Cardiology
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| Rheumatic fever definition | Multi-system disorder resulting from an abnormal autoimmune response to a preceding streptococcal upper respiratory tract infection (SURI); proliferative inflammatory reaction involving CT |
| Rheumatic fever: major criteria (JONES) | Carditis: Pancarditis/endocarditis/myocarditis/pericarditis Polyarthritis: >2 joints, painful w/ movements & tender Chorea minor: rapid uncoordinated jerking movements (hands, face, feet) Erythema marginatum: erythematous nodules/ normal centre, painless no itching (hands, inner legs, back, abdomen, face) subcutaneous nodules: firm painless 1mm-2cm, movable skin, not inflammed - coexists with carditis |
| Rheumatic fever: minor criteria (JONES) | Clinical: arthralgia, fever 38c for 1-2 weeks Laboratory: ESR, CRP >10mg/l, leukocytosis, ASO >250U Anamnesis: strep A infection (pharyngitis, angina, scarlet fever) ECG: PR prolonged |
| Rheumatic fever: treatment principles | Bed chair regime 2-6 wks (in case of carditis & diffuse myocarditis) 1. Antibiotics for strep for 10 days: PenIcillin G 2m U 4-6doses IV: Amoxicillin 2g/day; Cefadroxil 1.0/p (recurrent) if penicillin sensitive: erythromycin 250mg 4/day 2. NSAIDS- until ESR normal to relieve arthralgia & arthritis: Diclofenac 150mg/d 3.Glucocorticoids- until CRP normal. for HF, Recurrent attacks & cardiomegaly: oral prednisolone 1-2mg every 3-5days. Severe- IV pantoprazole 4. Diazepam 2.5mg 3/day for chorea minor 5. Surgical treatment for sever AR & MR (aortic/mitral valve repair or bio-prothesis, LV assist device in HF) |
| Rheumatic fever: Primary prevention | -accurate diagnosis -appropriate treatment of strep -Abx prophylaxis in high risk populations (children, doctors, teachers, soldiers, after heart surgery or prosthetic valves) |
| Rheumatic fever: Secondary prevention | Abx prophylaxis to prevent recurrence: Penicillin G benzathine 1.2m U IM every 3wks Penicillin V potassium 200mg orally BID Sulfadiazine 1g orally once daily Macrolide/ Azalide abx for penicillin + sulfadiazine allergy Duration: RHF w/out carditis: 5yrs or age 21 ; RHF w/ carditis& w/out VHD: 10yr or age 21; RHF w/ VHD: 10yrs after last attack, until 40 or lifelong |
| Rheumatic fever: pathogenesis | - Connective tissue disorganisation, fragmentation, exudative inflammation, interstitial and cellular edema, vasculitis, collagen fiber fragmentation - Aschoff bodies (plasma cells, lymphocytes, eosinophilic leukocytes, fibrinoid material, macrophages) in myocardium and interstitium - persist long time, subclinical rheumatic activity -Acute period: regurgitating valves - Chronic period: sclerosis, deformation, stenotic valves, commissural fusion |
| Infective Endocarditis: Definition & Epidemiology | - Infection of the endocardium, usually with bacteria (staphylococci, streptococci, enterococcus, HACEK group0 or fungi. - Forms: Acute, Subacute, Persistent - can occur at any age, but risk increases with age (peak: 70-80yrs) - Male:Female ratio 2:1 |
| Infective Endocarditis: Risk Groups | - Elderly (70-80yrs) - IV drug users - Immunocompromised individuals - Patients with prosthetic heart valves/ intra-cardiac devices |
| Infective Endocarditis: Pathogenesis | (A) cell apoptosis due to blood turbulence (B) Deposit of fibrin & thrombocytes (C) colonisation of microbes & neutrophils; chemoattraction (D) Neoangiogenesis,valve destruction |
| Infective Endocarditis: Forms | -Subacute: aggressive; develops insidiously & progresses slowly (weeks-months). Usually no source of infection or portal of entry evident (streptococci most common cause). - Acute: develops abruptly & progresses rapidly (days). Evident source of infection or portal of entry ( s.aureus, group A strep, pneumococci, gonococci). If massive bacteria - can affect normal valve, - Prosthetic: develops within1 year after valve replacement; aortic>mitral . Affects mechanical and biprosthetic valves equally |
