Cardiac failure ( long case approach ) summary

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  • 1. Cardiac Failure Definition: Compensatory changes in Heart Failure: State where the heart is unable to maintain an adequate cardiac output, or is only able Local changes Systemic changes to do so at the expense of an elevated filling pressure. Chamber enlargement Sympathetic activation Diagnosed whenever PT with heart disease devts S/S of low CO, pul. congestion or Myocardial hypertrophy RAAS activation systemic venous congestion. Increased heart rate ADH release Refers to a clinical syndrome rather than a specific Dx. May be caused by many heart Release of natriuretic peptides diseases. Mx requires Rx of underlying aetiology. Poor Px: many patients die suddenly due to malignant ventricular arrhythmias or MI. Precipitating / Aggravating factors in Heart failure: Cardiac Extracardiac Pathophysiology: Myocardial infarction Anemia e.g. secondary to GI bleed Starling’s Law: Cardiac output depends on preload (end-diastolic vol. & pressure), Arrhythmias – tachy/ brady Hyperthyroidism afterload (arterial resistance) & myocardial contractility. Infective endocarditis Sepsis Pregnancy Noncompliance with therapy Drugs Angiotensinog Drug noncompliance fluid-retaining e.g. NSAIDs, negatively ↓ Afterload Renin Fluid restriction noncompliance inotropic drugs (beta-blockers) ↑ Contractility Over-strenuous exercisesCardiac output Angiotensin I ACE Types of Heart failure: Angiotensin II Left-sided HF ↓ LV output ↑ LA or pul. venous pressure Direct Aldosterone o Acute ↑: Pulmonary oedema Preload vasoconstriction o Gradual ↑: reflex pul. vasoconstriction and pulmonary HPT + Right sided HF ↓ RV output Salt & H20 K loss CO= SV x HR retention Causes: Cor pulmonale, multiple Pul. emboli, pulmonary stenosis Biventricular Disease affecting both ventricles, or left heart dz leads to subsequent right HF heart failure ADH release ↑ Preload ↑ Afterload ↑ Contractility Causes: dilated CMP, IHD High output Causes: large AV shunt, beri-beri, severe anaemia, thyrotoxicosis failure Systolic dysf(x) Impaired myocardial contraction Sympathetic activation May be a/w diastolic dysfunction as well Neurohormonal changes: More likely in younger PTs, hx of MI, displaced apex beat, S3 gallop, o activates RAAS and sympathetic nervous system cardiomegaly on CXR o Initially optimizes CO by change in afterload, preload and contractility. Diastolic Defective diastolic filling due to decreased LV compliance – results in o Later, reduces CO by excessive increase in peripheral vascular dysf(x) impaired LV filling, elevated Lt atrial and pul venous pressures, and resistance – vicious cycle established. decreased ability to increase stroke volume Causes of pulmonary and peripheral oedema: o High atrial pressures Causes: LVH due to HPT or IHD o Impaired renal perfusion causing salt and water retention (heart failure Findings: LVH, dilated Lt atrium, normal ejection fraction, reversal of flow causes increased venous pressure which transmit to renal venous velocity across the mitral valve system. Decr pressure gradient btwn renal arterial and venous gradient More likely in hx of HPT, older PTs, sustained apex beat, S4 gallop, LVH results in decreased renal perfusion) on ECG, lack of cardiomegaly on CXR o Secondary aldosteronism
