4/13/20

Rehabilitasi
Jantung
Abdurrasyid, S.ST, M. Fis, FMSC

Bahan baca & belajar

• www.heartonline.org.au
• www.aacvpr.org
• www.bacpr.com
• www.cvphysiology.com

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Pengantar
• Rehabilitasi jantung adalah
intervensi kompleks yang
ditawarkan kepada pasien yang
didiagnosis dengan penyakit
jantung, yang mencakup
komponen pendidikan kesehatan,
nasihat tentang pengurangan
risiko kardiovaskular, aktivitas fisik
dan manajemen stres
• Bukti klinis menjelaskan bahwa
rehabilitasi jantung mengurangi
mortalitas, morbiditas, & rawat
inap dengan perbaikan kapasitas
latihan, kualitas hidup dan
kesejahteraan psikologis
meningkat.

Setiap tahunnya lebih dari 36 juta orang meninggal karena Penyakit

Tidak Menular (PTM) (63% dari seluruh kematian). Lebih dari 9 juta
kematian yang disebabkan oleh penyakit tidak menular terjadi
sebelum usia 60 tahun, dan 90% dari kematian “dini” tersebut
terjadi di negara berpenghasilan rendah dan menengah.

Mengapa Secara global PTM penyebab kematian nomor satu setiap tahunnya

rehablitasi adalah penyakit kardiovaskuler. Penyakit kardiovaskuler adalah

penyakit yang disebabkan gangguan fungsi jantung dan pembuluh
darah, seperti:Penyakit Jantung Koroner, Penyakit Gagal jantung
jantung atau Payah Jantung, Hipertensi dan Stroke.

diperlukan? Pada tahun 2008 diperkirakan sebanyak 17,3 juta kematian

disebabkan oleh penyakit kardiovaskuler. Lebih dari 3 juta kematian
tersebut terjadi sebelum usia 60 tahun dan seharusnya dapat
dicegah. Kematian “dini” yang disebabkan oleh penyakit
jantungterjadi berkisar sebesar 4% di negara berpenghasilan tinggi
sampai dengan 42% terjadi di negara berpenghasilan rendah.

http://bit.ly/309pnDK Info Datin DEPKES 2014

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Apa itu rehabilitasi jantung dan untuk

siapa?
• Layanan rehabilitasi jantung (dan pencegahan
sekunder)diberikan komprehensif, dengan program jangka
panjang yang melibatkan evaluasi medis, latihan yang
diresepkan, modifikasi faktor risiko jantung, pendidikan, dan
konseling
• Program ini dirancang untuk membatasi efek fisiologis dan
psikologis dari penyakit jantung, mengurangi risiko kematian
mendadak atau infark ulang, mengontrol gejala jantung,
menstabilkan atau membalikkan proses aterosklerosis, dan
meningkatkan psikososial dan status pasien yang dipilih

Target populasi untuk dapat berpartisipasi dalam program

rehabilitasi jantung

Penyakit jantung iskemik Kondisi Gagal Jantung Penyakit kronik lainnya

1. Post-MI, graft bypass arteri 1. Gagal jantung kompensasi 1. Stroke

koroner, perkutan angioplasti
koroner transluminal
2. Angina yang stabil
2. Dysrhythmias Terkontrol 2. Peripheral vascular disease
3. Implan otomatis cardioverter 3. Chronic heart failure
defibrillate/alat pacu jantung
4. Paska Penggantian katup
5. Cardiomyopathy
6. Reseksi aneurisma miokard
7. Transplantasi pra dan pasca
jantung
8. Kelainan jantung kongenital

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Apa manfaat rehabilitasi jantung?-kematian

• Tahun 2011 Lembaga Cochrane melakukan review
dan meta analisis RCT 47 data yang terdiri dari
10.794 pasien rehab jantung menunjukkan
penurunan mortalitas dengan nilai absolute risk
reduction (ARR) 3,2%
• Data lainnya berupa systematic review dan meta
analisis 34 RCT terdiri dari 6111 pasien myocard
infarc yang mengikuti rehab jantung memiliki
resiko rendah mortalitas dibandingkan dengna
ynag tidak mengikuti program. Program rehab jantung dapat
• Review dari Cochrane tentang rehab jantung Mengurangi resiko kematian
dengan latihan pada CHD menghasilkan penurunan dini bagi penderita CHD &
mortalitas jantung dari 10,4% menjadi 7,6% pada Myocard infark
pasien myocard infarc dan revascularisation.

Pengurangan kunjungan
rumah sakit
• Dalam ulasan Cochrane tahun 2015 dalam penyakit
jantung koroner melaporkan tidak ada pengurangan
dalam risiko infark miokard fatal atau non-fatal atau
revaskularisasi koroner (cangkok bypass arteri koroner
atau intervensi koroner perkutan), namun ada
penurunan risiko masuk rumah sakit (dari 30,7%
menjadi 26,1%, NNT 22).
• Dalam tinjauan Cochrane lain dari 33 percobaan
terkontrol acak dan 4740 pasien dengan gagal jantung,
rehabilitasi jantung berbasis latihan mengurangi risiko
keseluruhan rawat inap (risiko relatif 0,75 (0,62 untuk
0,92), ARR 7,1%, NNT 15) dan rawat inap untuk gagal
jantung (risiko relatif 0,61 (0,46 sampai 0,80), ARR
5,8%, NNT 18).

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Perbaikan dalam kesejahteraan

psikologis dan kualitas hidup
• Program rehabilitasi jantung awal hanya
menawarkan intervensi yang berfokus
terutama pada latihan, tetapi memberikan
hasil signifikan (P < 0.01) perbaikan dalam
nilai kecemasan dan depresi yang
dilaporkan dalam satu percobaan
terkontrol acak 210 laki-laki mengakui
dengan infark miokard menjalani latihan
latihan berbasis gym.
• Beberapa studi telah melaporkan
perbaikan dalam stres psikologis pada
pasien dengan penyakit jantung koroner
yang telah menghadiri rehabilitasi jantung:
satu studi pengamatan AS baru-baru ini
189 pasien dengan gagal jantung (fraksi
ejeksi ventrikel kiri < 45%) melaporkan
penurunan gejala depresi oleh 40% setelah
latihan rehabilitasi jantung (dari 22% untuk
13%, P < 0.0001).

Faktor risiko penyakit

kardiovaskular
• Ades et al melakukan uji acak terkontrol 74
pasien yang kelebihan berat badan dengan
penyakit jantung koroner dan menunjukkan
bahwa "berjalan sering dan berjalan jauh"
("tinggi kalori, pengeluaran tinggi") protokol
latihan 45-60 menit per sesi latihan intensitas
yang lebih rendah (70% penyerapan oksigen
puncak) mengakibatkan dua kali penurunan
berat badan (8,2 kg v 3,7 kg, P < 0.001)
dibandingkan dengan sesi latihan rehabilitasi
jantung standar dari 25-40 menit
• Penelitian ini juga melaporkan peningkatan yang
signifikan (P < 0.05) tekanan darah sistolik,
indeks massa tubuh, trigliserida serum,
kolesterol HDL, kolesterol total, glukosa darah
dan penyerapan oksigen puncak dalam kalori
tinggi, kelompok latihan pengeluaran tinggi

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Pasien dengan angina tidak stabil, aritmia ventrikel tidak

terkontrol, dan gagal jantung berat (New York Heart
Association (NYHA) tingkat 3 atau 4, fraksi ejeksi < 35%)
telah dipertimbangkan dengan risiko tinggi, dengan
stratifikasi risiko formal (untuk menyertakan faktor seperti
Riwayat aritmia dan kapasitas fungsional) yang dilakukan
Apa risiko dari oleh dokter berpengalaman sebelum mereka terlibat
dalam komponen latihan rehabilitasi jantung.
rehabilitasi
jantung? Namun, review Cochrane terbaru ditemukan "tidak ada
bukti yang menunjukkan bahwa program latihan
menyebabkan kerugian dalam hal peningkatan risiko
semua penyebab kematian baik dalam jangka pendek atau
panjang" pada pasien dengan gagal jantung kronis stabil
(tingkat NYHA 1 – 3).

