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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
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.
FAMILY HISTORY
(+) HPN (father) (-) cardiovascular disease (-) diabetes mellitus (-) asthma (-) thyroid disease (-) cancer (-) PTB (-) allergies
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. MI 2. CHF
ADMITTING IMPRESSION
CHF
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.
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.
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:
Biological stimuli for mechanical stretch of myocytes: Neurohormone = NE, angiotensinogen II Cytokine = TNF Growth factor = endothelin Reactive oxygen species = superoxide NO
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)
Diuretics= loop diuretics, thiazides, metolazone, Adverse effect of diuretics= electrolyte and volume depletion, worsen azotemia, hypo/hyper K
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%
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
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