic regurgitation
rheumatic fever, bicuspid valve, infective endocarditis, marfans, tertiary syphylis
what are signs of aortic regurge
pulse - collapsing, wide pulse pressure quinkes - capillary pulsation de Musset's - head nodding pistol shot femorals palpation - displaced apex beat ecg - left ventricular hypertrophy
describe the aortic regurge murmur
high pitched early diastolic murmur, best heard at the left sternal edge in the 4th ICS leaning forward with breath held
how do you work out rhythm on an ECG?
300/ big squares in R-R interval or rhythm strip x 6
describe the ECG in AF
irregular rhythm and no P waves
describe the ECG in atrial flutter
saw tooth p waves,
factors of 300
describe the ecg in VT
fast 120-180 bpm, broad complexes, always serious, may need cardioversion
describe v fib
patient arrested, look for capture or fusion beats, concordance
what are causes of left axis deviation?
left ventricular hypertrophy, left anterior hemiblock
describe the different types of heart block
1 - prolonged p-r interval
2a -progressive pr lengthening until one QRS dropped
2b - intermittent failure of AVN to conduc - 2:1, 3:1
3 - no relationship between p-p and R-R
Describe the ECG territories for MI
V1-V2 - septal V3-V4 - anterior V5-V6 - lateral I, aVL - high lateral II, III, aVF - inferior
describe the ECG changes in PE
S1, Q3, T3, right axis deviation, tachycardia
describe the ECG changes in hyperkalaemia
flat p waves, broad QRS, tall tented t
what are the three main causes of heart failure?
IHD (70%), non-ischaemic dilated cardiomyopathy (25%), hypertension (5%)
what are more niche causes of heart failure?
valvular disease congenital heart disease arrhythmias hyperdynamic circulation pericardial disease right heart failure alcohol and drugs
what are normal physiological changes in heart failure?
ventricular dilatation, myocyte hypertrophy, neurohumeral increased ANP, salt and water retention, sympathetic stimulation, peripheral vasoconstriction
what are early compensation mechanisms in heart failure?
normally if CO decreases, venous return increases leading to increased end diastolic volume restoring starlings law
if mild myocardial depression there is no decrease in cardiac output as it is maintained by an increase in venous pressure and sinus tachycardia, there is a decrease in ejection fraction
what are late compensatory mechanisms in heart failure?
cardiac output is maintained by large increases in venous pressure and sinus tachycardia at rest, they are unable to maintain a normal CO during excercise, increase VP leads to dyspnoea, hepatic enlargement, ascites and dependent oedema
what are the changes in severe heart failure?
decreased CO even at rest despite increased venous pressure and sinus tachycardia
what are causes of left heart failure?
IHD
non ischaemic dilated cardiomyopathy
hypertension
mitral/aortic valve disease
what are symptoms of left heart failure?
fatigue, exertional dyspnoea, orthopnea/PND
what are the physical signs of left heart failure
displaced apex beat (cardiomegaly)
gallop rhythm
features of mitral regurge
crackles at lung bases (pulmonary oedema)
dependent pitting oedema (activation of RAA)
what are causes of right heart failure?
chronic lung disease
PE or pulmonary hypertension
tricuspid/pulmonary valve disease
what are the symptoms of right heart failure?
fatigue, dyspnoea, anorexia
what are the physical signs of right heart failure?
increased jugular venous distension, cardiomegaly, hepatic enlargement (tender and smooth), ascites, dependent pitting oedema
describe the NYHA classification of heart failure?
class I - no limitation of physical activity class II - slight limitation of physical activity class III - marked limitation of physical activity class IV - symptoms at rest
what is the general management for heart failure?
low level exercise low salt diet stop smoking education vaccination
what is the medical management of heart failure?
