You are on page 1of 21

Irsad Andi Arso

Departemen Kardiologi dan Kedokteran


Vaskular FK UGM/ KSM Jantung RSUP Dr.
Sardjito Yogyakarta
Objectives
 Review the pathophysiology of ADHF.
 Describe the clinical presentation of ADHF.
 Apply effective therapeutic strategies using
consensus guidelines
 Evaluate the appropriateness of treatment.
Pathophysiology
LV Dysfunction:
Accumulation of fluid.
Decrease in CO Hypoperfusion.

 Reciprocal Activation of (RAAS)


Na, water retention.
AGII ET1 + Vasopressin.
Reflex activation of SNS: Epi, NE.
Processes mediating short-term effects Processes mediating long-term effects
Initiation phase Amplification phase

The Short-term and long-term Pathophysiogical consequences of AHF‡


O2 supply-demand
mismatch
Vaso- Decreased Fluid
constriction cardiac function overload Hemodynamic Neurohormonal Oxidative Inflammation
abnormalities activation stress

INCREASE INCREASE INCREASE INCREASE

Myocardial Myocardial
Renal
overload and Myocardial fibrosis and
Renal damage dysfunction
renal dysfunction damage remodelling as shown by
as shown by as shown by
as shown by ↑Cystatin C,
↑fibroblast ↑uric acid
↑hs-cTnT ↑Creatinine,
proliferation
↑BUN
and activation

INCREASE
INCREASE

Preload
NT- Afterload
proBNP
N T-p r Congestion Organ damage and
dysfunction

‡Proposed schematic of acute heart failure pathophysiology


Biolo et al. Circ Heart Fail 2010;3:44–50; Bott-Flügel et al. Eur J Heart Fail 2008;10:129–32; Cotter et al. Am Heart J 2008;155:9–18; Cotter et al. Eur J Heart Fail 2008;10:165–69;
Feng & Wang. J Geriatr Cardiol 2008;5:1–6; Hunt et al. J Am Coll Cardiol 2009;53:e1–e90; Oikonomou et al. Hellenic J Cardiol 2011;52:30–40; Tsutsui et al. Am J Physiol Heart Circ Physiol 2011;301:H2181–90
usually a hx of prog.
Classification of AHF worsening of known chronic HF on Rx,
and evidence of systemic/pulmonary
congestion.

high BP, +/- preserved LV systolic fxn;


increased sympathetic tone with ↑HR,
vasoconstriction; may be euvolaemic
or only mildly hypervolemic, and
frequently with signs of pulmonary or
systemic congestion

Severe respiratory distress, ↑RR,


orthopnea, rales. O2 sats <90% RA
prior to O2

Clinical and lab evidence of an


ACS; ~15% of patients with an ACS
have signs and symptoms of HF.
Episodes of AHF are frequently
assoc w/ or precipitated by Usually sys BP <90 mmHg or drop low output in absence of
arrhythmia (bradycardia, AF, VT). in MAP >30 mmHg and pulmonary congestion with
absent/low urine output. Organ increased JVP, w/ or w/out HSM,
hypoperfusion and pulmonary and low LV filling pressures
congestion develop rapidly
ESC 2012
Killip Classification
 Stage I: No clinical signs of decompensation.
 Stage II: Heart failure. Rales, S3, PVH.
 Stage III: Severe heart failure. Pulmonary edema with
rales throughout the lung fields.
 Stage IV: Cardiogenic Shock: Hypotension,
peripheral vasoconstriction, oliguria, cyanosis and
diaphoresis.
Forrester Classification
Cardiac Index
(L/min/m2) 18 mmHg
5 Subset I Subset II
4 (Normal) (Congestion)
Warm and Dry Warm and Wet
3
2.2L/min/m2
2 Subset III Subset IV
(Hypoperfusion) (Congestion and
1 Cold and Dry hypoperfusion)
Cold and Wet
10 20 30
Pulmonary Capillary Wedge Pressure (mmHg) Nohria A et al. JAMA.2002:287; 628-40
Goals of Therapy
 Inprove symptoms and signs of congestion
and/or hypoperfusion.
 Reverse hemodynamic abnormalities.
 Identify the etiology.
 Minimize side effects.
 Optimize therapy.
 Length of stay, mortality, time to hospital
readmission.*
 Educate patients on medications and self
assessment of HF.
The Principle
Reduce Fluid Overload
 Diuretics Reduced Preload: (E-DVf), PCWP

increase Contractility
 Inotropes
Increase CO, EF, Perfusion

 Vasodilators Reduce Preload


Reduce Afterload
Diuretics
 Class I, B
Summary of Vasodilators
Dopamine and Dobutamine
 Dopamine:  Dobutamine, Class IIa, C
 Vasodilator of Renal,  Hypotension and low Urine
Coronary, splanchnic and output
Cerebral Vascular beds  Beta 1 and 2 agonist
 Hypotensive patients  At high doses increases SVR
 Drawbacks: arrhythmia,  Additive effect with
increased pulmonary Phosphodiesterase inhibitors
vascular resistance and  Draw Backs- arrhythmia,
increased afterload reflex decrease in
sympathetic tone

You might also like