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If the patient is intubated and connected to a ventilator, the tidal volume is set at 6?mL/kg ideal bodyweight at 10 breaths/minute [7]. If hyperinflation is suspected, intermittent disconnection of the tracheal tube for 10 seconds [15] may relieve air trapping permitting return of venous flow and spontaneous circulation [7]. Dynamic hyperinflation increases transthoracic impedance and with shockable rhythms higher shock energies may be considered [7]. Always consider tension pneumothorax or bilateral pneumothorax in asthma-related cardiac arrest. In skilled hands, lung ultrasound is a faster and more sensitive diagnostic test than chest X-ray [7]. Myocardial stunning is due to ischaemia most often because of infarction [2]. After brief periods of myocardial ischaemia, prolonged myocardial dysfunction can occur, followed by gradual recovery and improvement in cardiac output typically within 2-3 days [7, 15]. Countermeasure. Percutaneous coronary intervention (PCI) should be conducted as soon as possible, when appropriate. Hyperkalemia prevents adequate efflux of potassium, and hence the resting membrane potential of the myocytes decreases, leaving the myocardium depolarized and the myocytes refractory to further stimulation (unexcitable). The cardiac conduction is slowed and the heart stops in diastole refractory to resuscitation. Voelckel hypothesized this as a mechanism of delayed ROSC [16]. The myocardium is also extremely sensitive to hypokalemia, which alters cardiac tissue excitability and conduction, and may induce malignant ventricular arrhythmias, resulting in cardiac arrest. Countermeasure. ABG taken early (or even in the prehospital setting) can confirm suspicion. Delayed delivery and action of administered medications (like epinephrine) can occur, when drugs are administered through a peripheral vein, as central delivery is slow due to impaired venous return. Presumably, some older cases of AR can be attributed to this mechanism, especially due to escalating doses of epinephrine used according to historic ALS guidelines [2]. Countermeasure. Use intraosseous line or central line if present. Transient asystole or PEA following defibrillation of prolonged VF is a well-known phenomenon and occurs in about 60% of patients [2, 17]. Surprisingly, it has a worse prognosis than primary asystole or PEA. This may be related to direct myocardial injury due to electrical current and because the fibrillating myocardium requires more oxygen and faster depletes high-energy phosphate stores [17]. Countermeasure. Use biphasic instead of monophasic defibrillators, using only energy levels specified by the manufacturer. Unobserved minimal vital signs likely represent another explanation, when the circulation is present again. Pseudo-PEA is the clinical situation in which contractile activity is Selleck Thiazovivin occurring, yet it is of minimal magnitude.