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Figure 2. Timing of Participation in Cardiac Rehabilitation

The number of days after incident myocardial infarction hospital discharge that patients
attended their first session of cardiac rehabilitation is shown

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STEMI= ST-segment elevation myocardial infarction

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Simpulan
• Rehabilitasi jantung adalah intervensi kompleks yang ditawarkan
kepada pasien yang didiagnosis dengan penyakit jantung, yang
mencakup komponen pendidikan kesehatan, nasihat tentang
pengurangan risiko kardiovaskular, aktivitas fisik dan manajemen
stress
• Program sekunder yang diberikan kepada pasien dengan target jangka
panjang
• Tidak semua pasien dengan masalah jantung dapat mengikuti
program rehab jantung
• Terapis harus terus mengedukasi pasien akan dampak positif dari
rehab jantung

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• Penyakit jantung iskemik:

suatu kondisi di mana
ketidakseimbangan antara
pasokan dan permintaan
oksigen miokard, paling sering
disebabkan oleh aterosklerosis
dari arteri koroner. Sehingga
hipoksia myocardial &
akumulasi sisa metabolisme.
• Sindrom koroner akut (ACS):
kondisi yang mengancam jiwa
dengan simtom angina
pectoris tidak stabil (UA)
berkepanjangan dicurigai
adanya kondisi nekrosis infark
ireversibel.
ISCHEMIC HEART DISEASE
http://www.pathophys.org/acs/#Pathophysiology_of_the_ischemic_process

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Acute Heart Attact – Ischemia-Miocard Infark

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Mekanisme iskemia
• Iskemia miokard adalah konsekuensi dari berkurangnya aliran darah di
arteri koroner, karena kombinasi dari penyempitan pembuluh tetap
dan abnormal denyutan akibat dari aterosklerosis dan disfungsi
endotel. Hal ini menyebabkan ketidakseimbangan antara pasokan
(supply) dan permintaan (demand) oksigen miokard.

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Penyempitan pembuluh
darah koroner
Beberapa faktor mempengaruhi hemodinamika dari lesi
stenotik:

• Panjangnya dari lesi penyempitan pembuluh menyebabkan

diameter menyempit & menyebabkan tahanan laju darah
• Kemampuan kompensasi pembuluh untuk dapat
bervasodilatasi resikonya lebih rendah, namun Pembuluh
koroner distal dapat bertindak sebagai cadangan pembuluh
agar dapat menyesuaikan denyutan vasomotor guna
menanggapi kebutuhan metabolismejantung.
• Permintaan oksigen miokard
Saat istirahat – pembuluh darah yang menyempit akan
berdilatasi sebagai bentuk kemampuan pembuluh
dalam memasok oksigen ke jantung.
Selama latihan – ketika permintaan oksigen meningkat
akan beriringan dengan kenaikan denyut jantung dan
kekuatan kontraksi, namun pembuluh coroner tidak
sanggup mengkompensasidilatasi sehingga berdampak
pada iskemia.

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Disfungsi endotel

• disfungsi endotel memberikan kontribusi untuk miokard iskemia dengan

cara berikut:
• Vasokonstriksi yang tidak tepat arteri koroner
• Gangguan pelepasan vasodilator endotel (misalnya NO, prostacyclins) sedemikian
rupa sehingga efek konstriktor katekolamin pada otot polos arteri saat stres dan
olahraga, sehingga menjadi resultan penurunan aliran darah koroner yang
berkontribusi iskemia
• Dalam konteks pecahnya plak dan trombus, endotelium menjadi disfungsi dan tidak
dapat melepaskan NO dalam menanggapi produk trombosit (serotonin, ADP),
sehingga terjadi Vasoconstricting
• Hilangnya sifat antitrombotik normal: Vasodilator endotel seperti NO dan prostacyclins
juga memiliki efek antitrombotik, namun ketika pelepasan antitrombus berkurang akan
menggangu dilatasi.

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Penyebab iskemia non-aterolerotik

1. Penurunan tekanan perfusi koroner karena hipotensi (misalnya hypovolemia,

septic shock)
2. Penurunan kadar oksigen darah (misalnya anemia ditandai, penyakit paru)
3. Peningkatan yang signifikan dalam permintaan oksigen miokard (misalnya
cepat tachycardias, hipertensi akut, stenosis aorta berat)
4. Kelainan koroner yang tidak biasa menyebabkan penurunan perfusi
miokardium
5. Emboli koroner dari Endokarditis atau katup jantung buatan:
• Peradangan arteri koroner dari sindrom vaskulitik (perubahan dinding pembuluh)
• Spasme koroner transien parah, baik primer atau disebabkan oleh
Penyalahgunaan Kokain
• Kelainan kongenital, trauma atau aneurisma arteri koroner

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Konsekuensi iskemia
pada miokardium
• Konsekuensi dari iskemia
mencerminkan oksigenasi
miokard yang tidak memadai
dan akumulasi produk lokal
limbah metabolik.
• Pada akhirnya, keparahan dan
durasi ketidakseimbangan
antara pasokan oksigen dan
permintaan akan menentukan
kematian miokardium.

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Stunned myocardium
• menunjukkan disfungsi sistolik berkepanjangan bahkan setelah
kembalinya aliran darah miokard normal
• besarnya serangan tergantung kondisi iskemia sebelumnya
• pemulihan fungsi Tertunda karena kelebihan kalsium myocyte dan
akumulasi dari oksigen yang diturunkan radikal bebas selama iskemia
• Kelainan yang dihasilkan dari iskemia yang reversibel dan fungsi
kontraktil secara bertahap pulih

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Hibernating myocardium
• disfungsi kontraktil ventrikel kronis dalam menanggapi suplai darah yang terus-
menerus dikurangi, biasanya dalam konteks penyakit arteri koroner multivessel
• Kerusakan ini adalah reversibel dan fungsi ventrikel dapat segera dipulihkan jika
aliran darah dinormalkan kembali

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Infark miokard

• Myocyte necrosis as a result of prolonged myocardial ischemia

• Amount of tissue that succumbs to infarction depends on:
• Mass of myocardim perfused by the occluded vessel
• Magnitude and duration of impaired coronary blood flow
• Oxygen demand of the affected region
• Adequacy of collateral vessels that provide blood supply from neighbouring
nonoccluded coronary vessels
• Degree of tissue response to the ischemic process

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Ischemic syndromes
• 1. Stable angina
• Pattern of chronic, predictable, transient angina during exertion or emotional stress
• Generally caused by a fixed obstructive atherosclerotic plaque in one or more coronary
arteries, in addition to inappropriate vasoconstriction resulting from atherosclerosis-
associated endothelial dysfunction
• Severity of symptoms usually related to degree of stenosis and compensatory capacity of
distant resistance vessels to vasodilate
• 2. Unstable angina (also part of acute coronary syndromes, see below)
• Represents an acceleration of symptoms from stable angina, such as a sudden increase in
the rate and duration of ischemic episodes, occurring with lesser degrees of exertion and
sometimes even at rest
• Can be a precursor to an acute myocardial infarction
• Underlying pathophysiologic mechanism typically involves rupture of an unstable
atherosclerotic plaque with subsequent platelet aggregation and thrombosis

