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ADMITTING CONFERENCE ( AUGUST 14-15, 2012) DR.

SUNGA, GUEVARRA, VILLANUEVA PGI HALILI

GENERAL DATA;
TE

58y/o
Male Filipino Married Angeles

City Admitted for the 1st time at our institution on August 14, 2012

CHIEF COMPLAINT:

Difficulty

Of Breathing

HISTORY OF PRESENT ILLNESS


Few

hours PTA

Patient experienced Difficulty of breathing especially on lying position, accompanied by chest pain, cough and easy fatigability. No other associated signs and symptoms. Prompted consult. Hence, admitted.

REVIEW OF SYSTEMS
*General. (-) weigt loss *Skin. No rashes, lumps, sores, dryness, color change *Head, Eyes, Ears, Nose, Throat. Head. No headache, dizziness, lightheadedness Eyes. No redness, no double vision, excessive tearing Ears. No earaches, tinnitus, discharge. Nose and sinuses. no itching, no nosebleeds, nasal stuffiness, discharge, colds Throat (or mouth and pharynx). No difficulty swallowing , no dry mouth. No hoarseness.

*Neck. No lumps, no swollen gland, no neck stiffness *Respiratory. (+) DOB, (+) orthopnea *Cardiovascular. No palpitations. *Gastrointestinal. (+) loss of appetite. No abdominal pain. No diarrhea, no constipation. No change in bowel habits *Urinary. No polyuria, nocturia, hematuria, *Genital. No lesions, no discharge, no itching, no sores.

Musculoskeletal. No muscle or joint pains. No stiffness. Neurologic. No blackouts, no seizures, no paralysis, no tremors nor tingling sensations. Endocrine. No excessive thirst or hunger. No temperature intolerance. No excessive sweating.

PAST MEDICAL HISTORY


Diagnosed case of Cardiomyopathy ( March 6, 2012) maintained on Aspirin 80mg OD Old anterolateral ischemia via ECG ? (+) HPN = HBP 140/100, UBP 130/80 - Maintained on Metropolol 50mg OD, Perindopril SL OD (-) DM (-) Asthma

FAMILY HISTORY
(+) HPN (father) (-) cardiovascular disease (-) diabetes mellitus (-) asthma (-) thyroid disease (-) cancer (-) PTB (-) allergies

PERSONAL & SOCIAL HX.


Previous smoker Previous alcoholic beverage drinker Denies elicit drug use

PHYSICAL EXAMINATION
General: Ambulatory, conscious, coherent, oriented to time, place and person, in respiratory distress Vital signs: BP: 130/80mmHg HR:82bpm RR: 28 T: 36.7C Skin: diaphoretic , no jaundice, no rashes, no scars

HEENT: pink palpebral conjunctivae, anicteric sclerae, no nasoaural discharge, no tonsillopharyngeal congestion, (+) distended neck veins, no anterior neck mass, (-) cervical lymphadenopathies Chest and Lungs: no masses or lesions, no deformities, (+) use of accessory muscles, symmetrical chest expansion, decreased vocal and tactile fremitus, tachypneic, (+) rales on all areas of both lung fields, occasional wheezes R > L

Heart: adynamic precordium, apex beat at 5th LICS along the MCL, no heaves, regular rate and rhythm,, JVP 7 cm, Hepatojugula reflex negative Abdomen: flat, no scars, normoactive bowel sounds of 8 per minute,(-) bruit, no tenderness, liver span is 5cm midsternal line and 9 cm midclavicular line, spleen was not palpable Extremities: cold clammy skin, full equal pulse , gr.2 bipedal edema

Neurologic:

GCS 15

NEUROLOGIC EXAMINATION
Oriented to time, place and person Cranial nerves: II: pupils 2-3 mm ERTL III,IV,VI: intact EOMs V: good masseter muscle strenght VII: no facial asymmetry VIII: can hear IX,X: (+) gag reflex XI: can shrug both shoulders XII: no tongue deviaation

Motor: 5/5 on all extremities Sensory: 100% on all extremities DTR: equal on both extremities (-) Babinski sign (-) meningeal signs

SALIENT FEATURES

Subjective 58 y/o Male Difficulty of breathing easy fatigability weakness non productive cough Hypertensive Previous smoker Previous Alcoholic beverage

OBJECTIVE FEATURES

Objective BP:130/80mmHg, HR:82 bpm, RR: 28cpm distended neck veins use of accessory muscles decreased vocal and tactile fremitus (+) ocassional wheezes R>L (+) rales on all areas of both lung fields Normal JVP Hepatojugular reflex negative (+) cyanosis, cold clammy skin, weak pulse, gr.2 bipedal edema

APPROACH
DOB

Respiratory

Cardiovascular

1. COPD 2. Pneumonia 3. Pulmonary mass

1. MI 2. CHF

ADMITTING IMPRESSION

CHF

III, Dilated Cardiomyopathy, HPN

II

AT THE ER
Patient came in ambulatory, conscious, awake, coherent, in cardiorespiratory distress assisted by his wife BP 130/80, RR 28, PR 82 , T 36.7 Initially given O2 via NC at 2-3 LPM & furosemide 40mg/IV and observed for improvement.

