9.Kuliah 2akhir Baru Kardiovaskuler Usila

8/12/2019 9.Kuliah 2akhir Baru Kardiovaskuler Usila

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PENY KITK RDIOV SKULER P DUSI L NJUT

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Principal Hospital Diagnoses of

Elderly Age 85+ (2006)

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Muscle

Strength

& Aerobic

Capacity

Vasomotor

Instability

Bone

DensityVentilation

Sensory

Continence

Altered

Thirst and

Nutrition

Fragile

Skin

Tendency

To Urinary

Incontinence

Immobilized

High Bed

Bed Rails

Plasma

Volume

Accelerated

Bone Loss

Closing

Volume

Sensory

Deprivation

Isolation

Barriers

Tether

Rx Diet

Immobilization

Sheering

Force

Diapers

Tether

Hazards of Bed Rest and Hospitalization

++ + + + + + + +

Dehydration Malnutrition

Tube

Pressure

Sore

Infection

Functional

Incontinence

CatheterFamily

Rejection

Aspiration

Nursing Home

Cascade to Dependency

Deconditioning

Syncope

Fall

Fracture

pO2 Delirium

Physical

Restraint

Chemical

Restraint

False LabelTardive

Dyskinesia

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DYSFUNCTION AND DISABILITY4


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Etiology of deconditioning/tdksehat

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Consequences of deconditioning

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Hospital associated

deconditioning

Loss of ambulatory function or ADL or both in atleast 1/3 of hospitalized patients

Increased risk of death

Demand for rehabilitation will increase

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Cardiovascular Aging 1

Resting LV systolic function normal in absenceof CAD, Hypertension

SBP and pulse pressure increase with age

Sedentary lifestyle may impact on CV systemand obscure impact of aging changes

Lifestyle alterations may delay and partially

reverse changes of cardiovascular aging

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Increased systemic vascularimpedence/menghalangi Systolic hypertension

LV hypertrophy Impaired ventricular diastolic relaxation and

compliance/pemenuhan Increased cardiac interstitial collagen

Compensatory myocyte hypertrophy Increased LVEDP, LA size

Predispose to atrial fibrillation

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Diminished responsiveness to beta-adrenergic stimulation Reductions in maximum HR

1 & 2 effect Impaired peripheral vasodilatation

2 effect

Altered myocardial energy metabolism Impaired mitochondrial capacity to increase ATP

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Clinical implications

Increased preload and afterload

Impaired augmentation of cardiac output Physiologic stress (exercise)

Pathologic stress (e.g. MI, infection, surgery)

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Echocardiography LV wall thickness and mass increase linearly with

age

LVEF correlates strongly with presence of CADand HTN

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Traditional medical approaches do not cater/melayani for

the heterogeneity/beda2 of disease in the elderly!

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Spectrum of CV Disease

in the Elderly

Arrhythmias atrial fibrillation

ventricular

Atherosclerotic vasculardisease

cerebrovascular disease

peripheral vascular disease

CAD

chronic stable angina acute ischaemic syndromes

Conducting SystemDisease

Congestive Heart Failure

Systolic

Diastolic

Hyperlipidemia Hypertension

Hypertrophic

cardiomyopathy

Valvular Heart Disease

Aortic sclerosis

Aortic stenosis

Mitral annular calcification

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CV Disease and theElderly CV disease rises sharply with age

85% of CHD deaths are in patients> 65 years of age

60 % of admissions for acute MI are in patients> 65 years of age

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Age, years Men Women

30-39 5% 1%

40-49 11% 5%

50-59 20% 12%

60-69 29% 15%

70-74 26% 20%

Source: Framingham Heart Study. Am J Hypertens 1993;6:309S-313S

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Atypical Presentation ofAcute Illness,elderly Only 40% of elderly fit the classic one

symptom

Acute myocardial infarction without chestpain

Acute hyperthyroidism without tachycardia,weight loss, etc.

