Card Set Information
Cardiology objectives for finals
Revise Anatomy + Physiology of heart [not question, just learn]
Coronoary Circulation → arises from coronary sinus [aortic root]
→ Left Main
-LAD [ant septum, ant lat + apircal walls LV]
-Circumflex system [lat post + inf LV]
→ SA + AV node
-Right Main → RA, RV + Inferopost LV
-Post descending → inf septum
Revise the conducting system of the heart
SA Node → junction of SVC + RA; depol at autonomic rate + circulating catecholamines
AV → slower conduction than SA slows HR
His-Purkinje system → bundle of His + bundle branches
-1 BB on R
-2 on L → ant + post fascicles
-End diastolic Volume
-EDV; vol of blood in V at end diastole [fullest the V gets] effect → filling time + venous return
-Preload; stretching of ventricle during diastole, proportional to EDV
-Afterload; force V must generate to overcome SVR + open SL to eject blood. Effect → any ^^SVR
as afterload ^^, SV decreases
CO = ?
CO = SV x HR
Mummy, how are atheromatous plaques made?
Know from years
accumulation of thrombus
decrease of lumen
Compare Stable Vs Unstable angina
i.e. features, features of high risk?
Fixed stenosis, demand led ischaemia
predictable, w symptoms develop over chronic
risk → minimal exertion, bad exercise test [^duration, ^^changes, ABN BP]
Dynamic stenosis, supply led ischaemia
acute symptoms, unpredictable
risk → frequent/nocturnal, ECG change w symptoms, ^^troponin
Acute coronoary syndrome
chest pain at rest/ minimal exertion, spectrum form unstable angina → evolving MI
[MI, unstable angina, coronary spasm (Cocaine)]
"evidence of myocardial necrosis in clinical setting consistent w myocardial ischaemia"
Rise of cardiac biomarker [Troponin] +1 of;
-CF of MI
- ECG changes [new ST^/Twave changes/LBBB]
-Patho Q waves
-Imaging suggesting wall motion abn
What are the symptoms + signs of ACS?
cardiac CP [central, crushing, neck + L arm]
n+v, SOB, LoC
^^symp tone [pallor, clammy, tachy]
impaired Myocardial function → hypotensive, cool, oliguria, narrow PP, ^^JVP, S3, lung creps
Complications → MVR, Pericarditis
Ix in ACS/MI?
12 lead ECG + repeats
-ST elevation [full thickness occlusion]
-hyperacute T waves [tall]
-T wave inversion [Later]
-Q waves [not time specific, acute = transmural]
Bloods → Troponin [base + 12hour]
CXR → pulmonary oedema
How does MI cause ST elevation?
ST = ventricular systolic depol + subsequent repol
damaged muscle has changed physiological + electrical properties
ST elevates due to early repolarisation/ premature end systole
What is the Initial Mx of ACS/MI?
Morphine, Oxygen, Nitrates, Interventional Cardiology [4hours STEMI], Aspirin 300mg
NSTEMI → Thrombolyse, admit, PCI later
Outline secondary prevention of MI
-ASSIGN [no prev CVD] GRACE [new ACS/MI]
-ETT as per bruce protocol
Lifestyle & risk modification
→ change modifiable factors [smoking, hyperlipidaemia, med diet, normotension]
→ early mobilise, aim to work by 4-6/52
-Aspirin + clopidogrel [antiplatelet therapy]
-ACEi [Enalapril/ramipril] → counteract remodelling + prevent HF onset
-BB → if tolerated
Give 5 complications of MI/ACS?
MI as complication for ACS ≠ acceptable
Arrythmia → VF, VT, AF [atrial overstretch], Sinus brady [Inf MI]
Acute circulatory failure
pericarditis [only MI] → day 2/3, Tx opiates, NSAIDS ^^aneurism nb Dressler Syndrome [fever, pericardiits, pleurisy → autoimmune → colchicine/steroids]
-Papillary Muscle rupture [Mitral] → shock, acute PulmOedema, emergency MVR
-Septal Rupture → LR shunt through VSD [haemodynamic unstable, loud pansystolic murmur]
-Ventricular rupture → transmural MI → tamponade
Impaired ventricular function
-thinning wall + stretch impaired area
-^^wall stress → dilation + hypertrophy
-ACEi help prevent
Draw outline of arrythmias
Define AF and give 6 causes?
