Cardiovascular

1. Infective

2. 3. Arrhythmias 4. Valvular disease 5. 6. Myocardial infarction 7. Coronary disease

8. 9. Vasculitis 10.

Editorial team Katie Newman, Rebecca Ng, Ashleigh Spanjers

Peer reviewed in 2012 by

Professor Joe Hung

Infective Endocarditis (IE) Ex1,2,4 Skin: clubbing, splinter haemorrhages, Oslers nodes on finger pulps (painful, embolic), Janeway lesions on palms, pulps, foot 1,2,3 Definition soles (painless, erythematous maculopapular lesions containing The invasion of the endothelial lining of the heart bacteria), petechiae () and cardiovascular structures by Eyes: Roths spots (boat-shaped retinal haemorrhage due to microorganisms, most commonly involving the valves, heart immune deposition, also in SLE), conjunctival wall, and intrathoracic vessels. petechiae/haemorrhages Acute: Normal valve, acute HF+/-emboli Heart: Regurgitant murmurs (IE cause destruction & perforation Subacute: Abnormal valves, prolonged course, low-grade of valve leaflets, so valves become floppy), esp new or changing fever, non-specific sx murmur, CHF (from severe regurg), heart block (valve ring - Prosthetic valve endocarditis divided into early (<60 days abscesses) post-surgery), and late (thereafter) Respiratory: dyspnea, tachypnea, pleuritic chest pain (septic PE in right sided IE) 1,2 Abdomen: splenomegaly (late sign) Presentation Renal: haematuria  Acute or subacute Neurological: embolic signs  Majority will have systemic constitutional symptoms: Joints: occasionally resembles pattern fever, chills, rigors, night sweats, fatigue, malaise, anorexia, wt loss 1,2,4,5,6  Symptoms suggesting embolic phenomena to large Ix vessels (brain, viscera), or small vessels (kidney, w/  Confirmation of organism by serial blood cultures: at haematuria or loin pain) least 3 sets at different times from different sites at peak Consider Dx of IE in the following presentations: fever BEFORE administration of antibiotics  Fever plus new murmur or change in existing murmur NB: 10% culture negative  Embolic event of unknown origin Causes of culture negative IE:  Sepsis of unknown origin  Previous antibiotics, fastidious GP cocci, Legionella sp,  Haematuria, glomerulonephritis and ARF Bartonella sp, Coxiella burnetti, or fungi including Candida albicans; use molecular methods for specific Dx 1,4,5 Bloods DDx  FBC: normochromic, normocytic anaemia, IE is a major differential in PUO polymorphonuclear leucocytosis, ↑ ESR/CRP (acute IE),  Libman-Sacks [non-bacterial thrombotic] endocarditis U&E (renal dysfunction), LFTs (↑ ALP)  Antiphospholipid antibody syndrome ABG  Endocarditis associated with malignancy, autoimmune  If septic PE suspected from right sided IE disease eg. SLE, surgery, eosinophilic HD, Urinalysis ruptured mitral chordea, myxomatous degeneration  Haematuria and proteinuria (immune mediated glomerulonephritis)

5 ECG Mx: Antibiotics-  AF or heart block, long PR interval (aortic root abscess)  Long courses 4-6/52 of high doses IV  New AV block suggestive of abscess formation Empirical  Administer 4-hourly  TOE>TTE for visualising mitral lesions and aortic root  Benzylpenicillin (cover streptococci) PLUS abscess  Di/flucloxacillin (cover staphylococci) PLUS  Vegetations must be >2mm to be seen  Gentamicin (cover GN sepsis) 4-6 mg/kg  Use to identify valvular dysfunction & mycotic NB: adjust dose in renal dysfunction aneurysms Proven streptococcal MIC up to <4 mg/L, enterococcal IE  NB: negative result does not exclude Dx of IE  Exclude di/flucloxacillin CXR  Dosage, frequency and duration depend on MIC and  Evidence of HF (cardiomegaly, Kerley B lines, upper whether complicated* or uncomplicated infection. lobe blood diversion [erect but not supine film])  *large vegetation, multiple emboli, symptoms >3m,  Pulmonary emboli secondary septic events Proven streptococcal MIC >4 mg/L, resistant enterococcal IE, 1,5,18 prosthetic valve IE Prophylaxis  Vancomycin, slow infusion PLUS No RCT to decide the role of antibiotic prophylaxis Pt with cardiac conditions assoc w/ highest risk of adverse  Gentamicin Staphylococcal IE (usually s.aureus, rarely s.lugdenesis) outcomes from IE undergoing specific dental or other procedures  Di/flucloxacillin  Prosthetic cardiac valve or recently implanted prosthetic NB: Gentamicin DOES NOT alter outcome material (eg. pacemaker wire, note excludes coronary HACEK IE stents)  Ceftriaxone OR Cefotaxime  Previous IE  Congenital HD: unrepaired cyanotic defects, prosthetic -Adjust for culture results, susceptibility material or devices, residual defects following repair -Gentamicin and vancomycin: monitor blood levels and adjust  Cardiac transplantation with valvular disease dose accordingly, clinically monitor for vestibular toxicity, Educate pts of importance of good oral hygiene, regular dental ototoxicity evaluation, sx, when to seek advice, & risk of invasive procedures incl tattooing

Mx: Surgery-2,7,8 Aetiology1,2,4,5 Make decision about need for cardiac surgery in consultation  Caused by wide variety of microorganisms, but GP with cardiologist and cardiothoracic surgeon (and monitor for major cause: 80% Strep & Staph the development of these indications over course of Rx) Native valve, Non-IVDU: Absolute indications (Level B evidence):  Staphylococcus aureus, viridans group streptococci,  Development of HF or cardiac decompensation from enterococci, coagulase negative staphylococcus, valve destruction (ie. valve regurgitation) Streptococcus bovis (assoc w/ bowel cancer)  Fungal or highly resistant organisms Rarely (native valve):  IE complicated by heart block, intra-cardiac abscess-  GN bacteria HACEK (more insidious course), coxiella annular, aortic; perforation, fistulous tracts, false burnetii, Chlamydia, fungi including candida, aneurysms aspergillus, histoplasma

IVDU:

Consider for pt w/ recurrent emboli, persistent vegetations,  Staphylococcus aureus persistent bacteriaemia, despite appropriate antibiotic Rx, also Prosthetic valves: to prevent embolisation in presence of large (>1cm) mobile  Staphylococcus epidermidis, corynebacterium sp, vegetations (Level C evidence) streptococcus sp, enterococci, enteric GN rods,

Pseudomonas aeruginosa, Candida albicans, other fungi

Risk Factors 1,8  Structural cardiac defects- Epidemiology o Acquired valvular HD with stenosis or  Men>women regurgitation eg. MVP  Mortality 5-50% treated, 100% untreated o Valve replacement

o Structural congenital HD except ASD, VSD, Pathophysiology 1,2,4,5 PDA, non-endothelialised intracardiac devices A complex interaction between damaged vascular  Hypertrophic cardiomyopathy, previous IE, RHD, endothelium, local haemodynamic abnormalities, circulating IVDU, indwelling pulmonary catheter, bacteremia (overt bacteria, and host immune system. Most commonly involves or covert), dermatitis, renal failure, organ aortic and mitral valves. In IVDU tricuspid valve is most transplantation, DM, post-op wounds, chronic frequently affected. alcoholism, well defined extra-cardiac focus of  Turbulent blood flow traumatizes the endocardium infection, agglutination antibodies  Damage to endocardium causes deposition of fibrin and platelets leading to non bacterial thrombotic Duke Criteria for Clinical Diagnosis1,9

endocardial lesion (NBTE)  2 major, 1 major + 3 minor, or 5 minor

 NBTE colonized by bacteria in the bloodstream Major criteria

 Vegetations may cause destruction to the valves they  +ve blood cultures

colonize, and may lead to regurgitation or obstruction o Typical microorganism consistent w/ IE from 2

 Emboli from the vegetation can form in various separate blood cultures, OR

organs, and may lead to infarction or abscess o Persistently +ve blood cultures (>2 +ve cultures

formation separated by >12hrs; or 3 or majority of 4+

o L-sided IE: brain, kidney, spleen, gut cultures w/ 1st & last at least 1hr apart) o R-sided IE: lungs  Evidence of endocardial involvement Complications: o +ve echocardiogram  Cardiovascular: heart failure, abscess formation, o Oscillating intracardiac mass on mycotic aneurysm, pericarditis, aortic valve valve/supporting structures, or path of dissection, fistula formation between aorta and atrium regurgitant jet or o Abscess  Neurological (25% of episodes): encephalopathy, o New partial dehiscence of prosthetic valve meningitis, stroke, brain abscess, cerebral o New valvular regurgitation haemorrhage from mycotic aneurysms, seizures  Embolic phenomena  Renal: infarction, antibiotic-induced interstitial nephritis, glomerulonephritis, renal abscess Minor criteria  Other: Metastatic abscesses of kidney, spleen, brain,  Predisposition (cardiac lesion, IVDU or soft tissues  Fever >38 degrees Celsius  Vascular phenomena (arterial emboli, septic PE, mycotic aneurysm, Janeway lesions, intracranial or

conjunctival haemorrhages)  Immunological phenomena (glomerulonephritos, Oslers HACEK1,6 nodes, Roth spots, rheumatoid factor) Haemophilus aphrophilus, paraphrophilus, and parainfluenzae  +ve blood cultures (not meeting major criteria) Actinobacillus acetinomycetemcomitans  +ve echocardiogram (not meeting major criteria) Cardiobacterium hominis Eikenella corrodens Kingella kingae

Hypertension Definition Sustained elevation of systemic arterial

Classification1,10,11 Ex1,4,10,13 sBP dBP Focus on end organ damage and causes of 2O HTN Grade 1 140-159 90-99 Moon face, upper body obesity, striae, buffalo hump (Cushing) Cardiac: Grade 2 160-179 100-109  Point of maximal intensity displaced laterally (LV Grade 3 ≥180 ≥110 hypertrophy) Malignant HTN=sBP>200, dBP>130mmHg+bilateral retinal  LV heave, S4, S3, pulmonary oedema, carotid , haemorrhages and exudates +/- papilloedema. Emergency! valvular murmurs (AS, MR) Mayacute RF, HF, encephalopathy. Untreated 90% die 1yr, Cerebrovascular: treated 70% survive 5yrs. Hallmark is fibrinoid necrosis.  Neurological deficit Eye:  Hypertensive retinopathy, see over Presentation1,4,12 GIT: Usually asymptomaticregular screening crucial  AAA, renal bruits (renovascular HTN), hepatomegaly, Secondary hypertension: palpable kidneys or renal mass (renal disease, polycystic  Renal disease: lethargy, LOA, ankle swelling, SOB kidneys), striae (Cushing syndrome)  RAS: sudden worsening of HTN, <30yo or >50yo Peripheral vascular:  Cushing syndrome: fatigue, weakness, wt ∆, striae, acne,  ↓, absent &/or delayed femoral or radio-femoral delay skin infn, bruising, ↑ thirst & urination, mood ∆ (CoA of aorta), or peripheral pulses (PAD), femoral bruits  Acromegaly: h/aches, vision ∆, tightness of rings, ↑ shoe (PAD), peripheral oedema (HF, renal disease) size, arthritis, poor sleep,

