Defini&on,Pathyophysiology and Hemodynamic Profile of AHF dr. Irmalita, SpJP(K) Department of Cardiology and Vascular Medicine Faculty of Medicine, Universitas Indonesia Harapan Kita Na?onal Cardiac Center
Acute Heart Failure Defini?on • Rapid symptoms and signs secondary to abnormal cardiac func?on (hours-days). • Cardiac dysfunc?on can be related to systolic or diastolic dysfunc?on, to abnormali?es in cardiac rhythm, orto preload and aHerload mismatch. • It is oHen life threatening and requires urgent treatment. • It may occur with or without previous cardiac disease
Subset Klinis Gagal Jantung Akut 1. ADHF :Worsening or decompensated Chronic HF 2. ACS & Heart Failure 3. Hypertensive AHF 4. Pulmonary Edema 5. Cardiogenc shock 6. Isolated right heart failure
Subset Klinis Gagal Jantung Akut • Gagal jantung akut dekompensata (dekompensasi gagal jantung kronik) • Terdapat tanda dan gejala GJA yang ringan dan ?dak memenuhi kriteria untuk syok kardiogenik, edema pulmoner, atau krisis hipertensi. • Sindroma koroner akut dan gagal jantung (de novo) • GJA hipertensif • Terdapat tanda dan gejala gagal jantung terkait dengan tekanan darah ?nggi dan fungsi ventrikel kiri yang masih baik disertai gambaran edema pulmoner akut dari foto toraks.
Subset Klinis Gagal Jantung Akut • Edema paru akut • Terdapat distress pernafasan yang berat, ronki kasar (crakles) diseluruh lapang paru, orthopnoea, saturasi O2 < 90% pada udara kamar sebelum terapi. • Syok kardiogenik • Keadaaan dimana ada tanda hipoperfusi jaringan akibat gagal jantung setelah koreksi preload. Parameter hemodinamik syok kardiogenik antara lain penurunan tekanan darah (TD sistolik < 90 mmHg atau turunnya tekanan arteri rerata (mean arterial pressure = MAP) > 30 mmHg dan / atau penurunan diuresis (< 0,5 cc/kg/jam), dengan laju nadi > 60 denyut per menit dengan atau tanpa buk? konges? organ. • Gagal jantung kanan akut • Ditandai sindroma output rendah dengan peningkatan vena juguler, hepatomegali dan hipotensi.
Mekanis AHF • Non Obstruc?ve - Pericardi?s • Obstruc?ve – MS, AS, HOCM
ADHERE study • • • • •
HF prevalence 10% in >75 yo 78% of AHF, ED ini?al point of care 80-88% pts in ED with AHF hospitalized Associated with significant morbidity and mortality Short term prognosis poor – 3 months : 61% readmiged or dead – 6 months : 30% readmiged for HF, 23 % die
Peacock WF etal. ADHERE Registry Data Ann Emerg Med 2003:
HF Situa?on in Indonesia • Any official data published ? • No mul?center data • Na?onal Cardiac Centre
– In 2005 : 1702 heart failure Emergency admission
FACT : • HF àCommon medical problem • HF àCommon cause of hospitaliza?on • HF àCommon cause of death
Mortality vs where Vasoac?ves Ini?ated 10.9
12
Patients (%)
10 8 6
4.3
4 2 0
ED (n=4096)
Hospital (n=3499) ADHERE registry Data Peacock WF etal. Ann Emerg Med. 2000;42:S26
Patients (%)
ICU Transfer vs where vasoac?ve started 20 18 16 14 12 10 8 6 4 2 0
20
4
ED (n=4096)
Hospital (n=3499) ADHERE registry Data Peacock WF etal. Ann Emerg Med. 2000;42:S26
Treatment of AHF
ADHERE subanalysis : Is quicker beger • N=46,599 • Pa?ents receiving IV vasoac?ves = 7596 – Dopamine, dobutamine, milrinone,niseri?de, nitroglycerin, nitroprusside – Excluded pa?ents with SBP <90 mmhg and/or ⇑cardiac enzymes
12 10 8 6 4 2 0
ED Inpatient initiation initiation (n-4096) (n=3500) LOS (days) Inpatient initiation ADHERE registry Data Peacock WF etal. Ann Emerg Med. 2000;42:S26
Improving Treatment • Time is everything – Quicker = beger outcome – Standardized protocol for acute HF • Consensus ? Guideline ?