Irregularly irregular tachycardia
Atrial arrythmia 350-600bpm, w ventricular escape of <200bpm
^^risk of embolism → stagnant flow
, MV disease, I
nfection, hyperthyroid, Post op
What are the CF and Ix of AF?
- Palpitations, SOB, LoC [syncope]
-Irregularly irregular pulse
-ECG → absent P waves, irregular QRS
-U+E, TnI, TFT
-Echo → LVSD
Outline the Mx of AF?
RACE → if haemodynamically stable
RACE = Rate/Rhythmn control, Anticoagulate, Cardiovert, Etiology
→ BB → >65, CAD, Antuarrythmic contraindicated, AF >1year
→ Amiodarone/Flicanide → young, symptomatic/CCF, 1st lone AF
→ asses stroke risk [CHADS2VASC], heparin if low risk, warfarin/Aspirin if high
- <48hours no anticoagulation
- >48hours anticoagulate 3/52 prior, 4/52 after
→ treat cause
How do you treat;
-AF in Heart Failure
Flicanide PRN + anticoagulation
-AF in HF
Digoxin + Amiodarone
What is sinus tachycardia, what cuases it and how is it Mx?
Sinus tachy= HR >100bpm
Due to ^^ symp tone; fever, hypotension, anaemia, thyrotoxicosis etc...
Mx → Tx cause, consider BB if symptomatic
What is SVT?
Narrow complex tachycardia
Dx of exclusion → paroxysmal aborrhant tachy from atria/ AV junction
What is Atrial Flutter, its ECG pattern and Mx?
Atrial Flutter = rapid, regular atrial depol ~300bpm w AV block [2:1/ 3:1]
→ CAD, thyrotox, PTE
→ sawtooth in inf leads [II, III, aVF]
-bring out P-waves [slow AV conduction → carotid sinus massage, valsalva, Adenosine]
-Unstable → DC cardioversion
-Stable → RACE
What is VT?
>3 ectopic ventricular complexes, rate >100bpm, sustained if >30s duration
ECG → wide QRS [>140msec]
- monomorphic → intraventricular re-entry circuit → acute MI, cocaine, scarring
-Polymorphic → constant changing → acute MI, silent ischaemia
Mx → >30s = emergency
-compromised → DC cardioversion
- stable → Lidocaine, amiodarone, electrical cardioversion, Type 1A antiarrythmic
What is sinus brady?
P waves, rate <60bpm
Causes → ^^ vagal tone [vomiting, inf MI, ^^ICP, Drugs]
Mx → Tx cause, ?atropine
What is sick sinus syndrome?
SSS → sinus node dysfunction → marked brady, sinus pause/arrest, SA block
Symptomatic → pacemaker
Can be assoc w atrial tachy → Tachy/Brady syndrome
What is 1st degree heart block?
common, no Tx
What is 2nd degree heart block?
some P waves no conducted to Ventricles
Type 1 [Wenkebach]
gradual prolonged PRi until QRS dropped
block = proximal [AV node]
triggers = reversible → ^^vagal tone [post-op], RCA mediated ischaemia
PRi constant w sudden drop of QRS
Block = distal [Bundle of His]
^^risk of 3rd degree → ?Pacing
What is 3rd degree heart block?
Complete failure of conducting impulses to ventricles → no relat P-QRS
Ventricular depol = escape rhythmn
wide complex [ventricular escape]
Narrow complex [junctional rhythmn]
Mx → Electrical Pacing
Define Heart Failure & give 3 risk factors?
