Admitting Conference CHF

7/31/2019 Admitting Conference CHF

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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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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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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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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



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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

Admitting Conference CHF

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