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• 3. Variant angina
• Episode of focal coronary artery spasm in the absence of overt atherosclerotic lesions
• Mechanism leading to intense vasospasm is not completely understood but thought to
involve increased sympathetic activity in combination with endothelial dysfunction
• Often occurs at rest since ischemia results from a transient reduction in coronary oxygen
supply rather than an increased myocardial oxygen demand
• 4. Silent ischemia
• Episode of cardiac ischemia that occurs in the absence of perceptible discomfort or pain
• Can occur in patients who experience typical symptomatic angina, or be the only
manifestation of coronary artery disease
• Pathophysiology is unknown, but thought to involve impaired pain sensation resulting
from peripheral neuropathy, since silent ischemia is particularly common among patients
with diabetes
• 5. Syndrome X
• Refers to patients with typical symptoms of angina pectoris who have no evidence of
significant coronary artery disease on angiograms
• Thought to be due to inadequate vasodilator reserve of coronary resistance vessels,
which do not dilate appropriately during periods of increased myocardial oxygen demand

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Pathophysiology of the ischemic process

Early changes in infarction (minutes to days)
• Drop in tissue oxygen levels
• Rapid conversion from aerobic to anaerobic metabolism
• Impaired glycolysis and ATP production → impaired contractile protein function
• Systolic dysfunction – loss of synchroneous myocyte contraction → compromised cardiac output
• Diastolic dysfunction – reduced ventricular compliance (i.e. impaired relaxation) and elevation of ventricular filling
pressures
• Accumulation of lactic acid and reduction in pH
• Impairment of transmembrane Na-K-ATPase due to impaired ATP production
• Increased intracellular Na → intracellular edema
• Increased extracellular K → alteration in transmembrane potential → electrical instability and susceptibility to arrhythmias
• Increased intracellular Ca → activation of degradative lipases and proteases → tissue necrosis
• Acute inflammatory response with infiltration of neutrophils leading to further tissue damage

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Late changes in infarction (days to weeks)

• Resorption of irreversibly injured/dead myocytes by macrophages
• Structural weakness of ventricular wall and susceptibility to myocardial wall rupture
• Fibrous tissue deposition and scarring
• Ventricular remodeling
• Infarct expansion – thinning and dilatation of necrotic tissue without additional
necrosis
• Increased ventricular wall stress
• Further impairment in systolic contractile function
• Increased likelihood of aneurysm formation
• Remodeling of non-infarcted ventricle
• Dilatation of overworked non-infarcted segments subjected to increased wall stress
• Enlargement initially compensatory to increase cardiac output via Frank-Starling mechanism,
but can eventually predispose to ventricular arrhythmias and lead to heart failure

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Complications of myocardial infarction

• Early complications result mainly from myocardial necrosis itself, while later complications reflect the
inflammation and healing of necrotic tissue.
• Arrhythmias
• In addition to arising from the electrical instability of ischemic myocardium, they can also be caused by
interruption of perfusion to structures of the conduction pathway (i.e. SA node, AV node, bundle branches)
• Congestive heart failure
• Can be directly caused by impaired contractility resulting in both systolic and diastolic dysfunction
• More rarely results from papillary muscle infarction or rupture causing moderate to severe mitral
regurgitation
• Thromboembolism
• Intra-ventricular thrombus formation can arise from stasis of blood flow in regions of impaired LV
contraction, especially when the infarction involves the apex or when an aneurysm has formed
• Pericarditis
• Can arise in the early post-MI period when necrosis and neutrophilic infiltrates extend from the myocardium
to involve the adjacent pericardium

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• Ventricular aneurysm
• Develops as the ventricular wall is weakened but not perforated by the
phagocytic clearance of necrotic tissue
• Cardiac tamponade
• Hemorrhage into the pericardial space due to ventricular free wall rupture
(structurally weakened by necrosis) leads to rapid filling of the pericardial
space and severe restriction of ventricular filling; often lethal
• Cardiogenic shock
• Severely decreased cardiac output and hypotension with inadequate
perfusion of peripheral tissues develops when more than 40% of the LV
mass is infarcted
• Self-perpetuating mechanism whereby impaired contractility results in
hypotension, decreased coronary perfusion, exacerbation of ischemic
damage, further decrease in contractile function, and so forth

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Symptoms Mechanism

Chest pain/discomfort Metabolic products such as lactate, serotonin

(typically retrosternal, and adenosine accumulate locally and may
“pressure”, “discomfort”, activate peripheral pain receptors in the C7 to
“tightness”, “burning” or T4 distribution
“heaviness”)

Clinical Tachycardia Dangerous arrhythmias can be precipitated by

transient abnormalities of myocyte ion

presentation transport and accumulation of local

metabolites; increased sympathetic tone

of myocardial during myocardial ischemia can also account

for an increased heart rate

ischemia Dyspnea Transiently impaired LV relaxation leads to

elevation of LV diastolic pressure which is
transmitted backwards into the pulmonary
capillaries and can precipitate pulmonary
congestion and symptoms of dyspnea

Diaphoresis Increased sympathetic tone during the

discomfort of an acute ischemic attack

Nausea/vomiting Increased parasympathetic tone during the

discomfort of an acute ischemic attack

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Treatment options and their role in the

management of acute coronary syndromes
Treatment Underlying mechanism of action
Immediate adjunctive treatment
Nitrates Decrease anginal symptoms by inducing coronary vasodilation and improving myocardial O2 supply, and by decreasing myocardial
O2 demand by decreasing preload through venodilatation
Beta blockers Decrease myocardial O2 demand by decreasing heart rate and contractility; in addition, also contribute to electrical stability

Calcium channel blockers Decrease myocardial O2 demand by decreasing heart rate and contractility, decreasing wall stress via decreased blood pressure, and
decreasing preload via venodilatation
Morphine Reduces myocardial oxygen demands by decreasing chest pain and anxiety
Oxygen Improves oxygen supply in patients with hypoxemia
Antiplatelet therapy
Aspirin Prevents further thrombus formation by inhibiting platelet synthesis of thromboxane A2 , an important mediator of platelet activation

Clopidogrel (or other ADP receptor blockers)
GP IIb/IIIa inhibitors
Unfractionated heparin (UFH) or low molecular weight
heparin (LMWH)
Recombinant tissue-type plasminogen activators
(tPA, rPA and TNK-tPA)
Plain old balloon angioplasty (POBA)
Bare metal stents
Drug-eluting stents
Coronary artery bypass graft (CABG)
Inhibit ADP-mediated activation of platelets, thereby preventing expansion of the existing thrombus; have superior outcomes when
used in combination with Aspirin
Potent antiplatelet agents that block the final common pathway of platelet aggregation; often used in patients undergoing PCI as they
are very effective in reducing cardiac events in these patients
Anticoagulant therapy
UFH an LMWH, which preferentially bind to antithrombin III and factor Xa, respectively, slow thrombin formation and impede clot
development
Fibrinolysis
Transform the inactive precursor plasminogen into the active protease plasmin, which lyses fibrin clots, thereby accelerating lysis of
the occlusive intracoronary thrombus and restoring blood flow
Primary percutaneous coronary intervention (PCI)
Inflation of a balloon within a stenosed coronary artery mechanically dilates the affected vessel to restore blood flow, both by
compressing the atherosclerotic plaque and stretching the underlying media
Mechanically maintain the patency of coronary arteries occluded by atherosclerotic plaques
In addition to maintaining patency, these stents release antiproliferative agents such as sirolimus or paclitaxel, which prevent
neointimal proliferation (migration of smooth muscle cells and production of extracellular matrix), thereby decreasing the rate of in-stent
restenosis
Surgical revascularization
Restores coronary blood flow by using a healthy patent artery to bridge circulation around an occlusive lesion within an atherosclerotic
coronary vessel

