53 Congestive Heart Failure & Acute Pulmonary Edema
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CONGESTIVE HEART FAILURE AND ACUTE PULMONARY EDEMA TINTINALLIS CHAPTER 53 MARK SERRA
EPIDEMOLOGY
550,000 NEW CASES PER YEAR LEADING CAUSE OF HOSPITALIZATION IN PEOPLE OLDER THAN 65 OVERALL COST IS ROUGHLY DOUBLE OF ANY CANCER DIAGNOSIS
PROGNOSIS
2 YEAR MORTALITY RATE 35% IF SYMPTOMATIC INCREASES TO 80% (MALES) AND 65% (FEMALES) WITHIN 6 YEARS PATIENTS DEVELOPING PULMONARY EDEMA SURVIVAL RATE 1 YEAR 85% OF PATIENTS IN CARDIOGENIC SHOCK DIE WITHIN 1 WEEK
TYPES OF PATHOLOGY
HIGH-OUTPUT, LOW-OUTPUT SYSTOLIC, DIASTOLIC RIGHT SIDED, LEFT SIDED COMBINATION OF TYPES
PATHOPHYISIOLOGY
INABILITY OF THE HEART TO SUPPLY BLOOD TO ADEQUATLY MEET THE METABOLIC NEEDS OF BODILY TISSUES MAY DEVELOP OVER LIFETIME OR PRESENT ACUTELY 3 MECHANISMS UTILIZED TO COMPENSATE – FRANK-STARLING LAW: INCREASING PRELOAD RESULTS IN INCREASED CONTRACTILITY – MYOCARDIAL STRUCTURAL CHANGES: HYPERTROPHY OF MYOCYTES (INCREASED MASS) – NEUROHORMONAL : RENIN-ANGIOTENSINALDOSTERONE SYSTEM, RELEASE OF NOREPINEHRINE, NATRIURETIC PEPTIDES AND ENDOTHELIEN RELEASE
PATHOPHISIOLOGY
HIGH-OUTPUT: CARDIAC FUNTION IS MAINTAINED, BUT INADEQUQTE TO MEET EXCESSIVE DEMANDS OF TISSUES – ETIOLOGY: ANEMIA, BERIBERI, THYROTOXICOSIS, PAGET’S DISEASE, ARTERIOVENOUS SHUNTS
LOW-OUTPUT: DECREASE IN MYOCARDIAL CONTRACTION FROM INHERENT OR AQUIRED ETIOLOGIES
– MANY CAUSES: ISCHEMIA, HYPERTENSION MOST COMMON
SYSTOLIC VS DIASTOLIC
SYSTOLIC DYSFUNCTION DEFINED AS EJECTION FRACTION <40% (AFTERLOAD SENSITIVE) – CAUSES AN INCREASE IN PULMONARY VASCULAR PRESSURES, PULMONARY CONGESTION AND EDEMA
DIASTOLIC DYSFUNCTION: IMPAIRED VENTRICULAR RELAXATION WITH PRESEVED CONTRACTILITY (PRELOAD SENSITIVE) – EXCESSIVE DIURESIS MAY EXACERBATE CONDITION
DISTINCTION MADE BY ECHOCARDIOGRAM
RIGHT SIDED VS LEFT SIDED
LEFT SIDED: INCREASING PRESSURES IN PULMONARY VASCULATURE – MANIFESTS AS PERIVASCULAR AND INTERSTITIAL TRANSUDATE – ALVEOLAR SEPTAL WIDENING – ACUMMULATION OF TRANSUDATE IN ALVEOLI
ETIOLOGY: HTN, ISCHEMIA, VALVULAR DISEASES
LEFT SIDED
KERLY B LINES -SIDEROPHAGES
RIGHT SIDED
ISOLATED RIGHT SIDED HF RARE – CHRONIC PULMONARY HYPERTENSION MOST COMMON CAUSE (COR PULMONALE)
LEFT SIDED HEART FAILUSE MOST COMMON CAUSE OF RIGHT SIDED FAILURE MANIFESTS AS: PERIPHERAL EDEMA, JVD, RUQ PAIN, HEPATOSPLEENOMEGALY
RIGHT SIDED
DIAGNOSIS
