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ADMITTINGCONFERENCE( AUGUST 14-15, 2012)DR. SUNGA, GUEVARRA, VILLANUEVAPGI HALILI
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GENERAL DATA;
TE
58y/o
Male Filipino
Married
Angeles CityAdmitted for the 1st time at our
institution on August 14, 2012
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CHIEF COMPLAINT:
Difficulty Of Breathing
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HISTORY OF PRESENT ILLNESS
Few hours PTA
- Patient experienced Difficulty of breathing
especially on lying position, accompaniedby chest pain, cough and easy fatigability.
No other associated signs and symptoms.
Prompted consult. Hence, admitted.
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REVIEWOFSYSTEMS
*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, excessivetearing
Ears. No earaches, tinnitus, discharge.
Nose and sinuses. no itching, no nosebleeds, nasalstuffiness, discharge, colds
Throat (or mouth and pharynx). No difficultyswallowing , no dry mouth. No hoarseness.
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*Neck.No lumps, no swollen gland, no neckstiffness
*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.
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Musculoskeletal. No muscle or joint pains. Nostiffness.
Neurologic. No blackouts, no seizures, noparalysis, no tremors nor tingling sensations.
Endocrine. No excessive thirst or hunger. No
temperature intolerance. No excessive sweating.
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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
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FAMILY HISTORY
(+) HPN (father)
(-) cardiovascular disease
(-) diabetes mellitus
(-) asthma(-) thyroid disease
(-) cancer
(-) PTB
(-) allergies
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PERSONAL & SOCIAL HX.
Previous smoker
Previous alcoholic beverage drinker
Denies elicit drug use
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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
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HEENT: pink palpebral conjunctivae,
anicteric sclerae, no nasoaural discharge,
no tonsillopharyngeal congestion, (+)
distended neck veins, no anterior neckmass, (-) cervical lymphadenopathies
Chest and Lungs: no masses or lesions, no
deformities, (+) use of accessory muscles,
symmetrical chest expansion, decreasedvocal and tactile fremitus, tachypneic, (+)
rales on all areas of both lung fields,
occasional wheezes R > L
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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 palpableExtremities: cold clammy skin, full equal pulse ,
gr.2 bipedal edema
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Neurologic: GCS 15
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NEUROLOGICEXAMINATION
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
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Motor: 5/5 on all extremities
Sensory: 100% on all extremities
DTR: equal on both extremities
(-) Babinski sign(-) meningeal signs
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SALIENT FEATURES
Subjective
58 y/o
Male
Difficulty of breathing easy fatigability
weakness
non productive cough
Hypertensive
Previous smoker
Previous Alcoholic beverage
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OBJECTIVEFEATURES
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.2bipedal edema
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APPROACH
DOB
Respiratory Cardiovascular
1. COPD
2. Pneumonia
3. Pulmonary mass
1. MI
2. CHF
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ADMITTING IMPRESSION
CHF III, Dilated Cardiomyopathy, HPN
II
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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
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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
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LABORATORY WORK UPS
Crea 91.72
K 4.76
Na 143.1
RBS 5.54
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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
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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, andshortened life expectancy.
Harrison's Principles of InternalMedicine, 17th edition
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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
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Prognosis:
1 year = 30-40%
5 years = 60-70%
NYHA class IV = 30-70% annual mortality rateNYHA class II = 5-10% annual mortality rate
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PATHOGENESIS:
Index Event = damages the heart muscle, withresultant 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
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PATHOGENESIS:
Basic Mechanism of HF:
LV remodeling= series of adaptive changes withinthe 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 desensitization5. abnormal myocardial energetics and metabolism
6. reorganization of the extracellular matrix with
dissolution of the structural collagen weaves
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PATHOGENESIS:
Basic Mechanism of HF: Biological stimuli for mechanical stretch of
myocytes:
Neurohormone = NE, angiotensinogen IICytokine = TNF
Growth factor = endothelin
Reactive oxygen species = superoxide NO
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BASIC MECHANISMOF 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)
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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
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CLINICAL MANIFESTATIONS:
Cardinal symptoms = SOB, fatigue, dyspnea
Orthopnea = dyspnea occurring in recumbentposition
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
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Cheyne-Stokes respiration = periodicrespiration or cyclic respiration=Common in advance HF with low CO
=Caused by diminished sensitivity ofresp. center for pCO2 producingapneic phase=Hyperventilation and hypocapnia,
recurrence of apnea=Perceived as severe dyspnea andtransient cessation of breathing
Clinical Manifestations:
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Paroxysmal Nocturnal dyspnea (PND) = acuteepisodes of SOB and coughing generally occur atnight and awaken the patient from sleep
Coughing, wheezing cardiac asthma wheezing2ndary bronchospasm
Others:=Anorexia, nausea, early satiety,
=Abdominal fullness = congested liver or boweledema
=Confusion, disorientation, sleep mood disturbance =reduced cerebral perfusion
Clinical Manifestations:
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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
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PHYSICAL EXAMINATION:JUGULAR veins:
=Estimation of right atrial pressure, normal < 8cmH2O
=Giant v waves indicates tricuspid regurgitation
