Cardiogenic Shock Case Studies

Question 1:
Airway:
Patient’s airway is patent and protected, a lack of noisy breathing or stridor rules out partial obstruction, the ability to talk in full sentences rules out silent complete airway obstruction, and also indicates the patient is ventilating and oxygenating sufficiently (Robertson & Al-Haddad, 2013). Cardiogenic shock does not result in airway collapse, obstruction, or hypoventilation (Van Thielen & Price, 2010).
High priority: monitor the patient’s level of consciousness and cognizance using the Glasgow Coma Scale (GCS) (Urden et al., 2014). The GCS measures consciousness by evaluating the patient’s ability to open their eyes, respond verbally, and perform motor tasks. A reduced level of consciousness indicates a compromised airway, as the patient is unable to clear secretions or protect the airway from aspiration (Thim et al., 2012). Important, as this patient may decompensate suddenly.
Breathing:

Impaired ejection fraction from the left ventricle reduces cardiac output. A reduced cardiac output impairs tissue perfusion, and causes pulmonary vascular congestion. Hypoxemia secondary to impaired gas exchange and cardiac output shifts cell metabolism to anaerobic, causing an accumulation of lactic acid, thus increasing metabolic acidity (Urden et al., 2014). This results in tachypnoea and dyspnoea as the body attempts to eliminate carbon dioxide to correct pH imbalance. Poor oxygen saturation relative to FiO2 and crepitation are secondary to pulmonary congestion and oedema. Backwards cardiac effects increase hydrostatic pressure, causing fluid filtration into the lungs, resulting in impaired alveolar gas exchange and oedema in the lung. Thus, causing reduced oxygen saturation and crepitation as alveoli pop open after being collapsed by oedema (Murray,