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Approach to the management of patients

with ACS
UA/NSTEMI All patients STEMI

•Aspirin •Nitrates •Aspirin

•Heparin (UFH or LMWH) •Beta blocker •Heparin (UFH or LMWH)
•Clopidogrel •± Ca channel blocker •Clopidogrel
•Morphine
In high risk patients: •Oxygen Reperfusion method selected
•Primary PCI based on timing:
•GP IIb/IIIa inhibitor Additional therapies shown to •Primary PCI + GP IIb/IIIa inhibitor if
have long-term outcome benefits performed within 90 mins of
•ACE inhibitor presentation
•Statin •Fibrinolysis within 30 mins of
presentation if timely PCI not
possible

http://www.pathophys.org/acs/#Pathophysiology_of_the_ischemic_process

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• it is important to note that heart failure is not a

Heart Failure diagnosis. Rather, it represents a constellation of
signs and symptoms resulting from the inability of
the heart to pump blood forward at a sufficient rate
to meet the metabolic demands of the body
(forward failure) or the ability to do so only if the
cardiac filling pressures are abnormally high
(backward failure), or both. Often, it is the final and
most severe manifestation of almost any form of
cardiac disease.
• Extra-cardiac conditions resulting in inadequate
tissue perfusion, such as severe hemorrhage, or
increased metabolic demands, such as in
hyperthyroidism, can also cause the above definition
to be met, but will not be addressed here.

http://www.pathophys.org/heartfailure/

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Etiology
• Predominantly systolic dysfunction is seen in a majority of patients, while others
exhibit mainly diastolic dysfunction. Components of both can also be found.
• Systolic dysfunction – diminished ability to eject blood due to:
• Impaired ventricular contractility: destruction or abnormal function of myocytes,
fibrosis
• Increased afterload – increases resistance to flow
• Diastolic dysfunction
• Impaired ventricular relaxation
• Impaired ventricular filling due to increased ventricular wall stiffness
• This classification may help distinguish causes in terms of their impact on normal
heart physiology, heart failure can also be thought of clinically as right- versus
left-sided heart failure.

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Left-sided heart failure Right-sided heart failure

Systolic dysfunction
Impaired ventricular contractility
•Myocardial infarction, or transient
myocardial ischemia
•Chronic volume overload (mitral or aortic
regurgitation)
•Dilated cardiomyopathy (see
cardiomyopathy chapter for etiology of
dilated cardiomyopathy)
•Myocardial infarction, or transient
myocardial ischemia
•Chronic volume overload (tricuspid or
pulmonic regurgitation)
•Dilated cardiomyopathy

Increased afterload •Uncontrolled systemic hypertension •Uncontrolled pulmonary hypertension

Diastolic dysfunction
Impaired ventricular relaxation
Impaired ventricular filling
•Aortic stenosis
•Ventricular hypertrophy
•Cardiomyopathy (hypertrophic or restrictive)
•Transient myocardial ischemia
•Mitral stenosis
•Pericardial constriction or tamponade
•Pulmonic stenosis
•Chronic obstructive pulmonary disease
(COPD)
•Interstitial lung disease
•Acute respiratory distress syndrome
(ARDS)
•Chronic lung infection or bronchiectasis
•Pulmonary embolism
•Tricuspid stenosis
•Pericardial constriction or tamponade

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Pathogenesis
Myocyte loss and/or dysfunction
• In addition to global mechanical dysfunction in heart failure, another key
player in this process may be dysfunction at a cellular level.
• Myocyte loss
• Necrosis – resulting from insults such as MI or exposure to cardiotoxic drugs
• Apoptosis (programmed cell death) from elevated catecholamines, angiotensin II,
inflammatory cytokines, and mechanical strain from increased wall stress
• Changes activated in expression of contractile proteins, ion channels,
enzymes, receptors and secondary messengers
• Reduced cellular ability to maintain calcium homeostasis
• Changes in handling of high-energy phosphates
•

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Compensatory mechanisms
• Frank-Starling mechanism
• Frank-Starling relationship: Ventricular output increases in relation to
preload, i.e. with a greater stretch of myocardial fibers (larger diastolic
volume), there will be a greater force of contraction generated
• In heart failure, a decreased stroke volume results in reduced chamber
emptying, with higher than normal diastolic volume
• This induces a greater stroke volume for the subsequent contraction to help empty
the ventricle and preserve forward cardiac output
• However this mechanisms has limits, and at markedly elevated diastolic
volumes, the stretch of myofibers becomes too great and suboptimal for
generating a strong contraction

43

Myocardial hypertrophy
• Wall stress is often increased in heart failure due to either ventricular
dilatation or the need to generate high systolic pressures to overcome
excessive afterloadWall stress is estimated from LaPlace’s
relationship, in which the wall stress (σ) is proportional to ventricular
pressure (P) and ventricular chamber radius (r), and inversely
proportional to ventricular wall thickness (h)

44

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• In response to a sustained increase in pressure and chamber radius,

hypertrophy of the ventricular myocytes is stimulated
• The increased mass of muscle fibers serves to maintain contractile force and
counteract the elevated ventricular wall stress
• Eventually, the chamber may dilate out of proportion to wall
thickness, resulting in excessive hemodynamic burden on the
contractile units, rapid deterioration of ventricular function and
worsening of symptomatology
• Lowering wall stress as a way to slow the remodelling process is a
common therapeutic target

45

Neuro-hormonal mechanisms
• In the early stages of heart failure, these mechanisms help maintain a near normal perfusion to
vital organs by increasing systemic vascular resistance as a way to balance the fall in cardiac
output (blood pressure (BP) = cardiac output (CO) × total peripheral resistance (TPR)). In addition,
activation of neuro-hormonal mechanisms leads to salt and water retention with a consequent
increase in intravascular volume and preload, which maximizes stroke volume via the Frank-
Starling mechanism.
• Renin-angiotensin-aldosterone system (RAAS): (See Nephrology for details of physiology). The
pathway leads to the activation of angiotensin II.
• Angiotensin II
• Vasoconstriction: Increases TPR to maintain BP.
• Increased intravascular volume to increase preload to raise the SV via Frank-Starling mechanism. Angiotensin II does this by (i)
stimulating thirst at hypothalamus and (ii) increasing aldosterone secretion at adrenal cortex.
• Aldosterone
• Increased water retention via increased sodium resorption. This increases preload, in turn increasing the SV
• Antidiuretic hormone (ADH, aka vasopressin)
• Increased secretion thought to be induced by arterial baroreceptors (detecting decreased CO) and increased
angiotensin II levels.
• Promotes water retention in the distal collecting tubule, in order to increase preload.

