objectives - internal medicine define diastolic and systolic heart

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  • 1.Objectives- Internal Medicine Define diastolic and systolic heart failure Heart failure is present when cardiacoutputfails to meet the metabolic demands of the body or meets those demands only if the cardiac fillingpressures areabnormally high. Systolic Heart Failure: In systolic dysfunction,theaffected ventriclehas a diminished capacity to eject blood because of impaired myocardial contractility or pressureoverload (i.e. excessiveafterload). Loss of contractility may resultfrom destruction of myocytes, abnormal myocyte function, or fibrosis. Pressureoverload impairsventricular ejection by significantly increasingtheresistanceto flow. In impaired contractility,the end systolic pressure-volume relationship (ESPVR) is shifted downward such that systolic emptyingceases at a higher-than-normal end-systolic volume. When normal pulmonary venous return is added to the increased end-systolic volumethat has remained in the ventriclebecause of incomplete emptying, the diastolic chamber vol umeincreases,resultingin a higher- than-normal end-diastolicvolumeand pressure. Whilethat increases in preload induces a compensatory risein stroke volume (via the Frank-Starlingmechanism),impaired contractility and the reduced ejection fraction cause the end-systolic volumeto remain elevated. Duringdiastole,the persistently elevated LV pressureis transmitted to the left atrium(through the open mitral valve) and to the pulmonary veins and capillaries. An elevated pulmonary capillary pressure(>20mm Hg) results in the transudation of fluid onto the pulmonary intersititumand symptoms of pulmonary congestion. Diastolic Heart Failure: Abnormalities of impaired diastolic function includeeither impaired early diastolic relaxation (an active,energy- dependent process),increasingstiffnessof the ventricular wall ( a passiveproperty), or both. Acute myocardial ischemia is an exampleof a condition that transiently inhibitsenergy delivery and diastolicrelaxation. Conversely, left ventricular hypertrophy, fibrosis,or restrictivecardiomyopathy causes theLB walls to become chronically stiffened. In diastole,fillingof the ventricleoccurs athigher-than-normal pressures becauseof reduced complianceof the ventricle. Patients with diastolicdysfunction often present with signs of vascular congestion because the elevated diastolic pressureis transmitted retrograde to the pulmonary and systemic veins. Discuss the underlying pathophysiology of heart failure Heart may not provide tissues wadequate blood for metabolic needs Systolic or diastolicfunction abnormalities pulmonary or systemic pressures organ congestion - Systolic dysfunction:ventriclecontracts poorly,and doesnt empty fully diastolic volumeand pressure, EF - Diastolicdysfunction:difficulty fillingventricle end-diastolic volume, end-diastolic P (EF normal) - LV failure:LV dysfunction CO and pulmonary vein P extravasation fromcapillaries into interstitial spaceand alveoli = work of breathing - RV failure: BP extravasation into periphery = edema, liver highly affected ( conjugated and unconjugated bilirubin,PT,ALP, AST, ALT)