CLINICAL FINDINGS: RESPIRATORY DISTRESS ORTHOPNEA, JVD, HTN, DIAPHORESIS, PERIPHERAL EDEMA, ELEVATED PCWP Chest X-RAY: VASCULAR REDISTRIBUTION, CARDIOMEGALY (CARDIOTHORACIC RATIO > 0.6 PA), INTERSTITIAL EDEMA, KERLY B LINES, PLEURAL EFFUSIONS CLINICAL SYMPTOMS MAY PRECEDE IMAGING EVIDENCE BY UP TO 6 HOURS, DONOT WITHHOLD THERAPY ECHOCARDIOGRAPHY GOLD STANDARD
CLINICAL DIAGNOSIS
DIAGNOSIS
ELEVATED BNP LEVELS NON HF PATIENTS LEVELS AVG 38 pg/ml HF PATIENT AVG 1076 pg/ml BNP INCREASED IN ELDERLY, RENAL FAILURE, WOMEN, CIRRHOSIS BNP LEVELS 100-250 pg/ml CONSIDER OTHER DIAGNOSIS
TREATMENT
AIRWAY MANAGEMENT: CADIAC MONITORING, PULSE OXIMETRY, ECG, IV ACSESS CARDIAC ENZYMES (14% HAVE POSITIVE SERUM MARKERS) CBC,BMP,BNP, CHEST XRAY, LIVER ENZYMES, DIGOXIN LEVEL
TREATMENT PHARMACOLOGY
REDUCTION OF AFTERLOAD – SUBLINGUAL NITROGLYCERIN: 0.4 mg REPEAT 1-5 MIN – IV NITROGLYCERIN: 10-30 micg/min TITRATE TO 200 micg/min – IV NITROPRUSSIDE: 2.5 micg/kg/min TITRATE – NESIRITIDE: ANTAGONIST TO RENIN- ANGIOTENSIN AXSIS, 2 micg/kg BOLUS, IV DRIP 0.01 micg/kg/min
VASODIALATORS NOT RECOMMENED FOR HYPOTENSIVE PATIENTS, PATIENTS WITH CARDIOGENIC SHOCK
CONTRAINDICATIONS TO VASODIALATORS
PRELOAD DEPENDENT STATES – – – –
RIGHT VENTRICULAR INFARCTION AORTIC STENOSIS VOLUME DEPLETION HYPERTROPHIC CARDIOMYOPATHY
REDUCTION OF HEART RATE AND CONTRACTILITY WITH IV BETA BLOCKERS IS THERAPY OF CHOICE
TREATMENT PHARMACOLOGY
FUROSEMIDE: – NO PRIOR USE: 40 mg IVP – PRIOR USE: DOUBLE LAST 24 HOUR USAGE: 80-180 mg – NO RESPONSE IN 20-30 MIN RE-DOUBLE DOSE
BUMETANIDE: – 1-3 MG DIURESIS BEGINS WITHIN 10 MIN
MONITORING OF ELECTROLYTES ESSENTIAL
TREATMENT PHARMACOLOGY
ACE INHIBITORS – DECREASE MORTALITY AND HOSPITALIZATIONS – ALL HF PATIENTS SHOULD BE DISCHARGED WITH ACEI (DECREASES MORTALITY IN CLASS 4 HF BY 31%)
BETA BLOCKERS – DECREASE MYOCARDIAL HYPERTROPHY, AFTERLOAD AND MYOCARDIAL OXYGEN DEMAND – METOPROLOL DECREASES 1 YEAR MORTALITY IN CLASS II-III BY 34%
CLASSIFICATION OF HF
PHARMACOLOGY
DRUGS CONTRAINDICATED IN HF CALCIUM CHANNEL BLOCKERS NSAIDS: INHIBIT EFFECTS OF DIURETICS AND ACEI ANTIARRHYTHMICS: PROPHYLACTIC USE IS NOT EFFECTIVE, AND MAY INCREASE MORTALITY
DISPOSITION
MOST PATIENTS WITH ACUTE PULMONARY EDEMA REQUIRE ICU ADMISSION PATIENTS WITH RESOLVED HYPERTENSION AND DYSPNEA MAY BE ADMITTED TO MONITORED NON-ICU BED FOLLOW ENTRY PROTOCOL GUIDELINES FOR OBSERVATION, ACUTE CARE OR SHORT-STAY UNIT ADMISSION
LONG TERM MANAGEMENT
OUTPATIENT FOLLOW-UP BY PHYSCIAN TRAINED IN HF MANAGEMENT
SOCIAL SERVICE EVALUATION – – –
MEDICATION COMPLIANCE DIETARY EDUCATION SMOKING CESSATION (REDUCES MORTALITY AS EFFECTIVLY AS BEST MEDICATION)
EPIDEMOLOGY
550,000 NEW CASES PER YEAR LEADING CAUSE OF HOSPITALIZATION IN PEOPLE OLDER THAN 65 OVERALL COST IS ROUGHLY DOUBLE OF ANY CANCER DIAGNOSIS
PROGNOSIS
2 YEAR MORTALITY RATE 35% IF SYMPTOMATIC INCREASES TO 80% (MALES) AND 65% (FEMALES) WITHIN 6 YEARS PATIENTS DEVELOPING PULMONARY EDEMA SURVIVAL RATE 1 YEAR 85% OF PATIENTS IN CARDIOGENIC SHOCK DIE WITHIN 1 WEEK
TYPES OF PATHOLOGY
HIGH-OUTPUT, LOW-OUTPUT SYSTOLIC, DIASTOLIC RIGHT SIDED, LEFT SIDED COMBINATION OF TYPES
PATHOPHYISIOLOGY
INABILITY OF THE HEART TO SUPPLY BLOOD TO ADEQUATLY MEET THE METABOLIC NEEDS OF BODILY TISSUES MAY DEVELOP OVER LIFETIME OR PRESENT ACUTELY 3 MECHANISMS UTILIZED TO COMPENSATE – FRANK-STARLING LAW: INCREASING PRELOAD RESULTS IN INCREASED CONTRACTILITY – MYOCARDIAL STRUCTURAL CHANGES: HYPERTROPHY OF MYOCYTES (INCREASED MASS) – NEUROHORMONAL : RENIN-ANGIOTENSINALDOSTERONE SYSTEM, RELEASE OF NOREPINEHRINE, NATRIURETIC PEPTIDES AND ENDOTHELIEN RELEASE
PATHOPHISIOLOGY
HIGH-OUTPUT: CARDIAC FUNTION IS MAINTAINED, BUT INADEQUQTE TO MEET EXCESSIVE DEMANDS OF TISSUES – ETIOLOGY: ANEMIA, BERIBERI, THYROTOXICOSIS, PAGET’S DISEASE, ARTERIOVENOUS SHUNTS
LOW-OUTPUT: DECREASE IN MYOCARDIAL CONTRACTION FROM INHERENT OR AQUIRED ETIOLOGIES
– MANY CAUSES: ISCHEMIA, HYPERTENSION MOST COMMON
SYSTOLIC VS DIASTOLIC
SYSTOLIC DYSFUNCTION DEFINED AS EJECTION FRACTION <40% (AFTERLOAD SENSITIVE) – CAUSES AN INCREASE IN PULMONARY VASCULAR PRESSURES, PULMONARY CONGESTION AND EDEMA
DIASTOLIC DYSFUNCTION: IMPAIRED VENTRICULAR RELAXATION WITH PRESEVED CONTRACTILITY (PRELOAD SENSITIVE) – EXCESSIVE DIURESIS MAY EXACERBATE CONDITION
DISTINCTION MADE BY ECHOCARDIOGRAM
RIGHT SIDED VS LEFT SIDED
LEFT SIDED: INCREASING PRESSURES IN PULMONARY VASCULATURE – MANIFESTS AS PERIVASCULAR AND INTERSTITIAL TRANSUDATE – ALVEOLAR SEPTAL WIDENING – ACUMMULATION OF TRANSUDATE IN ALVEOLI
ETIOLOGY: HTN, ISCHEMIA, VALVULAR DISEASES
LEFT SIDED
KERLY B LINES -SIDEROPHAGES
RIGHT SIDED
ISOLATED RIGHT SIDED HF RARE – CHRONIC PULMONARY HYPERTENSION MOST COMMON CAUSE (COR PULMONALE)
LEFT SIDED HEART FAILUSE MOST COMMON CAUSE OF RIGHT SIDED FAILURE MANIFESTS AS: PERIPHERAL EDEMA, JVD, RUQ PAIN, HEPATOSPLEENOMEGALY
RIGHT SIDED
DIAGNOSIS
CLINICAL FINDINGS: RESPIRATORY DISTRESS ORTHOPNEA, JVD, HTN, DIAPHORESIS, PERIPHERAL EDEMA, ELEVATED PCWP Chest X-RAY: VASCULAR REDISTRIBUTION, CARDIOMEGALY (CARDIOTHORACIC RATIO > 0.6 PA), INTERSTITIAL EDEMA, KERLY B LINES, PLEURAL EFFUSIONS CLINICAL SYMPTOMS MAY PRECEDE IMAGING EVIDENCE BY UP TO 6 HOURS, DONOT WITHHOLD THERAPY ECHOCARDIOGRAPHY GOLD STANDARD
CLINICAL DIAGNOSIS
DIAGNOSIS
ELEVATED BNP LEVELS NON HF PATIENTS LEVELS AVG 38 pg/ml HF PATIENT AVG 1076 pg/ml BNP INCREASED IN ELDERLY, RENAL FAILURE, WOMEN, CIRRHOSIS BNP LEVELS 100-250 pg/ml CONSIDER OTHER DIAGNOSIS
TREATMENT
AIRWAY MANAGEMENT: CADIAC MONITORING, PULSE OXIMETRY, ECG, IV ACSESS CARDIAC ENZYMES (14% HAVE POSITIVE SERUM MARKERS) CBC,BMP,BNP, CHEST XRAY, LIVER ENZYMES, DIGOXIN LEVEL
TREATMENT PHARMACOLOGY
REDUCTION OF AFTERLOAD – SUBLINGUAL NITROGLYCERIN: 0.4 mg REPEAT 1-5 MIN – IV NITROGLYCERIN: 10-30 micg/min TITRATE TO 200 micg/min – IV NITROPRUSSIDE: 2.5 micg/kg/min TITRATE – NESIRITIDE: ANTAGONIST TO RENIN- ANGIOTENSIN AXSIS, 2 micg/kg BOLUS, IV DRIP 0.01 micg/kg/min
VASODIALATORS NOT RECOMMENED FOR HYPOTENSIVE PATIENTS, PATIENTS WITH CARDIOGENIC SHOCK
CONTRAINDICATIONS TO VASODIALATORS
PRELOAD DEPENDENT STATES – – – –
RIGHT VENTRICULAR INFARCTION AORTIC STENOSIS VOLUME DEPLETION HYPERTROPHIC CARDIOMYOPATHY
REDUCTION OF HEART RATE AND CONTRACTILITY WITH IV BETA BLOCKERS IS THERAPY OF CHOICE
TREATMENT PHARMACOLOGY
FUROSEMIDE: – NO PRIOR USE: 40 mg IVP – PRIOR USE: DOUBLE LAST 24 HOUR USAGE: 80-180 mg – NO RESPONSE IN 20-30 MIN RE-DOUBLE DOSE
BUMETANIDE: – 1-3 MG DIURESIS BEGINS WITHIN 10 MIN
MONITORING OF ELECTROLYTES ESSENTIAL
TREATMENT PHARMACOLOGY
ACE INHIBITORS – DECREASE MORTALITY AND HOSPITALIZATIONS – ALL HF PATIENTS SHOULD BE DISCHARGED WITH ACEI (DECREASES MORTALITY IN CLASS 4 HF BY 31%)
BETA BLOCKERS – DECREASE MYOCARDIAL HYPERTROPHY, AFTERLOAD AND MYOCARDIAL OXYGEN DEMAND – METOPROLOL DECREASES 1 YEAR MORTALITY IN CLASS II-III BY 34%
CLASSIFICATION OF HF
PHARMACOLOGY
DRUGS CONTRAINDICATED IN HF CALCIUM CHANNEL BLOCKERS NSAIDS: INHIBIT EFFECTS OF DIURETICS AND ACEI ANTIARRHYTHMICS: PROPHYLACTIC USE IS NOT EFFECTIVE, AND MAY INCREASE MORTALITY
DISPOSITION
MOST PATIENTS WITH ACUTE PULMONARY EDEMA REQUIRE ICU ADMISSION PATIENTS WITH RESOLVED HYPERTENSION AND DYSPNEA MAY BE ADMITTED TO MONITORED NON-ICU BED FOLLOW ENTRY PROTOCOL GUIDELINES FOR OBSERVATION, ACUTE CARE OR SHORT-STAY UNIT ADMISSION
LONG TERM MANAGEMENT
OUTPATIENT FOLLOW-UP BY PHYSCIAN TRAINED IN HF MANAGEMENT
SOCIAL SERVICE EVALUATION – – –
MEDICATION COMPLIANCE DIETARY EDUCATION SMOKING CESSATION (REDUCES MORTALITY AS EFFECTIVLY AS BEST MEDICATION)
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