1) diuretics - furosemide, bumetanide, add thiazide
2) ace inhibitor, swap to arb if dry cough
3) beta blocker
4) spironolactone
5) inotropic agent - dopamine, dobutamine, digoxin
6) nitrates
7) anticoagulation
describe the pathophysiology of atherosclerosis
endothelial injury
oxidation of lipoproteins which are taken up by macrophages to make foam cells
release of cytokines leads to an accumulation of fat and smooth muscle proliferation
plaque formation
describe the physiology of acs
rupture of coronary artery plaque, platelet aggregation and adhesion, localised thrombus, vasoconstriction, myocardial ischaemia
what are risk factors for ACS?
non modifiable - increased age, male hender, family history, ethnic origin
modifiable - smoking, diabetes, hypertension, hypercholesterolaemia
initial management of ACS?
ABC IV access 12-lead ECG morphine oxygen nitrates aspirin bloods - FBC, U&E, LFTs, glucose, lipids, CK, troponin
ECG findings in a STEMI
ST elevation Anteroseptal = V1-4 (LAD) Lateral = V5-6 (Cx) High Lateral = I, aVL (Cx) Inferior = II, III, aVF (RCA) new LBBB T wave inversion pathological Q waves
What are indications for thrombolysis?
<12 hours onset of pain
+ any 1 of the following
- ST elevation >1mm in 2+ consecutive limb leads
- ST elevation >2mm in 2+ consecutive chest leads
- posterior infarct
- new onset LBBB
what are thrombolysis contraindications?
absoloute: haemorrhagic or ischemic stroke < 6 months CNS neoplasia recent trauma or surgery GI bleed <1 month bleeding disorder aortic dissection relative: warfarin pregnancy advanced liver disease infective endocarditis
what are possible complications of thrombolysis?
bleeding hypotension intracranial haemorrhage reperfusion arrythmias systemic embolaisation of thrombus allergic reaction
what are indications for PCI?
same as thrombolysis
if does not fill thrombolysis criteria or thrombolysis contraindicated
if symptomatic post thrombo-lysis or develops
what are complications of a STEMI?
s- sudden death p - pump failure r - rupture papillary muscles or septum e - embolism a - aneurysm d - dressler's syndrome
what are the discharge medications and advice post STEMI?
Dual antiplatelet - aspirin and clopidogrel ACE inhibitor B-blocker Statin Address modifiable risk factors 1 month off work inform DVLA - no driving for 4 weeks
how to you distinguish between NSTEMI and unstable angina?
check troponin I 12 hours after onset of pain to distinguish, NSTEMI will have positive troponin I and unstable angina will have a negative troponin
Describe the management of NSTEMI/ UA
morphine
nitrates, ACE inhibitor, beta blocker, calcium channel blocker, statins
antiplatelet - aspirin and clopidogrel
LMWH
when would you consider PCI as the management for NSTEMI/UA?
raised troponin I recurrent angina/ ischaemic ECG changes features of heart failure poor LV function haemodynamic instability PCI <6 months/previous CABG
describe the presentation of acute pulmonary oedema
acute breathlessness
cough and frothy pink sputum
orthopnoea, PND
collapse, arrest, cardiogenic shock
describe signs you’d find in acute pulmonary oedema
distressed, pale, sweaty
tachycardic
fine crepitations bilaterally
gallop rhythm, 3rd heart sound
what are the commonest causes of LVF?
myocardial ischemia
hypertension
aortic stenosis or aortic incompetence
what are the radiological signs of heart failure?
airspace shadowing kerley B lines cardiomegaly diversion of blood to upper lobes effusions
what are the mechanisms causing tachyarrythmias?
accelerated automaticity - an area of myocardial cells depolarises faster than the SAN
triggered activity - myocardial damage
re-entry - propagating action potential keeps meeting excitable myocardium, must be 2 pathways around area of conduction block
what are precipitating factors for VT?
metabolic IHD cocaine cardiomyopathy MI
what are precipitating factors for SVT?