46

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Adrenergic nervous system

• Decreased CO results in decreased perfusion pressure sensed by
baroreceptors in carotid sinus and the aortic arch. Central and peripheral
chemoreflex activation induces epinephrine, norepinephrine, and
vasopressin release. This results in an increased sympathetic outflow to
heart and peripheral circulation, and decreased parasympathetic tone.
• Increased HR and contractility directly increase cardiac output (CO = HR × SV)
• Peripheral vasoconstriction
• Venous: Increases preload (venous return).
• Arteriolar: Raises peripheral vascular resistance, to maintain BP.
• Unfortunately, despite these compensatory mechanisms, there is
progressive decline in the heart’s ability to contract and relax in the face of
persistent hemodynamic challenges. Furthermore, chronic activation of the
above mechanisms ultimately becomes maladaptive and induces further
worsening of cardiac performance.

47

Deleterious consequences of compensatory

mechanisms
• Continuous sympathetic activation results in downregulation of β-
adrenergic receptors with decreased sensitivity to circulating
catecholamines and less inotropic response.
• Increased heart rate augments metabolic demands and can further reduce
performance by increasing myocardial cell death.
• Increased circulating volume and preload ultimately overwhelm Frank-
Starling mechanism and heart’s ability to maintain forward flow, resulting
in worsening of lung vasculature congestion.
• Increased total peripheral resistance results in higher afterload, impeding
the left ventricle’s stroke volume and reducing cardiac output.
• Chronically elevated angiotensin II and aldosterone trigger production of
cytokines, which activate macrophages an stimulate fibroblasts resulting in
adverse heart remodelling.

48

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Exacerbating factors in compensated heart

failure
• Heart failure can be clinically silent (i.e. asymptomatic) if
compensatory mechanisms are sufficient to balance the degree of
cardiac dysfunction, or alternatively if it is adequately managed
medically. However, patients can become symptomatic, if
decompensation occurs.

49

Precipitants Mechanism of exacerbation

Fever, infection, anemia, tachyarrhythmia,
hyperthyroidism
Excessive salt content in diet, excessive fluid
administration, renal failure
Uncontrolled hypertension, pulmonary embolism
Negative inotropic medications (β-blockers, calcium Impaired contractility: Reduced contractility impairs
channel blockers), ischemia
Bradyarrhythmia
Increased metabolic demands: Inability to
sufficiently increase cardiac output to match
disproportionately elevated demand of organ
systems
Increased circulating volume (preload): Promotes
systemic and pulmonary congestion as the heart is
unable to accommodate a larger preload (Frank-
Starling mechanism overwhelmed)
Increased afterload: Increased resistance against
which ventricle must pump with consequent
decrease in stroke volume
stroke volume and consequently decreases cardiac
output
Direct drop in cardiac output (CO = HR × SV)

Medical non-adherence Multifactorial; e.g. if diuretics not taken adequately,

can result in increased circulating volume (as above)

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Pathophysiology
Left-sided heart failure
Symptoms
Shortness of breath Increased pulmonary capillary oncotic pressure from left-sided backflow causes extravasation of fluid into the pulmonary interstitium,
which then leads to reduced pulmonary compliance and increased airway resistance. There is also an increased ventilatory drive
secondary to hypoxemia, a consequence of increased pulmonary capillary pressures and ventilation/perfusion mismatch due to
inadequate CO.

Orthopnea Redistribution of extravascular fluid from the periphery into dependent areas when supine (i.e. lungs) exacerbates dyspnea as the
Paroxysmal nocturnal dyspnea ventricles cannot adapt to the acute increase in volume; this results in increased pulmonary capillary pressure and worsening of
interstitial pulmonary edema.

Cough +/- frothy blood-tinged sputum Caused by pulmonary congestion. Rupture of engorged bronchial veins can lead to hemoptysis.

Confusion and/or impaired memory Manifestations of inadequate cerebral blood supply

Decreased urine output Decreased renal perfusion during the daytime can sometimes lead to acute kidney injury and eventually renal failure.

Nocturia At night when supine, blood flow is redistributed to the kidney, promoting perfusion and diuresis.

Signs
Pulmonary crackles Opening of small airways that were closed by interstitial edema prior to inspiration; initially present at lung bases where hydrostatic
forces are greatest, but worsening pulmonary edema is associated with crackles in higher lung fields

Cardiac “asthma” Coarse ronchi and wheezing caused by compression of conduction airways by pulmonary congestion

Accentuated P2 Reflects increased pulmonary vascular pressures caused by elevated left-heart filling pressures

Mitral regurgitation murmur May be auscultated if dilation of the left ventricle has excessively stretched the mitral valve annulus and spread the papillary muscles,
preventing full closure of the mitral leaflets

Pulsus alternans May present as a sign of advanced ventricular dysfunction

51

Right-sided heart failure

Symptoms
Peripheral edema, sacral edema, ascites Various manifestations of increased hydrostatic venous pressures
and/or anasarca
Hepatosplenomegaly (+/- right upper Portal and splenic circulation engorgement from inadequate right-sided forward flow
quadrant pain)
Anorexia/weight loss Hepatic and intestinal congestion result in diminished appetite; there can also be occasional
impaired intestinal fat absorption, and more rarely, protein-wasting enteropathy; total
metabolism can also be increased secondary to increased myocardial oxygen consumption
and excessive work of breathing

Signs
Elevated JVP Reflects elevated right-sided pressures and inadequate right-sided forward flow

Kussmaul sign
Palpable right ventricular heave
Tricuspid regurgitation murmur
Paradoxical elevation of JVP with inspiration (as opposed to decrease) reflects increased
right atrial pressure
Represents right ventricular enlargement and approximation of the chamber to the chest
wall
May be auscultated if dilation of the right ventricle has excessively stretched the tricuspid
valve annulus and spread the papillary muscles, preventing full closure of the tricuspid
leaflets

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Right- or left-sided heart failure

Symptoms
Chest pain/pressure Can occur as a result of primary myocardial ischemia from CAD or secondary to increased
filling pressures, poor cardiac output (with consequent poor coronary diastolic filling) or
hypoxemia

Palpitations Can be secondary to sinus tachycardia due to decompensated heart failure, or

atrial/ventricular tachyarrhythmias arising in dilated heart chambers

Chronic Likely a result of the chronic state of hypoxemia from inadequate oxygen delivery to
fatigue/weakness peripheral tissues, with generalized decreased muscle strength, decreased endurance and
multi-organ system dysfunction

Cachexia In part due to poor appetite, along with increased metabolic demands of increased work of
breathing
Signs
S3 gallop Caused by abnormal filling of a dilated ventricle, often in systolic heart failure
S4 gallop Results from forceful contraction of the atria into a stiffened ventricle; common in diastolic
dysfunction
Cardiomegaly Chronically increased workload and excessive volume cause ventricular dilatation and
hypertrop

53

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Chronic management
• Non-pharmacologic management
• Lifestyle modification:
• 10% weight loss
• Sodium < 2gm/day
• Fluid restriction (<2L/day)
• Smoking and drinking cessation