Acute infection without rising WBC count ortypical fever

Fatigue as chief presenting complaint ofCHF

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Non-Specific Symptoms Confusion

Self-neglect/mengabaikan

Falling

Apathy

Anorexia/weight loss

Dyspnea

Fatigue

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Hidden Illness:

You Must Ask, They Wont Tell!

Sexual dysfunction

Depression

Musculoskeletal stiffness Alcoholism

Hearing loss

Memory loss

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Normal Aging vs. Disease

Aging is NOT a disease

Learn to separate pathologic processes

from the aging process

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Normal Aging vs. DiseaseContd

Normal aging Crows feet/keriput

pojok mata

Presbycusis /kurangpendengaran

Seborrheickeratoses; loss of

skin elasticity Benign forgetfulness

Increase in % bodyfat

Disease Macular

degeneration

Tympano-sclerosis

Basal cell CA

Dementia

Athero-sclerosis

Hypertension

Obesity

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61%19%

6%

14%

53%

12%

5%

30%

CHANGES IN BODY COMPOSITION

with AGING

SOLID CELLS

BONE MINERAL

FAT

H2O

25 YEARS OLD 70 YEARS OLD

(Merriman, 1989)


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Laboratory Values that Do Not

Change with Aging

Hepatic function (ALT, AST, GGPT, Bilirubin)

Coagulation tests

Chemistries: electrolytes, total protein,calcium, phosphorus

ABGs: pH, PaCO2

Hemoglobin, RBC indices, platelet count

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The Hospital Cascade

of Disasters/petaka Hospitalizationnew environment and new

medicationsacute deliriummore newdrugs more agitation; Foley inserted poororal intakedehydrationIV fluids increased

and/or NG tube placed for feeding We now have the potential for congestive heart

failure, thrombophlebitis, pulmonaryembolism, aspiration pneumonia, falls andfractures, pressure sores, urosepsis, septicshock, etc . . .

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The Hospital is aHazardous/bahaya,penuh risikoPlace...

Drugs:

Polypharmacy

Alterations in drug disposition and tissuesensitivity

Drug-to-drug interactions

Changes in renal/hepatic elimination Medications errors

Medication side effects

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The Hospital is aHazardous Place... Contd

Bed rest and immobility

General cardiac and muscle deconditioning

Postural lightheadedness, hypovolemia,hypotension

Constipation/fecal impaction

Atelectasis and pneumonia

Thrombophlebitis and thromboembolism

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Th H it l i


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Therapeutic and diagnostic procedures

Angiography

GI endoscopy and its preparation Surgery and anesthesia

Nosocomial Infections

Pneumonia, C. difficile, MRSA

The Hospital is a

Hazardous Place... (Contd)

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Medications

Make an accurate list of all medications onadmission, including OTCs and herbals

Always consider adverse drug effects as the

cause of new symptoms Monitor appropriate blood levels (Digoxin)

Try to control pain without narcotics first

Monitor/review need for medications daily

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Nutrition Albumin and total cholesterol signal poor

nutritional state

Provide vitamin supplementation

Adjust fluid therapy on an individual basis

Ask about nausea/anorexia, foodsatisfaction daily

The hospital is an excellent place to obtaina professional nutritional consultation

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Emotional Status Address anxiety, pain and insomnia early

Depression common: 20-60% of

hospitalized elderly; treat it Frequently update family; hold

patient/family conferences to

allay/menghilangkan fears and clarifythe plan

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Goals of GeriatricAssessment Improve diagnostic accuracy

Define functional impairment

Recommend optimal living situation

Monitor clinical change over time

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PERUBAHAN ANATOMIPADA JANTUNG Secara alami,elastisitas pada manusia akan

menurun dengan bertambahnya umur.

Akibat adanya perubahan dinding media

aorta,bukan karena perubahan intima,ok arterosklerosis yg memang sering terjadi.

Secara histologis,ok perubahan yg progresifpada fungsi jaringan elastis pada aorta.