IHD thyrotoxicosis caffeine alcohol smoking
what are precipitating factors for AF?
same as SVT + mitral vlave disease hypertension lung disease post op pericardial disease cardiomyopathy
describe the management of SVT
ABC, O2, IV access vagal manoeuvres adenosine SEEK HELP antiarrythmic DC cardioversion if haemodynamically unstable
what are the differences between SVT and VT?
SVT is slowed/terminated by vagal manoeuvres or adenosine, there is atrial and ventricular coupling
VT has QRS >160ms, indipendent atrial activity, presence of fusion/capture beats
what is the management for broad complex tachycardia?
ABC - if pulseless = arrest protocol
no adverse signs
amiodarone/lidocaine, K/Mg as needed, sedation and DC cardioversion
adverse signs
sedation, DC cardion, amidoarone/lidocaine
what is the causative organism in infective endocarditis?
usually strep viridans
can be staph aureus - skin infections, abscesses, central lines, IV drug users
describe the pathophysiology of infective endocarditis
1 - endothelial damage/damaged valve
2 - platelets and fibrin are deposited - sterile fibrin-platelet vegetation
3 - bacteraemia - delivers bacteria to surface of the valve
4 - adherence and colonaisation of bacteria
5 - fibrin aggregates protect the bacteria and vegetation from host defence mechanisms
leads to disruption of the valve cusps (regurgitation), vegetations embolise, deposition of immune complexes
describe the clinical presentation of infective endocarditis
HEART MURMUR AND FEVER
systemic infection - malaise, pyrexia, myalgia, weight loss, fatigue
valvular/cardiac damage - changing murmur, heart failure, conduction abnormals
embolaisation - cerebral, pulmonary, coronary, renal
immune vasculitis - roth spots, oslers nodes, janeway lesions, clubbing, splinter haemorrhages, glomerulonephritis
what is the criteria for diagnosing infective endocarditis?
Duke criteria
Major - Positive blood culture and evidene of endocardial involvement
Minor - predisposition, fever, vascular/immunological signs, positive blood criteria (doesn’t fit major criteria), postivie echo (doesn’t fit major)
need 2 major or 1 major, 3 minor or 5 minor
what is the management for infective endocarditis?
ABC
involve micro and cardiology
empirical treatment is benpen and gent
who’s at risk of infective endocarditis?
structural congenital heart disease
acquired valve disease
prosthetic valves
previous endocarditis
what should you explain to a patient with infective endocarditis?
why antibiotic prophylaxis is no longer recomended
importance of maintaining good oral health
symptoms and when to seek help
risks of undergoing invasive procedures inc body piercing and tattoo
describe the drainage of pericardial fluid
via thoracic duct and right lymphatic duct into right pleural space
describe the pathophysiology of pericarditis
the pericardium is acutely inflamed
there is infiltration of polymorphonuclear leukocytes and pericardial vascularaisation which can lead to constrictive pericarditis or pericardial effusion
what are causes of pericarditis?
viral - most common (coxsackie) idiopathic tuberculosis bacterial (causes purulent pericarditis) neoplams cardiovascular disease - MI, dressler's renal failure inflammatory - RA, sarcoidosis, SLE
describe the features of pericardial pain
sharp worse on inspiration central chest pain radiating to left shoulder eased sitting forwards \+/- dyspnoea/ fever
what signs would you see when examining a patient with pericarditis?
tachycardia + tachypnoea + fever
pericardial friction rub
if constrictive - right heart failure, hypotension, pulsus paradoxus, loud high pitched S3
describe the ECG changes in pericarditis
1 - saddle shaped SST elevation
2 - ST returns to baseline, followed by T wave flattening
3 - T wave inversion
4 - ECG returns to pre-pericarditis baseline weeks to months after onset
what is the treatment for pericarditis?
treat cause bed rest and oral NSAIDs unless its post MI when no NSAID (as assoc with myocardial rupture) corticosteroids pericardial window pericardiectomy
what is a pericardial effusion?
it is an abnormal accumulation of fluid in the pericardial cavity
what is cardiac tamponade?