Laboratory Work Ups done

LABORATORY WORK UPS


CBC Hct 0.47 Hgb 160 Leukocyte 10.49 N 0.77 L 0.17 M 0.04 E 0.02 PC 192

LABORATORY WORK UPS


Crea 91.72 K 4.76 Na 143.1 RBS 5.54

2D ECHO
Dilated left Ventricle with normal wall thickness and generalized hypokinesia with only the basal interolateral and anterolateral showing adequate contractility. Findings consistent with dilated cardiomyopathy ischemic in etiology

CHF

clinical syndrome due to an inherited or acquired abnormality of cardiac structure and/or function, develop constellation of clinical symptoms (dyspnea and fatigue) and signs (edema and rales), that lead to frequent hospitalization, poor QOL, and shortened life expectancy.

Harrison's Principles of Internal Medicine, 17th edition

CHF
Epidemiology: Prevalence=2% 6-10% > age 65 2 groups = systolic failure and diastolic failure

Etiology: CAD = 60-75% Hypertension = 75% Unknown = 20-30% RHD = Africa and Asia Chagas diseases = South America

Prognosis: 1 year = 30-40% 5 years = 60-70% NYHA class IV = 30-70% annual mortality rate NYHA class II = 5-10% annual mortality rate

PATHOGENESIS:

Index Event = damages the heart muscle, with resultant loss of functioning cardiac myocytes or alternatively disrupts the ability of the myocardium to generate force (affect contraction) = MI, pressure/volume overload, cardiomyopathy = Decline in pumping capacity of heart

PATHOGENESIS:
Compensatory mechanism: 1. activation of rennin-angiotensin-aldosterone (RAA) and adrenergic nervous system = responsible for maintaining CO thru retention of Na and H2O 2. increase myocardial contractility Activation of vasodilatory moleciules: ANP, PGe2/PGI2, NO

PATHOGENESIS:
Basic Mechanism of HF: LV remodeling = series of adaptive changes within the myocardium 1. myocyte hypertrophy 2. alteration in the contractile properties of myocyte 3. progressive loss of myocyte through necrosis, apoptosis and autophagic 4. B adrenergic desensitization 5. abnormal myocardial energetics and metabolism 6. reorganization of the extracellular matrix with dissolution of the structural collagen weaves

PATHOGENESIS:

Basic Mechanism of HF:

Biological stimuli for mechanical stretch of myocytes: Neurohormone = NE, angiotensinogen II Cytokine = TNF Growth factor = endothelin Reactive oxygen species = superoxide NO

BASIC MECHANISM OF HF:


Systolic Dysfunction: Sustained neurohormonal activation result in post transcriptional changes in the genes and proteins that regulate excitation-contraction coupling and cross bridge interaction

Diastolic dysfunction: Slowed myocardial relaxation = ischemia LV filling is delayed LV compliance is reduced (hypertrophy and fibrosis)

LV remodeling: Changes in LV mass, volume. Shape and composition of the heart that occur following cardiac injury and/or abnormal hemodynamic loading condition Increase sphericity of LV, pappilary muscle are pulled apart = functional MR further overloading of the LV

CLINICAL MANIFESTATIONS:
Cardinal symptoms = SOB, fatigue, dyspnea Orthopnea = dyspnea occurring in recumbent position Redistribution of fluid from the splanchnic circulation and LE circulation into the central circulation resultant increase in pulmonary capillary pressure Nocturnal cough, generally relived when sitting upright or by sleeping with additional pillows

Clinical Manifestations:
Cheyne-Stokes respiration = periodic respiration or cyclic respiration =Common in advance HF with low CO =Caused by diminished sensitivity of resp. center for pCO2 producing apneic phase =Hyperventilation and hypocapnia, recurrence of apnea =Perceived as severe dyspnea and transient cessation of breathing

Clinical Manifestations:
Paroxysmal Nocturnal dyspnea (PND) = acute episodes of SOB and coughing generally occur at night and awaken the patient from sleep Coughing, wheezing cardiac asthma wheezing 2ndary bronchospasm Others: =Anorexia, nausea, early satiety, =Abdominal fullness = congested liver or bowel edema =Confusion, disorientation, sleep mood disturbance = reduced cerebral perfusion

PHYSICAL EXAMINATION:
General appearance and vital signs: =Labored breathing, shortness of breath when talking =Diminished pulse pressure = reduction in stroke volume =Sinus tachycardia = increased adrenergic activity =Cool peripheral extremities and cyanotic lips and nailbeds = adrenergic activity