 Thyroid disease: fatigue, weakness, wt ∆, 10 tachy/, palpitations, tremor, dry skin/hair, DDx hair loss, diarrhea/constipation, menstrual irregularities,  False elevation of BP-improper technique (eg. cuff too small), (calcified artery) mood ∆, temp intolerance  Phaeochromocytoma: h/ache, palpitations, sweating,  Physiologic causes: exercise, anxiety, pain, pregnancy anxiety  Exogenous causes: meds, caffeine, intoxications  Sleep apnea: snoring, pauses in breathing during sleep,  White coat hypertension fatigue, morning h/aches  CoA of aorta: cold legs, SOBOE, chest pain, syncope Mx4,10 PMH Goal: BP<140/90 mmHg or <130/80 mmHg if DM or CKD  DM, CAD, HF, obesity, hyperlipidaemia, renal disease, Lifestyle Modifications-ALL pts w/ HTN thyroid disease  Regular physical activity (≥30 min/day mod-intensity, most Med Hx days)  NSAIDs, corticosteroids, OCP, phenylpropanolamines,  Smoking cessation cyclosporine, tacrolimus, erythropoietin, others  Sodium restriction (<4g/day=65mmol/day)-low salt foods, no Family Hx added salt)  HTN  Wt ↓/maintenance (waist circumference <94cm M, <80cm F; Social Hx BMI 18.5-24.9)  Cocaine, cocaine w/drawal, “herbal ecstasy”  Limit ETOH (<20g/day w/ ≥2 ETOH-free days/wk) (phenylpropanolamine analogs), nicotine, nicotine Tailor advice, realistic goals, specific written instructions, provide w/drawal, anabolic steroids, others encouragement and review progress regularly  ETOH, sodium, cholesterol, and calorie intake Symptoms that suggest end organ disease: Medications (50-75% pts require 2+)  Chest pain Vision changes -Immediately when grade 3 HTN, assoc conditions, end-organ  TIA Left heart failure damage, high absolute CV risk (using markers of high risk or NZ  Claudication CV risk calculator, see below). -Initial drug choice based on age, presence of assoc clinical conditions or end-organ damage, potential drug interactions, Ix1,4,10 implications for adherence, cost. st Quantify absolute CV risk, ID end-organ damage, exclude 2O NHF recommended 1 line drugs: causes  ACE inhibitors (=efficacy to ARB) esp. stroke, CHF Bloods: U&E, Ca2+, creatinine, fasting BG, lipid profile  Dihydropyridine calcium channel blockers, or Urinalysis: Proteinuria, haematuria  Low-dose thiazide diuretics (if age≥65yo) NB: ↑ risk DM ECG: LV hypertrophy, past MI  Beta-blockers no longer 1st line (unless pregnant or Imaging: Echocardiogram-gold standard for LVH associated CAD) NB: ↑ risk DM If the following are suspected:  Start low dose  RAS-renal US/arteriography  If initial not well tolerated then change class. Target BP not  Cushing syndrome-urinary free cortisol, dexamethasone reached ≥6 wks, add 2nd agent from different class. Then if suppression test BP still above target, ↑ dose of one agent incrementally  Acromegaly-IGF-1, GH  Follow-up in 4/52  Parathyroid disease-serum PTH  Sleep apnea-sleep study  Thyroid disease-TSH  CoA of aorta-CT angiography  Phaeochromocytoma-24-hr urinary metanephrine and  Primary aldosteronism-plasma aldosterone, renin, potassium normetanephrine  White coat HTN-24hr ambulatory BP

Aetiology1,4,10,12 Epidemiology1,4,10 >95% Essential HTN (aka primary, no identifiable cause)  >50% 60-69yo 5% Secondary Causes:  75% ≥70yo Suspicion should be in pt <35yo, no family Hx, severe rapid  Associated with ↑ all-cause mortality onset, HTN refractory to standard therapy  Renal (most common) o Any cause of CKD eg, GN, PAN, systemic sclerosis, High CV Risk Groups10 chronic pyelonephritis, polycystic kidneys Following groups can be assumed to have high CV risk w/out o Renovascular disease eg. Atheromatous, fibromuscular using risk calculator: dysplasia 1. Pts ≥75yo  Endocrine a. >15% in next 5yrs o Cushing syndrome 2. Pts w/ existing CV disease o Primary hyperaldosteronism eg. Conn’s syndrome a. Symptomatic CV disease eg. , MI, CHF, stroke, o Acromegaly TIA, PAD o b. LV hypertrophy Dx w/ECG or echo o Hyperparathyroidism c. >20% in next 5yrs  Neurogenic 3. Pts w/ assoc clinical conditions and end-organ disease o Brain tumour a. >15% in next 5 yrs o Bulbar poliomyelitis b. Requires antihypertensive drug Rx o Intracranial hypertension For all pts estimate absolute risk using modified NZ CV risk  Drugs- NSAIDs, OCP, MAOI, steroids, cyclosporine, calculator tacrolimus, erythropoietin, adrenergic meds, ephedrine, ETOH, cocaine, amphetamines Causes: APE ERECTIONS  Pregnancy-nb Pre-eclampsia/eclampsia is a special high-  Anxiety risk hypertensive condition  Pregnancy (esp pre eclampsia)  Other  Exertion o Phaeochromocytoma  Essential o OSA  Renal (GN, chronic pyelonephritis, PCKD, RAS, o CoA obstructive uropathy)

 Endocrine (DM, thyrotoxicosis, Cushings, Conns, ovarian tumor, phaeochromocytoma)  Coarctation of aorta Hypertensive Retinopathy Hypertensive Emergencies  Toxaemia I: silver or copper wiring  HT encephalopathy  Iatrogenic II: A-V nipping (cerebral oedema)  OCP( and other meds: steroids, analgesics, NSAIDs, anti II: Flame haemorrhages,  Aortic dissection depressants) cotton wool spots  Rapid lowering of BP  Neurogenic (raised ICP, bulbar disease/polio, head injury, IV: Papilloedema required (urgent hypothalamic lesion)

hospitalization)  Sleep apnoea

Pathophysiology 11 Normal BP

 Function of CO and PVR, influenced by multiple genetic, environmental, and demographic factors

o CO is highly dependent on BV, which is greatly influenced by sodium intake

o PVR determined mainly at level of arterioles and affected by neural and hormonal factors. Reflects balance b/w

vasoconstrictors (angiotensin II, catecholamines, endothelin) and vasodilators (kinins, PGs, NO). of vessels,

whereby ↑BF, also plays a role.

 Local factors (eg. pH, hypoxia, alpha- and beta-adrenergic systems) also influence HR, cardiac contraction, & vascular tone

Role of Kidneys-Renin-angiotensin system:

 Juxtaglomerular cells secrete renin when ↓ BPconverts angiotensinogen to angiotensin I, then converted to angiotensin II by ACE ↑PVR (via vascular SM cells) and ↑BV (via aldosterone) Vasodilator substances (eg. PGs, NO)  ↓BV ↓GFR↑sodium reabsorption↑BV Essential HTN A complex, multifactorial disorder, likely influences by interactions of mutations or polymorphisms at several loci, and variety of environmental factors.  Accelerates atherogenesis: o Hyaline arteriolosclerosis-plasma ptn leakage, ↑SM cell matrix synthesis o Hyperplastic arteriolosclerosis-in malignant HTN, “onion-skin lesions”, concentric laminated thickening of walls and luminal narrowing, SM cells w/ thickened reduplicated BM, fibrinoid deposits, vessel call necrosis, esp in kidney Uncontrolled or poorly controlled HTN leads to complications in a number of systems:  Cardiac (CAD, MI, HF, RAD, aortic regurgitation, atrial flutter)  Cerebrovascular (TIA, intracerebral haemorrhage)  Peripheral vascular (limb)  Renal (A/CRF)  Ophthalmologic (retinal haemorrhage, blindness)

Arrhythmias Disturbance in normal and/or rhythm

 Important to elicit whether benign or haemodynamically severe or indication of underlying heart disease  Can arise from cardiac abnormalities, most commonly MI, CAD, valvular disease, cardiomyopathy, pericarditis, or myocarditis  Other non-cardiac causes: Drugs (nicotine, ETOH, caffeine), meds (beta2-agonists, dixogin, +++), and metabolic imbalances + 2+ 2+ (K , Ca , Mg , ↑O2, ↑CO2, thyroid disease)  May be asymptomatic

Hx4,12 Ix1,4,12,14,16  PC: palpitations, CP, dizziness, syncope, dyspnea,  Blood tests: FBC, U&E, inorganic chemicals (Ca, Mg, fatigue, confusion, anxiety phosphate), glucose, TFT, cardiac enzymes (troponin I,  Hx HD, arrhythmias, angina, MI, HTN, ↑ chol, DM BNP, ?CKMB)  Drugs (see DDx)  ECG  ETOH, smoking. recreational drug use o Atrial : abnormal shaped P wave, +/- # P  Family hx HD waves > # QRS o Multifocal atrial tachycardia: 3+ P wave morphologies, irregular QRS o Atrial flutter: 250-350 bpm, negative directed saw-tooth Ex1,3 deflections in leads II, III, aVF, positive directed saw-

 Vital signs-temp, HR, BP, RR, O2sats tooth deflections in lead V1, +/- usually 2:1 or higher  Palpation - grade AV block o : weak, thready (tachycardia), o AF: fibrillary waves >300/min, irregular narrow QRS, irregularly irregular (AF) usually fast rate o WPW syndrome: short PR interval, wide QRS w/ delta  Cardiac of cardiac disease (see ‘Heart wave (slurred upstroke), ST-T changes Failure’) o Junctional tachycardia: 150-250bpm, P wave within QRS or after QRS o VT: regular wide QRS complex tachycardia, either complete AV dissociation or 1:1 retrograde atrial capture o Hypokalaemia: U waves