  • 2. Causes of Heart Failure: Look out also for the precipitating factors, and screen for depressionPump failure Heart muscle disease Ischemic HD / CAD (cause of up to 75% of cases of heart failure) Diagnosis Cardiomyopathy Boston Criteria for Diagnosing Heart Failure Myocarditis (Sensitivity 50%, specificity 78%) Criterion Point value Restricted filling Category I: History Pericarditis/ effusion Rest dyspnoea 4 Orthopnea 4 Drugs PND 3 Negative inotropes – beta-blockers Dyspnoea while walking on level area 2Excessive preload Valve disease Dyspnoea while climbing 1 MR, AR Category II: Examination Heart rate 1 (if HR 91-110bpm); 2 (if >110bpm) Fluid Retention JVP 2 (if JVP >6cm H2O); 3 (if JVP >6cm H2O + NSAIDS, steroids hepatomegaly or edema)Excessive afterload AS Lung crackles 1 (if basilar); 2 (if more than basilar) nd Wheezing 3 Systemic hypertension (2 most frequent cause) Third heart sound 3High output CF Thyrotoxicosis Category III: CXR Anemia Alveolar pulmonary edema 4 Interstitial pulmonary edema 3Clinical Features Bilateral pleural effusion 3Low CO Cardiothoracic ratio >0.5 3 Fatigue / altered mental Cold peripheries Upper zone flow redistribution 2 state Low BP Scoring Listlessness Pulsus alternans Max 4 points per category, scored upon a max of 12 points: Poor effort tolerance Cachexia 8-12 points: definiteVentricular Displace left apex beat Function MR / TR 5-7 points: possibledysfunction RV heave Tachycardia <5 points: unlikely S3 / S4Poor renal Oliguria Complicationsperfusion Uraemia Depression In the past 2 weeks, have you:Pul. oedema SOB Inspiratory basal (in 15-40% of Often been bothered by feeling down/ depressed/ hopeless? crepitations patients) Have you had little interest in doing things which previously Orthopnea Cough (usually nocturnal) Cheyne-Stokes resp interested you? (periodic breathing) HypoK+ Due to K+ losing diuretics, hyperaldosteronism (due to RAAS PND activation) & impaired aldosterone metab due to hepatic congestionRight HF / fluid Raised JVP Hypo Na+ Due to diuretics, inappropriate water retention, failure of cellretention Hepatic congestion – progresses to cirrhosis due to venous membrane ion pump congestion Impaired liver Hepatic venous congestion and poor arterial perfusion causes Peripheral oedema / ascites / Pleural effusion / nocturia function jaundice and abN LFTs and reduced clotting factor synthesisChronic HF LOW due to anorexia and impaired absorption due to GI Thromboembolism DVT & PE due to low CO, immobility, arrhythmias, AF, intracardiac congestion thrombus due to MS or LV aneurysms Poor tissue perfusion Arrhythmias Common, and due to electrolyte changes, structural heart dz, Skeletal muscle atrophy due to immobility pro-arrhythmic effects of increased catecholamines and drugs
  • 3. eg digoxin. Sudden death common and usually due to VF NYHA classification of Heart Failure Ventricular ectopic beats and vent. Tachycardias common and I No undue dyspnoea from ordinary activity a/w poor Px. Px is not changed by using anti-arrhythmic drugs II Comfortable at rest, dyspnoea on ordinary activities III Less than ordinary activities causes dyspnoea, which is limitingInvestigations: IV Dyspnoea at rest, all activities cases discomfort to confirm diagnosis of CF and exclude other differentials to look for precipitating causes of CF Management: to look for complications of CF Concise summaryBloods FBC Anemia Acute Sepsis U/E/Cr Electrolyte abnormalities esp. K+, Na+ ABCs + monitoring Cardiac enzymes MI Oxygen – 100% if no COPD BNP Investigations o ECG TFT Hyper/Hypo-thyroidism if clinically o CXR suspected o U/E LFT Cardiogenic liver cirrhosis o Cardiac enzymesECG MI, ischemia, arrhythmia o +/- ABGRadiological CXR Pulmonary edema Drug management upper lobe diversion o Frusemide 40mg IV slowly o GTN S/L or disc (if sys BP>90) blunting of costophrenic angles o Diamorphine + antiemetic Bat’s winging o If systolic BP>90 give IV GTN Kerley’s B lines (interstitial edema) If systolic BP<90 treat as cardiogenic shock alveolar shadowing If systolic BP>180 treat as hypertensive LVF Heart size (may be normal in diastolic Chronic dysfunction) Non