| Infective Endocarditis: Major Criteria | 1- Blood culture +ve for IE (a) + 2 separate blood cultures (every 30 mins). Typical: s. aureus, s. viridans, s.gallolyticus, HACEK gr. or enterococci (b) + 2 separate blood cultures (12 hours apart): (c) + 1 blood culuture (C. burnetii) or phase 1 IgG Ab titre >1:800 2- Imaging: (a) echo: vegetation, abscess, pseudoaneurysm, fistula, valvular perforation/aneurysm, prosthetic valve defect (dehiscence) (b) PET: abnormal activity around prosthetic valve (18F-FDG PET/CT if >3m, or radio-labelled leukocytes SPECT/CT) (c) Cardiac CT: definite paravalvular lesions |
| Infective Endocarditis: Minor Criteria | 1- Anamnesis (predisposition): underlying heart disease, IV drug abuse 2- Clinical: Fever ≥ 38° 3- Vascular phenomena: emboli, septic pulmonary infarcts, infectious aneurysm, intracranial/conjunctival haemorrhages, Janeway's lesions 4- Immunological phenomena: Glomerulonephritis, Osler's nodes, Roth's spots, Rheumatoid factor 5- Microbiological evidence: + blood culture but doesn't meet major criteria |
| Infective Endocarditis : Streptococcal treatment | NVIE 4 weeks (6 weeks if Prosthetic): -Penicillin G 12-18mln U/day IV (6 doses or cont.)or - Amoxicillin 100-200mg/kg/day IV (4-6 doses) or -Ceftriaxone 2g/day IV/IM (1 dose) If NVIE 2 weeks: One of above + Gentamycin 3mg/kg/day IV/IM (to avoid renal failure) OR if B-lactam allergic: Vancomycin 30mg/kg/day in 2 doses for 4 weeks |
| Infective Endocarditis: Staphylococcal Treatment | - Native 4-6 weeks: Oxacillin / Cloxacillin 12g/day IV in (4-6 doses >6 weeks) -if methicillin susceptible - Prosthetic > 6 weeks: Oxacillin/ cloxacillin 12g/day IV (4-6 doses) + Rifampin 900-1200mg IV or orally (2-3 doses) + Gentamycin 3mg/kg/day IV/IM (1or 2 doses for 2 weeks) - MRSA: Vancomycin + Rifampin + Gentamycin for >6weeks (alternative: Daptomycin) |
| Infective Endocarditis: Enterococcus treatment | -MOST SAFE: Ampicillin 200mg/kg/day IV (4-6 doses for 6wks) + Ceftriaxone 4g/day IV/IM (2 doses for 6 weeks) or - Ampicillin/ Amoxicillin + Gentamycin or - Vancomycin + gentamycin |
| Infective Endocarditis: Empirical treatment | Before and w/out pathogen identification: - Native / Late prosthetic: Ampicillin + Oxacillin + Gentamycin / Vancomycin + Gentamycin - Health care native / Early prosthetic: Vancomycin + Gentamycin + Rifampin |
| Primary Arterial Hypertension: Classification | Classification: - Optimal: Systolic <120, Diastolic <80 - Normal: Systolic 120-129, Diastolic 80-84 - High Normal: Systolic 130-139, Diastolic 85-89 - Hypertension grade 1: Systolic 140-159, Diastolic 90-99 - Hypertension grade 2: Systolic 160-179, Diastolic 100-109 - Hypertension grade 3: Systolic >180, Diastolic >110 - Isolated systolic hypertension: Systolic >140 but diastolic <90 |
| Primary Arterial Hypertension: Risk factors | - Hereditary & Age >35 years -↑ BMI - Excess Na+ intake - Alcohol abuse & Smoking - Dislipidemia - Chronic stress - Diabetes Mellitus - Drugs: NSAIDs, Glucocorticoids, Amphetamines, Oral contraceptives, Adrenomimetics |
| Primary Arterial Hypertension: Treatment principles | Treatment plan according to grade: - High normal: Lifestyle advice, Consider drug treatment in high risk patients with CVD - Grade 1: Lifestyle advice, Immediate drug treatment in high (or >) risk patients with CVD, Renal disease or HMOD/ Drug treatment in low risk patients if 3-6 months lifestyle change does not work - Grade 2: Lifestyle advice, Immediate drug treatment and control within 3 months - Grade 3: Lifestyle advice, Immediate drug treatment and control within 3 months |
| Primary Arterial Hypertension: Lifestyle changes | -Exercise -Reduce salt -Reduce alcohol intake (<14U for men, <8U for females) -Stop smoking -Fruits and vegetables intake -Weight control (BMI <30kg/m2) -Reduce stress |
| Primary Arterial Hypertension: Medications | Mono-therapy: considered for low risk G1HTN or very old >80yrs/ frail patients ACE I or ARB or B-blocker or CCB or Diuretic Dual Combination: if high risk ie many risk factors ; start immediately at FULL dose ACEI or ARB + CCB or Diuretics TRIPLE combination: if BP is not controlled ACEI or ARB +CCB +Diuretic For RESISTANT HTN; add B-blocker or Spironolactone 25-50mg or a-blocker (consider referral) |