Vasovagal manoeuvres1  Echocardiogram - holding breath o - carotid sinus massage  Provocation tests - valsalva o Cardiac stress test (exercise ECG) - coughing  Holter monitor-ambulatory ECG worn around neck for 24hr  ↑ AV block  Invasive investigations can include electrophysiological testing and cardiac catheterization

CHADS2 score 1,14,15 Sick sinus syndrome1,14 For predicting risk of thromboembolic stroke in pts w/ AF  Sinus bradycardia, sinus pauses, or alternating tachy- . Congestive heart failure and bradycardia syndrome. Requires pacing if . Hypertension symptomatic . Age ≥75yo  Usually idiopathic, rarely caused by conduction defects . Diabetes mellitus (eg. amyloidosis, Chagas disease), meds (eg. digoxin) . Stroke or TIA Torsades de pointes14 1 point for each of the above risk factors except for stroke (2  VT with varying axis, due to ↑ QT interval points). Max score out of 6. Pts w/ score ≥2/6 are  "Twisting of the peaks" morphology on ECG recommended to be put on oral anticoagulation eg. warfarin  May  VF (target INR 2-3):  Drug-induced, including- Score 0-aspirin or nothing; score 1-warfarin or aspirin o Procainamide, quinidine, sotalol, amiodarone,  AF is the most common arrhythmia, and is common arsenic, methadone particularly in the elderly o Antibiotics (eg. clarithromycin, erythromycin)  May be asymptomatic, or pts may experience palpitations, o Antiemetics (eg. domperidone, dizziness, LOC metoclopramide)  Contraindications to anticoagulants are bleeding diathesis, o Antipsychotics (chlorpromazine, haloperidol) 3 thrombocytopenia (<50x10 /microL), non-adherence to Long QT14 treatment and monitoring, previous intracranial, retinal or  Characterised by prolonged QT on ECG GIT bleeding, and pregnancy (teratogenic).  Assoc w/ ventricular tachyarrhythmias and resulting sudden cardiac death  Can be genetic or acquired (eg. drugs, electrolyte imbalance, starvation) Bradycardia Resting heart rate <60bpm

DDx14 Mx of bradycardia1 May be due to rhythm disturbances resulting from sinus node  Address underlying cause & stop any associated drugs dysfunction, AV conduction disturbance or heart block  Asymptomatic, HR >40bpmno specific treatment  Physiological eg. athlete required  Drugs-beta blocker, antiarrhythmics eg. flecainide,  Symptomatic, or HR<40bpmtreat digoxin, TCA, lithium, cholinesterase inhibitors eg. o Atropine 0.6-1.2 mg IV (≤3mg) neostigmine, heroin (and many more...) o If no response, insert temporary pacing wire  Poisoning-many, including opiate overdose o May require isoprenaline infusion or use external cardiac pacing toxidrome, insecticide/organophostphate  CVS-Heart block, HD, MI, arrhythmia, cardiomyopathy, neurogenic shock, hypothermia  Infection-bacterial overwhelming sepsis Side-effects of amiodarone12,14  Metabolic-Electrolyte disturbances (eg.  Corneal deposits hyperkalemia), diabetic autonomic neuropathy  Photosensitivity syndrome, malnutrition, starvation  Hepatitis  Endocrine-hypothyroidism, adrenocorticoid  Arrhythmias deficiency  Pulmonary fibrosis, pneumonitis  Allergies-anaphylaxis  Hyper-/hypothyroidism  Trauma-brain injury, traumatic brain haemorrhage  Increased INR  Psych-anorexia nervosa  Nightmares

Must monitor LFT and TFT!

Tachycardia Resting heart rate >100bpm

1,4,12 14 Classification DDx Narrow complex (rate>100bpm, QRS width <120ms)-  Physiological eg. Exercise, fear, stress, pregnancy electrical signal passes through AV node  Drugs-amphetamines, ecstasy, cocaine, ETOH,  caffeine ++  SVT [Rx: vagotonic maneouvres, IV adenosine or  CVS-Heart block, heart disease, MI, arrhythmia, verapamil, DC shock if compromised] cardiogenic or hypovolemic shock o Atrial tachycardia  cardiomyopathy o Multifocal atrial tachycardia-most commonly in  Electrolyte disturbances-hypokalemia COPD; ≥3 morphologically distinct P waves,  Poisoning-botulism, carbon monoxide irregular P-P intervals  Infection-pericarditis, acute infective illness, o Atrial flutter (macro-reentrant atrial tachycardia; 2:1 overwhelming sepsis AV block common)  Metabolic-hypokalemia, acidosis, hypoxia, o AF dehydration . Paroxysmal: recurrent, terminates spontaneously  Endocrine-hyperthyroidism, adrenocorticoid excess <7d (eg. Cushing syndrome), hypoglycaemia . Persistent: >7d or <7d but requires cardioversion  Vascular-Anaemia . Longstanding: >1yr  Neoplastic-phaemochromocytoma . Holiday Heart Syndrome-binge drinking in pt with normal heartAF (DDx: marijuana use). [Rx:  Malignant hyperthermia ETOH abstinence, verapamil, beta-blocker,  Psych-anxiety, mania, hyperactive delirium amiodarone, digoxin (nb 2nd-line unless AF w/ HF]  NMS syndrome o Junctional tachycardia 1. AV nodal re-entry tachycardia (ANNRT) Mx of tachyarrhythmias1 2. AV re-entry tachycardia (AVRT) 3. His bundle tachycardia  Address underlying cause o WPW syndrome-congenital accessory conduction  If compromised use DC conversion pathway b/w atria and ventricles arrhythmias esp.  For AVRT, vasovagal maneouvres, if unsuccessful then nd rd AVRT, AF, atrial flutter try IV adenosine (CI in asthma, 2 /3 degree AV block, Broad complex (rate>100bpm, QRS width >120ms)-AV node sinoatrial disease), failing that then IV verapamil or conduction system dysfunction. Supraventricular or  Amiodarone loading dose (200mg/8h po 7d, then ventricular in origin. 200mg/12h 7d), followed by maintenance Rx (200mg od)  VT (>3 ventricular ectopics, HR>100bpm, QRS duration  In regular broad complex tachy-assume VT until proven >120ms) [Rx: IV amiodarone or lidocaine, no response otherwise, give O2, obtain IV access and draw bloods then DC shock] (U&E, cardiac enzymes, Ca2+, Mg2+), obtain 12-lead o Torsades de pointe ECG, do ABG  SVT- abnormal conduction or ventricular pre-excitation o VT: amiodarone or lidocaine, failing that or if can any SVT to produce a broad complex tachycardia compromised, use DC shock o VF: use asynchronised DC shock

Valvular Heart Disease Definition Congenital or acquired valvular defects leads to restriction to blood flow (stenotic) or incompetency of the valves and backward flow (regurgitation/insufficiency)

1,4,13 4 Presentation DDx  AS: exertional angina or weakness, SOBOE, effort-related Systolic murmur- syncope, CHF  AS, HOCM, PS, VSD, MR, TR; innocent flow  AR: SOBOE , CHF, palpitations murmur- hyperdynamic state (eg.  MS: SOBOE , exertional weakness, palpitations, orthopnea, PND, thyrotoxicosis, anaemia, infection, pregnancy, AF, haemoptysis, CHF after exercise)  MR: SOBOE, orthopnea, PND, cough, palpitations, haemoptysis Diastolic murmur-  All assoc w/ fatigue  AR, PR, MS, TS  Elicit hx of rheumatic heart disease in pt  Known or presumed CAD may accentuate or mask symptoms  (*CHF- for S&S see CHF document)

1,4,6,12,13 Ex AS AR MS MR Age Childhood/adolescence- Younger person-RHD, 10-50-depends on prevalent Depends on aetiology eg. middle age-bicuspid aortic Marfan’s, ankylosing rates of rheumatic fever. RHD, Marfan’s, valve spondylitis Severe MS can occur at myxomatous mitral valve, >65yo-calcific Older age--degenerative AV, young age if recurrent bouts mitral valve prolapse, (degenerative), aortic dilated aortic root/aortic of RF functional MR due to MI, stenosis aneurysm from HTN, cystic cardiomyopathy or HF medical necrosis or atheroma Ex Sustained forceful apical Increased Loud S1, opening snap, AF, Soft S1, AF, brisk carotid impulse (water-hammer pulse) RV heave, hepatomegaly upstroke w/ ↓ volume, S3 Weak/delayed carotid pulse Corrigan’s pulse, Hill’s sign, (pulsatile), pulmonary gallop, hyperdynamic Carotid upstroke (delayed) pistol-shot femoral pulses, oedema, malar flush apex, RV heave Single S2 (valve static) Duroziez’s sign, de Musset’s LV heave sign, Quincke’s pulse Murmur Crescendo-decrescendo Early decrescendo diastolic Non-radiating apical Pansystolic, radiating from systolic ejection, radiate to murmur diastolic rumble apex to axilla neck w/ assoc thrill, ↓ Mid to late systolic if MVP intensity w/ valsalva ECG LV hypertrophy, left anterior Increased LV mass LA enlargement (broad Increased LV mass, AF hemiblock notched P waves), RV hypertrophy, R axis deviation, AF CXR Poststenotic aortic dilatation, Cardiomegaly, left HF LA enlargement, RA Cardiomegaly, left HF boot shaped heart enlargement, Kerley B lines, prominent pulmonary  Echocardiogram for Dx and assessment of severity  Cardiac catheterization to confirm DX, estimate severity, measure pressure gradient and intrachamber pressures, and if valve replaceme nt surgery is to be undertaken

Mx1,4,5  Symptomatic severe AS managed purely medically has worst prognosis (50% 1 yr)  In remainder, medical (echocardiography monitoring) is initial approach, with surgery reserved for progression of symptoms  If lesion arises acutely, surgery is necessary earlier in the course To relieve symptoms:  Digoxin (esp if AF)  Diuretics

 Vasodilators for AR or MR (contra-indicated in AS)  Anticoagulation esp in AF, and also in MS Valve repair or replacement  Bioprosthesis {tissue valves-10-15 yr lifespan; used in elderly)}  Mechanical prosthesis (exceed human life span; used in young pt)  Decision based on the need for anticoagulation with its risks when mechanical valves are used and on the durability-before symptoms, or for ventricular decompensation Percutaneous balloon valvuloplasty (stenotic cases) Antibiotic prophylaxis no longer routinely recommended against IE for dental and surgical procedures unless high risk features