pharm Weight loss if obese Infections Fluid restriction + daily weight monitoring TTE (2D echo) Ventricular dysfunction Ejection fraction (Avoid gain of >2kg in 1 week) Valvular lesions Dietary salt restriction (2-3g daily)Special tests to Exercise stress test Exercisediagnose Non-exercise stress For those unable to exercise Regular low-moderate intensity aerobic exerciseunderlying IHD test (pharmacologic) Dipyramidole Avoid lifting heavy weights >10kg Dobutamine Cut down other risk factors Radionuclide imaging Thallium scintigraphy Smoking Technitium-99m sestamibi Hyperlipidemia Coronary Angiography For CAD, and KIV PCI if suitable Learn to monitor symptoms of deterioration Cardiac Catheterization Pharm DiureticsSuper-specialised Plasma B-type Plasma concentration of BNP reflects sttests ) natriuretic peptide ventricular pressure Spironolactone – 1 choice, shown to reduce mortality High negative predictive value: low BNP Loop suggests that if patient is dyspneic, Thiazide cause is highly unlikely to be CF ACE-I/ A2RB Endomyocardial biopsy To diagnose rare forms of CMP or Beta-blockers – started with low doses, up-titrated slowly infiltrative heart diseases Digoxin – may not reduce mortality but reduces hospitalization
  • 4. episodes There is NO vol. overload per se, thus main Rx is with vasodilators End point of Rx is resolution of symp. overdrive, as indicated by pulse rate, BP,Treat associated AF, hyperlipidemia, CRF etc restoration of warm dry extremities & PT comfort.comorbidities Features to aid clinical diagnosis: i. Severe resp distress, orthopneaDetailed Summary ii. Cold clammy extremities iii. Thready pulsePresentations: iv. ↓ SpO21. Acute decompensation of chronic left HF - Decreased effort tolerance / pedal oedema / Features of impending resp failure: wheeze (“cardiac asthma”) i. Altered mental state2. Acute cardiogenic pulmonary oedema ii. Poor and uncoordinated respiratory effort3. Cardiogenic shock iii. Progressive desaturation iv. PaO2 <50mmHg, PaCO2 >50mmHg1) Acute Mx of Acute Decompensation of Chronic HF 1. Monitoring + attach defibrillator 1. Monitoring: vital signs, pulse oximetry, continuous ECG 2. ABC assessment: intubate in impending respiratory failure 2. Maintain airway, supplemental O2 3. 100% O2 / CPAP in alert PT, but of limited utility 3. IV access 4. IV access 4. Blood invxs: FBC, U/E/Cr, Cardiac enzymes 5. ECG: exclude inferior/right ventricular infarct which is a CI to use of nitrates 5. Position patient: seated upright with legs hanging down to reduce venous return 6. Bloods: RBC, U/E/Cr, cardiac enzymes, Troponin T 6. ECG: concomitant MI, dysrhythmias, LVH, old MI, chronic HPT 7. ABG: baseline 7. CXR: cardiomegaly & features of pul. edema (eg upper lobe diversion) 8. CXR 8. Diuretics: IV frusemide 40-60 mg 9. Catheterize: assess urine output 9. Nitrodisc 5-10mg: relieve symptoms of pul. congestion 10. Drugs: 10. IV GTN: lower LV end-diastolic volume and pressure rapidly for resolution of Nitroglycerine 10-200 μg/min, starting at 10μg/min, increasing by 5μg/min every 5 symptoms mins until MAP = 90mmHg. Continuous BP monitoring required. 11. Monitor urine output to assess response to Rx. Nitroprusside 0.25-10μg/kg/min. invasive monitoring required to prevent 12. Admit / discharge precipitous drop in BP. Admit Symptomatic dysrhythmias Hydralazine IV 10mg every 30 mins. Monitor PT New MI Frusemide 40-80mg IV bolus. Onset of effects from 20min-2h Rapid onset of new symptoms of HF Morphine 0.1mg/kg, starting with IV 3-5mg incremental boluses of 1 mg. GTN 0.5-1.5mg SL stat Decompensation of chronic HF Captopril 6.25 or 12.5mg SL Ppting factors require inpatient Mx Combination regimes Anasarca / severe oedema IV GTN + frusemide Frusemide stat