• Different approach for different risk – Risk stra?fica?on ? – Op?mizing treatment modali?es
Heart Failure • Clinical state in which the ability of the heart to pump blood is reduced, • Leaving the body’s oxygen and metabolic demands unmet. • Usually caused by an underlying heart problem. • Characterized by inadequate blood flow (perfusion) to the ?ssues and symptoms such as fa?gue.
Conges?ve Heart Failure Can Be Defined Based on: • How rapid the symptoms onset • Which ventricle is primarily involved • Overall cardiac output
E?ology and Pathophysiology • syndrome usually results from LV dysfunc?on and compensatory mechanisms, except in obstruc?ve AHF • cardiac performance is a func?on of 4 primary factors. What are they?
4 Factors Determine Cardiac Performance Contrac?lity + Heart Rate
Preload + Stroke Volume
+
+
“Cardiac Output”
AHerload -
Usual Cardiac Causes of AHF • • • • • •
Decompensa?on of chronic CHF Coronary ischemia/ infarc?on Severe Hypertension & Arhythmias Valvular Heart Disease Cardiomyopathy/ Myocardi?s Circulatory Failure
Compensatory Mechanisms to Maintain Cardiac Output: • The Frank-Starling mechanism • Neurohormonal ac?va?on – Increase Renin Angiotensin Aldosterone system – Increased sympathe?c tone
• Myocardial hypertrophy – All result in increased myocardial O2 demand!
Acute Pulmonary Conges?on/ Pulmonary Edema • May be CARDIAC or NON-CARDIAC in origin. • Results from condi?ons that: – Increase pulmonary capillary pressure – Increase pulmonary capillary permeability
Patophysiologi AHF INITIATION - AMPLIFICATION - VICIOUS CYCLE – Systolic Diastolic Failure – Backward-Forward Failure – Symphate?c Nervous System and Renin AgiotensinAldosterone system – Natriure?cpep?de – Endothelin Cytokines
Ini?a?on phase of AHF Neurohormonal & Inflammatory ac?va?on LV ↓ contrac?lity
+
SVR ↑
AHerload mismatch CO↓
LV pressure↑
Amplifica?on phase of AHF Neurohormonal & Inflammatory ac&va&on LV ↓ contrac?lity
+
SVR ↑
AIerload mismatch CO↓
LV pressure↑
Alveolar ↑ Capillary permeability
Wedge pressure↑↑
Decreased Fluid clearance
Pulmonary Edema
Obstruc?ve AHF Mitral Stenosis
For op?mal CO need • AV synchrony, • adequate diastolic filling ?me Conditions ↓ CO • •
•
Not a pump problem Diseases progression Atrial fibrillation
– Loss atrial contraction → LA pressure ↑ → congestion
Increase Venticular rate – Diastolic filling time ↓
Aor&c stenosis
For optimal CO need • •
AV synchrony high LV pressure (adequate preload)
Conditions ↓ CO •
Diseases progression
•
Change in preload
– Diare, bleeding • • •
Atrial fibrilation Heart Rate ↑ – Systolic ejection time ↓ Myocardial ischemia – ventricle relaxation ↓
Clinical Findings of AHF Low Perfusion
Conges?on
Hypotension Cool extremi&es Narrow pulse pressure Sleepiness, obtunda&on Elevated BUN, crea&nine Hyponatremia
Orthopnea Paroxysmal Nocturnal Dyspnea Neck vein disten&on Ascites, edema Hepatojugular Reflux Rales
Assessment of Hemodynamic Profile 4 Possible Hemodynamic Profiles of AHF NO
Sign of low perfusion: Narrow pulse pressure,cool ex tremities,sleepy, suspect from ACEI hypotension, low Na, re nal worsening
NO
Low Perfusion? YES
YES
A
B
Warm/Dry
Warm/Wet
Cold/Dry
Cold/Wet
L
C
Conges&on?
Sign of congestion: Orthopnea, elevated JVP, edema,pulsatile hepatomegaly ascites, rales,louder S3, P2 radiation left ward, abdomino-jugular reflex, valsava square wave
Adapted from LW Stevenson
Dry
Wet
Warm
A
B
Cold
L
C
Fluid Challange
Diure&c Vasodilator
Inotropic drugs :