Aetiology4,11 Epidemiology1  In adult population due to acquired defects (congenital in paeds),  Most 7th decade (MS usually 3-5th decades) most commonly affecting AV and MV.  Rheumatic fever was initially most common  ARF: scarring of the valve apparatus and fusion of the valve aetiology, but now RF ↓ in incidence cusps  more prone to mechanical degeneration and failure  Wear and tear degeneration assoc w/ ageing is (stiffening and thickening of the valve leaflets as well as the now the more common cause resultant turbulent flow) and more prone to become involved in IE causing further valvular damage  Several valvular entities have particular specific aetiologic

associations o AS: congenital bicuspid valve, calcific (senile) degeneration o AR: congenital bicuspid valve, IE, rheumatic fibrosis, syphilitic aortitis, RA, Marfan syndrome, cystic medial necrosis o MS: RHD (mitral annular calcification), rarely endomyocardial fibroelastosis, malignant carcinoid syndrome, SLE o MR: MV prolapse, abnormal leaflets and commissures postinflam (RHD, IE), papillary muscle dysfunct (MI), LV enlargement (myocaditis, hypertrophic cardiomyopathy), idiopathic myxomatous degeneration

11,13 Pathophysiology  Leads to restriction to blood flow (stenotic) or incompetency of the valves and backward flow (regurgitation/insufficiency). o Stenotic lesions: pressure overload on the upstream cardiac and vascular structuresconcentric LV hypertrophy is AS o Regurgitant lesions: volume overloadLV dilatation & eccentric hypertrophy ↑ contractility (Starlings’ Law)

The following pathogenic responses result:  AS o Concentric LV hypertrophy (initial) o LA hypertrophy (secondary to ↑ role of atrial contraction in diastolic filling of the hypertrophied LV) o ↓ LV (late) Complications: LV hypertrophy (concentric), exacerbation of CAD, arrhythmia, syncope, IE  AR o LV dilation (early) o LV hypertrophy (secondary) o ↓ LV contractility (late) causing HF  MS o Fusion of commissures, leaflet thickening, shortening of chordae tendinae o Cusps fuse↑ LA pressure LA enlargement (early) with subsequent development of AF o Pulmonary venous congestion (early) o ↑ pulmonary and pulmonary HT N(late) o RV hypertrophy and RHF (late) Complications: AF, IE, atrial flutter, pulmonary HTN, emboli from LA , RVH, RVF, CHF, pressure from enlarged LA on local structures may cause hoarseness, dysphagia, bronchial obstruction  MR o ↑ LA pressureLA enlargement (early) causes AF o Pulmonary congestion (late) o Pulmonary HTN (late) o LV failure (late, as LV no longer able to compensate for regurgitant flow by ↑ systolic emptying) Complications: LVH, LA dilation, hyperdynamic cardiomegaly, LHF, RHF, atrial flutter, AF

 These changes will only occur if the valvular lesions develop slowly over time (eg RHD). Initially compensatory, but usually at the eventual cost of chamber failure  If rapid valvular lesion (in acute AR or MR from IE or acute MR in setting of AMI) abrupt congestive failure results  Abnormal valve surfaces are thrombogenic (esp when associated with AF): emboli (stroke)

Chest Pain (CP) Funny feeling in chest!

Questions to ask on Hx1,4,12 DDx1,4,12  Determine the severity, location, duration, and-  Common aetiologies in 1O care setting are musculoskeletal Character: (36%), GIT (19%), stable angina (10.5%), unstable angina  Central, crushing -MI or MI (1.5%)  Constricting -angina, oesophageal spasm, anxiety Life threatening causes must always be excluded:  Sudden, tearing -aortic dissection  Acute coronary syndrome (AMI, unstable angina)-severe  Sharp, pleuritic -pneumonia, PE, pericarditis central chest pain radiating to jaw or upper extremities, Radiation: assoc w/ nausea, vomiting; may have life-threatening  Arms, neck/jaw -MI arrhythmias, , pulmonary oedema  Shoulder -MI, cholecystitis, GORD, PUD  Aortic dissection-sudden, severe pain, “tearing” sensation  Interscapular -aortic dissection radiating to mid-back  Back -pancreatitis, GORD, PUD  Tension pneumothorax-acute, sharp, pleuritic pain assoc Exacerbating and relieving factors: w/ dyspnea, tachycardia, tachypnea, hypoxia; mediastinal Cardiac (also psychogenic)- shift with compression of great vessels causes ↓ BF to  ↑ by exercise, emotion heartshock  ↓ by rest, nitrates  PE-acute SOB, pleuritic pain, syncope, imminent Pleuritic- cardiopulmonary arrest  ↑ by deep breathing  -suddenly as result of trauma or aortic Oesophageal disease- dissection, or gradual, with muffled , distended neck ,  ↑ by food, lying down, hot drinks, ETOH  Oesophageal rupture-localised abrupt onset lower thoracic  ↓ by antacids pain ↑ w/ swallowing, neck flexion, preceded by vomiting Musculo- Cardiac:  ↑ by movement or local pressure Note-Pericarditis, pancreatitis, oesophageal disease may be  Angina, MI, pericarditis, myocarditis, , aortic dissection relieved by sitting forwards Respiratory: Associated sx:  PE, pneumothorax, pneumonia, pleuritis, pleurodynia  Dyspnea -LVF, PE, pneumothorax, pneumonia, GIT: anxiety  Oesophagitis, hiatus hernia, oesophageal spasm, PUD,  N&V -MI, oesophageal rupture, acute acute cholecystitis, pancreatitis, splenic infarction, cholecystitis, pancreatitis hepatitis  Palpitations -arrhythmias, thyrotoxicosis, anxiety Chest wall:  Syncope -cardiac events, vasovagal ‘faints’  Ribs-fracture, costrochondritis  Prodrome viral illness -viral pleuritis or pericarditis  Nerves-herpes zoster, trauma PMHx  Muscles-rheumatic  Specific cardiac risk factors-known cardiac disease, ↑ chol, Psychogenic: HTN, smoking, family Hx  Anxiety, panic attack  Risk factors for DVT-prolonged immobilization, recent Pleuritic pain-↑ w/ inspiration or cough, aggravated by surgery, hospitalization, travel, smoking, OCP movement or position (pulmonary aetiologies, pericarditis, Med Hx musculoskeletal)  NSAID use may suggest gastric aetiology Visceral pain-dull ache, tightness, burning pain, poorly Social Hx localized (MI, oesophageal disease)  Cocaine use (cardiac ischaemia)

Ex1,4,12,13 Vitals  Dyspnea, tachypnea (pneumothorax, PE)  BP-unequal b/w arms (aortic dissection) Inspection  ↑ JVP (cardiac tamponade)  Rash in region of dermatological burning pain (herpes zoster) Palpation  Reproduction of CP by palpation (musculoskeletal eg. costochondritis)  Examine legs for DVT-LL oedema, erythema, with tender firm calf Auscultation  Cardiac auscultation for ↓heart sounds (cardiac tamponade), MR murmur (ACS, heart failure)  Respiratory auscultation- o ↓ breath sounds (pneumothorax, collapsed lobe) o Crepitations in lung bases (pneumonia, HF) o Pleural rub (pulmonary infarct, pneumonia) o Hyperresonance, tracheal deviation to opposite side (pneumothorax)

Acute Mx1,4,12 Ix1,4,12  Continuous monitoring of vitals (temp, PR, BP  Continuous monitoring of vitals (temp, PR, BP [both arms [both arms initially], RR, O2 sat) initially], RR, O2 sat) o O2 saturation <90% high-flow O2 Bloods  Take bloods (see ‘Ix’) and insert IVC  FBC (anaemia, infection), U&E (renal profile), cardiac  Administer analgesia, antiemetics as required biomarkers (CK, CK-MB, troponin I & T), BNP, D-dimer (exclude PE), & LFT, serum lipase, ABG if acute cholecystitis  See ‘Ix’ for more info on imaging etc or pancreatitis suspected Pharmacological o CK peaks @ 48hrs  Analgesia - o Troponin T or I peaks @ 12-24hrs, more sensitive and o NSAIDs in suspected musculoskeletal specific for cardiac damage. Nb Consider non-AMI aetiologies or pericarditis causes for +ve troponin eg. HF arrhythmia, myocarditis, o Severe painmorphine IV PE renal failure, septic shock  AMI-antiplatelet (ASA, clopidogrel, and/or ECG GPIIb/IIIa inhibitor) and antithrombotic Rx CXR (heparin/LMWH). Consider B-blocker & IV GTN  Look for signs of heart failure o STEMI acute reperfusion therapy with o ↑ cardiac silhouette, dilated upper lobe vessels, alveolar and primary angioplasty (<6hrs) or thrombolytics, perihilar shadowing, Kerley B lines, pleural effusions if primary PCI unavailable o NSTEMI -stabilize with B-blocker, nitrates.  Widened mediastinumdissecting aorta Angiography+PCI within 24 hours  Large globular heartcardiac tamponade  Aortic dissectionIV beta-blockade for HR and BP Echocardiography control  TTE for Dx cardiac tamponade, and pts w/ high suspicion for  PE systemic anticoagulation with heparin or PERV hypokinesis and paradoxical septal motion indication LMWH of acute RVF  GORD PPI  CT chest w/ IV contrast or TOE to confirm Dx aortic dissection Non-Pharmacological V/Q scan  Tension pneumoneedle decompression followed  In presence of pleuritic pain and clinical suspicion of PE by tube thorarostomy to prevent acute Abdo Imaging decompensation  US or CT in suspected acute cholecystitis or pancreatitis  CAD Coronary angioplasty Exercise treadmill test or stress test with imaging  In probable angina Barium swallow  Oesophageal spasm,corkscrew or rosary bead appearance

BMJ Editorial Team. Chest pain [Internet]. BMJ Evidence Centre: BMJ Publishing Group Limited; 2011 [cited 2011 Apr-Jun]. Available from: BestPractice