| Primary Arterial Hypertension: Drug classes and representatives | - ACEI: Perindopril 5-10mg/day - ARB: Valsartan 160-300 mg/day - Thiazide diuretics: Hydrochloride thiazide 12.5-50mg/day; - Thiazide-like: Indapamide 1.5-2.5mg/day - B-blocker: Metoprolol 25-200mg - Central acting agents: Doxazosin 4-16mg/day ; Moxonidine 0.2-0.6 mg/day - Ca2+ blocker: Amlodopine 5-10mg/day; Verapamil 40-320mg/day |
| Primary Arterial Hypertension: Drug principles | - B-blockers should be considered at any step where there is a specific indication: HF, angina, post MI, atrial fibrillation, younger women planning on/are pregnant - ACEI & ARBs should not be administered together-> Orthostatic hypotension |
| Primary Arterial Hypertension: target values | -CKD -> SBP <140/90 (130 if tolerated) -HTN, DM CAD+ Stroke: SBP: 18-65yrs <130 (not <120) ; >65yrs: 130-39 & DBP: 70-79mmHg |
| Mitral Regurgitation: Etiology | Etiology: Primary (1&2 because its valvular) vs. Secondary (3. because its functional) 1- Acute - trauma, IE, AMI (chordal/papillary rupture), Acute Rheumatic Fever, Spontaneous chordal rupture, degeneration of valves 2- Chronic Organic changes of leaflets, rings, chords, papillary muscles 3- Chronic Functional (LV & Mitral annulus dilatation) - Dilated/ Ischemic/ Hypertensive Cardiomyopathy |
| Mitral Regurgitation: Pathophysiology | Systolic reversal of blood flow to LA causes 1) LA volume overload and hypertrophy -> Pulmonary hypertension/edema (venous congestion) -> RV hypertrophy& dysfunction 2) LV dilation &hypertrophy -> LV systolic & diastolic dysfunction |
| Mitral Regurgitation: Symptoms | (*Chronic can be asymptomatic, acute has:) - Fatigue - Weakness - Palpitations - Dyspnea (↓ stroke volume) - Atrial fibrillation (↑LA pressure) (maybe : diaphoresis & peripheral edema) |
| Mitral Regurgitation Diagnosis: Physical & ECG | Physical exam: - ↓ S1, audible S3 - Holosystolic murmur (at apex) spreading to the armpit - Systolic thrill on palpation (LVD) ECG: -LVH &volume overload -Atrial fibrillation, Old MI (ischemic MR), - LAH(P mitrale) |
| Mitral Regurgitation Diagnosis: Xray & Echo | Chest Xray: - Heart chamber dilation: left heart enlargement (LA,LV) -Pulmonary HTN, edema Echo: - Evaluation of the Mitral valve leaflets, annulus, chords, papillary muscles: Primary vs Secondary etiology - LA, LV systolic and diastolic diameter and volume (LV-ESD <40 mm) - LV systolic and diastolic function, PH (LV EF >60%) - Mitral regurgitation quantification (Volume, fraction, regurgitant orifice, vena contracta) |
| Mitral regurgitation: Treatment | - Prophylaxis of IE and rheumatic fever -Asymptomatic: no meds or physical restriction 1- Medication- if LVD or dysfunction present a) ACEI/B-blockers b)HR Control: RAAS inhibitors, Beta blockers, CCB, amiodarone - A.fib c) Anticoagulants eg Vit.K antagonists, warfarin -thromboembolic complication. 2- Surgical/Interventional: a) Repair: Open or Mitraclip b) Replacement: Open with CPB |
| Mitral Stenosis : Etiology | - Rheumatic fever (95%) - Congenital - Degenerative: Annulus calcification - SLE - Myxoma - RA - Fabry disease |
| Mitral Stenosis: Pathophysiology | 1- Diastolic pressure gradient between LA and LV 2- ↑ LA pressure, dilatation and hypertrophy 3- Blood regurgitates back into venous system = Raise pulmonary venous and capillary pressures 4- Pulmonary artery hypertension 5- RV hypertrophy, dilatation and dysfunction + TR |
| Mitral Stenosis: Symptoms | Symptoms depend on degree of stenosis: - Weakness - fatigue - palpitation - dyspnea (exertional, orthopnea, paroxysmal, nocturnal) - peripheral edema - chest pain/syncope (thromboembolic complications) -dysphagia/hoarseness |
| Mitral Stenosis: Physical findings | Facies mitralis Mitral melody (accentuated S1, opening snap following S2) Protodiastolic murmur at apex Graham-Steel diastolic murmur of pulmonary regurgitation |
| Mitral Stenosis: ECG & Xray findings | ECG: P mitrale (LA enlargement) RV hypertrophy (in V1; R axis, QRS deviation, tall R waves) Atrial fibrillation Right heart overload signs (big prominent R on V1-V3, deep S on V4-V6) Chest Xray: enlarged LA displaces oesophagus + straightening of left cardiac border Exercise test: to evaluate hemodynamic significance of MS |
