APO

Question 1

RED FLAGS

Question 2

DIFFERENTIALS

Answer 2

• Pneumonia
• Asthma
• Anaphylaxis
• Chest infection

Question 3

DEFINITION

Answer 3

Severe LV failure with pulmonary venous hypertension & alveolar flooding.

Question 4

PATHOPHYSIOLOGY

Answer 4

Non-cardiogenic (1st)
- Causes: septicaemia, anaemia, thyrotoxicosis (these are high), hypoalbuminemia, pancreatitis, eclampsia, DIC, burns, submersion, toxic inflammation, high altitude, decompression illness, head injury (intracranial haemorrhage), PE, renal failure.
- Pathophysiology: Due to pathological processes causing capillary permeability in the lungs –> protein leak into alveoli –> oncotic pressure draws fluid out.

Cardiogenic (2nd)
- Causes: ACS, LVF, arrhythmias, peri/myo/endocarditis, valve dysfunction/stenosis, fluid overload (non-compliance with diuretics).
- Pathophysiology: If LV filling pressure increases suddenly, plasma fluid moves rapidly from pulmonary capillaries into interstitial spaces & alveoli, causing pulmonary oedema. ACS –> LV HF –> increases pulmonary pressure –> increased hydrostatic pressure outweighs oncotic pressure in vessels –> fluid leak/shift into alveoli –> v/p mismatch –> hypoxaemia & hypercapnia from impaired gas exchange (respiratory acidosis) –> manifestations: Cough, crackles, cyanosis, pink frothy sputum, tachypnoea, tachycardia, hypertension (compensatory)/hypotension (decompensation of LVF), anxiety, sympathetic activation.
- Increase pulmonary hydrostatic pressure –> increase R heart pressure –> manifestations: Raised JVP, peripheral oedema –> leads to R HF/cardiogenic shock (dependent on cause)

Question 5

TREATMENT

Answer 5

Cardiogenic: DRAB: O2, IPPV/PEEP/CPAP. C: IV access + fluids. D(drugs): GTN, Aspirin. E: Posture Pt. sitting up, 12-lead ECG, manage dysrhythmias/ACS/cardiogenic shock.
Non-cardiogenic: O2, 12 lead ECG, IPPV, PEEP, CPAP.

Inotropic support from CCP drugs, fluids with caution if needed

Question 6

PHARMACOLOGY

Answer 6

• GTN in smaller doses dilates the coronary arteries via smooth muscle relaxation  in higher doses it dilates systemic veins & arteries  reducing pre/afterload which reduces the pressure on the heart from both the systemic & pulmonary circuit ** decrease hydrostatic pressure in the lungs as well **  continue to give GTN in APO even when chest pain ceases.
• Aspirin (antiplatelet) inhibits platelet aggregation by irreversibly inhibiting COX  reduce synthesis of thromboxane A2 (an inducer of platelet aggregation)  platelets do not aggregate to exposed collagen fibres at the site of injury
  Give aspirin because you can’t rule out ACS

Question 7

DEFINITIVE CARE

Answer 7

• Assessments/tests: Identify cause & manage. Bloods for troponin, arterial blood gasses, chest radiography (identify causes), CT scan, whole blood count, echocardiogram.

Treatment
- Manage ACS with pPCI or thrombolysis, continued CPAP, IV infusion of GTN.
- Lifestyle review to manage cardiac conditions.
- Drugs: antihypertensives, vasopressors, diuretics, inotropes, analgesic for anxiety, pain, SOB.