Failure of heart to pump blood
at sufficient rate to meet metabolic requirments of tissues. Associated with abn of cardiac function w
characteristic heamodynamic + neurohumeral changes
Outside UK → Valve disease/ Congenital Malformations
What is the pathophysiology of heart failure?
Primary insult → pump dysfunction leads to;
remodelling [dilation, hypertrophy]
neurohumeral activation [oedema, tachy, vasoconstrict]
leads to further damage
^End-daistolic pressure → peripheral vasoconstriction → hypertrophy
^EDV → cardiac dilation
Systemic response to ineffective circulating volume →
Activate SNS + RAAS
salt + water retention → intravascular expansion
^HR + myocardial contractility
Name 3 types of HF?
Systolic dysfunction → impaired ventricular ejection
Diastolic dysfunction → impaired filling of Vent
High output failure → demand for ^^CO
Outline systolic dysfunction
Impaired myocardial contractility
decreased ejection fraction & SV
→ Displaced apex beat [
], S3, LV dilation
extensive CAD, prev MI
Non-ischaemic → HTN, DM, Alcohol, Myocarditis, DCM
Outline Diastolic Dysfunction?
30% of HF have normal systolic function
poor filling of ventricles → decreased compliance
^Ventricular filling pressure → ^venous congestion [pulmonary + systmic venous congestion]
→ HTN, S4, LVH, apex beat = N
Transient → ischaemia [cardiac relaxation requires ATP]
Permanent → severe hypertrophy [HTN, AS, HCM], Restrictive cardiomyopathy, MI
Outline high output failure?
demand for ^^CO
exacerbates existing HF/ decompensate Pt w other cardiac pathology
anaemia, thiamine deficit, hyperthyroid, AV fistula
What are the causes of acute heart failure?
i.e. precipitants of exacerbations?
Endocarditis/ Environment [heatewave]
Rheumatic heart disease [other valves etc]
Failure to comply
In general what are the CF of HF?
Dyspnoea [SoB, ??at rest?]
Orthopnoea + PND
Peripheral pitting oedema [ankles/sacrum]
Displaced apex beat [cardiomegaly]
Basal crackles [coarse = Pulm Oedema]
What are the CXR features of heart failure?
eart enlargement [Cardiomegaly]
edistribution of fluid [alveolar oedema/ upper lobe diversion → batwing]
Ix for HF?
ECG → LVH, Previous MI [Patho Q waves]
Echo → chamber size, wall motion Abn, sytolic + diastolic function [EF]
Bloods → FBC, U+E, LFT, Natriuretic peptides [ANP, BNP]
CXR → exclude pulmonary cause for Pc, HERB-B
What are the featuers of LVH on ECG?
≥ QRS amplitude (voltage criteria; i.e., tall R-waves in LV leads, deep S-waves in RV leads)
Delayed intrinsicoid deflection in V6 (i.e., time from QRS onset to peak R is ≥ 0.05 sec)
Widened QRS/T angle (i.e., left ventricular strain pattern, or ST-T oriented opposite to QRS direction)
Leftward shift in frontal plane QRS axis
How does one classify HF?
stage 1 = no symp/limitations
stage 2 = mild symp/limitations
stage 3 = marked limitations due to symptoms, comfortable at rest
stage 4 = severe limitations, symptoms at rest
What is the acute management of HF?
[same for acute pulmonary oedema]
Fuck My NOPP!!!
Furosemide 40-80mg IV [slow, nb vasodilation]
Morphine [decrease PCWP, may not help]
Nitrates → GTN, 2 puff if sys >90mmHg
Positive airway pressure → CPAP/BiPAP NIV
Position Patient → sit up, legs over bed
Chronic Mx of CF?
Conservative measures → lifestyle advice
Symptomatic Tx → O2, night time pillows, Diuretics
Outline Pharmacological Mx of HF?