| Mitral Stenosis: Echo | -Calcification/ fibrosis of mitral valve leaflets -Decreased motion of mitral valve leaflets -Doming/hockey-stick deformity of anterior leaflet - Posterior leaflet restricted - Reduced mitral valve orifice area (fish mouth) - Damage of sub-valvular structures; calcification, fibrosis - Dilation of LA + right heart chambers - LA thrombosis , TV insufficiency |
| Mitral Stenosis: Treatment - medications | A) Prophylaxis for B-hemolytic streptococcal infection, IE, Rheumatic fever b) HR control: B blockers (metoprolol, bisoprolol), CCB ( verapamil, diltiazem) c) For Permanent AF, HF: Digoxin/ Nitrates/ Diuretics d) Prophylaxis of thromboembolic events: VitK antagonists, warfarin |
| Mitral Stenosis: Surgical Treatment | Indications: -MVOA< 1.5cm2 (C+D stages)- hemodynamically significant MS -Severe symptomatic MS (D stage), NYHA III-IV when MVOA <1.5cm2 + percutaneous commissurotomy can't be performed + recurrent sys embolisation - Moderate MS: MVOA 1.6- 2.0 cm2 Intervention: -Percutaneous balloon commissurectomy (for younger + not heavily calcified valves) - Surgical commissurotomy ( for severe subvalvular disease, valvular calcification or LA thrombi) - Valve replacement (for severe morphological changes not suitable for balloon or surgical commissurotomy) |
| Aortic Regurgitation: ACUTE Etiology | - Aortic dissection - IE - Trauma |
| Aortic Regurgitation: CHRONIC Etiology | (a) Cusp pathology: - Congenital diseases - unicuspid/ bicuspid/ quadricuspid aortic valve, AV prolapse, - Inflammatory - IE, rheumatic fever/disease - Degenerative - atherosclerosis, calcinosis (b) Abnormalities of aortic root & ascending aorta geometry: - Idiopathic anuloaortoectasy, Inflammatory CT diseases (Spondyloarthritis, ulcerative colitis), Arterial HTN, Aneurysm of sinus vasalva, Marfan's syndrome & Ehler's Danlos - syphilis aortitis, degenerative aneurysm of ascending aorta, bicuspid AV w/ aorthopathy |
| Atherosclerosis: Unmodifiable Risk Factors | Family predisposition (premature atherosclerosis eg MI<55yrs) age : >40yrs M >50yrs F male gender genetic abnormalities |
| Atherosclerosis: Modifiable Risk Factors -1st line | Dyslipidemia Hyperfibrinogenemia Cigarette/ cigar smoking Arterial Hypertension Diabetes Mellitus (NB: MI risk ↑es 4x, if >3 ↑es 10x ) |
| Atherosclerosis: Modifiable Risk Factors - 2nd line | Obesity (BMI >30% above normal) Physical inactivity Mental stress + Type A personality Hyperuricemia - strengthen the impact of 1st line factors |
| Atherosclerosis: Pathogenesis | 1- Endothelial injury due to risk factors or trauma 2- LDLs accumulate & aggregate, entering tunica intima 3- Macrophages oxidise LDLs via free radicals 4- Oxidised LDLs stimulate further leukocyte recruitment via chemoattractants releases by endothelial & SM cells 5- Monocytes engulf LDLs; accumulation of lipids and fatty streak development; cause cytotoxic damage to endothelial cells and cause dysfunction 6-Intimal smooth muscle proliferation &↑leukocyte recruitment result in atherosclerotic plaque formation 7- If plaque reaches coronary arteries, it can keep growing and cause stenosis OR rupture off; thrombosis/ embolism OR cause aneurysm by wall damage 8- ↓ O2 supply to myocardium, cellular acidosis and lactate release; in time it can cause ischemia and is called IHD |
| Stable Angina Pectoris : definition | Pain >1month, not progressing & no exact time of disease beginning |
| Stable Angina Pectoris : PAIN symptoms | PAIN 1) type: pressure/heaviness/squeezing/tightness/burning/numbness 2) when: physical or emotional exertion/cold/rich meals/tobacco/anger 3) where: sub/parasternal; mostly left or both sides/ levine's sign (between epigastrium and neck) 4) radiation: inner arm to forearm/wrist/left shoulder/epigastrium, sometimes neck/mandible/upper back 5) duration: 0.5-5 mins but sometimes 10-15 mins 6) relief: rest/sublingual nitroglycerine (1-3mins), elimination of factor |
