DECOMP CORDIS

PATOPHYSIOLOGY
A

C
 PRELOAD AFTERLOAD
3 CO ↓
Overload cairan 3
CHF PHT

1. Overload Cairan JVP 4

2 & 3. Edema Paru
4. JVP 1
HR
5. Edema tungkai
6. Hepatomegali 1 X CO X TPR = BP 2
CO
7. Ascites 2 SV
1. CO ↓
2. T ↓
6 7
3. Edema Paru Akut
R/ 4. Edema tungkai
Diuretik 5. PND
Aminophilin
Vasodilator R/
Bronkodilator Aminophilin
UF 5 4
Vasodilator
Morphin
Respirator
 R/ Central Acting

CNS
R/  Blocker
HR
X CO X TPR = BP
SV H2O & Na CCB & α Block
R/ Diuritik R/ Vasodilator

RAA
R /ACE. I / ARB
 R/ Central Acting

CNS
R/  Blocker
HR
X CO X TPR = BP
SV H2O & Na CCB & α Block
R/ Diuritik R/ Vasodilator

RAA
R /ACE. I / ARB
Pulmonary Edema

(Silbernagl & Lang, 2000: Color Atlas of Pathophysiology)

(Ware LB and Matthay MA, 2005: Acute Pulmonary Edema, NEJM 353:2788-96)
(Ware LB and Matthay MA, 2005: Acute Pulmonary Edema, NEJM 353:2788-96)
ROC of BNP
 B type Natriuretic Peptide (BNP)
BNP pg/ml Sensitivity Specificity PPV NPV Accuracy

50 97 62 71 96 79

80 93 74 77 92 83

100 90 76 79 89 83

125 87 79 80 87 83

150 85 83 83 85 84

N Engl J Med 2002;161-7

CT Ratio (Cardiomegaly)

CTR =
(A+B) ÷ C

CTR =
(3.2 + 6) ÷ 14.8
= 9.2 ÷ 14.8
A = 63%

B
C
CXR in HF
Pulmonary Congestion

BAT’s WING SIGN

Acute Pulmonary Edema
Acute MI – Pulmonary Edema
Severe Heart Failure
Cardiomegaly, Pl Effusion
Pulmonary Plethora in HF
Cardiomegaly – Cong HD
Algorithmic Diagnosis of HF LV dysfunction Suspected HF because
Suspected because of of symptoms & signs
signs

Assess & confirm Cardiac Normal : HF or

Disease by ECG, CXR, BNP LV dysfunction unlikely

Tests Abnormal

Normal: HF or
Imaging by Echo, MRI, NAG
LV dysfunction unlikely

Tests Abnormal

Assess etiology, Staging, Additional Dx Tests

precipitating factors, LVD Example CAG

Choose Therapy
ESC - BMJ Vol . 320, 22 Jan 2000
Precipitating Causes of HF
1 • AMI, Arrhythmias especially AF

2 • Recurrent Ischemia, Anemia

3 • Infections (CAP),  Ethanol

4 • Poor drug compliance, HT Rx.

5 • IV Fluids, Steroids, NSAIDS

6 • Thyrotoxicosis, PE, Pregnancy

 Complications of HF
• Arrhythmias: AF; V Tach, VF, Brady arrhythmias
• Thromboembolism: Stroke; DVT, PE, VTE
• Gastrointestinal: Hepatic congestion and hepatic
dysfunction; malabsorption
• Musculoskeletal: Muscle wasting
• Respiratory: Pulmonary congestion; respiratory
muscle weakness; pulmonary hypertension (rare)

BMJ Vol . 320, 22 Jan 2000

 Prognosis of Heart Failure
• The prognosis of Heart failure is poor
• Mortality from CHF after 5 years - 32 years
of follow up in the Framingham study
– 62% in Men; 42% in Women
• Mortality rate >> Ca Breast, Prostate, Colon
• Survival better with NEF HF
• Disability extreme – recurrent hospital adm.
• HF quality of life is much worse
• HF is an expensive condition
• Trends: increasing incidence & prevalence
 Predisposing Factors
Ventricular Arrhythmias
• Recurrent or continued coronary ischemia
• Recurrent myocardial infarction
• Hypokalemia and Hyperkalemia
• Hypomagnesaemia
• Psychotropic drugs—for example, TCA
• Digoxin toxicity
• Anti arrhythmic drugs cardio-depressant
inotropism) and pro arrhythmic