55

Pharmacologic management
• β-blockers: (Lancet. 1999 Jun 12;353(9169):2001-7, Lancet. 1999 Jan 2;353(9146):9-
13. Lancet. 2003 Jul 5;362(9377):7-13)
• Counteract the harmful effects of sympathetic nervous system activation, may also assist in preventing
tachyarrhythmias and myocardial ischemia
• Of all beta blockers, only metoprolol succinate (MERIT-HF trial), carvedilol (COMET trial),
and bisoprolol (CIBIS-II trial) have demonstrated mortality benefit
• COMET – carvedilol superior to metoprolol reducing mortality in NYHA II+ & EF <35%
• CIBIS II – significant reduction in all-cause mortality and hospitalization in NYHA II+
• ACE inhibitors (ACEi) / angiotensin receptor blockers (ARBs): (N Engl J Med. 1992 Sep
3;327(10):685-91)
• Counteract the activated mediators of the RAAS to prevent their deleterious consequences and ultimately
minimize cardiac remodelling
• Enalapril shown to have significant morbidity and mortality benefit (SOLVD & CONSENSUS trials)
• For patients unable to tolerate ACEi, both candesartan and valsartan have been studied and have been shown
to have mortality benefit (CHARM & V-HeFT trials) – no added benefit to ACEi
• Hydralazine + nitrates (N Engl J Med. 2004; 351:2049-2057)
• Consider if patients unable to tolerate ACEi/ARBs or in African American patients with NYHA class III/IV
• A-HEFT trial – 40% reduction in mortality

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• Aldosterone antagonists (N Engl J Med. 2011 Jan 6;364(1):11-21, N Engl J Med. 1999 Sep 2;341(10):709-
17.)
• Aldosterone antagonist counteracts the harmful effects of aldosterone including salt retention, myocardial hypertrophy and
potassium excretion
• Spironolactone: RALES trial – 34% mortality benefit in patients with heart failure NYHA Class III+ (patients already optimized
on beta blocker and ACEi therapy)
• Epleronone: EMPHASIS-HF trial – 37% reduction in death from CV causes or hospitalization for HF NYHA Class II+
• Digoxin (N Engl J Med. 1997 Feb 20;336(8):525-33):
• Enhances cardiac contractility, but also blunts the compensatory sympathetic drive by increasing the sensitivity of
baroreceptors, which decreases afterload
• No mortality benefit; only decreased hospitalizations (DIG trial)
• ICDs and cardiac resynchronization therapy (N Engl J Med. 2005 Jan 20;352 (3):225-37, N Engl J Med. 2009
Oct 1;361 (14):1329-38.):
• Pacemaker-based approach to treat patients with a wide QRS complex
• Purpose is to provide electromechanical coordination and improve ventricular synchrony in patients with severe systolic
dysfunction and significant intraventricular conduction defects such as left bundle-branch block
• ICDs in patients with NYHA II/III HF & EF<35% significantly reduced mortality (SCD-HEFT)
• CRT, when further added to ICDs, reduces HF exacerbations by 41%. Similar benefits for ischemic and non-ischemic
cardiomyopathy as well as significant reduction in LV volume & EF improvement (MADIT-CRT)
• Mechanical circulatory support (i.e. intra-aortic balloon pump, IABP)
• An IABP deflates in diastole and inflates in systole to decrease impedance to LV ejection of blood and increase coronary
perfusion
• Used in extreme cases of unstable hemodynamics
• Diuretics
• Mainstay of symptomatic congestion control; may help improve stroke volume by eliminating excessive circulating volume
and decreasing preload, therefore reducing “backup” of fluid into pulmonary interstitium and peripheral tissues. Diuretics
have not shown mortality benefit.

57

Acute decompensation
• It is important to identify the precipitant of heart failure and treat as the HF episode is being
treated.
• Diuretics: Lasix (furosemide)
• Helps eliminate excess fluid that the heart cannot accommodate (preload) and improve stroke volume,
thereby decreasing pulmonary and peripheral edema
• Morphine:
• Decreases preload by acting as a venodilator, and reduces sympathetic activation and consequently demand
on heart by procuring pain relief
• Nitrates:
• Decrease preload via venodilation, and improve oxygen delivery to the heart
• Oxygen:
• Oxygen +/- noninvasive ventilation – preserve ventilator drive and maintaining blood oxygen saturation
• Positioning:
• Sit patient upright with legs dangling down to promote blood pooling in the lower extremities and decrease
preload

http://www.pathophys.org/heartfailure/

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REHAB JANTUNG
• Rehabilitasi jantung adalah proses dimana pasien dengan kondisi
penyakit jantung, bekerjasama dengan tim kesehatan professional
multidisiplin untuk memulihkan dan mempertahankan kesehatan fisik
dan psikososial yang optimal.

Scottish Intercollegiate Guidelines Network (SIGN) Cardiac rehabilitation: a national clinical guideline, 2002

59

multidisciplinary team approach

• Cardiologist/Physician and co-coordinator to lead cardiac rehabilitation
• Clinical Nurse Specialist
• Physiotherapist
• Clinical nutritionist/Dietitian
• Occupational Therapist
• Pharmacist
• Psychologist
• Smoking cessation counsellor/nurse
• Social worker
• Vocational counsellor
• Clerical Administration

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Target populasi untuk dapat berpartisipasi dalam program

rehabilitasi jantung

Penyakit jantung iskemik Kondisi Gagal Jantung Penyakit kronik lainnya

1. Post-MI, graft bypass arteri 1. Gagal jantung kompensasi 1. Stroke

koroner, perkutan angioplasti
koroner transluminal
2. Angina yang stabil
2. Dysrhythmias Terkontrol 2. Peripheral vascular disease
3. Implan otomatis cardioverter 3. Chronic heart failure
defibrillate/alat pacu jantung
4. Paska Penggantian katup
5. Cardiomyopathy
6. Reseksi aneurisma miokard
7. Transplantasi pra dan pasca
jantung
8. Kelainan jantung kongenital

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Capaian Rehab Jantung

Body Function Activity Participation Enviromental & Personal Factor
& Structure

Capaian Medis Capaian Fungsi Capaian Sosial Capaian Capaian Capaian

tubuh Psikologis Kebiasaan layanan
Kesehatan
Meningkatkan Berjalan Kembali Mengembalika Berhenti Menekan biaya
fungsi jantung bekerja pada n rasa percaya merokok medis
Mengangkat level aktifitas diri
Mengurangi beban sebelum sakit Diet Mempromosika
resiko infark Mengurangi n mobilisasi dini
Naik turun ADL mandiri rasa khawatir Aktif fisik agar cepat
Mengurangi tangga dan depresi lepas dari RS
simtom sesak Mengikuti
dan angina Mengontrol program Mengurangi
stress pengobatan masuk RS
Meningkatkan menyeluruh akibat serangan
kerja fisik Mengembalika jantung ulang
n aktifitas
Mencegah seksual
peningkatan
aterosklerosis

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Individual Risk Assessment (profile)

Tak dapat diubah Dapat diubah
Usia Konsumsi Alkohol
Jenis Kelamin Merokok
Riwayat Jantung Hipertensi
Riwayat Keluarga Dyslipidemia
Diabetes Obesitas
Sedentary
Depresi/cemas
stress

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Cardiac Rehabilitation Participation