| Stable Angina Pectoris : other symptoms & signs | Other symptoms (Dyspnea, nausea, anxiety, cold sweats, general weakness, tremor, clouding of consciousness) Signs (pallor, ↑ HR/BP, diffuse apex beat, gallop rhythm, paradoxical S2 due to prolonged LV ejection & mid-late systolic apical murmur due to ischemia of papillary muscles) on palpation: ectopic systolic bulging / paradoxic movement |
| Stable Angina Pectoris : Classification | Class I (only rapid/strenuous/ prolonged exertion); Rare Class II (high but usual everyday physical load ); More frequent w/ nervous tension Class III (low/moderate physical load); sometimes 1st hours of awakening Class IV (slight tension, even at rest) |
| Stable Angina Pectoris: Diagnostic Criteria | 1- Typical anginal pain 2- Ischemia on ECG at rest or exertion 3- Significant CA stenosis >75% |
| Stable Angina Pectoris: Diagnosis | - Clinical signs - Blood test (for risk factors/causes & DDx): CBC, lipids, electrolytes, Thyroid, Troponin, CRP, sugar, liver enzymes, Creatinine kinase & uric acid - ECG (rest+24 hr - ST changes, T inversion,↓R, arrhythmia, BBB) - Exercise Stress test: pathological if ST changes >1mm + anginal pain - Xray (heart): degree of myocardial hypertrophy, the signs of left ventricular failure - Echo (regional wall abnormality) - SPECT w/Thallium, PET, multi-slice CT - Angiography (MRI or Invasive) |
| Stable Angina Pectoris: Treatment objectives | - To alleviate /prevent angina attack & improve QoL - To perform timely diagnosis of acute MI - To prevent sudden ischemic death |
| Stable Angina Pectoris : Treatment - lifestyle changes | Change lifestyle to improve prognosis: - quit smoking - nutrition: reduce fat/salt/alcohol intake & more fruit/veg, - if obese: reduce calories + exercise - if HTN: reduce salt/alcohol - exercise Modify RFS: ( Lipid management: diet & anti-lipid drugs, BP: antihypertensives, DM, Weight, thromboses: reduce fats/smoking/aspirin) |
| Stable Angina Pectoris : Drug therapy & Revascularisation | Drug therapy (nitrates + anti-ischemic improve quality of life, others for prognosis) 1- ↑O2 supply, = Nitrates (nitroglycerin, glycerol trinitrate, isosorbide mono/di nitrate), ACE inhibitors (captopril),Revascularization procedures (PCI, CABG) 2-↓ O2 demand = Nitrates, B-blockers (B1-metaprolol / B1&2-propanolol), Ca+ channel blockers (amlodapine), IF inhibitor (Ivabradine), Non-nitrate Anti-anginals (Ranolazine) 3- Myocyte metabolism adaptation= Anti-ischemic drugs (Trimetazidine, mildronate) 4- Prevention of adverse outcomes= Antiplatelet therapy to prevent TE (aspirin/clopidogril), Influenza vaccine, Statins (fluvastatin), RAAS blockade therapy 5- improve QoL + Prognosis( B-blockers, ACEI, Statins, Aspirin, CCBs) |
| Unstable Angina: Definition | Myocardial ischemia at rest or w/ minimal exertion in the absence of myocardial necrosis ECG: ST segment depression + inverted T wave (acute ischemia) |
| NSTEMI: Definition | Myocardial necrosis in clinical setting consistent with acute myocardial ischemia |
| Acute Coronary Syndromes : Types | - Unstable Angina - Non-ST-Segment Elevation MI (NSTEMI) - ST-Segment Elevation (STEMI) |
| NSTE- ACS: Pathogenesis | 4 processes: 1- rupture of unstable atheromatous plaque 2- coronary arterial vasoconstriction 3- imbalance between the supply and demand of myocardium for oxygen 4- gradual intra-luminal narrowing of an epicardial coronary artery because of progressive atherosclerosis or post-stent restenosis can occur simultaneously in any combination |
| Unstable Angina: Clinical presentation | -Prolonged (>20mins) anginal pain at rest: retrosternal sensation of pressure/ heaviness radiating to left arm, neck or jaw - sweating, pallor - nausea, abdominal pain, vomiting - dyspnea, syncope - Atypical symptoms: epigastric pain, indigestion - Physical exam: stable or in shock; excited/flashy/sweaty , BP↓ or↑, tachy/bradycardia auscultation : gallop rhythm,, systolic murmur, pericardial friction sound (if pericarditis) |
| MI: Clinical Presentation | - Pressure/ tightness in chest with radiation. - shortness of breath - diaphoresis (ex. sweating due to sympathetic innervation) - nausea and vomiting (parasympathetic response) - anxiety |