Myocardial Infarction Definition Death of myocardium from coronary ischaemia

Classification 1,4 Ex4,13 1. ST-segment elevation (or new onset LBBB)  Can be entirely normal 2. NSTEMI incl non-Q wave, subendocardial MI-ECG may  Anxious, restless, uncomfortable show ST depression, inversion, non -specific  Ashen, diaphoretic, cool, cyanosis changes, or may be normal  Tachycardia, bradycardia (inferior wall MI) Acute coronary syndrome includes unstable angina, STEMI,  Irregular pulse NSTEMI  BP usually ≥110mmHg, often hypertensive (anxiety) or hypotensive (shock) Presentation4,12  4th sound (↓ compliance of ischaemic myocardium)  Acute retrosternal chest pain: Complications suggested by: oreaches max over several minutes, lasts >20 mins  ↑ JVP, 3rd HS, basal crepitations (signs of HF) oprolonged or recurrent  Pansystolic murmur (papillary muscle dysfunction, VSD) omay radiate to back, neck, arms or jaw  onitrates may provide relief, but generally not resolution  No pain (‘silent’ infarct) in elderly (dementia), diabetics, post op (analgaesics)-may have pulmonary oedema, epigastric pain, post-op hypotension or oligouria, acute confusional state, stroke, diabetic hyperglycaemic states DDx4,12  Palpitations, diaphoresis, anxiety  Angina, pericarditis, myocarditis, aortic dissection  Dyspnea, numbness  PE, tension pneumothorax  Nausea, vomiting Oesophageal spasm, reflux or rupture, cholecystitis,  Light-headedness, syncope pancreatitis)  Fatigue  PMH of new-onset angina or angina w/ increasing severity, duration, or frequency; Hx MI, IHD, HTN, hyperlipidaemia, DM, hypothyroidism Mx1 Medical emergency: prompt therapy to limit infarct size + Ix4,16 preserve ventricular function post infarct Bloods Pre-hospital:  Aspirin 300mg po, GTN sublingual, analgesia IV  FBC, U&E, glucose, lipid profile, troponin T or I, CK-MB, At hospital: myoglobulin, prothrombin time with INR Cardiac biomarkers  Rapid clinical assessment w/ 12-lead ECG and CXR  Troponin T and I-  Administer O2 (↑ myocardial oxygen delivery result in ↓ o ↑ 3-12hr, peak 24-48hr, ↓ to baseline 5-14days. pain) Nb Can detect elevated levels even earlier with the new  Analgesia w/ morphine IV high sensitive troponin assays o Pain relief↓ adrenergic tone↓ oxygen demand  CK (CK-MM {skel muscle}, CK-BB {brain}. CK-MB o Opiates (morphine): pain and anxiolysis; also ↓ HR ↓ {heart})- BP thus improve haemodynamics o ↑ 3-12hr, peak ≤24hr, ↓ to baseline 48-72hr  Administer antiplatelet and antithrombotic therapy for o Sensitivity 95%, high specificity (CK-MB only) coronary thrombosis o Note low sensitivity very early MI (<6hr after Sx Goals of acute care onset), or later (>36hrs after Sx onset)  Relief of pain, ↓ myocardial oxygen demand,  Myoglobulin- improve/restore myocardial . recognition & o Rise w/in 1-4h, highly sensitive but not specific treatment of complications ECG – check early and recheck frequently (see over page)-acute Therapies Mx algorithm based on presence (STEMI) or absence of ST- Monitor for complications, institute secondary prevention, segment elevation (NSTEMI) assess/treat residual atherosclerotic disease, physical CXR rehabilitation  Signs of HF, heart size usually normal unless previous  STEMI: primary angioplasty or thrombolysis MIs/HF  NSTEMI: stabilize with aim of angiography plus/minus  Other causes of chest pain: pneumonia, PE, aortic PCI with 1-2 days dissection  Proven evidence-based therapies for secondary prevention Cardiac echocardiography (transthoracic and transoesophageal) after MI include,  Regional wall motion abnormalities indicative of ischaemia 1. Beta-blockers (esp if HF, ventricular or infarct arrhythmia)  Structural complications such as aneurysms, pericardial 2. ACE-inhibitors (esp if HF) effusions, valvular incompetence, mural thrombi 3. High-dose statins 4. Anti-platelet therapy-note need dual  Assess LV function and segmental wall motion antiplatelet therapy for 12m if received stent Coronary angiography – usually performed in setting of AMI with goal of mechanical revascularisation  After discharge pt gradually ↑ activity over 8/52  Identify precise location of a thrombus  Educate! Cardiac rehab program, identify & modify risk  Detect other atherosclerotic lesions factors

Aetiology and Pathophysiology1,4,12 Complications1,12  Plaque rupture, thrombosis, inflammation, irreversible Early death:1/12- myocyte death and necrosis  Arrhythmias (VFs/V tachy, complete heart block)  Most often occurs by occlusion of a coronary artery by a  HF (cardiogenic shock) thrombus that forms as a result of the spontaneous rupture  Ventricular rupture (peak 3-5 days)

of a pre existing atherosclerotic plaque  Other mechanical complications (VSD, mitral  Spontaneous fissuring and rupturing or a coronary papillary rupture) atherosclerotic plaque exposes a highly thrombogenic Death after 1/12- surface leads to platelet aggregation and fibrin formation,  Reinfarction thus thrombus  Progressive HF  Large thrombus completely occlude lumenSTEMI;  Sudden arrhythmias coronary thrombus w/ subtotal occlusionNSTEMI o Transmural or Q wave infarct involves entire thickness of myocardium Epidemiology1,4 o Subendocardial or non Q wave infarct from subtotal  50% die w/in 2hr onset sx or transient occlusion (thrombus), followed by  Worse prognosis if elderly, LV failure, ST changes spontaneous lysis before occurrence of full thickness infarct; also in setting of vessel occlusion Risk Factors with extensive distal collateralisation Non-modifiable:  Coronary artery dissection (often in setting of dissecting  Age>40yo, male, family hx IHD ) Modifiable:  Coronary vasospasm (either idiopathic or drug induced,  Smoking, HTN, DM, hyperlipidaemia, obesity, e.g., cocaine) sedentary lifestyle  In situ thrombus formation (hypercoagulable state)  Other: coronary embolism, vasculitis (Kawasakis disease), CO poisoning

ECG and MI1,16 Horizontal plane:  V1, V2: RV  V3, V4: IVS & anterior wall LV  V5, V6: anterior & lateral walls LV Vertical plane:  Left lateral heart: I, VL

 Inferior heart: II, III, VF  Right atrium: VR Infarct patterns: Longmore M, Wilkindon IB, Davidson EH, Foulkes A, Mafi AR. Oxford  Antero septal: V1 to V4 (LAD) th Handbook of Clinical Medicine. 8 ed. Oxford: Oxford Univeristy Press; 2010.  Anterolateral: V5-V6, I, aVL (LCX) Fig 1, Sequential ECG changes following acute MI; p. 113

 Inferior: II, III, aVF (RCA)  Posterior V1-V2 {tall R, not Q}(RCA) Blood Supply of the Myocardium1,2,11 Anteroseptal/Anterior infarct  LCA –between LA and pulmonary trunk to reach AV  Artery: LAD and branches groove, dividing into  Leads: V1-V4 . LAD: in anterior IV groove toward cardiac apex  Possible abnormalities: ST elevation, Q waves, T wave o Septal br supply ant 2/3 IVS, apical part of ant inversion in leads V1-V4 papillary muscle Anterolateral infarct o Diagonal br supply ant LV  Artery: LCX . LCX: continues in L AV groove, passes around L  Leads: V5-V6, I, aVL border of heart to posterior surface  Possible abnormalities: ST elevation, Q waves, T o Large obtuse marginal br supply lateral and inversion in leads I, aVL, V5-6 posterior wall of LV (and variable parts of Inferior infarct posterior heart)  Artery: RCA . RCA – in R AV groove, passing posteriorly between RA  Leads: II, II, VF and RV  Possible abnormalities: ST elevation, Q waves, T . Acute marginal br supply RV inversion in leads II, III and VF . posterior descending artery (85% from RCA; 8% from LCX) o Travels from inferioposterior aspect to the apex o Supplies inferior and posterior walls of RV and variable portions of LV . AV nodal artery given off usually prior to posterior descending branch . SA nodal artery (70% from RCA, 25% from LCX)

Coronary Artery Disease Definition Thickening and hardening with focal narrowing (aka. atherosclerosis) of large and medium epicardial coronary arteries

Presentation4 Ex1,3  Chest pain or discomfort-stable or unstable angina NB: May have a normal Ex, esp if asymptomatic at time of o Stable=by exertion or emotion; pain ↑ over exam mins and ↓ by rest over mins  Obesity o Unstable=pain at rest, or significant change Vitals: in pattern of existing chronic angina  HTN o Atypical=atypical pain characteristics or Auscultation: dyspnea only (esp underlying diabetes)  S3, S4 (HTN), MR  Substernal or central pressure, heaviness, squeezing, Findings due to predisposing conditions or atherosclerosis or choking outside of coronary arteries:  Rarely described as sharp localized pain or of sudden oRetinal vascular damage (see “Hypertension”) onset oArterial bruits (peripheral atherosclerosis) eg.  Radiation to jaw, shoulder, back or arms carotid, renal  Sx of co-existing peripheral artery disease such as oAbsent or diminished peripheral pulses intermittent claudication (peripheral atherosclerosis)  Meds: OCP oXanthelasmata, tendon xanthomas (familial  PMH: ↑LDL, ↓HDL, HTN, DM hyperlipidaemia)  FHx: HD, HTN, DM  Social Hx: Smoking, type A personality Mx1,17 DDx4 Goals: Control symptoms, stop or limit progression, and • MI, aortic dissection avoid MI, improve prognosis • PE, pneumothorax (tension) Pt Education • GIT: oesophageal spasms, cholecystitis, pancreatitis  Recognizing sx of MI, action plan • Nonatherosclerotic CAD: collagen (eg. Risk Factor Mx Kawasaki disease, Takayasu arteritis), ID (septic emboli)  Smoking cessation  Treat hyperlipidaemia (↓ intake sat’d fats; statin) Ix1,4,12  Treat HTN For RFs and assoc conditions:  Control diabetes  Lipid profile, glucose, creatinine, urine microalbumin  Weight management (BMI 18.5-24.9) Resting ECG  ↑ physical activity  Normal in 50%  Moderate ETOH  Old infarct: Q waves, inverted T waves  Reduce emotional and physical stress  Ischaemia: ST depression > 1mm depression in 2 Meds-goals are control sx and secondary prevention leads  Aspirin 75-162 mg/day  Evidence of LV hypertrophy  ACE inhibitors-↓ mortality, MI, hospital admission Stress ECG testing-diagnostic, risk assessment, best utility in for HF patients w/ intermediate pre-test likelihood of CAD (Bayes  Beta blockers-if hx angina, MI, ACS, or LV theorem) dysfunction  Exercise (preferred)-treadmill, bicycle ergometer with  Statins-↓ mortality, MI standardized increasing workload  Nitrates (nitroglycerin, isosorbide dinitrate);  Discontinue if chest pain, dizziness, severe dyspneoa, o Systemic venodilation↓ ventricular wall > 2mm ST depression, ↓ sBP > 15mm Hg, ventricular tensionrelieving cardiac workload tachys o Coronary artery dilatation↑ myocardial  Diagnostic ST depression positive test blood flow  Nb Exercise or pharm stress echo or perfusion o Sublingual (acute ischaemia); patches, slow imaging more sens and spec than EST but also more $ release oral (long acting to limit frequency and Coronary arteriography – diagnostic, 1st line high risk pt severity of attacks); IV nitroglycerin for  Determine if mechanical revascularisation (bypass or severe acute. angioplasty) possible and to guide this therapy o SE: hypotension, lightheadedness, headache (depends on number of vessels, coexisting illness, age, o Other antianginal agents are calcium channel functional status, severity and nature of sx) blockers and nicorandil Perfusion imaging (SPECT) Coronary Revascularization  If resting ECG has pre-excitation or >1mm ST  PCI/stent or CABG-depends on coronary anatomy depression, abnormal exercise test, worsening Sx and LV dysfunction