Inklusi
• Paska Myocard Infark (dinyatakan stabil medis)
• Paska Bedah Pintas Arteri (CABG)
• Percutaneous Coronary Intervention
• Angina Stabil
• Gagal Jantung Stabil (NYHA I-III)
• Cardiomyopathy
• Tranplantasi Jantung
• Implantable Cardioverter Defibrillator
• Valve Repair/Replacement
• Insertion of Cardiac Pacemaker (with one or more
other inclusion criteria)
• Peripheral Arterial Disease
• Post Cerebral Vascular Disease
• At risk of coronary artery disease with diagnosis of
diabetes, dyslipedemia, hypertension
64
Ekslusi
• Angina Tak Stabil
• Iskemia ditandai dengan perubahan EKG
• Sistolik istirahat >200mmHG atau diastole istirahat
>110mmHG
• Orthostatic BP drop >10mmHg with symptoms
• Critical aortic stenosis (peak pressure gradient
>50mmHg with aortic valve orifice <0.75cm2
• Acute systemic illness or fever
• Uncontrolled atrial or ventricular arrhythmias
• Uncontrolled sinus tachycardia (>120bpm)
• Uncompensated CHF
• Acute systemic illness
• 3rd degree AV block with no pacemaker
• Acute pericarditis/myocarditis
• Recent embolism
• Thromobophlebitis
• Uncontrolled diabetes
• Severe orthopediac problems
• Other metabolic problems such as acute thyroiditis,
hypo-hyperkalaemia, hypovolemia

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Strategi billing/pembiayaan

• 18 minggu dengan 36 pertemuan

65

Dosis Rehab Jantung

• Berdasarkan METS

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67

• https://www.ncbi.nlm.nih.gov/books/NBK499903/figure/article-30557.image.f1/?report=objectonly

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klasifikasi Fungsional
New York Heart Association (NYHA) classification

Derajat klasifikasi Fungsional METS

Kelas I Tidak ada gejala dengan aktivitas biasa >7
Kelas II Sedikit keterbatasan aktivitas fisik yang 5
nyaman ketika istirahat, tapi biasanya setelah aktivitas fisik terjadi :
kelelahan, palpitasi, dispnea, atau angina
Kelas III Ditandai pembatasan aktivitas fisik yang nyaman saat istirahat, tetapi 2-3
setelah melakukan aktivitas fisik yang ringan diikuti :
kelelahan, palpitasi, dispnea, atau angina
Kelas IV Tidak dapat melakukan aktivitas fisik tanpa gejala ketidaknyamanan 1,6
dan insufisiensi jantung dapat hadir bahkan pada saat istirahat

Clinton D. Kemp, John V. Conte, 2011

69

intensitas

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Proses Pelaksanaan Rehab Jantung

Pemeriksaan Monitoring Monitoring

Perencanaan Pelaksanaan Akhir
resiko Awal

71

Pelaksanaan Rehab Jantung

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Safety 1-target HR
• Hitung target kerja Denyut Jantung pakai Karvonen berdasarkan USIA
{(Max HR - rest HR) x %intensitas}+ rest HR

73

Safety 2- Borg Scale

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Safety 3
• EKG
• VAS/VDS/NRS
• Tekanan Darah

75

TAHAPAN REHAB JANTUNG

FASE 2: RAWAT JALAN (PERIODE

FASE 1: RAWAT INAP PRA LATIHAN) dengan monitor
EKG

REHAB JANTUNG

FASE 3: PROGRAM LATIHAN FISIK & FASE 4: PEMELIHARAAN KONDISI

EDUKASI

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Fase 1- capaian
• Tidak adanya masalah skeletal seperti ROM, pectus excavatum,
carinatum, scoliosis, bengkak sendi, kelemahan otot, dll
• Tidak ada masalah paru seperti obstruktif, restriktif, suara gangguan
napas (crackles, wheeze, dll)
• Mengurangi rasa nyeri dan rasa khawatir untuk bergerak
• Meningkatkan kapasitas fungsional

77

FASE 1 – program RAWAT INAP (2-5 hari)

• Dimulai 2-5 hari paska serangan/operasi di ICU atau CVICU
• Program Rehab jantung Fisio dimulai setelah 12-24 jam paska operasi
• Dosis 1-3 Mets
• Program FT: mobilisasi (Mi-Ka, Mi-Ki), Chest FT, aktifitas fungsional

Kontraindikasi
• Isometrik
• Latihan beban

Kriteria masuk Fase 2:

• Mampu melakukan latihan 3-4 Mets (6MWT)
• Skala Nyeri 0

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Batasan aktifitas fisik pada pasien Bedah vs. pasien

medis
• Post-MI: HR < 120 beats/min atau naik 20 bpm denyut istirahat
• Pasca bedah: boleh naik 30 bpm di atas nadi istirahat
• Pasien bedah mungkin memiliki tindakan pencegahan sternal

79

Activity Progression in Cardiac Rehabilitation

Example of Activity Progression

Day Location Activity MET Level HR response

1 CCU OOB to chair (sitting) 1.5-2 MET 5-15 bpm above resting
Bedside commode
2 Telemetry ADL/self care 2-3 MET 10-15 bpm above
Sitting leg and arm range of motion resting

Walking in room
3 Tele OOB as tolerated 2-3 METs 15-20 bpm above
Standing warm up exercise resting

Walking 5-10 minutes

4 Tele Shower seated 3-4 METs 15-20 bpm above
Ambulate level, up stairs ½ level or resting
down 1 level

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Fase 1- contoh panduan protokol

Level 1 – hari 1 paska bedah (complete bed Level 2- hari 2-3 (partial bed rest Level 3 hari 3-5
rest)

1. Relaksasi – breathing control Tahap 1 Tahap 1

2. Latihan pernapan – Pulsed lip breathing
3. Stretching/latihan LGS aktif ankle & wrist
Repetisi : 5 kali/1 set
Frekuensi: 3 kali/hari
1. Posisi duduk (1-2 jam/hari) dan makan
mandiri
2. Relaksasi – breathing control
3. Latihan pernapan – Pulsed lip breathing
4. Stretching/latihan LGS aktif ankle, knee,
hip & wrist
5. Mobilisasi/stretching ektremitas atas
Repetisi : 5 kali/1 set
Frekuensi: 3 kali/hari
Tahap 2
1. Penambahan lama duduk 3-4 jam/hari
2. Latihan pernapan – Pulsed lip breathing
3. Latihan pernapan – Pulsed lip breathing
1. STOP relaxation
2. Level 2(b)— progress exercises to 10
repetitions
3. *Walk within room (thrice a day)
4. Standing — Upper limb flexion (five
repetitions thrice a day)
Tahap 2
1. Walk-standing — lower limb flexion (five
repetitions thrice a day)
2. Stride-standing — hip and knee flexion
(five repetitions thrice a day)
3. *Walking outside the room (thrice a day)

an 4. Quad set & Glute (tanpa menahan napas) Tahap 3

atas nsi 5. Toileting mandiri 1. Bend standing — elbow circling

B ra an 2. Trunk bending
e u
Tol amp !!!!
Repetisi : 5 kali/1 set 3. *Walking outside the room with arm
Frekuensi: 3 kali/hari swings
!!
kem sien
4. Climbing one flight of steps

pa
PROGRESSIVE with TOLERANCE

81

Fase 1 - Safety
• Gunakan Borg Scale untuk mengetahui tingkat kemampuan pasien
• mengontrol denyut jantung & Tekanan Darah

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• Tuan F mngeluhkan nyeri dada ketika melakukan exercise stress test,

kemudian dirujuk ke unit jantung coroner dan dilakukan kateterisasi
berupa angioplasty dan stenting, namun pasien masih mengeluhkan
jantungnya dan segera dilakukan CABG di pagi hari. Hasil stress test
menggunakan protocol bruce test, setelah 8 menit target HR
mencapai 128 x/menit, capaian ini mencapai submaksimal dibawah
usianya. 3 Menit awal latihan segmen ST dari EKG ada tanda
peningkatan pada sisi inferior. Disimpulkan ada kondisi acute inferior
infarc. Tes dihentikan dan mengeluhkan nyeri dada.

