Please enable JavaScript.

Coggle requires JavaScript to display documents.

ISCHAEMIC HEART DISEASE (ACUTE CORONARY SYNDROME (RF (66 M >70 F risk…

- - - - atorvostatin 20mg for primary prevention of CVD with greater risk than 10% 10 yr risk
      - LFT measured within 3 months of starting treatmentand at 12 months
- - - - Neck: raised JVP
      - Palpation: displaced apex beat (due to cardiomegaly)
      - Pulse: tachycardia, pulsus alternans
      - Auscultation: S3, S4 or gallop rhythm. Crackles in lung bases (pulm oedema)
      - Hands: cool peripheries, cyanosis
      - Legs: pitting oedema
  - - - CXR:
        A- alveolar oedema (batwing)
        B - kerley b lines (interstitial oedema)
        C - cardiomegaly
        D - diversion to upper lobes = prominent upper lobe vessels
        E - pleural effusion
      - ECG changes in HF non-sepcific: LV hypertrophy, AF, LBBB, pathological Q waves
      - ECHO done if abnormal ECG or BNP.
  - - - FRANK STARLING LAW:
        As myocardial contractility reduces, SV reduces=inc end diastolic vol due to incomplete emptying of ventricle during systole = fibres stretched inc SV in following contraction to generate CO - result in ventricular remodelling, inc wall stress and dec CO as mechanism fails
      - SNS: As CO declines = early activation of SNS = causes tachycardia, inc Na and fluid reabsorption by kidney and inc periph vasc resistance
      - RAAS: Late compensatory mechanism. Mediated primarily by angiotensin II - aim to achieve adequate tissue perfusion by attempting to inc CO. Actions inc preload and afterload. As heart inc in workload = further activation of RAAS = vicious cycle = fluid overload and worsening wall stress
        
        effects on ang II:
        
        aldosterone activation = Na reabsorption => inc preload
        
        ADH activation = water retention => inc preload
        
        arteriolar vasoconstriction = inc systemic vasc resistance and afterload
        
        persistently high causes fibrosis of heart [lead to further activation of SNS] and kidneys
        
        inc sympathetic activity = inc HR and contractility
  - - - 1st line:
        
        beta blockers - BISOPROLOL/CARVEDILOL - decreases HR = more time to fill = inc ejection fraction
        
        Diuretics - FUROSEMIDE (loop) then METOLAZONE (thizaide-like) - monitor K+ and renal function. REDUCES PRELOAD AND PULM CONGESTION AND OEDEMA
        
        ACEi [RAMIPRIL- SWITCH TO ARB - LOSARTAN/CANDESARTAN IF COUGH NOT TOLERATED]
      - 2nd line:
        
        aldosterone antagonist [SPIRINOLACTONE] added if still symptomatic despite 1st line meds [risk of hyper K+ when with ACEi]
        
        vasodilators [HYDRALAZINE/ISOSORBIDE DINITRATE] reduce preload and afterload. Especially useful in individuals of Afro-Caribbean origin who are resistant to treatment
      - Others:
        
        digoxin
        
        used if 1st and 2nd line flop. improves cardiac contractility. used in those with systolic dysfunction. monitor for hyperK+
        
        ivabridine
        
        blocks funny channels in SAN to dec HR used if 1st 2nd and aldost antag dont work
        
        inotropes
    - - pneumococcal and annual influenza vaccine
    - - CRT
        
        indicated in severe symptoms. LVEF<35% broad QRS
        
        cause both ventricles to contract simultaneously - placed on LV
        
        2 types: pacing and defibrillator
      - ICD
        
        used to prevent ventricular arrhythmias. recommended with LVEF <40% who have exp prev VT with haemodynamic instability or VT with syncope
      - cardiac transplantation commonly done in young with CAD or dilated cardiomyopathy
      - LVAD - bridge to transplant
  - - - poor ventricular contraction causes back up in the lungs
      - increases pulmonary vein hydrostatic pressure = result in extravasation of fluid into the interstitium - known as pulmonary oedmea
      - Usually affected first
      - PULM OEDEMA, CARDIOMEGALY, PERIPH OEDEMA+
    - - RHF is compensated by ventricular hypertrophy = lead to progressive dilatation and failure
      - less commonly, isolated RHF is caused secondary to lung disease such as pulmonary HTN or pulmonary emboli - cor pulmonale
      - inc in press of pulm vessels causes R side of heart to pump against inc resistance
      - rarer causes are related to pulmonary and tricuspid valve pathology
      - most commonly caused by left heart failure
      - ELEVATED JVP, HEPATOMEG, ASCITES, PERIPH OEDEMA
    - - DIASTOLIC HF
        