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PERUBAHAN ANATOMIPADA JANTUNG Penambahan usia tdk menyebabkan

jantung mengecil(atrofi),at terjadi justru

hipertrofi. Pada batas umur 30-90 tahun,masa

jantung bertambah(+/- 1 gr/thn pd

laki,1,5gr pd wanita)(Lakatta,1987).

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The Electrical System

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GEJALA,TANDA,DIAGNOSIS PENYAKITJANTUNG PADA USIA LANJUT

Sifat penyakit pd usila yg bersifat umum,yi patologimultipel,gejala dan tanda yg tersembunyi,tdkkhas,atipik,bervariasi,asimptomatik,progresif,kadangbersifat kronis,shg menimbulkan invaliditas cukup lamasblm meninggal(Stieglitz,1954,Boedi-Darmojo,1982).

Nyeri dada,sesak nafas,dirasa ringan.angina pektorisjarang,ok hilangnya rasa pd ujung syarafsensorik(Caird dkk.1985).

Gejala kebingungan(cofusion),muntah,nyeriperut,akibat bendungan hepar/insomnia,harusdipikirkan dek.kordis.

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Hamm Lancet 358:1533,2001


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No ST Elevation ST Elevation

Acute Coronary Syndrome

Unstable Angina NSTEMI STE MI

NSTEMI

Myocardial Infarction

Davies MJ

Heart 83:361, 2000

Ischemic DiscomfortPresentation

Working Dx

ECG

Biochem.

Marker

Final Dx


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PENYAKIT JANTUNG KORONER PADAUSIA LANJUT PJK paling sering

ditemukan,pria(20%),wnita(12%)pd usila>65thn(Kennedy dkk.1977)

Angina pektoris,rasa nyeri lebih ringan.Operasipintas koroner menunjukkan keberhasilan95%)Knapp dkk,1985.Ketahanan hidup 5 thnsebasar 80%.

IMA pd usila tidak khas(bingung akut,episodesinkope,hemiplegi,oklusi,emboli,gagalginjal,muntah,kelemahan hebat,dalampenelitian,25% gejala khas,40% atipis,31%silent(Caird dkk 1985).

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PENYAKIT JANTUNG KORONERPADA USIA LANJUT Pengobatan IMA,sama,at pd usila masih

menjadi perdebatan u pemberian betabloker,trombolitik.

Hal ini ok pengobatan IMA didasarkan ataspengalaman pd usiapertengahan(Goodman,Amstrong,1994)

Riwayat alamiah IMA pd usila menunjukkansecara signifikan lbh buruk dari usia muda dgkomplikasi lbh banyak di RS dan mortalitas lbhtinggi.Pengobatan trombolitik bukan kontraindikasi pd usila.Meskipun pd usila komplikasilbh banyak at pd golongan ini trombolitik lbh

menguntngkan(Goodman,Amstrong,1994) 40


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Components of Risk StratificationTarget Organ Damage/Clinical CardiovascularDisease

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Target end-organs should be assessed

by history and physical examination

Brain

HeartKidneys

Eyes

Arteries

Adapted from: JNC VI. Arch Intern Med 1997;157: 2413-46


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RINGKASAN DAN SIMPULAN

Penyakit kardiovaskuler sbg penyebabkematian,baik di negara berkembang maupun dinegara sedang berkembang.

Urutan penyakit kardiovaskuler pd usila,PJK,PJ

hipertensif,kardiomiopati,dg komplikasinya algagal jantung kongestif,aritmia kordis. Faktor

risiko:merokok,hipertensi,dislipidemia,DM,inaktifitas fisik,obesitas.

Tujuan utama pengobatan al menghindaridisabilitas,mortalitasprematur,mempertahankan fungsi danperbaikan kualitas hidup.

42THE END


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Health is notEverything,

but Life without Healthis Nothing.


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Thanks for your attention

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9.Kuliah 2akhir Baru Kardiovaskuler Usila