Principles; Block RAAS + SNS, make comfortable
ACEi → Cardioprotective → ramipril
AIIRB → 2nd line ACEi → Losartan, Candesartan
AldosAntag → Block Ald, decrease Na reabsorption → Spironalactone, Epleranone
BB → start low and go slow → propanolol, atenolol
Diuretics → furosemide, bumetinide
Dificult dificult, lemon dificult
140/90 = abritrary
200/130 = malignant
What are the causes of HTN? Give5
Primary → Essential [no one knows why] →95%
intrinsic renal disease →75% →GN, PCKD, polyarteritis nedosa
Renovascular disease → 24% →renal artery stenosis, RA atheroma, fibromuscular dysplasia [rare]
Cushings + Conns
Coarctation of Aorta
What are the CF of HTN?
For HTN retinopathy give the 4 stages.
Occiptal headache on waking
End organ damage →LVH, Proteinuria, retinal disease
1 → tortuous arteries w copper wiring sign
2 → AV nipping
3 → flame haemorrhages + cotton wool spots
4 → papilloedema
How does one investigate HTN?
BP Measure → Nb white coat
Basic → U+E, creatinine, eGFR, Cholesterol, glucose, ECG, Urinalysis [protein/blood]
Exclude 2ndry → Renal USS, retinal angiography, urinary free cortisol, renin + aldosterone, Echo
Mx of HTN?
Target pressure <140/90 [diabetic 130/80, proteinuria 125/75]
lifestyle changes → low salt, stop smoking, low fat diet, rduce alcohol, ^^exercise, weight loss
Step 1 → <55 = ACEi/AIIRB, >55/Black CCB [amlodipine nb oedema]
Step 2 →ACEi/AIIRB + CCB
Step 3 →ACEi/AIIRB + CCB + Thiazide like diuretic [bendro]
Step 4 → add further diuretic/Alphablocker/BB, consider referral
What is cardiomyoapthy and what are the different types?
Diseases of heart muscle
Acute myocarditis →inflamm of myocardium [viral/bacterial/toxic]
Dilated Cardiomyopahty →big baggy heart, unknown aetiolgy →^^ETOH, consider transplant
Hypertrophic cardiomyopathy → LV outflow tract obstruction [assymetrical septal hypertrophy] →sudden death
Restrictive CM →features of RVF → causes = amyloid haemochrom, sarcoid
Classify IE? And give likely organisms for each.
Native valve → acute [staph aureus] sub-acute [strepviridans/enterococci]
Prosthetic Valve → CoagNeg Staph, Gram negatives
IVDU → tricuspid, Staph aureus
Q-fever → coxiella burnetti
What are the clinical features of IE?
I caught IE, FROM JANE
Acute → normal valves → acute heart failure
Sub-acute → suspect in Hx damaged valves + fever
Fever + Murmur = IE
oth Spots [emboli on retina]
slers nodes → painful, red raised
aneway Lesions → small non-tender palms/soles
ail haemorrhages [splinter]
What are the diagnostic criteria of IE?
Blood cultures → typical org in 2 BC or persistently +ve >12h apart
Endocardial involvement → +ve echo [veget/abscess], new valve regurge
Predisposition [cardiac lesion/IVDU]
Vascular/ immunological signs
+ve BC [nt meeting maj]
+echo [not meeting maj]
Dx = 2 Maj OR 1 Maj +3Min OR 5Min
Mx of IE?
Early recog, liase w Micro + Cardiology
Consult local guidelines on empirical antibiotics
Consider Surgical Mx if → HF, Valve obstruction, repeated emboli, fungal cause, persistent bacteraemia, abscess
Mid-systolic murmur [crescendo-decrescendo]
Aortic area, radiates down left sternal border + carotids
?S1 ejection click
Causes; congenital bicuspid aortic valve, calcification, rheumatic heart disease
Low frequency diastolic rumble [bell @ apex]
does not radiate
causes: rheumatic fever, infective endocarditis
early diastolic, high pitched + blowing
patient sitting up + leaning forward
causes: Rheumatic heart disease, IE, Marfans, Syphyllis, AnkSpond
Pansystolic harsh murmur, loudest at apex
radiates to axilla
causes: Rheumatic fever, IE, MI, Cardiac Myxoma