        preserved ejection fraction
        
        preserved LV systolic function
        
        ventricles unable to relax due to stiffness = inadequate filling of heart during diastole (EF >50%)
        
        seen in restrictive cardiomyopathy and constrictive pericarditis
      - LOW OUTPUT HF
        
        caused by either failure of the pump (heart), inc preload or inc afterload
        
        low output states are seen in IHD and aortic stenosis
        
        Compensatory mechanisms eventually fail resulting in reduced CO
        
        characterised by cool peripheries and weak pulses
      - SYSTOLIC HF:
        
        reduced ejection fraction
        
        impaired LV systolic function
        
        poor ventricular contraction leads to reduced ejection fraction (<40%)
        
        commonly seen as a result of IHD or MI
      - HIGH OUTPUT HF (MISNOMER AS BOTH DONT MEET METABOLIC DEMANDS)
        
        rare and seen in thyrotoxicosis, AV fistula, beriberi (thiamine deficiency), preg, severe anaemia
        
        conversely this form is instead characterised by warm peripheries and normal pulses
        
        unable to meet metabolic demands despite normal or inc CO
  - - - slight limitation
      - mild symptoms with ordinary activity
    - - marked limitation
      - symptomatic with less than ordinary activity such as walking short distances (20-50 mins)
    - - physical activity not limited
      - no symptoms
    - - symptoms present at rest. mostly bed bound pts
      - symptoms present at rest
- - - - PHYSIOLOGICAL - during sleep, athletes, young people
      - cardiac - inf MI (RCA affected that supplies the SAN), sick sinus syndrome
      - drugs - beta blocker, CCB, digoxin, opiates
      - metabolic - hypothyroid, hyperK+, hypothermia
      - Neuro- brain stem pathology (eg raised ICP, infarction) - CUSHING'S REFLEX - VAGAL COMPRESSION - HERNIATION
        
        Cushing's Reflex
        
        response to increased intracranial pressure (ICP) that results in Cushing's triad of increased blood pressure, irregular breathing, and bradycardia
    - - No need to treat if asymptomatic
      - stop offending meds
      - atropine may be indicated in acute setting with severe brady
      - if unresponsive to atropine then consider isoprenaline and temporary pacing
    - - Encompasses sinus brady/sinus pause/sinoatrial block
      - often assoc with other SVTs: AF and atrial flutter. when atrial arrhythmia terminates there is prolonged sinus node recovery time => syncope termed tachycardiac-bradycardia-syndrome
      - More common in elderly
      - AETIOLOGY:
        
        infiltrative conditions -sarcoidosis, amyloidosis
        
        drugs- beta blocker, digoxin, CCB, amiodarone
        
        MI
        
        metabolic - hypothyroid, hyperK+
        
        idiopathic fibrosis of SAN (Ageing)
        
        cardiomyopathies
      - CLINICAL FEATURES
        
        palpitations
        
        dizziness or syncope
        
        Chronic frequent episodes of intermittent bradycardia and tachycardia
        
        ON ECG: Normal SAN impulse but conduction to atria is impaired. Sinus node pause (>3sec) is seen as a result of SAN failure - the subsequent beat is a junctional escape
        
        Sinus node exit block - there is a missing P wave - the node has 'fired' but the impulse has failed to propagate into the atrium
      - MANAGEMENT
        
        treat underlying cause if present
        
        intravenous atropine may be useful in pts with severe symptoms
        
        dual chamber pacemaker implantation recommended if have symptomatic chronic disease
  - - - indicated in sinus node disease and AVN disease
      - Single chamber (RA or RV) or dual (RA + RV)
      - prevent brady
    - - INDICATED IN HF
      - CRT pacemaker. CRT ICDs for pts at high risk of ventricular arrhythmia
      - Coordinate and synchronise atrila, RV and LV contractions
    - - Used to treat VT
      - Delivers overdrive pacing and/or DC shocks to restore sinus rhythm
      - Single chamber (RV) OR Dual chamber (RA and RV)
      - chemical cardioversion - antiarrhythmic drugs - amiodarone, procainamide
- - - - if there is complete occlusion of the coronary vessel by the resultant thrombus, infarction and necrosis develop rapidly
      - ST elevation >/ 1mm in atleast 2 adjacent limbs OR
        /2mm ST elevation in 2 contiguous precordial leads OR
        New onset LBBB
      - ADVANCED MANAGEMENT
        
        STEMI
        
        Primary Percutaneous Coronary Intervention
        
        indicated if symptom onset within 12hr and procedure performed within 120mins of diagnosis
        
        POST PROCEDURE
        
        Aspirin continued indefinitely and the P2Y12 inhibtor (clopidogrel) continued 12 months post-procedure
        