Complications4  Angina pectoris  ACS including MI 1,4  Sudden cardiac death (VF/asystole) Epidemiology  HF  Majority of infarcts occur in vessels <50%  Arrhythmias particularly VT/VF stenosed; 40% infarcts lead to sudden death  Kidney function decline  >50% stenosed vessels lead to exertional angina  Depression (early warning)

Aetiology and Pathophysiology11 Fatty streak  Longitudinal accumulation of lipid-filled foamy macrophages  Multiple minute flat yellow spotscoalesce into elongated streaks ≥1cm  Earliest lesions in atherosclerosis  Can happen early in life <1yo, seen in virtually all children >10yo, regardless  Same anatomic sites that later tend to develop into plaques  Not all destined to become advanced lesions  Atheroma (atherosclerotic plaque)  Fibrofatty plaque within intimaimpinge on lumen of artery  Raised lesion w/ soft, yellow necrotic core of lipid (cell debris, cholesterol, cholesterol esters, calcium) covered w/ fibrous cap (smooth muscle, collagen, lipid, foam cells)  Response-to-injury hypothesis oChronic inflammatory and healing response of arterial wall to endothelial injury oInteraction of modified lipoproteins, macrophages, T lymphocytes, with normal cellular constituents of arterial wall 1. Endothelial injury/dysfunction (hyperlipidaemia, HTN, smoking, toxins, haemodynamic factors, immune reactions, viruses)↑ vascular permeability, leukocyte adhesion, thrombosis 2. Accumulation of lipoproteins (mainly LDL)oxidised 3. Monocyte adhesion to endotheliumemigration to intimatransformation to macrophagesingest oxidized LDLfoam cells 4. Platelet adhesion 5. Factor release from activated platelets, macrophages, vascular wall cellssmooth muscle cell recruitment, other inflam cells 6. Smooth muscle cell proliferation and ECM production 7. Lipid accumulation 8. Areas of cell necrosis and calcification within the plaque occur 9. Formation of fibrous cap results in narrowing of lumen of coronary artery 10. Blood flow reduced to the distal myocardium; oxygen supply becomes limited 11. Under increased demand, ischaemia occurs in myocardium (CSA <30% of normal) 12. Progressive luminal compromise

th Kumar V, Abbas Abul, Fausto N, Ater J. Robbins and Cotran Pathologic basis of disease. 8 ed. Saunders Elsevier US; 2010. Fig 11-5, Natural hx, morphologic features, main pathogenic events, and clinical complications of athersclerosis; p. 505

Risk Factors for CAD Risk Factors for Mortality1,4,11

 A – age, activity, A-type personality  Extent of coronary disease-# vessels affected

 B – blood pressure, bloke  Extent of LV damage-result of previous MIs 2  C – cigarette or cigar smoking, cocaine  Renal impairment (GFR<60mL/min/1.73m ) and  D – diabetes, dyslipidaemia (↑TG, ↑ total chol, proteinuria (≥1+ dipstick) ↑LDL, ↓HDL)  Depression  E – early menopause  Low functional support  F – family hx, fatty boomba  Limited social support  G – silent G  H – hyperhomocysteinaemia, hyperuricaemia

Heart Failure Definition The inability of the heart to pump blood at a rate that meets metabolic demands.

Classification1,4 DDx1 Classified according to If known CVD, Dx generally made clinically  The predominance of the ventricle affected (RHF vs LHF) Rule out common causes for dyspnea: o Cor pulmonale=RHF 2o lung disease  COPD, asthma, pneumonia, arrhythmia, IS LD, anaemia, PE o Together as congestive cardiac failure (CCF) Rule out other causes for peripheral oedema:  The predominant form of myocardial dysfunction  ARF, CKD, hepatic disease, venous insufficiency, endocrine o Systolic-inability of ventricle to contract disease, drugs normally↓CO, EF<40% o Diastolic-inability of ventricle to relax and fill normally↑ filling pressures, EF>50% Ix4,6 o Usually co-exist Bloods  Time course  FBC, U&E, Ca2+, Mg2+, BNP, lipid profile, LFTs, TSH o Acute-new onset, or decompensation of chronic; ECG characterized by pulmonary and/or peripheral oedema  Ischaemia, arrhythmia, MI, hypertrophy +/- signs of peripheral hypoperfusion CXR o Chronic-progresses slowly; venous congestion  Enlarged cardiac silhouette (cardiothoracic ratio >50%), common, arterial press well maintained until late dilated prominent upper lobe vessels, diffuse IS or alveolar shadowing, perihilar ‘bat’s wing’ shadowing (alveolar Hx1,3,4 oedema), Kerley B lines (IS oedema), pleural effusions LHF Echocardiography  Dyspnea (initially exertional, then at rest), orthopneoa,  Valve function and overall ventricular function PND, nocturnal cough, wheeze (cardiac ‘asthma’)  Systolic dysfunction: ↓ ejection fraction, cardiomegaly  Poor exercise tolerance, fatigue  Diastolic dysfunction: ejection fraction normal and  Nocturia ventricular wall thickening without dilatation may be present  Cold peripheries  Weight loss, muscle wasting Mx1,17 RHF Lifestyle Modifications  Peripheral oedema (up to thighs, sacrum, abdominal wall)  Regular physical activity tailored to pts capacity (10-30  Nausea, anorexia, abdominal pain (liver distension) min/day, 5-7/7)  Facial engorgement (HF in children), venous pulsation  Nutrition- (“v” wave) in neck (tricuspid regurgitation) o Limit saturated fat intake

o High-fibre diet (constipation common due to relative Ex4,13 GIT hypoperfusion) Pts w/ compensated chronic HF may be normal on examination o Sodium restriction (Class II≤3g/day, III/IV≤2g/day) LHF  Fluid Mx  Tachypnea (↑ pul pressures), central cyanosis (pul o Daily weights (morning, before breakfast) oedema), Cheyne-Stokes breathing, peripheral cyanosis o ↑/↓ ≥2kg over 2 dayscontact GP or specialist w/out (low CO), hypotension (low CO), cardiac cachexia delay o Fluid restriction (<1.2-2.0L/day)  Sinus tachycardia (↑ sympathetic tone), low pulse pressure o ETOH restricted to 10-20g/day (low CO), pulsus alternans o Limit to 1-2 cups caffeinated beverages a day  Laterally displaced and/or dyskinetic (esp w/  Smoking cessation systolic dysfunction)  Flu vaccination  3rd heart sound (systolic dysfunction)  Depression and social isolation are important associated  Functional mitral regurgitation (2O to valve ring dilatation) factors and shown to have direct causal relationship. Turn  Dullness at lung bases, basal inspiratory crackles and that frown upside down! wheezes (↑ , pleural effusions)  Pts are at increased risk of DVT-long flights may predispose Signs of underlying or precipitating cause: to accidental omission of meds, lower limb oedema,  IHD, cardiomyopathy, aortic or mitral regurgitation, dehydration, and DCT, therefore pt should be counseled prior systolic HTN, anaemia, thyrotoxicosis, rapid arrhythmia to travel and DVT prophylaxis considered RHF Pharmacological  Pitting ankle and/or sacral oedema, ascites (Na+ & water ACE-I* retention, ↑ venous press)  LV systolic dysfunction  Cool peripheries, peripheral cyanosis (low CO)  If cough, use ARB  Low volume arterial pulse (low CO)  Up-titrate to doses shown to be benefit in major trials  Raised JVP (↑venous pressures, ↑ R heart preload), Beta-blockers* Kussmaul’s sign (↑JVP on inspiration), large V waves  NOT initiated during a phase of acute decompensation, only (function TR 2o to valve ring dilatation) after pt has stabilized  RV heave (pulmonary HTN) Aldosterone antagonists (spironolactone, epleronone)*  RV S3, pansystolic murmur (TR) Diuretics  Tender hepatomegaly (↑ venous press), pulsatile liver (TR)  To achieve euvolaemia in fluid-overloaded pts Signs of underlying or precipitating cause:  Loop SE: ↓K+, renal impairment  COPD, LHF, TR, right MI, cardiomyopathy  Thiazide-consider in refractory oedema *improves LV function and long-term prognosis Mx Cont… New York Classification of HF1,2,4 Second-Line Agents: I HD present, no sx Digoxin II Comfortable at rest, but fatigue, palpitation, dyspnea on  LV systolic dysfunction, signs and symptoms w/ ordinary physical activities standard therapy III Fatigue, palpitations, dyspnea provoked by less then  For symptom relief and to reduce HF hospitalization ordinary activity, which is limiting  Especially beneficial in CHF pts w/ AF IV Sx of cardiac insufficiency at rest, all activity causes discomfort Pt Education is essential  Educate about underlying condition, beneficial lifestyle changes, function of medication, possible SE of therapy, signs of deterioration of their condition, importance of Pathophysiology11 adherence to therapy CO determined by  Exercise rehab reduces sx and improves effort tolerance 1.Preload (LVEDP): pressure required to distend the ventricle to a given end diastolic volume 2.Contractility: the stroke work (CO) the heart generates at a given preload – describes functional state of Epidemiology 1,4 myocardium; ↑ preload↑ stroke work  1-3 % general population, 10% >70yrs 3. (sBP): the dynamic resistance against which  5yr mortality 25-50% the heart contracts