| NSTE-ACS: Diagnostic Criteria | 1- Troponin elevation (not specific) 2- typical ischemic symptoms or ECG ischemic changes (ST depression of T wave inversion) 3- Imaging tests: echocardiography , coronary angiography |
| NSTE- ACS: Diagnosis | 1- Clinical signs 2- ECG: ST changes - >1mm height), T inversion (if LBBB, ECG not useful) for MI: pathological Q waves 3- Biomarkers - < x5 ↑ troponin = Unstable Angina > x5 ↑ troponin = NSTEMI 4- Chest Xray - acute left ventricular insufficiency (due to stasis or edema) & heart dilation 5- Transthoracic echo - check LV structure (volume, size) and function (segment contractility, diastolic dysfunction), MI complications (rupture, aneurysm, thrombus, heart valves, pericardial effusion) |
| NSTE-ACS: GRACE Risk Score (Mnemonic - CBCSTEAK) | - Creatinine - Systolic BP - Cardiac arrest at admission - ST deviation - Troponin, (elevated cardiac biomarkers) - Elevated pulse rate - Age - Killip classification (I- no HF, II- rales/JVD, III- Pulmonary edema, IV- Cardiogenic shock/hypotension) |
| NSTE-ACS: TIMI Risk Score | TIMI (each one is 1 point) - Mnemonic - AASSKPR Age ≥65, ≥3 CAD risk factors (hypertension, hypercholesterolemia, diabetes, current smoker,family history of CAD) Known CAD (stenosis >50%) Aspirin use in past 7 days Severe angina (>2 episodes in 24 hrs) ST changes ≥ 0.5 mm Positive cardiac marker |
| NSTE-ACS: High Risk Patients | - Recurrent ischemia - Dynamic ST changes - Early post-infarction angina, - Elevated troponins - Hemodynamically unstable - Major ventricular arrhythmias - Diabetes, - GRACE score >140 (Death/MI 30d. 12-30%) |
| NSTE-ACS: Low Risk Patients | - No recurrent ischemia - Isoelectric ST segment - Only negative T wave or normal ECG - Normal biomarker levels at baseline & after 6-12 hours - GRACE score <109 (Death/ MI 30d. <2%) |
| NSTE-ACS : Invasive strategy criteria | - Immediate (<2hrs) for very high risk criteria - Early (<24hrs) for High risk criteria - Invasive (<72hrs) for intermediate risk criteria - Selective invasive for low risk criteria |
| MI: Definition | Evidence of myocardial injury (elevated cTn values) w/ necrosis in a clinical setting consistent with myocardial ischemia |
| MI: Criteria | CTn >99th percentile & at least one of the following: - symptoms of ischemia - ECG changes indicative of ischemia: sig ST/T changes or LBBB - Pathological Q wave - Imaging: new loss of myocardium or new regional wall abnormality -angiography/ autopsy: intracoronary thrombus |
| MI: CLASSIFICATION | Type I : SPONTANEOUS MI- ischemia due to primary coronary event eg plaque rupture/erosion/fissure, coronary dissection, distal platelet embolism Type II: ischemia due to ↑O2 demand eg HTN or ↓supply eg coronary artery spasm/embolism/arrhythmia/hypotension Type III: related to sudden unexpected cardiac death ( w/ symptoms of myocardial ischemia + new ECG changes: ischemia or LBBB) Type IVa: associated with PCI (w/ symptoms of MI+ cTn values >5x URL) Type IVb: associated with documented stent thrombosis Type V: associated with CABG (w/ symptoms of MI+ cTn >5x URL) |
| MI : etipathogenesis | - disruption of atherosclerotic plaque - leads to activation of thrombogenesis pathways: thrombus forms from platelet aggregates, fibrins & RBCs - complete occlusion of epicardial vessel leads to large zone of ischemia - if ischemia prolongs -> necrosis -> MI |
| Other causes of elevated troponin: Cardiac disorders | - Heart failure - Cardiomyopathy ( hypertrophic, viral ) - Hypertension - Myocarditis, pericarditis - Infiltrative disorders eg amyloidosis - Injury - Cancer |
| Other causes of elevated troponin: Systemic disorders | - Pulmonary embolism - Rhabdomyolysis - Toxicity eg anthracycline - Trauma - Renal failure - Sepsis - Stroke - Subarachnoid haemorrhage |
| ACS w/ ST elevation: Treatment | - Stabilse patient : MONA - if <120 mins: Primary PCI strategy + Re-perfusion - if >120 mins: Fibrinolytic therapy for re-perfusions ( bolus of fibrinolytic eg Tenecteplase, alteplase, reteplase, streptokinase ) then either Routine or Rescue PI & Re-perfusion - Long term : B-blockers/ ACEI (if patient w/ HF, LV dysfunction or DM) & Statins- should be continued indefinitely |