Pulmonary Examination:=Crackles - transudation of fluid from intravascularspace into the aveoli
=Expiratory wheeze (cardiac asthma)
=Pleural effusion - biventricular failure - - commonlyoccurs bilateral, unilateral=right side
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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
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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
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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
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DIAGNOSIS:
Laboratories: CBC, electrolytes, BUN, crea, liverenzymes, UA, work up for FBS, lipid profile, thyroidfunction test
ECG: Rhythm= LV hypertrophy, prior MI, QRS width
CHEST XRAY: Cardiac size= pulmonary vasculature
ASSESSMENT OF LV FUNCTION
2decho with DopplerMRI =Gold standard for assessing LV mass andvolume
EF =Stroke volume divide by end diastolic volume
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BIOMARKERS:
-BNP and N-terminal pro BNP= sensitive marker forheart failure with low EF
-Troponin T and I, CRP, TNF receptor, and uricacid= prognostic information
EXERCISE TESTING:
-Assessing the need for cardiac transplantation inpatients 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)
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TREATMENT
Stage A: high risk for HF but without structural heartdisease or symptoms of HF (DM, HPN)
Stage B: structural heart disease but withoutsymptoms 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)
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DEFINING APPROPRIATE THERAPEUTIC
STRATEGY FOR CHRONIC HF
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DEFINING APPROPRIATE THERAPEUTIC
STRATEGY FOR CHRONIC HF
Class I: slow disease progression by blockingneurohormonal system that lead to cardiac
remodeling
Class II-IV: alleviate fluid retention= diuretic withneurohormonal interventions
MANAGEMENT OF HF WITH
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MANAGEMENT OF HF WITH
DEPRESSED EF (
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PREVENTING DISEASE
PROGRESSION
Drugs= can interfere with the excessive activation ofthe 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
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PREVENTING DISEASE
PROGRESSION
ANGIOTENSIN RECEPTOR BLOCKER (ARB)Action= Used in symptomatic and asymptomatic
patients with EF
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PREVENTING DISEASE
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PREVENTING DISEASE
PROGRESSION
ALDOSTERONE ANTAGONISTS (spironolactoneand 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
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MANAGEMENT OF PATIENTS WHO
REMAINED SYMPTOMATIC
Maximize ACE/ARB, Beta blockers, diureticsDigoxin= symptomatic LV systolic dysfunction with
AF, dose= 0.125 mg/day
ANTICOAGULATION AND ANTI-PLATELETStroke risk= 1.3 2.4% / year
Treatment= warfarin with INR goal 2-3recommended with HF and chronic AF or history of
TIA, or systemic or pulmonary emboli
=Aspirin recommended in HF patients with ischemicheart disease for the prevention of MI and death;
dose= 80 mg/day
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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
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DEVICE THERAPY: CARDIAC
RESYNCHRONIZATION
1/3 with depressed EF and NYHA class III-IVmanifest QRS duration > 120ms
Mechanical consequence of ventriculardyssynchrony= suboptimal ventricular filling,
reduction in LV contractility, worsen MR, paradoxicalseptal wall motion
Treatment= biventricular pacing/ CRT (cardiacresynchronization therapy) stimulates bothventricles near- simultaneously thereby improving
the coordination of ventricular contraction andreducing severity of MR
MANAGEMENT OF HF WITH
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MANAGEMENT OF HF WITH
PRESERVED EF (>40-50%)
No proven and/ or approved pharmacologic anddevice 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 depressedcardiac output
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PHARMACOLOGIC MANAGEMENT
OF ACUTE HF
Vasodilators IV= stimulating guanylyl cyclasewithin smooth muscle cells results in loweringLV filling pressure, reduction on MR. improveforward CO,
Ex: nitoglycerines, nitroprussides, nesiritides=
common side effect hypotension
Inotropic agents= produce direct hemodynamicbenefits by stimulating cardiac contractility andperipheral vasodilation, improvement in CO and
fall in LV filling pressure
Dobutamine= most common used inotropicagents stimulates beta 1 and 2 receptors
Inotropic agents:
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Inotropic agents:Milrinone= phosphodiesterase III inhibitor
*most appropriately used in patients with poor
systemic perfusion, cardiogenic shock,hemodynamic support after MI or surgery, awaitingcardiac transplant, palliative for advance heartfailure
Vasoconstrictors Agents:support systemic BPDopamine= endogenous cathecolamine that
stimulates beta 1 alpha 1 receptors anddopaminergic receptors leading to increase in SVR,
LV filling pressure and HR Ex: epinephrine, phenylephrine, vasopressin
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MECHANICAL SURGICAL INTERVENTION
For advance refractory heart failure with failure of
pharmacologic therapy:
IABP, LVAD, Cardiac Transplant
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COR PULMONALE
Definition: pulmonary heart disease= dilation andhypertrophy of RV in response to diseases of the
pulmonary vasculature and lung parenchyma
Etiology and epidemiology:
COPD and Chronic bronchitis= 50% of cases
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Pathophysiology and basic mechanism
Pulmonary hypertension RV dilation with or
without concomitant RV hypertrophysustained
pressure overload impose by pulmonary hpn and
increase pulmonary vascular resistance RVfailure hypoxia, hypercapnea, acidosis,
polycythemia, increase salt and water retention
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Clinical manifestations
Symptoms: dyspnea, orthopnea, PND
Signs: tachypnea, elevated jvp, hepatomegaly,
lower extremity edema, palpable RV heave,
cyanosis
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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
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DIAGNOSIS
2DECHO:
Measures RV thickness and dimensions
MRI:
Assess RV structure and function
RIGHT HEART CATHETERIZATION:
Useful for confirming dx of pulmonary HPN
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TREATMENT
Goal= to decrease in pulmonary vascular resistanceand relieve pressure overload in RV
=NIMV, Bronchodilators, steroids, O2 therapy,
phlebotomy for HCT > 65%
=Diuretic, Digoxin
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THANKYOUFORYOURATTENTION
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