BMJ Vol . 320, 22 Jan 2000

 Predictors of Poor Prognosis
1. Men, Elderly, Winter 1. QRS > 0.10, V
2. CRF, IHD, Anemia tachycardia
3. DM, Depression 2. T-wave alternans
4. ? AF (no clear view) 3.  LV EF%, LV Dilatation
5.  NYHA class 4.  PCWP,  LV Mass
6.  Heart rate 5.  Cardiac index
7.  Blood Pressure 6. Hyponatremia
8. Cardiac cachexia 7.  NE &  BNP levels
9. S3 Gallop,  JVP 8.  Troponin T and I
10.  UA, Poor LFT 9. 6 minute walk test
10. Poor VO2,  CA 125
BMJ Vol . 320, 22 Jan 2000
NT-pro BNP, All cause mortality

Kaplan Meier Survival curves

Gardner, R. S. et al. Eur J Heart Fail 2005 7:253-260;
Copyright restrictions may apply.
Survival of Patients of HF
Months
Survival %
after HF

1 81

3 75

6 70

12 62

18 57
BNP is Predictive of Death in MI
Non Pharmacological Measures
Lifestyle Measures
Smoking and Alcohol
Salt and Fluid restriction
Immunization and antibiotics
Diet and Nutrition
Exercise training & Rehabilitation
Underlying Diseases, Co morbidities
 Principles of Treatment
• Identification and treatment/removal of
precipitating factors
• Improvement, where possible, of cardiac
function
• Prevent progression from Stage 1 - Stage 4
• Control of problems, resulting from HF e.g.
edema, arrhythmias
• Reduction of morbidity and mortality
• Improvement of the patient’s quality of life
Algorithm for Primary Care
Algorithm for Drug Rx. in HF
HF Dx.

ACE-I ARB
as Blocker

A-A Diuretic Digoxin Specialist

 Referral to a specialist
• Diagnosis in doubt or • Renal impairment
• Significant murmurs • Severe associated
• Valvular heart vascular disease
disease • ACE-I in Reno VD
• Arrhythmias - AF
• Relative hypotension
• Secondary cause - SBP < 90 mm Hg
thyroid disease
• Poor response to
• Severe LVD EF <20% treatment
• Hyponatremia
 Drugs used in  EFHF
Class of
Drug Class Indication in HF NYHA Class
Evidence

ACE Inhibitors All patients of HF Class I – IV Class I Level A

ARB ACE-I intolerant or

Class II – III Class I Level A
(Candesartan) persisting Symptoms

Beta Blockers All patients* Class I – IV Class I Level A

Aldosterone Severe symptoms on

Class III – IV Class I Level A
Antagonists ACE-I / non response
All pts of congestive
Diuretics Class III – IV Class I Level B
symptoms and signs
 ACE-I in Heart failure
• These are FIRST line agents in Heart failure
• Both in symptomatic or asymptomatic LVSD
• ACE-I are mandatory unless contraindicated
•  Morbidity and mortality unequivocally
• Use with caution in renal disease - check weekly
• Previous H/o Angioedema is a contraindication
• Start at low dose, up titrate. Check for  K+
• Stop K+ sparing diuretics, if needed Furosemide
• Nocturnal dosing preferred. Caution in AS
 Guidelines for ACE-I Use in HF
• Stop K supplements and K sparing diuretics
• Omit /reduce diuretics for 24 h before first dose
• Advise patient to sit or lie down for 24 hours
• Start low doses; Review after 12 weeks to
reassess symptoms, blood pressure, serum
creatinine and electrolytes
• Increase dose unless there has been a rise in
serum creatinine; Titrate to max. tolerated dose
• If patient is “high risk” consider admission
 Why ACE-I Vasoprotective ?
 of circulating AT-II and Aldosterone

 of tissue AT-II (Endothelium, Kidney)

 Vasodepressor KK-Bradykinin system

 Sympathomimetic Amines – Anti Adrenergic

 Vagomimetic Effect – Anti arrhythmic, NHR

Alteration in prostanoid metabolism

Mechanisms of ACEI Benefits
• Reduction of arrhythmias
• Prevention of reperfusion arrhythmias
• Prevention of cardiac remodeling
• Modification of endogenous fibrinolysis
• Antihypertensive effects
• Regression of Left ventricle hypertrophy
• Inhibition of neuro-hormonal activation
• Renoprotective & anti proteinuric effects
Mechanisms of ACEI Benefits
• Vasodilatation
• Reduction in sympathetic tone
• Free radical scavenging
• Direct anti-atherogenic effect
• Improvement in insulin sensitivity
• Neo Angiogenesis (in humans?)
• What not – all excellent benefits !!