Systolic Dysfunction=abnormality in force generation (contractility)  ↓ contractility or lowered inotropic state (due to loss of viable myocardium or dysfunction of myofibrils 1,4,11,13 Aetiology  For a given preload, get ↓ inotropic state, ↓ ventricular Systolic HF function, ↓ ejection fraction  IHD, MI, systemic HTN, valvular HD (incl AS, MR),  ↓ ejection fraction↑ end diastolic volume, thus ↑ end myocarditis, arrhythmia, IE, dilated cardiomyopathy diastolic pressure (preload) and restorating ventricular (genetic, viral, ETOH, chemotherapy), hypertrophic function

cardiomyopathy,  A limit exists to which preload can ↑ to compensate for ↓

Diastolic HF inotropy or ↑ afterload

 Systemic HTN, constrictive pericarditis, tamponade,  Once the preload> pulmonary capillary oncotic pressure,

restrictive cardiomyopathy (sarcoidosis, fluid passes into the alveolar space leading to pulmonary

haemochromotosis, amyloidosis) congestion RHF  Activation of RAA and SNS: systemic vasoconstriction and  LHF (commonest causes) ↑ afterload further impairing systolic function o o Severe chronic LHF↑ pulmonary pressures2  Accumulation of salt and water (expansion of intravascular RHF volume) further impairs systolic function, also causes  COPD, pulmonary HTN peripheral oedema  Volume overload-

o ASD, primary TR Diastolic Dysfunction=decreased ventricular compliance,  Other causes of pressure overload- contractile function usually normal o Mitral stenosis, pulmonary stenosis, idiopathic  Due to abnormalities in active relaxation during or pulmonary HTN abnormalities of elastic properties of the heart itself  Myocardial disease- (surrounding tissues) o RV MI, cardiomyopathy  ↓ compliance↑ LVEDP for a given end diastolic volume, LVF: Pulmonary in nature due to ↑ LVEDPpulmonary and pressure transmitted across pulmonary capillaries venous congestion  If place ↑ demand on heart, need still higher pressures  Myocardial disease- required to produce the greater ventricular filling to meet the o IHD, cardiomyopathy increased output demand  Volume overload-  Once filling pressure> oncotic pressure of pulmonary o Aortic or mitral regurgitation, PDA capillaries, fluid moves into alveolar space causing  Pressure overload- pulmonary congestion o Systolic HTN, aortic stenosis  Avid salt and water retention and vasoconstriction are not Precipitating factors: noncompliance w/ meds, excess fluid commonly seen in pure diastolic dysfunction intake, high output states w/ increased metabolic demands (fever, infection, hypothyroidism, anaemia, AV fistula, Complications: pregnancy, cocaine)  Cardiac arrhythmias, salt and water retention, end-organ damage (hypoxic liver injury, worsened renal function, sleep disorder, depression

Vasculitis Definition Heterogeneous group of disorders characterized by inflammation of blood vessels

Classification4,12,14 Ex4,12,14 Classified by the size of the blood vessels involved: Takayasu Large-vessel  HTN (from RAS), ↑ BP in legs, painful skin nodules,  Takayasu’s arteritis (“pulseless disease”): aorta and major retinal haemorrhages, carotid, subclavian or abdominal branches aorta bruits, AR (aortic root dilation), ↓ peripheral pulses  Temporal (Giant cell) arteritis (GCA): carotid, temporal, GCA - Medical emergency! vertebral, ophthalmic, aortic arch  H/ache, scalp tenderness, amaurosis fugax (painless Medium-vessel vision loss), ↓ BP in 1 or both arms, carotid, axillary or  Polyarteritis nodosa (necrotizing vasculitis) (PAN): small brachial bruits and med muscular incl renal and visceral NOT pulmonary PAN or splenic  HTN, uremia, splenomegaly, RF, foot/wrist drop  Kawasaki’s disease (acute febrile mucocutaneous LN (infarction of radial or peroneal nerve, respectively), syndrome): coronary, other extraparenchymal muscular large cutaneous ulcers esp. over lower extremities incl celiac, femoral, mesenteric, renal, iliac, axillary Kawasaki Small vessel (venules and arterioles)  Irritability, extensive erythematous rash <5d following  Churg-Strauss disease (allergic granulomatosis angiitis) fever onset, bilat conjunctival injection, red, dry and (CS): pulmonary +/- any organ system esp skin, NS, heart, peeling oral cavity, , tachycardia, diffuse kidneys, abdominal viscera erythema and oedema of hands and feet  Wegener’s granulomatosis (WG): renal, pulmonary CS  Behcet syndrome: multisystem-oral, genital, eye, CNS,  Erythrematous maculopapular rash, palpable purpura* GIT, synovium, veins, arteries, meninges, brain esp. lower extremities and buttocks (hydrostatic press  Hypersensitivity angiitis greatest), livedo reticularis, , nasal polyps, bloody nasal o Cutaneous vasculitis aka. palpable purpura discharge, wheeze, haematuria, peripheral neuropathy o Disseminated lesions: Henoch-Schonlein Purpura WG (HSP), cryoglobulinaemic vasculitis, serum sickness  Otorrhoea, ear pain, sinus pain, nasal discharge, epistaxis, nasal ulcers, nasal septal perforation, saddle nose deformity, haemoptysis (pulmonary haemorrhage) Behcet syndrome  Cutaneous lesions, erythema nodosum, ulcers Presentation4,12,14 Hypersensitivity angiitis  Generally sub-acute  Palpable purpura, petechiae, urticaria, ulcers  Differ in clinical severity and organ involvement Palpable purpura: red-purple, raised, do not blanch, lower  Constitutional sx: Fever, wt loss, malaise, myalgia, extremities arthralgia +/- accompanying organ specific symptoms Small-med vascilitides assoc w/ livedo reticularis: lace-like Takayasu’s bluish discolouration of skin esp lower limbs, aggravated by  Cool peripheries, claudication of upper arm(s), headache, cold visual Δs, dizziness, stroke, angina pectoris, hemiparesis GCA 4  New onset headache, scalp tenderness, pain when eat, DDx blurring vision, assoc w/ polymyalgia rheumatica  Embolic disease-endocarditis, atrial myoma, chol PAN embolisation  Episodic painful red skin nodules, headache, abdo pain,  Vessel stenosis or spasm-atherosclerosis, fibromuscular N&V, peripheral neuropathy dysplasia, drug-induced spasm Kawasaki  Venous thrombosis-DIC, TTP, Coumadin-associated  Erythematous polymorphous rash, erythema, dryness of necrosis, antiphospholipid antibody syndrome oral cavity and extremities, abdo pain, vomiting, diarrhea,  Small to med vessel-Inflammatory rheumatic diseases, cervical LN swelling less common hep B, hep C, HIV CS  Palpable Purpura-Disseminated meningococcal,  Recurrent asthma attacks, allergic rhinitis, sinus polyposis, gonococcal infection peripheral neuropathy DDx for specific vasculitides WG  Takayasu: carotid artery dissection, syphilis, Ehlers- Triad of- Danlos 1. acute necrotizing granulomas of RTsinus pain, bloody  GCA: RA, inflammatory arthritidies, amyloidosis nasal discharge, nasal septal perforation and ‘saddle  PAN: subacute bacterial endocarditis, SLE deformity’, hearing loss  Kawasaki: viral infections (incl enterovirus, EBV, 2. necrotizing or granulomastous vasculitis of small to med measles), bacterial infections (scarlet fever, vessels esp. lungs &URTIdyspneoa, cough, haemoptysis leptospirosis), SJS 3. Progressive focal necrotizing and cresentic  CS: allergic bronchopulmonary aspergillosis, sarcoidosis, GNproteinuria, haematuria, RF hypereosinophilic syndrome), other causes of Behcet eosinophilia (eg. drug, parasite)  Intermittent arthritis, recurrent oral and genital ulcers  WG: septic arthritis, lymphomatoid granulomatosis Hypersensitivity angiitis  Hypersensitivity angiitis: cryoglobulinaemia, malignancy  Sx depend on organ involvement, incl palpable purpura, (1% vasculitis assoc w/ lymphoproliferative diseases) petechiae, urticaria, ulcers. May be hx of offending toxin Associated disease: SLE, RA, chronic Hep C +/-arthropathy, IgA nephritis and abdo pain (intususseption)

Ix4,12 Mx12 Bloods  Withdraw offending drug if serum sickness  ↑ ESR, ↑ CRP, U&E (N/↑), HBsAg, LFT (↑ ALP in GCA),  HSP-supportive care, often remits on its own ANCA (WGc-ANCA, PANp-ANCA), IgE (↑ in CS) Pharmacological  Normochromic, normocytic anaemia, leukocytosis,  Corticosteroids PLUS thrombocytosis, eosinophilia (CS)  Bone protective agents (eg. Ca2+/vit D,  Hep C antibody (in mixed cryoglobulinaemia), Hep B surface biphosphonates) PLUS antigen (30% PAN)  Immunosuppressant if life-threatening disease Urinalysis or risk to vital organs (eg. Cyclophosphamide 3-  Haematuria, proteinuria, RBC casts 6/12 [SE cystitis, bladder cancer, ECG myelodysplasia, infertility])  Ischaemic pattern (Takasayu), tachy, arrhythmia, ↑ PR, ↓ QRS OR (Kawasaki)  Anti-metabolite (eg. Methotrexate)-1st line in CXR pts in the absence of life-threatening disease or  Pulmonary infiltrates (WG, CS); widened aorta (Takayasu) risk to vital organs, and after 3-6/12 for Biopsy remission maintenance  Definitive test to show inflammation and destruction of vessels with direct immunofluorescence; vasculitis is focal/segmental, therefore easy for biopsy to miss affected area (≥3cm) o GCA: biopsy of temporal artery, see focal granulomatous 4 Aetiology inflammation w/ mural lymphocytes, macrophages, and  Systemic autoimmune disorders of unknown giant cells which engulf and disrupt elastic lamina aetiology Conventional angiography  May be associated with immune complex deposition  For medium - and large-vessel vasculitis esp Takayasu’s, GCA, (Type III hypersensitivity); others have a more PAN prominent granulomatous involvement, suggesting a o Takayasu: see stenosis & dilatation in aorta & subclavian cell-mediated pathology o PAN: see beaded appearance of aneurysms and segmental  Kawasaki has a likely infectious aetiology which stenosis of the mesenteric arteries triggers an abnormal inflammatory response MRA (significant cytokine cascade stimulation,  For large -vessel vasculitis endothelial cell activation) in genetically Echocardiography predisposed  In pts w/ suspected Kawasaki: coronary aneurysms esp LAD,  Hypersensitivity angiitis assoc w/ exogenous RCA, LMCA, ↓ LV contractility, pericardial effusion, mild MV antigens incl drugs (esp sulfa), certain foods, (less commonly aortic) regurgitation viruses; also assoc w/ CT disease and cancer  HLA-DR is associated with Takayasu, GCA, and Behcet syndrome