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diskusi
• Setelah CABG, apa edukasi yang dapat diberikan terkait dengan luka
sternal?
Perawatan luka dan Sternal
• Mandi (10 menit atau kurang) diperbolehkan jika sayatan kering dan penyembuhan.
• Hindari suhu air yang ekstrem.
• Sabun dan air yang lembut diperbolehkan, tetapi jangan menggosok keras sampai kulit yang luka.
• Lotion, salep, atau dressing tidak dianjurkan.
• Sedikit gatal, mati rasa, atau sesak dari daerah sayatan normal.
• pemulihan sternum waktu 6 untuk 8 minggu untuk menyembuhkan. Hindari mengangkat benda yang lebih besar dari 10
lbs/5kg atau aktivitas apapun yang
menyebabkan klik dari sternum. Sesekali mengklik normal.
• Gunakan bantal untuk memetat tulang dada selama batuk atau bersin.
• Lakukan latihan ROM progresif untuk leher, tungkai (termasuk sabuk bahu), dan batang sebagai

Ditoleransi.
• Postur simetris dan tepat sangat penting.
• Jangan gunakan lengan untuk mendorong saat masuk dan keluar dari tempat tidur atau kursi.
• Hindari berbaring di perut sementara di tempat tidur.
• Hindari aktivitas lengan sepihak untuk meminimalkan torsi pada luka sternal.
• Jika vena kaki digunakan untuk cangkok, jaga kaki yang terkena terpengaruhi atau kenakan stoking yang mendukung.
• Tidak mengemudi.
Beri tahu dokter jika pasien mengalami gejala infeksi berikut:
• Peningkatan drainase atau pembukaan sayatan.
• Peningkatan kemerahan atau kehangatan di sekitar sayatan.
• Demam > 38 ° C atau 100 ° F.

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• Pada hari 1 & 2 pasca-CABG di ICU operasi jantung, Anda diminta untuk melihat pasien. Tanda
vital stabil, dan kontrol nyeri optimal. Buatkan Garis besar rencana perawatan ICU untuk pasien
ini. Hari 1 Hari 2
• Duduk pasien di sisi tempat tidur, dan • Latihan pemanasan: pernapasan
membuatnya berdiri. dalam, relaksasi, dan latihan
• dari atelectasis, mengoptimalkan peredaran darah yang lembut
pertukaran gas, dan membantu menjaga
• Program latihan inti '. Leher, bahu
kekuatan dan mobilitas kaki.
• Pasien masih akan memiliki selang dada, girdle, latihan ekstremitas atas
dan berdiri memfasilitasi drainase darah. bilateral, batang, dan
• Setelah berdiri, pasien berjalan di tempat • latihan ROM ekstremitas bawah
dan mengambil beberapa napas dalam- • Cool-down periode '. Pernapasan
dalam. Beberapa pasien dapat menoleransi dalam, relaksasi, dan latihan
berjalan kaki singkat. peredaran darah yang lembut.
• Ajak pasien keluar dari tempat tidur dan
duduk di kursi.
• Instruksikan pasien dalam latihan
pernapasan dalam. lakukan 10 kali.
• Latihan batuk dengan melindungi area luka
menggunakan bantal.
• Melatih kaki dan pergelangan kaki latihan
per jam sementara di tempat tidur.
• melatihan bahu bilateral ROM.

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Fase 2- capaian
• Aktifitas fisik mencapai 5 METS
• Respons hemodinamik normal untuk latihan
• Absen atau stabil Angina Pektoris
• HR istirahat yang stabil dan terkendali, BP
• Tingkat kebugaran fisik yang memadai untuk setiap hari
• aktivitas dan tugas pekerjaan
• Program dilakukan 6-8 minggu
• Jika pre exc tes ditemui iskemia maka tidak bisa
diberika latihan

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Proses Fase 2

Perencanaan
Pre Test Pelaksanaan Evaluasi
Capaian

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Pre Exercise Test

• Bruce Test Protocol

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Perencanaan fase 2 berdasarkan hasil bruce

test
• The Adapted Karvonen's Formula is :
• (Max HR - rest HR) x (.4 -.8 + (Max METs/100)) + rest HR

Tn, James
resting HR = 80 bpm ;
maximal exercise HR = 180
resting BP = 120/80 ;
maximal exercise BP = 180/90
maximal METs obtained = 8 METs
Capaian HR:
(Max HR - rest HR) x (.4 -.8 + (Max METs/100)) + rest
HR
Training Exercise Heart Rate (TEHR) = (180 - 80 ) x (.5
+ 8/100) + 80
TEHR = ((100) x .58) + 80 = 138 bpm
Kategori intensitas =
138/180 = 76% à moderate

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• Capaian Tekanan darah

(max Systolic BP - resting Systolic BP) x (.4 - .8 + (max METs/100)) +
resting Systolic BP
• Training Exercise Blood Pressure (TEBP) = [(180 - 120) x (.58)] + 120
• TEBP = [(60) x (.58)] + 120 = 155 systolic BP

• Tekanan darah sistol Mr. James untuk latihan fase 2 tidak boleh
lebih dari 155 mm Hg.

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• Capaian METS

• (Max METs Achieved) x .5 = 4 METs

• 8 x 0,5 = 4 Mets

• Capaian METS mr. james tidak boleh lebih dari 4 METS (moderate/
sedang)

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intensitas

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Penentuan intensitas Jika tanpa Pre Exc Test

• Hitung target kerja Denyut Jantung pakai Karvonen berdasarkan USIA
{(Max HR - rest HR) x %intensitas}+ rest HR

• Kenaikan denyut. Jantung yang diperbolehkan dari Resting HR

– + 20 bpm
– Secara bertahap meningkatkan THR : 20 à 30 à 40
– Progression : Duration (>30 min à naikkan Intensity)
– Menyesuaikan intensitas (speed) by supervised exercise
• with telemetry
• • 20-35 bpm moderate intensity
• 30-55 bpm high intensity
• • RPE ≤ 13

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Pelaksanaan

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Phase III Outcomes

• Functional capacity goals > 8 METS or 2x energy requirements of
work
• Training effects expected
• No cardiac symptoms
• EKG monitoring happens occasionally, or when increasing activity
parameters
• Patients learn self-monitoring of HR and symptoms

• Program 8-12 minggu

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Pelaksanaan fase 3

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Aerobic Capacity and Endurance Goals

• Improved with appropriately prescribed and supervised exercise training program

• Peak VO2 Increased + 11-66% after 3 months training
• Increased submaximal exercise endurance (longer at given rate with lower HR &
BP)
• Decreased exercise induced ischemia at same cardiac work (Rate-pressure
product)
• Increased participation in exercise (does not continue after end of rehab
program)

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Resistance Training in Cardiac Rehabilitation

• AACVPR states patients may begin:

• Minimum of 5 weeks post MI, including 3 weeks of
participation in cardiac rehab
• Minimum 8 weeks post CABG, including 3 weeks of
participation in cardiac rehab
• Resistance training defined at > 50% of 1RM
• Theraband, light weights (1-3#) may be initiated sooner if
indicated

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q Fase IV (maintenance)
§ Pasien yang telah menyelesaikan fase III dianjurkan utk
mengikuti program ini scr individual (fittness center,
health club, RS, di rumah)
§ Biasanya pasien lebih senang melakukannya scr
berkelompok
§ Jaga METS 8-10
§ Program 12-18 minggu

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