APO: What is pulmonary oedema and how is it caused?
- accumulation of fluid within interstitial space and alveoli
- occurs when the amount of filtration from pulmonary capillaries is greater than what can be absorbed and managed by lymph
APO: How does left ventricular failure cause pulmonary oedema?
-left ventricular and atrial end-diastolic pressure increases
=>increased pressure in pulm. caps. from venous side
=>increased hydrostatic pressure, decreased reabsorption and increased filtration on arterial side
=>oedema & decreased gas exchange = hypoxaemia
APO: How does hypoxaemia cause a cycle of oedema through effects on the myocardium and sympathetic nervous system?
- reduced oxygen = reduced ATP levels so myocardium cant relax and stiffens, leading to increased end-diastolic pressure and less blood entering ventricles = backing up of pressure causing oedema
- hypoxaemia causes sympathetic response, leading to increasing force of contraction and HR, and higher oxygen demand of the myocardium & more hypoxia
APO: Signs and symptoms of pulmonary oedema?
- shortness of breath: tachypnoeic, feeling of drowning, maintaining upright posture, pink/white sputum, crackles on lung auscultation
- hypoxia: reduced Sp02, cyanosis, irritability (cerebral hypoxia)
- sympathetic response: anxious, pale, sweating, tachy, hypertensive (can progress to hypotension as cardiogenic shock develops), chest pain, ECG signs
APO: How would you treat a patient with suspected pulmonary oedema?
- oxygen: improves gas exchange and reduces hypoxia
- CPAP: decreases WOB, provides 100% O2, splints opem airways
- ECG: confirm cardiac ischaemia
- GTN: if indicated by BP, reduces cardiac workload
- Transport: potential to deteriorate quickly
PE: What is a pulmonary embolism and what are the main factors contributing to it’s formation?
- occlusion of blood supply to part of the lungs, usually caused by a thromboembolism
- hypercoagulability (pregnancy, dehydration, cancer, SIRS), statis (stagnation of blood flow - bed bound, long haul flights), endothelial damage (vessel wall injury - trauma, atherosclerosis).
PE: What are the respiratory and haemodynamic consequences of a PE?
Respiratory: -increased dead space (ventilated but not perfused), hypoxaemia (V/Q mismatch), hyperventilation, lung infarct
Haemodynamic: -decreased cross-sectional area of pulm. vascular bed => increased pulm. resistance => increased RV afterload => RV failure, obstructive shock and decreased cardiac output => worsed hypoxaemia
What two factors will determine the effect the PE will have on the patient?
Size and location of the emobolis
A large embolus occludes a large portion of pulmonary circulation, and symptoms will have a sudden onset.
PE: How would a patient with a PE appear?
- Resp: dyspnoea, tachypnoea, normal to lowering Sp02, normal breath sounds
- Cardiac: chest pain, tachy, hypotension, arrhythmias, RV dysfunction
- Concious levels consistent with levels of hypoxia
- Appearance: pale/cyanotic, coughing up blood (haemoptysis), evidence of DVT
PE: How would you treat a patient with a suspected PE?
- Oxygen: helps with dyspnoea, offset any developing V/Q mismatch
- Posture: upright/sitting
- Pain relief
- GTN: not indicated if PE confirmed or cardiac caused excluded