Pathophysiology4,12 Epidemiology4  Pathophysiology not clear cut Depends on type of vasculitis, and pt specific factors  Majority due to immune mechanisms including age, gender, and ethnicitiy  Immune complex deposition in vessel wallactivation of  Takayasu: 86% F, 15-45yo, Asian complement cascade & circulating antibodies (cell-mediated T-  GCA: 80% F, 90% >60yo, Northern European cell response to antigen)directly attack vessel walls  PAN: young adults esp. M o Fibrinoid necrosis of BV wall  Kawasaki: young children, 85% <5yo leading o Karyorrhexis oRBC extravasation cause of acquired HD in young children, esp Japanese  Systemic symptoms due to circulating cytokines  CS: 30-40yo, slight M>F  Organ specific symptoms due in part to ↓ luminal diametertissue ischaemia  WG:: age 50-60yo, M>F  Behcet: young adults esp F, Eastern European  May also be thrombus formation in inflamed vessel and aneurysms between inflamed segments 4,12 ANCA More handy info  PAN, WG & microscopic polyangiitis, typically assoc w/ anti-  Granulomatous arteritis includes CS, WG, nØ cytoplasmic auto-antibodies (ANCA) temporal, and Takayasu  ANCA  directly activate nØdegranulate  release of O2-  Pts w/ systemic inflammatory disorders often have free radicals and proteolytic enzymes  endothelial cell-nØ family hx of identical or related disorders interactions  endothelial cell damage including RA, SLE, AI thyroid disease, MS or o c-ANCA w/ WG myasthenia gravis o p-ANCA w/ PAN  In consideration of rheumatic syndrome, be sure Vasculitis Pathology to enquire about sicca symptoms, uveitis, pleurisy, Takayasu’s Usu not biopsied! CP, oral or genital ulcers, urethral or vaginal GCA granulomas discharge, skin rash, hair loss, diarrhea, PAN Mononuclear, PMNs, fibrinoid necrosis dysphagia, Raynaud’s phenomenon Kawasaki Mononuclear, CD8+ T cells, IgA plasma cells  Vasa nervorum are small arteries which supply CS Granulomas with eosinophils blood to peripheral nerves. ↓ blood supply through WG Necrotizing and granulomatous vasa nervorummononeuritis multiplex or Hyperensitivity Leukocytoclastic, IgA in H-Sch polyneuropathy

12 Shock Decreased end-organ oxygenation caused by an imbalance between tissue O2 delivery & demand O2 debt.

Classification1,4,12 Ix1,4,12  Hypovolaemic  Arterial line-to monitor vitals (see Mx)  Cardiogenic Urine Output  Obstructive  <0.5mL/kg/hr indicates ↓ organ perfusion; record hrly  Distributive-includes anaphylactic, septic, neurogenic, Bloods adrenal crisis  FBC: ↑ WCC (septic shock)  U&E: ↓ Na+, ↑K+, ↓ glucose, ↑ Ca2+, eosinophilia (adrenal insufficiency), ↑ urea/Cr, ↑ ammonia (GI haemorrhage) Presentation1,4,12  Amylase, LFTs, CRP if suspect pancreatitis  May have chest or abdo pain  Cardiac markers eg. troponin, creatine kinase  Haematemesis, melena, haematochezia  Lactate-indicator of regional perfusion  Prolonged vomiting, diarrhea o >4mmol/L assoc w/ ↑ mortality  ↓ or no UO (renal dysfunction) o Measure from an arterial gas sample 2-3x per day, to  Worsening mental status (may make Hx tricky!) monitor response to Rx Med Hx-  Blood cultures  Hx CHD, ACS, HTN, ↑ chol, DM (cardiogenic) ECG  Blood transfusion (anaphylaxis)  AMI: ST changes, Q waves may suggest previous AMI, Meds and allergies- predisposition to cardiogenic shock  Recent use of corticosteroids (adrenal crisis)  PE: ↑ HR, RBBB (RVF)  NSAIDs, anticoagulants CXR  Allergies & recent exposure eg. bee stings  Bilateral infiltrates (pul oedema) Social Hx-  Enlarged cardiac silhouette (tamponade, cardiomyopathy)  Exposure to new foods or drugs  Mediastinal shift (tension pneumo) Echocardiogram Ex1,4,12  MI: Regional wall and valvular abnormalities  Usually ↓ BP BUT normal BP does not necessarily  Pericardial tamponade: moderate to large pericardial mean normal perfusion, as adequate pressure≠adequate effusion, diastolic collapse of RA/V CO  PE: RHF Vitals  Fever (septic shock) Mx-Time is tissue! 1,4,12  Hypoxia (tension pneumothorax) Goal: Restore O delivery to tissues and restore O debt Inspection 2 2 Monitor vitals-  Dehydration-dry skin & mucosa, ↓ skin turgor, ↓ UO  Hamodynamic monitoring (eg. MAP, sBP, & dBP, w/  Facial oedema, tongue swelling (anaphylaxis) arterial line & confirm w/ hrly noninvasive BP monitoring  Assess JVP (volume status) o MAP= 2/3(dBP) + 1/3(sBP)  Following trauma look for signs of external bleeding,  ↑ HR, ↑ RR open fracture, unstable pelvis is fractured o Failure to ↑ HR in presence of ↓ BP suggests  Look for evidence of bites and stings, rash (anaphylaxis) conduction disturbance  Look for source of infection eg. wound site (septic  Pulsus paradoxus (↓ sBP >10mmHg w/ inspiration) shock) (cardiac tamponade) Palpation  Hourly urine output-best indicator of  Epigastric tenderness (upper GI haem, trauma, Hypovolaemia pancreatitis)  Control source of bleeding (to quote Naughty Morty “turn  Calf tenderness (PE) water off from tap, don’t’ ring Mundaring Weir”)! Auscultation o Local haemostatic measures, tourniquets Cardiacmuffled heart sounds (cardiac tamponade) o Coagulation support and monitoring in setting of Respiratory major trauma  Absent unilateral breath sounds, hyperresonance to  Volume resus w/ IV fluids percussion on affected side, tracheal deviation to o Coagulopathies may result from high-volume blood opposite side (tension pneumothorax) transfusion (deficient in clotting factors) or  ↓ breath sounds & dullness to percussion may indicate consumption of factors if continued bleedinguse haemothorax following trauma) FFP & platelets  Rales (cardiogenic shock) Cardiogenic  Wheezing (anaphylaxis)  Immediate Mx MI (revascularization, anticoagulation by  Pulsus paradoxus (cardiac tamponade) 1O angioplasty or thrombolysis) Rectal Ex (if suspect GI haemorrhage)  Acute HF may require resp support (noninvasive or  Upper haem: melaena (consider doing FOBT) invasive mech vent, urgent diuresis)  Lower haem: fresh blood +/- clots Obstructive  Tension pneumo: immediate needle thoracostomy Beck’s Triad (cardiac tamponade) drainage followed by formal chest drain 1. Muffled heart sounds  Cardiac tamponade: urgent echo evaluation, 2. ↑ JVP pericardiocentesis 3. ↓ HR  PE: anticoagulation or thrombolysis

Mx Cont…1,4,12 Distributive  Anaphylaxis: subcut epinephrine immediately, stop all potentially offending agents

 Septic shock: volume resuscitation, immediate empirical Abs AFTER collection of appropriate cultures, consider (eg. norepinephrine, dobutamine) after adequate resus if pt remains hypotensive; low-dose IV hydrocortisone in pts who develop corticosteroid insufficiency (Dx by ACTH stimulation test or based on high vasopressor requirement)

BMJ Editorial Team. Shock [Internet]. BMJ Evidence Centre: BMJ Publishing Group Limited; 2011 [cited 2011 Apr-Jun]. Available from:  Neurogenic: immediate imaging, possible intervention BestPractice to reverse permanent deficits From BestPractice, adapted with permission from Dr M. Rady

 Adrenal crisis: hydrocortisone IV 1,4,12 Pathophysiology  Imbalance between O2 delivery and cellular metabolic demand O2 debt  Oxygen delivery determined by CO and O2 content of blood o CO=HRxSV 1,4,12 Aetiology and DDx . SV affected by preload (filling), LV contractility Hypovolaemic (pump function), afterload (SVR) ↓ preload↓ CO with diversion of blood from splanchnic o O2 content a compositve of Hb and arterial O2 circulation to vital organs and ↑ SVR saturation  Haemorrhage-  ↓ CO or ↓ TPR↓ BP↓ perfusion and O2 delivery o GI bleeding or trauma, AA rupture, retroperitoneal  Initially compensated shock- bleeding, long-bone fractures o Early reversible stage where homeostatic mechanisms  Fluid depletion- compensate for ↓ perfusion by ↑ HR o GIT losses (eg. diarrhea, vomiting)  Evolves to overt shock (loss of 20-30% plasma volume)- o Insensible losses (eg. full-thickness burns) o Manifested by ↓ BP, ↓ UO, ↑ RR, altered mental status rd o 3 space losses (eg. major surgery, pancreatitis,  Lack of tissue oxygenationaccumulation of products of intestinal obstruction) anaerobic metabolism eg. lactatesystemic pro- inflammatory state with excess cytokine release and other Cardiogenic inflammatory mediators Heart pump dysfunction↓ CO in setting of ↑ preload;  Can evolve to irreversible cell death and organ damage compensatory surges in catecholamines↑ SVR  MIventricular dysfunction &/or structural Cardiogenic complications (rupture of papillary muscle(s),  ↓ CO, ↑ PCWP*, ↑ SVR, ↑ CVP ventricular septum, myocardium)  Compensatory mechanisms include-  Cardiomyopathies-viral, ETOHic o Release of ADH, RAA system activation, endogenous O  CHF (eg. RHF 2 to PE) catecholamines  Cardiac valvular lesions Hypovolaemic Obstructive  ↓ circulating volume↓ preload, ↓ SV, ↓ CO, ↓ PCWP*  Outflow restriction: PE, severe pul HTN, AS or MS  Compensatory mechanisms include-  Filling restriction: cardiac tamponade, tension pneumo o Vasoconstruction (↑ output from SNS) o Fluid shift into IV space (↓ capillary hydrostatic press) + Distributive o Renal Na & H2O retention (↑ secretion ADH & Significant in setting of relative hypovolaemia activation RAA system) & ↓ SVR  Anaphylaxis Septic  Septic shock (low SVR)  Bacterial products stimulate host defense cellssystemic  Neurogenic shock-spinal anaesthesia, spinal cord injury, inflammation (from eg. activation serum ptroeins, fainting (vasovagal reaction) cytokines, leukocyte extravasation) & activation pro-inflam  Adrenal insufficiency mediators (eg.TNF-alpha, IFN-alpha & –gamma,  Also thiamine deficiency, AV fistula bradykinin) tissue damage)

Neurogenic  Lack of neuronal controlhypotension  ↓/normal/↑ CO, ↓ PCWP, ↓ SVR  Normal circulatory volume *PCWP=pulmonary capillary wedge pressure

Reference List: Cardiovascular

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