| Peri-procedural anti-thrombotic medication in PCI | - Aspirin: LD 162-325 mg/day then 75-100mg/day - P2Y12 inhibitor- Clopidogrel: LD 300-600mg/day then 75mg/day for at least 12m - Anti-coagulants: LMWH 1mg/kg or Unfractionated heparin or Bivalrudin - Glycoprotein IIb/IIIa inhibitors for high risk patients (recurrent ischemia, dynamic ECG changes or hemodynamically unstable) eg Abciximab, Tirofiban, Eftifibatide for 6-24hrs |
| Fibrinolytic therapy : contraindications | - Aortic dissection - Previous hemorrhagic stroke - Previous ischemic stroke w/in 1 yr - Active internal bleeding - Intracranial tumour - Pericarditis |
| Myocardial Revascularisation | Restoration of blood supply to ischemic myocardium to limit ongoing damage, reduce ventricular irritability & improve long-term and short-term outcomes in ACS patients Modes: - Fibrinolytic therapy, - PCI w/ or w/out stent placement - CABG |
| Myocardial Revascularisation: Unstable Angina NSTEMI | - immediate perfusion not urgent - Angiography w/in 24-48hrs of hospitalisation to identify coronary lesions requiring PCI or CABG - Non-interventional approach & trail of medical management if angiography shows ( small area of myocardium at risk, lesion morphology not amenable to PCI, CA stenosis <50% or significant left main disease in CABG candidates) or patients are at high risk of procedure- related morbidity and mortality - if persistent chest pain despite meds -> Immediate PCI or CABG |
| MI: Early complications (<48hrs) | 1) Arrhythmias: ventricular fibrillation/flutter, ventricular extrasystoles, atrial fibrillation/flutter/premature beats , AV block( if inferior infarct), bradyarrhythmias 2) LV insufficiency/ Cardiogenic shock (SBP <90mmHg) 3) RV insufficiency 4) Acute pulmonary edema |
| MI: Late complications (>48hrs) | 1) Cardiac aneurysm 2) Pericarditis 3) Remodelling (hypertrophy) 4) Rupture of the heart 5) Arrhythmias 6) Heart failure - Stroke (emboli from LV) - Venous thrombosis |
| Atrial Fibrillation: Definition & symptoms | - DEF: rapid, irregularly irregular atrial rhythm - Symptoms: often asymptomatic; palpitations or HF (weakness, light-headedness + dyspnea) - HR: 400-600bpm |
| Atrial Fibrillation: Classification | 1- Paroxysmal - self-limiting within 7 days (usually 48 hours) + sinus rhythm resolves spontaneously 2- Persistent - continuous, lasts >7 days, needs therapy to restore to sinus rhythm 3- Longstanding Persistent - lasts >1 year, possibility of restoring sinus rhythm 4- Permanent - cannot be converted back to Normal sinus rhythm 5- Lone - w/o identifiable cause for ages <60 |
| Atrial Fibrillation: ECG diagnostic criteria | - Absent P waves - Irregular/narrow QRS <120 ms - Irregular f waves (<0.1mv = fine, >0.1mv= coarse) - Irregularly irregular R-R intervals - LV hypertrophy (Axis deviation, high QRS voltage >15) |
| Atrial Flutter: Definition & Symptoms | - DEF: regular atrial tachycardia - HR: >250bpm - Symptoms: dependent of ventricular rate if VR <120bpm: few/no symptoms if VR >150bpm: palpitations, reduced cardiac output, chest discomfort, dyspnea, weakness, syncope |
| Atrial flutter: Classification | - Type 1: Typical - Macroreentrant tachycardia (2:1 AV block, 250-350 bpm) involves idioventricular rhythm & tricuspid isthmus in reentry circuit: a) Anticlockwise flutter: -ve F waves in Inf. leads( II, III, avF) b) Clockwise +ve F waves in Inf. leads - Type 2 - Atypical: (3:1 or 4:1 blocks, 350-450 bpm): * mostly for people with previous heart surgery or catheter ablasion |
| Atrial Flutter: ECG diagnostic criteria | - 'sawtooth' shape of P waves: Inf. leads (-) II, III avF +V6 & (+)V1 - No isoelectric line - Always Regular - Narrow QRS <120 ms NB:Adenosine slows the ventricular rate (doesn't for Afib/AVNRT) |
| A.fib/A. flutter: Anticoagulants indications + contraindications | Indications: recommended for all patients unless: - specifically contraindicated - at slow risk of stroke ( CHA₂DS₂-VASc score <2) AIM: to prevent thromboembolisms & stroke |
| A.fib/A. flutter: CHA₂DS₂-VASc score | - Congestive HF : 1 point - Hypertension: 1 point - Age >75: 2 points - Diabetes: 1 point - Stroke/ TIA : 2 points - Vascular disease: 1point - Age 65-74: 1point - Sex: 1 point |