2. List the main risk factors for heart failure. The 5 most common causes of CHF are: CAD (and other cariac risk factors),HTN, idiopathic,Valvularheartdisease (AS, AR, MR) and alcohol (which may causedilated cardiomyopathy). Patients areoften asymptomactic for long periods of time becauseof mild impairement or because compensatory mechanisms are present (adrenergic nervous system, RAAS) to balancethe dysfunction. Manifestations of HF occur when factors increasecardiac workload or tip the state of balance= decompensation. Think in terms of preload,afterload,cardiac output, contractility. Think of HEART FAILED (risk factors and precipitants of heartfailure) o Hypertension (increased afterload) o Environment/endocarditis o Anemia (cardiacoutput) o Rheumatic heart diseaseand other valvediseases o Thyrotoxicosis (increased metabolic demand with insufficientCO) o Failureto take medications o Arrhythmia (with tacchy,decreased diastolicfillingtimeand increased heart O2 demand) o Infection, Ischemia or Infection o Lung problems (PE (hypoxemia because of decrease O2 supply to heart), pneumonia, COPD- emphysema is associated with right-sided failure) o Endocrine (pheo, hyperaldosteronism=increased metabolic demand) o Dietary indiscretions (too much salt=increased preload = congestion) Also: age (over 65) gender (male) ethnicity (higher rate in African american) genetics, family history chronic alcohol abuse(thiamineinsufficiency) =impaired contractility CAD (associated with smoking, obesity) Demonstrate an appropriate physical examination for heart failure Symptoms Signs (Physical Findings) LEFT-SIDED Dyspnea, orthopnea, paroxysmal nocturnal dyspnea, fatigue, dulled mental status (from decreased perfusion), decreased urineoutput in daytime (decreased renal perfusion),nocturia LEFT-SIDED Cachexia,diaphoresis (increased SNS activity), cool extremities, sinus tachycardia, tachypnea (+/- Cheyne Stokes breathing), pulmonary rales, loud P2, S3 gallop +/- S4, mitral regurgitation, pulsus alternans(alternatingstrongand weak contractions in peripheral pulse), dullness in baseof lungs on percussion (pleural 3. effusion) RIGHT-SIDED Peripheral edema (especially calves to feet), weight gain (from fluid), abdominal discomfort(liver becomes engorged), anorexia and nausea (edema of GI tract) Jugular venous distention, hepatomegaly, peripheral edema (ankles and presacral regions), right-sided S3 or S4, tricuspid regurgitation, dullness in baseof lungs on percussion (pleural effusion) Implement emergency management for heart failure Removal/correction of precipitatingcause o Infection/arrhythmia/valvular disease/MI/PE Prevention of deterioration of cardiac function o ACE inhibitors o -blockers o Digitalisglycosides Control of congestive HF state o Diuretic (+ weigh daily and adjustdose) o Liquid and saltrestriction Tx. of acute pulmonary edema LMNOP o Lasix o Morphine o Nitrates o Oxygen o Position (situpright) Write a series of appropriate ordersto treat heart failure Acute CHF (presenting with pulmonary edema) 1. O2 and intubation 2. Nitroglycerin 0.4 mg sublingiual (may be repeated every 1-5 min) 3. Potent IVdiuretic.E.g. Furosemide 40-80 mg IV a. Monitor electrolytes, especially K+ 4. Morphine 2-5 mg IV PRN ** Dopamine 5-10 /kg/min should be started for hypotensive pt or pt in need of additional inotropic support Long term tmt of CHF (accordingto ACC/AHA HF classification) Stage Description Tmt A No structural heartdiseaseand no symptoms but risk factors:CAD, HTN, DM, cardio toxins,familial cardimyopathy 1) Lifestyle modification (diet,exercise,smoking cessation) 2) Treat hyperlipidemia (Lipitor,Crestor) 3) ACE inhibitor for HTN (Ramipril,Enalapril) 4. B Abnormal LV systolicfunction,MI, valvular heartdiseasebutno HF symptoms 1) Lifestyle modifications 2) -blockers (Bisoprolol,Carveditol,Metoprolol) C Structural heart diseaseand HF symptoms 1) Lifestyle modifications 2) ACE inhibitors 3) -blockers 4) Diuretics (HCTZ, Bumetamide, Furosemide) 5) Digoxin D Refractory HF symptoms to maximal medical management 1) Therapy under A, B, and C 2) Mechanical assisted device 3) Heart transplantation 4) Continuous IV inotropic infusion 5) Hospicecarein selected pt Identify the pharmacological agents likely to increase survival with heart failure Long Term Management of Heart Failure Pharmacological Therapy: Vasodilators: o ACEis: standard of care slowprogression and improvesurvival All symptomatic patients functional classII-IV(gradeA) All asymptomatic patients with LVEF 5.2mmol/L Diuretics: symptom control management for fluid overload Furosemide for potent dieresis Metolazone may be used with furosemide to increasedieresis 5. List the valvular heart diseases associated with syncope Aortic stenosis:calcification of aortic cusps (resultingfromcongenital abnormality or rheumatic inflammation or age-related degenerative calcific) - Symptoms: asymp until S in V1 + right axis deviation (lead I ve, II positive) LVH S in V1 + R in V5 or V6 > 35mm + left axis deviation (lead I +ve, II ve) Interpret an ECG with atrial fibrillation (AF) - atrial rate350-600 discharges/minute(cannotsee distinctp waves) - ventricular rate140-160 bpm - ventricular (QRS) rhythm is irregularly irregular Recognize the various forms of heart block on an ECG AV CONDUCTION BLOCKS 1st degree AV block - PR interval - Found in otherwise healthy aduls - No tmt required 2nd degree AV block - TYPE I - Gradual PR interval preceeding QRSdrop - Due to failure of conduction of a Pwave - Frequentlybenign - TYPE II - Constant PR interval - Abrupt QRS drop - Block is usuallydistal to AV node - risk ofhighgrade 3rd degree AV block 9. 3rd degree AV block - Variable PR intervals - Narrow or wide QRS - Variable PPandPR intervals - No relationshipbetween P and QRS - Management electrical pacing BUNDLE BRANCH BLOCKS LBBB - Wide QRS - InitialR wave absent in V1 - Absent small Q wave in V6 RBBB - Wide QRS - R in V1 - Terminal deepS inV6 LAFB - Left axis deviation - Small Q in aVL andI - Small R ininferior leads (II, III, aVF) LPFB - Right axisdeviation - Small R inaVL and I - Small Q in inferior leads (II, III, aVF) Bifascicular block - RBBB plus either LAFB (common) orLPFB (uncommon) - Featuresof RBBB plus frontalplane features ofthe fascicular block (axisdeviation, etc.) Interpret an ECG consistent with ischemia One of the most useful tools for diagnosingischemia isobtainingan ECG duringan ischemic episode. During myocardial ischemia,STsegment and T wave changes often appear. Acute ischemia usually resultsin transient horizontal or downslopingST segment depressions and Twave flatteningor inversions. Occasionally,STsegment elevations areseen, suggesting more severe transmural myocardial ischemia,and can also beobtained duringthe intense vasospasmof variantangina. In contrastto the EC

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