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Revise Anatomy + Physiology of heart [not question, just learn]
Coronoary Circulation → arises from coronary sinus [aortic root]
- LCA → Left Main
- -LAD [ant septum, ant lat + apircal walls LV]
- -Circumflex system [lat post + inf LV]
- RCA → 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
Mummy, how are atheromatous plaques made?
Know from years
- Endothelial damage
- oxidised FFA
- Foam cells
- 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]
- angor animi
- 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
Lifestyle & risk modification
- -ASSIGN [no prev CVD] GRACE [new ACS/MI]
- -ETT as per bruce protocol
→ 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]
- Mechanical Complications;
- -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
- -Heart failure, MI, HTN, PTE, MV disease, Infection, 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
- Rate → BB → >65, CAD, Antuarrythmic contraindicated, AF >1year
- Rhythmn → 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
- ECG → 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]
- variable PRi
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
- Toxins [booze]
- 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
- Increased afterload
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
- decreased CO
→ Displaced apex beat [cardiomegaly
], S3, LV dilation
- Ischaemic → 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
- Pagets/Renal/Hepatic disease
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
- Infection/ Infarction
- Lung problems
- Endocrine problems
- Dietary Indiscretion
In general what are the CF of HF?
- Dyspnoea [SoB, ??at rest?]
- Orthopnoea + PND
- Ankle swelling
- Peripheral pitting oedema [ankles/sacrum]
- Displaced apex beat [cardiomegaly]
- Basal crackles [coarse = Pulm Oedema]
- Pleural Effusion
What are the CXR features of heart failure?
- Heart enlargement [Cardiomegaly]
- Pleural Effusion
- Redistribution of fluid [alveolar oedema/ upper lobe diversion → batwing]
- Kerley B-Lines
- Broncho-alveolar Cuffing
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
- LT Steroids
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
- Roth Spots [emboli on retina]
- Oslers nodes → painful, red raised
- Janeway Lesions → small non-tender palms/soles
- Nail haemorrhages [splinter]
- Embolic events
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
Dx = 2 Maj OR 1 Maj +3Min OR 5Min
- Predisposition [cardiac lesion/IVDU]
- Vascular/ immunological signs
- +ve BC [nt meeting maj]
- +echo [not meeting maj]
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