dose + titrate IV GTN titratable infusion Hypotension IV GTN + captopril SL Captopril stat + titrate IV GTN titratable infusion Lack of home support Frusemide + morphine D/C If patient is well and responsive to diuretics – TCU 2/52 If not on medication: start Lasix 40mg om + Span K 1.2mg om 11. Hypotension in Pul. oedema If already on med, increase diuretic dose Indicates severe HF If concurrent HPT present, add ACEI – Captopril 6.254-12.5mg IV dobutamine or dopamine (5-20μg/kg/min) tds or hydralazine 25mg tds 12. Admit: Diet advice: salt restriction, fluid restriction (~1 L/day; titrate CCU: PTs with acute coronary syndrome or if intubated against weight gain/loss and fluid output) HDU: PTs on CPAP General Wd: the rest2) Acute Mx of Acute Pulmonary Oedema Main pathogenic mechanism is sympathetic overdrive leading to elevated LV end- 3) Long term Management of CCF diastolic vol. & pressure Bed rest
  • 5. Stamina building exercise treat with ACEI (change to ARB if cough occurs, change to Diet: low salt diet, fluid restriction (~1L/day; monitor with weight, urine output and hydralazine + nitrate if worsening renal insufficiency or symptoms of pedal oedema/ascites) angioedema occurs) Beta blockers: for NYHA Class II or III Pharmacotherapy Spironolactone: for NYHA Class III or IV o Reduce preload in backward failure (pul. or systemic congestion) Digoxin: for symptomatic NYHA Class III or IV o Reduce afterload and increase myocardial contractility in forward failure (low Diuretics: for fluid overload in NYHA Class III or IV CO) If refractory to above treatment, add dobutamine or milrinone & o For patients with LVEF <40% IV diuretic ACE-I for all PTs o Diastolic dysfunction: treat underlying cause (eg IHD or HPT) with beta β-blockers for all PTs who are haemodynamically stable blockers, CCB, ACEI +/- diuretics Spironolactone for all PTs with rest dyspnoea Digoxin for PTs who are symptomatic despite ACEI + diuretics + β- blockers, and Pts with rest dyspnoea Diuretics Reduce preload Excessive diuretic Rx may cause fall in CO. Combination of different classes of diuretics (loop, thiazides and K+ sparing) prevents hypo K+. eg Frusemide + spironolactone. Symptomatic. Does not improve survival. ACE-I Reduce afterload mainly, + some reduction in preload Prevents RAAS & sympathetic activation Eg Captopril, enalapril, lisinopril. SE: postural hypotension, renal failure (therefore check renal function one mth after starting), catastrophic fall in BP on first dose of ACEI (therefore give at night before PT sleeps), hyperK+, cough, neutropenia, altered taste. ARB Similar action to ACE-I. Blocks effect of AT II on heart, peripheral bld vsls & kidneys. Eg losartan nd Usually 2 line Rx if PT does not tolerate ACE-I Advantage: does not cause cough β-blockers Reduce sympathetic stimulation to increase ejection fraction Non-cardioselective β-blockers better as they do not decrease CO as much Vasodilators Venodilators (nitrates) reduce preload Arterial dilators (hydralazine) reduce afterload Limited by SE of hypotension Digoxin For AF in HF Controls ventricular rate + small positive inotropic effect No effect on survival, but reduces hospitalisation Digitally signed by DR WANA HLA SHWE Amiodarone DN: cn=DR WANA HLA SHWE, c=MY, Anti-arrhythmic drug for PTs with symptomatic arrhythmias o=UCSI University, School of Medicine, KT- Anticoagulants Prevent thromboembolism Campus, Terengganu, ou=Internal Medicine Group, email=wunna. hlashwe@gmail.comSystolic vs Diastolic dysfunction: Long term Mx different, therefore impt to differentiate Reason: This document is for UCSI year 4 students.btwn the two. However, both may be concomitant in the same patient. Date: 2009.02.24 10:04:48 +0800 o Systolic dysfunction: