T9 - Insuficiência Cardíaca Aguda Flashcards
Acute HF - Concept?
Rapid onset or worsening of symptoms and/or signs of HF.
It’s life-threatening and requires urgent therapy typically leading to urgent hospitalization.
Delay in delivery of care for AHF?
Associates with increases in mortality, hospital length of stay, and treatment Costs.
AHF in Europe?
The main cause of hospitalization above 65y
10% of the patients admitted in European wards
HF in-hospital mortality?
12.5%
Acute Exacerbations may contribute to the Progression of HF?
With each event, there may be myocardial injury that may contribute to progressive ventricular dysfunction and dilatation
Acute HF - Economic burden?
HF consumes 1-2% of health resources, in developed countries, where it is the single most expensive disease
Acute Heart Failure - Subtypes?
‘De novo’ HF - 37%
Descompensação de HR Crónica - 63%
Acute Heart Failure - Clinical presentations?
- HF Crónica Agudamente Descompensada
- HR Aguda Hipertensiva
- Edema Pulmonar
- Choque cardiogénico
- ACS and HF
- Right HF
Acute Heart Failure - Clinical/Hemodynamic Classification?
Warm-Dry = No Congestion , No Hypoperfusion (melhor prognóstico) Warm-Wet = Congestion , No Hypoperfusion Cold-Dry = No Congestion , Hypoperfusion Cold-Wet = Congestion , Hypoperfusion (pior prgonóstico)
Etiology AHF?
Coronary artery disease is the main etiology of AHF (60-70% of patients)
Other possible causes/ precipitating factors: • Hypertension • Arrhythmia • Valvular or Congenital heart disease • Myocarditis/cardiomyopathy • Decompensating factors of CHF • Others
Main primary cardiac causes?
- Acute Coronary Syndromes,
- Tachy or bradyarrhythmias
- Acute cardiac mechanical cause
Main causes of decompensation of Chronic HF?
- Hypertensive emergency
- Acute pulmonary embolism
- Infection
- Non-adherence to treatment/diet
- Anemia
- other
Pathophysiology?
Low CO (Hypoperfusion) and congestion Neurohormonal and Inflammatory Activation
Frequency of Low cardiac output?
Low CO leading to symptomatic hypotension and hypoperfusion, is relatively rare, present in CCU/ICU and associated with a particularly poor outcome.
The clinical presentation of AHF?
Most patients have normal or high BP at presentation, and are admitted with congestion.
Most frequent mechanisms of acute congestion?
acute decompensations of chronic HF
abrupt onset of dyspnoea due to significant HTN
Congestion - Definition?
Clinical congestion • Increased LVEDP • Signs and symptoms of HF (dyspnoea, rales, and edema). Hemodinamic congestion • Increased LVEDP • No signs and symptoms of HF
Often, haemodynamic congestion precedes clinical congestion by days or even weeks.
Congestion (Increased LVEDP) in AHF?
Not always due to volume overload • Volume overload due to o RAAS activation o Dietary sodium o Cardio-renal Syndrome • Vascular mechanisms without volume overload o Arterial stiffness o Volume redistribution
Arterial compliance: HFrEF vs HFpEF?
Compliance arterial HFpEF < HFrEF
Resting blood volume distribution?
25% in splanchnic vasculature.
Under SNS control splanchnic blood volume can be recruited in seconds to effective circulatory volume.
Acute Hypertensive HF?
Common and with little volume overload
Patients improve rapidly with vasodilators with minimal diuresis.
There may be a disconnect between increased LVEDP and weight gain
Melhor preditor de mortalidade em AHF?
Congestion - vicious cycle
Acute HF - Therapy?
AHF Is life-threatening and requires urgent therapy
Pre-hospital management - Within minutes of patient contact in the ambulance?
• Non-invasive Monitoring
o pulse oximetry, BP, respiratory rate, and continuous ECG
• Oxygen therapy
o If SpO2 < 90%
o Non-invasive ventilation, in patients with respiratory distress.
• Treatment initiated based on BP and/or the degree of congestion
o vasodilators and/or
o diuretics (i.e. furosemide)
• Rapid transfer to the nearest hospital
o preferably to a site with a cardiology department and/or CCU/ICU
Early hospital management - On arrival in the ED/CCU/ICU?
Initial clinical examination, investigations and treatment should be started immediately and concomitantly.
AHF therapeutic strategy - The 3 steps?
A. Clinical and hemodynamic stabilization
B. Diagnostic investigation (early)
C. Definitive treatment/correction of precipitating factor
Early hospital management - Diagnosis of AHF?
Dyspnea is the most common symptom in AHF.
It is largely unspecific.
Confirmation AHF as the cause of dyspnea - 1. History and physical Examination?
- Prior HF was the most useful historical parameter
- The most relevant symptoms and signs are:
• Paroxysmal nocturnal dyspnea and orthopnea
• Cardiomegaly, S3, and cardiac murmurs
• Hepatojugular reflux, jugular venous distension, and peripheral edema
Confirmation AHF as the cause of dyspnea - 2. Ancillary examination?
- Chest X-Ray:
• up to 20% of AHF patients have no congestion on their ED chest radiograph - ECG:
• not useful for diagnosis of AHF
• but may suggest a specific cause or precipitant - Natriuretic Peptides:
• They are the most established AHF diagnostic biomarkers. - 2D-Echo:
• valuable in determining the etiology of dyspnea
• assessment of LV function
• volume status of AHF - Lung sonography:
• pulmonary ultrasound is accurate in detecting AHF with sensitivities of 86%–100% and specificities of 95%-98%
Clinical and hemodynamic - Stabilization?
Class I indication
• Oxygen therapy (if SpO2 < 90%)
• Diuretics (if congestion with normal/low BP is present)
Class IIa/IIb indication
• Morphine (in APE if severe anxiety/distress is present)
• Vasodilators (SBP > 110mmHg is present)
• Inotropes / Vasopressors (if congestion with low-output and SBP <90 mmHg is present)
Using the clinical/hemodynamic classification?
- Presence of congestion?
2. Adequate peripheral perfusion?
Correction of the causal/precipitating factor?
- ACS
- Taquiarritmia (ex: FA, Taquicardia ventricular)
- Aumento excessivo da PA
- Infeção (ex: pneumonia, endocardite infeciosa, sepsis)
- Non-adherence with salt/fluid intake or medications
- Bradiarritmia
- Toxic substances
- Drugs
- Exacerbation of DPOC
- Pulmonary embolism
- Surgery
- Increased sympathetic drive
- Metabolic/hormonal derangements
- Cerebrovascular insult
- Acute mechanical cause
