ACLS:

Las principales causas del paro cardíaco son hipoxemia, acidosis hipovolemia (por fluido
terapia o pérdida sanguínea)

Se relaciona con problemas cardíacos congestivos, alteraciones vasculares pulmonares,

alteraciones vasculares periféricas, insuficiencia renal terminal o alteraciones hidro
electrolíticas.

*imporatete identificar pulmonary embolism (S1Q3T3 pattern, new right bundle branch block,
or anterior T-wave inversion).

La perdida de pulso por > 10 segundo indica paro.

CPR in the prone position is a reasonable alternative to supine CPR when the airway is already
secured; defibrillation in the prone position is also posible.

in the pregnant patient, left lateral uterine displacement is necessary if fundal height is at or
above the umbilicus, to minimize aortocaval compression, optimize venous return (preload),
and generate adequate stroke volume during CPR. Manual uterine displacement is preferred
so that supine positioning of the upper torso is preserved to facilitate optimal chest
compression vector forces.

Compressions that result in a diastolic blood pressure (BP) between 30 to 40 mmHg have a
higher chance of successful (medidas con la arterial invasiva).

EtCO readings >20 mmHg during CPR are associated with better outcome and survival, while
EtCO readings <10 mmHg for 20 minutes are associated with failure. (atients who have
metabolic acidosis or increased intracranial pressure, a lower target for PaCO may be selected
(approximately 35 mmHg). However, more aggressive hyperventilation is avoided as this may
decrease cerebral blood flow, causing cerebral vasoconstriction and exacerbating any cerebral
ischemic injury)

Low tidal volumes (6 to 8 mL/kg) and mild permissive hypercapnia (partial pressure of carbon
dioxide [PaCO ] 40 to 45 mmHg). Higher PaCO levels might contribute to vasodilation,
hyperemia, or cerebral edema after cardiac arrest. Sat O2 94 % o mas, pero posterior a salir del
para limitar la hiperoxia. Apuntar a frecuencia de 10 resp/min..

*MAP is maintained at ≥65 mmHg, and sometimes increased to 80 to 100 mmHg to optimize
cerebral perfusion since the upper and lower limits of cerebral autoregulation may be shifted
upward after cardiac arrest.

*Norepinephrine is typically the first-line vasopressor in most

post-arrest patients, since epinephrine or dopamine have greater potential to

increase myocardial O consumption and induce arrhythmias, while phenylephrine may

decrease ventricular performance and cardiac output, and dobutamine may cause tachycardia
or exacerbate hypotension due to decreased systemic vascular resistance.