PHYSICAL EXAMINATION:

JUGULAR veins: =Estimation of right atrial pressure, normal < 8cm H2O =Giant v waves indicates tricuspid regurgitation Pulmonary Examination: =Crackles - transudation of fluid from intravascular space into the aveoli =Expiratory wheeze (cardiac asthma) =Pleural effusion - biventricular failure - - commonly occurs bilateral, unilateral=right side

PHYSICAL EXAMINATION:
Cardiac Examination: -Cardiomegaly - PMI displaced below 5th ICS or lateral to MCL -Severe LV hypertrophy - sustained PMI -S3 gallop = apex -S4 = diastolic dysfunction -Mitral regurgitation and Tricuspid regurgitation = advance heart failure

PHYSICAL EXAMINATION:
Abdomen and Extremities: -Hepatomegaly = tender and pulsate during systole if TR is present -Ascites = increased pressure in the hepatic veins -Jaundice = impairment of hepatic function 2ndary to hepatic congestion and hepatocellular hypoxia

PHYSICAL EXAMINATION:

Peripheral edema = symmetric, pretibial and ankle regions, presacral edema and scrotum in bedridden patients Cardiac Cachexia: -Marked weight loss and cachexia = elevation of resting metabolic rate, anorexia, nausea and vomiting due to abdominal fullness, elevations in TNF, impairment of intestinal absorption due to congestion of intestinal veins -Poor prognosis

DIAGNOSIS:
Laboratories: CBC, electrolytes, BUN, crea, liver enzymes, UA, work up for FBS, lipid profile, thyroid function test ECG: Rhythm= LV hypertrophy, prior MI, QRS width CHEST XRAY: Cardiac size= pulmonary vasculature ASSESSMENT OF LV FUNCTION 2decho with Doppler MRI =Gold standard for assessing LV mass and volume EF =Stroke volume divide by end diastolic volume

BIOMARKERS: -BNP and N-terminal pro BNP= sensitive marker for heart failure with low EF -Troponin T and I, CRP, TNF receptor, and uric acid= prognostic information

EXERCISE TESTING: -Assessing the need for cardiac transplantation in patients with VO2 < 14ml/kg/min
DIFFERENTIAL DIAGNOSIS: 1. congestion 2ndary to Na and H2O retention (renal failure) 2. non cardiac cause of pulmonary edema (ARDS)

TREATMENT
Stage A: high risk for HF but without structural heart disease or symptoms of HF (DM, HPN) Stage B: structural heart disease but without symptoms of HF (previous MI, asymptomatic LV dysfunction) Stage C: structural heart disease with symptoms (previous MI with dyspnea and fatigue) Stage D: refractory HF requiring special intervention (cardiac transplant)

DEFINING APPROPRIATE THERAPEUTIC STRATEGY FOR CHRONIC HF

DEFINING APPROPRIATE THERAPEUTIC STRATEGY FOR CHRONIC HF


Class I: slow disease progression by blocking neurohormonal system that lead to cardiac remodeling

Class II-IV: alleviate fluid retention= diuretic with neurohormonal interventions

MANAGEMENT OF HF WITH DEPRESSED EF (<40%)


General measures= screen for co-morbidities, avoid certain drugs (NSAIDS, COX2 inhibitors), and immunizations Activity= modest exercise NYHA class I-III like walking, stationary bicycle ergometer Diet= Na restriction (2-3 gms/day); fluid restriction (< 2l/day); caloric supplementation (cardiac cachexia)

Diuretics= loop diuretics, thiazides, metolazone, Adverse effect of diuretics= electrolyte and volume depletion, worsen azotemia, hypo/hyper K

PREVENTING DISEASE PROGRESSION


Drugs= can interfere with the excessive activation of the RAA system and the adrenergic nervous system ACE INHIBITORS Action= interfere with renin-angiotensin enzyme by inhibiting the conversion of angiotensin I to angiotensin II; inhibit kinninase II=upgregulation of bradykinin causing suppression of angiotensin -Stabilize LV remodeling, and improve symptoms -Adverse Effects= decrease in BP, K retention, azotemia, non productive cough 10-15%, angioedema 1%,

PREVENTING DISEASE PROGRESSION


ANGIOTENSIN RECEPTOR BLOCKER (ARB) Action= Used in symptomatic and asymptomatic patients with EF <40% =Block effect of angiotensin II on angiotensin type I receptor Adverse Effects= decrease in BP, K retention, azotemia BETA ADRENERGIC RECEPTOR BLOCKER Action= interfere with the harmful effects of sustained activation of the adrenergic nervous system Adverse Effects= bradycardia, exacerbate heart block *Avoid in asthma with active bronchospasm