| A.fib/A. flutter: Anticoagulation principles | - 0 score = Low risk: no anticoagulants - 1 score = low-moderate risk: anti-platelet (aspirin OR combination therapy: aspirin + clopidogrel & warfarin INR 2-3 - >2 score = moderate-high risk :oral anticoagulation (warfarin INR 2-3, dabigatran, rivaroxaban, apixaban, edoxaban) - Use long-term anticoagulation for patients with persistent or paroxysmal AFib/AF - Persists for longer than 48 hours / Post-cardioversion = 4 weeks of adequate anticoagulation |
| A.fib/A.flutter: Antiarrhythmic treatment | Rate control: can completely resolve symptoms - 1st line : Beta-blockers (metoprolol) & CCBs ( verapamil, diltiazem) - 2nd line: Digoxin if HF present - if ineffective: Amiodarone (and cannot tolerate first line) Rhythm control: to restore sinus rhythm / if rate control unsuccessful - Cardioversion: electrical or chemical by anti-arrhythmic drugs eg Class 1a /9quinidine, procainamide), Class 1b( flecainamide) Class III (Amiodarone/sotalol ) |
| A.Fib/ A.flutter: Anti-arrhythmic treatment (procedures) | Nonsurgical : - For A.fib: after anti-arrhythmic drugs: Pulmonary vein isolation ablation (Cryoablation or RDA)+ Pacemaker - A. flutter: AV node ablation (RDA or Isthmus block) - initially before drugs Surgical: Pacemaker, Open-heart maze procedure |
| First Degree AV block | - AV conduction delay but w/out skipped beats - 1:1 (every P is followed by QRS) - Consistently prolonged PR >200ms - Rate 79bpm - BENIGN: young w/ high vagal tone - Causes: idiopathic conduction, tissue disease, ischemia, drugs (digoxin, B-blockers, Calcium antagonists) |
| Type 1 Second Degree AV block | I Type (Wenckebach): - Progressive prolongation of the PR interval until a ventricular beat is dropped, repeats in clusters. - Associated with AV node disease - Usually BENIGN if associated w/ high vagal tone OR pacemaker needed |
| Type 2 Second Degree AV block | II Type (Mobitz) : - Regularly dropped ventriicular beats (2:1) with no lengthening of PR interval - Associated w/disease in His-Purkinje system - can progress to complete heart block -Pacemaker required |
| Type 3 Second Degree AV block | III Type (advanced/high grade) : - Several consequent P waves are blocked in the AV node - before every QRS, P wave is "tied" to the QRS - PR interval constant (looks like complete heart block) - If HR is low, after progression to complete AV block, it can be followed by asystole |
| Third Degree AV block | Third Degree (complete block): - No impulse conduction from atria to ventricles, - hence independent atrial and ventricular rates - AV dissociation: no relationship between A-V complexes -QRS: If Narrow- indicates ventricular pacemaker at that level of AV node / If Broad (>120ms)- pacemaker below AV node - PERMANENT PACEMAKER to prevent mortality & reduce morbidity from Morgangni-Adams-Stokes attacks |
| Modes of Permanent Pacemaker | Designated by 3-5 letters representing: I - Chambers placed: O (None), A (atrial), V (ventricle), D (dual) II - Chambers sensed: O (None), A (atrial), V (ventricle), D (dual) III - Response to sensing: O (None), T (trigger), I (inhibit), D (dual) IV - Rate modulation: O (none), R (rate modulating) V- whether pacemaker is multisite: in both atria, both ventricles or >1 pacing lead in a single chamber |
| Pacemaker: Principles | 1st class indications: Sinus node dysfunction, AV blocks, chronic bifascicular blocks, after acute phase of MI, after cardiac transplantation & pacing to prevent tachycardia) 1- Indications for single chamber pacemakers - permanent A. fib (VVI: a.fib w/ bradycardia, AAI: sinus bradycardia, sinus arrest) 2- Indications for dual chamber pacemakers - Sick sinus syndrome caused by sinus node dysfunction, AV blocks |
| Stable Angina: Nitrates | Eg. Long-acting glycerol trinitrate, isosorbide dinitrate, isosorbide mononitrate M.O.A: - vasodilation: reduce SBP& myocardial wall tension -> reducing oxygen. demand - increase contractility and exercise tolerance - transfer blood from non-ischemic to ischemic site |