Acute Cardiogenic Pulmonary Oedema Flashcards
(32 cards)
definition
-Leakage of fluid from the pulmonary capillaries and venules into the alveolar space as a result of increased hydrostatic pressure
-Inability of left ventricle to effectively handle its pulmonary venous return
pathophysiology
- decreased CO increased PCWP (symptomatic decompensation)
- activation of renin angiotensin system. activation of S/S system
- increased HR, increased systemic vascular resistance, increased preload
- cardiac ischemia. decreased left ventricular function
causes
FAILURE
-F orgot medication (poor compliance)
-A rrhythmia / Anaemia
-I schaemia / Infarction / Infection
-L ifestyle: high sodium diet
-U pregulation of cardiac output: pregnancy, thyroid storm
-R enal failure / Retention of fluid: steroids, NSAIDS
-E ndocardium : valvular pathology
clinical features
SOB
Orthopnoea
PND
Tachycardia
BP
Wheezing
Crepitations
relevant history
-Assess clinical severity by history and physical exam
-Assess cardiac structure and function
-Determine cause, pay attention to reversible causes
-Evaluate for coronary disease and myocardial ischeamia
-Evaluate risk of life threatening arrhythmia
-Identify exacerbating factors and comorbidities
-Establish treatment compliance
-Assess for exertional dyspnoea, PND and orthopnoea
New York Heart Association functional Classification (NYHA)
-Class I : No limitation of physical activity. Ordinary activity causes no undue fatigue, palpitations or dyspnoea.
-Class II : Slight limitation of physical activity. Comfortable at rest, symptomatic with ordinary activity.
-Class IIIA : Marked limitation of physical activity. Comfortable at rest, symptomatic at less than ordinary activity
-Class IIIB : Comfortable at rest, symptomatic with minimal activity.
-Class IV : symptomatic at rest, discomfort increased with any activity
Killip Classification – only with AMI
-Scoring system to assess severity of heart failure in patients with acute myocardial infarction
-Killip I: no clinical signs of heart failure,
-Killip II: crackles in the lungs, third heart sound (S3), and elevated jugular venous pressure
-Killip III: acute pulmonary oedema
-Killip IV: cardiogenic shock or arterial hypotension (measured as systolic blood pressure < 90 mmHg), and evidence of peripheral vasoconstriction (oliguria, cyanosis, and diaphoresis)
physical examination
-Assess weight and vital signs, manage accordingly
-Presence and severity of crackles, S3 gallop, elevated JVP, hepatic enlargement and tenderness, positive hepatojugular reflex, peripheral oedema and ascites
-Thorough clinical examination on cardiovascular and respiratory systems
investigations
- Blood
- Electrocardiography
- Radiology – CXR, echo, bedside cardiac ultrasound
blood investigations
-Arterial Blood Gas
-FBC – anaemia, infection
-U&E
-Troponin – when indicated (suspected myocardial ischaemia or infarction)
ECG
Advisable to do an ECG on all patients presenting with acute pulmonary oedema
Possible Findings:
*Ischaemia / infarction (ST segment changes)
*Arrhythmia – atrial fibrillation, atrial flutter, SVT
*LVH
*Prolonged QRS
chest radiography
FINDINGS IN HEART FAILURE
-Cardiomegaly
-Vascular redistribution
-Interstitial oedema
-Pleural effusions (right sided/bilateral)
chest X ray
Not all patients with acute heart failure have “typical features”
*No longstanding HF- Normal size heart
*Longstanding CCF -lymphatics
*COPD – minimal findings
other investigations: Echo/ bedside cardiac ultrasound
1.Identify reversible cause eg tamponade
2.Distinguish between systolic and diastolic dysfunction
3. Assess valvular function
differential diagnosis
-Acute Renal Failure
-Acute Respiratory Distress Syndrome
-COPD
-Myocardial Infarction
-Pneumonia
-Pneumothorax
-Neurogenic Pulmonry Oedema
-Pulmonary Embolism
-Pulmonary Fibrosis
management
*ABCs
*Decrease Preload (right-sided filling)
*Increase left-sided emptying
*↓ Afterload, Cardiac output
*± improve LV contractility – inotropes
*Main goal is to redistribute fluid out of the lungs
initial emergency management
-Attach patient to monitors, acute care setting (resus)
-Address airway – ensure patency. Apply supplemental oxygen if needed. Consider non-invasive positive pressure ventilation (NPPV) or intubation if necessary
-Breathing
-Circulation – establish IV access, consider inotropes if clinically shocked or significantly hypotensive (LV contractility)
-Disability – may have reduced level of consciousness due to hypoxia
specific management
-OXYGEN
-PHARMACOTHERAPY
-INOTROPIC SUPPORT (if needed)
-NONINVASIVE POSITIVE PRESSURE VENTILATION
-INVASIVE VENTILATION
supplemental oxygen
-Consider in patients with sats <94% on room air, or with signs of respiratory distress
-Titrate oxygen to symptoms
-Administer via nasal cannula, facemask or partial non- rebreather mask
-Assess efficacy, determine need for NPPV or intubation
preload reduction- give nitrates
*Isordil 5mg s/l or GTN spray (one dose) can be used, repeated every 5-10 minutes
*Nitrate Infusion: mix 50mg GTN (Tridil) in 200ml normal saline. Rate 0-48ml/hour, start at 20ml/hour and titrte to blood pressure.
*Avoid lowering systolic BP <90-100mmHg
Nitrates are more effective and safer than morphine or furosemide for preload reduction
nitrates
NITROGLYCERIN
MECHANISM OF ACTION
-Venodilation (low dose)= ↓ PRELOAD
-Arteriolar dilatation (higher dose)= ↓ AFTERLOAD
-↓pulmonary hydrostatic pressure
other considerations: furosemide
-Consider Furosemide
-Mainly indicated if pulmonary oedema due to fluid retention. No added benefit in normovolaemic patients
-Diuretic naïve: IV furosemide 1mg/kg
-Patient already on diuretics: usual dose in IV form
-Preload is decreased through diuresis, but overall effect is delayed.
other considerations
furosemide
morphine
other considerations: morphine
-Consider Morphine
-No good evidence to support immediate reduction in preload centrally
-May provide anxiolysis
-May reduce BP and respiratory drive
-If used, titrate in small doses (2,5mg IV as needed, max 0,1mg/kg)