it is a pericardial effusion causing haemodynamically significant cardiac compression, the increased pressure impedes venous return to the heart resulting in reduced cardiac output, hypotension and shock
describe the presentation of cardiac tamponade
depends on how fast the fluid accumulates
commonly - cardiac arrest, hypotension, confusion, shock
slow developing - SOB, cough, hiccoughs, dysphagia
what are the signs of cardiac tamponade
Beck’s triad - increasedJVP, low BP, muffled heart sounds
tachycardia
kussmauls sign (JVP increase with inspiration)
pulsus paradoxus (decrease in palpable pulse and decrease in systolic BP on inspiration)
describe the management of effusion/tamponade
MEDICAL EMERGENCY
pericardiocentesis - needle tip inserted at level of xiphisternum, aim for tip of left scapula, aspirating continously
Describe the class I antidysrhytmics
Na channel blockers
Ia - qunidine - delays
Ib - lidocaine - opes channels, aborts premature beats
Ic - flecanide - not specefic to damage cells, suppresses re-entrant rhythms
Class II antidysrhythmics
beta blocker e.g. bisoprolol, atenolol, propanolol
negatively chronotropic and ionotropic
indications - hypertension, angina, post MI, AF
SE - GI disturbances, , bradycardia, fatigue, cold peripheries, heart failure, hypotension, dizziness, sexual dysfunction, peripheral vasoconstriction, bronchospasm
CI - asthma, marked bradycardia, heartblock, uncontrolled heart failure, PVD, prinzmetals angina, hypotension, cardiogenic shock
what should beta blockers not be used in conjunction with?
verapamil and diltiazem (non-dihydropyridines) in heart failure due to their additive effects (decrease HR, contractility, CO)
What are class III antidysarythmics?
K+ channel blockers e.g. amiodarone
What are class IV antidysarrythmics?
calcium channel blockers e.g. verapamil, diltiazem (non dihydropyridines)
amlodipine, felodipine, nifedipine
(dihydropyridines)
SE - v
describe the nitrates
e.g. isosorbide mononitrate, GTN infusion, GTN spray
indications - stable angina,unstable angina, acute heart failure, chronic heart failure
CI - hypersensitivity, hypotension, hypertrophic cardiomyopathy, AS, MS, cardiac tamponade, constrictive pericarditis, marked anaemia
describe ACE inhibitors
e.g. ramipril, lisinopril
inhibit conversion of agiotensin 1 into angiotensin 2 inhibiting its effects:
-increasing sympathetic activity
- fluid retention by kidney (via increase aldosterone and direct)
- arteriolar vasodilation
- stimulate ADH secretion
indications - hypertension, HF, post MI, IHD risk, diabetic nephropathy, progressive renal insufficiency
side effects - renal impairment, dry cough, , angioedema, rash, hypotension, pancreatitis, hyperkalaemia, GI effects
CI - hypersensitivity, renal artery stenosis, pregnancy, AS,
describe statins
e.g. atorvastatin, simvastatin
MOA - block HMG-CoA-reductase so inhibit liver cholesterol synthesis and upregulation of LDL receptors
SE - myositis, rhabdomyolysis, headache, altered LFTs, parasthesia, GI effects
CI - active liver disease, pregnancy, breast feeding
Aspirin
Supresses production of prostaglandins and thromboxane by irreversibly inactivating the COX enzyme, irreversibly blocks formation of thromboxane A2 in platelets, inhibiting platelet aggregation
describe clopidogrel
inhibits ADP induced aggregation through n active metabolite
describe dipyridamole
phosphodiesterase inhibitor
compare UFH and LMWH
LMWH - inhibits factor Xa but not thrombin, LMWH not fully reversible with Protamine
UFH - binds to ATIII which is an endogenous inhibitor of coagulation, increases ATIII ability to inhibit factors IXa,Xa, XIa, XIIa and thrombin, fully reversible with protamine
MOA of warfarin
inhibits vitamin k dependent clotting factors - II,VII, IX, X, protein C& S