PREVENTING DISEASE PROGRESSION


ALDOSTERONE ANTAGONISTS (spironolactone and eplerenone) Action= K sparing diuretic Adverse Effects= life threatening hyperK, gynecomastacia *Not recommended with creatinine >2.5 mg/dl or crea clearance < 30ml/min, k >5

MANAGEMENT OF PATIENTS WHO REMAINED SYMPTOMATIC


Maximize ACE/ARB, Beta blockers, diuretics Digoxin= symptomatic LV systolic dysfunction with AF, dose= 0.125 mg/day ANTICOAGULATION AND ANTI-PLATELET Stroke risk= 1.3 2.4% / year Treatment= warfarin with INR goal 2-3 recommended with HF and chronic AF or history of TIA, or systemic or pulmonary emboli =Aspirin recommended in HF patients with ischemic heart disease for the prevention of MI and death; dose= 80 mg/day

MANAGEMENT OF CARDIAC ARRYTHMIA AF= 15-30% amiodarone class III anti-arrythmic with no negative inotropic or pro-arrythmic effect= preferred drug for restoring SR IMPLANTABLE CARDIAC DEFIBRILLATOR Highly effective in treating life threatening cardiac dysrrythmias (V-tach, V-fib) Considered for patients with NYHA class II-III with depressed EF < 30%

DEVICE THERAPY: CARDIAC RESYNCHRONIZATION


1/3 with depressed EF and NYHA class III-IV manifest QRS duration > 120ms Mechanical consequence of ventricular dyssynchrony= suboptimal ventricular filling, reduction in LV contractility, worsen MR, paradoxical septal wall motion Treatment= biventricular pacing/ CRT (cardiac resynchronization therapy) stimulates both ventricles near- simultaneously thereby improving the coordination of ventricular contraction and reducing severity of MR

MANAGEMENT OF HF WITH PRESERVED EF (>40-50%)


No

proven and/ or approved pharmacologic and device therapy Treatment efforts focused on underlying disease process ACUTE HF Defining appropriate therapeutic strategy stabilize hemodynamic derangement identify and treat reversible factors that precipitated decompensation re-establish an effective medical regimen *2 primary hemodynamic determinants of Acute HF =Elevated LV filling pressure and depressed cardiac output

PHARMACOLOGIC MANAGEMENT OF ACUTE HF


Vasodilators IV= stimulating guanylyl cyclase within smooth muscle cells results in lowering LV filling pressure, reduction on MR. improve forward CO, Ex: nitoglycerines, nitroprussides, nesiritides= common side effect hypotension Inotropic agents= produce direct hemodynamic benefits by stimulating cardiac contractility and peripheral vasodilation, improvement in CO and fall in LV filling pressure Dobutamine= most common used inotropic agents stimulates beta 1 and 2 receptors

Inotropic agents:
Milrinone= phosphodiesterase III inhibitor *most appropriately used in patients with poor systemic perfusion, cardiogenic shock, hemodynamic support after MI or surgery, awaiting cardiac transplant, palliative for advance heart failure Vasoconstrictors Agents: support systemic BP Dopamine= endogenous cathecolamine that stimulates beta 1 alpha 1 receptors and dopaminergic receptors leading to increase in SVR, LV filling pressure and HR Ex: epinephrine, phenylephrine, vasopressin

MECHANICAL SURGICAL INTERVENTION For advance refractory heart failure with failure of pharmacologic therapy: IABP, LVAD, Cardiac Transplant

COR PULMONALE
Definition: pulmonary heart disease= dilation and hypertrophy of RV in response to diseases of the pulmonary vasculature and lung parenchyma Etiology and epidemiology: COPD and Chronic bronchitis= 50% of cases

Pathophysiology and basic mechanism Pulmonary hypertension RV dilation with or without concomitant RV hypertrophy sustained pressure overload impose by pulmonary hpn and increase pulmonary vascular resistance RV failure hypoxia, hypercapnea, acidosis, polycythemia, increase salt and water retention

Clinical manifestations Symptoms: dyspnea, orthopnea, PND Signs: tachypnea, elevated jvp, hepatomegaly, lower extremity edema, palpable RV heave, cyanosis

DIAGNOSIS
Most common cause of Right HF is Left HF ECG: In severe pulmonary HPN= P pulmonale, RAD, RV hypertrophy CHEST XRAY: Enlargement of main pulmonary artery HIGH RESOLUTION CT SCAN: Most accurate means of dx emphysema and ILD

DIAGNOSIS
2DECHO: Measures RV thickness and dimensions MRI: Assess RV structure and function RIGHT HEART CATHETERIZATION: Useful for confirming dx of pulmonary HPN

TREATMENT
Goal= to decrease in pulmonary vascular resistance and relieve pressure overload in RV =NIMV, Bronchodilators, steroids, O2 therapy, phlebotomy for HCT > 65% =Diuretic, Digoxin

THANK YOU FOR YOUR ATTENTION