        ANTICOAG
        
        unfractionated heparin or bivalirudin agents of choice prior to reperfusion therapy
        
        glycoprotein IIb/IIIa inhibitors (TIROFIBAN) may be added to heparin
        
        THROMBOLYSIS
        
        Only performed in pts unable to receive pPCI within 10mins of diagnosis or where its contraindicated
        
        fibrin specific agents - TPA: tenecteplase, alteplase
        
        contraindications
        
        recent ischaemic stroke
        
        haemorrhage
        
        trauma or surgery
        
        coma
        
        aortic dissection
        
        cerebrovascular neoplasms
        
        bleeding diatheses
        
        ECG performed 90mins after thrombolysis to assess for reperfusion
        
        a 50% fall in ST elevation or the development of an idioventricular rhythm
        
        if not occurred, rescue PCI indicated within 6hrs of thrombolysis
    - - rise in troponin
      - ADVANCED MANAGEMENT FOR NSTEMI/UA
        
        glycoprotein IIb/IIIa inhibitors
        
        abciximab recommended for pts undergoing PCI who are at intermedite or higher risk of adverse CV events
        
        IV GPII in pts with intermediate or higher risk of adverse CV events and who are coronary angiography within 96hrs of admission
        
        anticoagulation
        
        fondaparinux - preferred anticoag for pts managed conservatively
        
        unfractionated heparin or bivalirudin to manage pts with a view to coronary angiography and PCI due to the increased risk of haemorrhage assoc with these procedures
        
        Dual antiplatelet therapy
        
        aspirin
        
        and either: clopidogrel/ticagrelor/prasugrel
        
        coronary angiography +/- PCI is indicated:
        
        within 96hrs of admission if intermediate or higher risk of adverse CV events
        
        Assessment of risk of future adverse CV events
        
        conservative approach
        
        coronary angiography offered if ischaemia is subsequently experienced or is demonstrated by ischaemia testing
  - - - Oestrogen is a protective factor in pre-menopausal women
      - women with endogenous oestrogen deficiency are 7x more likely to develop CAD
      - HRT not recommended in secondary prevention of CAD
  - - - epigastric pain
      - pulmonary oedema/syncope/oliguria
      - silent MI - no chest pain
      - HTN and acute confusional state
  - - - OXYGEN
      - NITRATES
      - MORPHINE
      - ASPIRIN
    - - GTN
        
        reduces pulmonary congestion, provides symptomatic relief of chest pain. Avoid if systolic bp <90mmHg
        
        ISOSORBIDE NITRATE INFUSION IF SYST >100
      - Aspirin
        
        300mg
      - oxygen
        
        if SpO2 <94%
      - Antiplatelet agents
        
        clopidogrel/ticagrelor/prasugrel
        
        300mg (600mg in pPCI) also given in addition to aspirin
      - Continuous cardiac monitoring
      - Morphine
        
        IV for pain, anxiety and pulmonary oedema. May be given with metoclopramide for nausea
      - Blood glucose control
      - Early risk stratifiation
    - - beta-blockers - metoprolol/bisoprolol
      - nitrates - sublingual GTN
      - statin therapy - started within 24hrs of admission and should be continued long term - atorvastatin 80mg
      - ACEi started within 36hrs on acute MI or in those with LV failure
      - antiplatelet agents for 12 months
      - structured cardiac rehab
      - long term aspirin 75mg given in all pts that had ACS
      - lifestyle modification
      - restrict sex and driving for 1 month and work and air travel for 2 months
    - - 3-vessel disease
      - 2-vessel disease in diabetics
      - significant left main stem disease +>50% stenosis
      - however not the mainstay of revascularisation
  - - - FBC, U&E, glucose, lipid profile, LFT, serial cardiac troponins
    - - ST elevation eventually resolves, giving rise to deep T wave inversion and emergence of Q waves
      - ST elevation - hours
      - T wave inversion - days
      - pathological Q waves - days to months
    - - elevated as early as 2 hours
      - peaks at 12-18 hours
      - remains elevated for approximately 14 days
      - request to be done on presentation and 12hrs after onset
      - can be elevated for several other conditions: acute heart failure, myocarditis, pericarditis, PE, renal failure and sepsis.
    - - performed in medium to high risk individuals with NSTEMI and unstable angina
  - - - cardiogenic shock
      - acute pericarditis
        
        early 2-3days - treat with aspirin and colchicine
        
        NSAIDs contraindicated - interfere with myocardial healing
      - Death from VF, LV failure or stroke
      - cardiac tamponade
      - mitral regurg due to papillary muscle rupture
      - ventricular septal rupture
      - arrhythmia
    - - systemic embolism
      - dressler's syndrome
        
        recurrent pericarditis/pleural effusions/anaemia/fever/raised ESR
        
        treat with colchicine
      - ventricular aneurysm - treat with anticoag +/- excision
      - chronic HF