Cardiac Arrest in Pregnancy
Cardiac arrest in pregnancy is rare and carries a poor prognosis .
Almost 10% of overall maternal deaths reported in the United
Kingdom result from cardiac arrest.
Successful resuscitation of the mother requires prompt and
effective CPR with some alterations in BLS and ACLS principles.
After 20 weeks’ gestation, the gravid uterus may compress the
inferior vena cava and impede venous return when in the supine
position.
The effects of aortocaval compression must be minimized by left
lateral uterine tilt using manual uterine displacement or insertion
of a wedge under the right hip.
Modification of Basic Life Support
Continuous cricoid pressure during positive-pressure ventilation
for any unconscious pregnant patient.
chest compressions should be performed higher than usual,
slightly above the midpoint of the sternum.
Defibrillation should be performed as directed by standard ACLS
guidelines.
Fetal and maternal monitors should be removed before delivering
any electric shocks.
Modification of Advanced Cardiovascular Life Support
The airway should be secured as early as possible.
smaller endotracheal tube may be required (0.5-1.0 mm smaller).
Pregnant patients can develop hypoxemia at a quicker rate than
nonpregnant women:
reduced FRC
increased oxygen requirements
The tidal volume to be reduced because of elevation of the
diaphragm.
Differential Diagnosis
Include:
amniotic fluid embolism, massive blood loss, complications of
preeclampsia, acute coronary syndromes, aortic dissection, lifethreatening pulmonary embolism, iatrogenic drug overdose (e.g.,
magnesium sulfate), or local anesthetic toxicity.
Calcium gluconate, 1 g intravenously, is the drug of choice for
magnesium toxicity.
Cardiac arrest due to local anesthetic toxicity includes standard
ACLS measures, and one should consider the use of 20% lipid
emulsion therapy.
Perimortem Cesarean Section
The best chance of fetal survival at 24 weeks’ gestation and
beyond is when delivery occurs no more than 5 minutes after the
onset of maternal cardiac arrest.
There is little chance of maternal resuscitation until the uterus is
emptied.
Emptying of the uterus will also improve thoracic compliance and
thus ability to improve maternal ventilation.
Drowning
each year,drowning is responsible for an estimated 500,000
deaths around the world.
Among those aged 5 to 14 years,drowning is the leading cause
of death worldwide for males and the fifth leading cause for
females.
Drowning is a process that begins when the airway goes
below a liquid surface and, if uninterrupted, may lead to
death.
PATHOPHYSIOLOGY
there are no important differences in humans between
drowning infresh water and drowning in salt water.
Surfactant destruction, alveolitis, and noncardiogenic
pulmonary edema, resulting in an increased intrapulmonary
shunt and hypoxia.
Hypoxia produces: tachycardia, bradycardia, pulseless electrical
activity, asystole
↓CO, ↓BP, ↑PAP, ↑PVR
It should be noted that the heart and brain are the two
organs at greatest risk for permanent, detrimental changes
from relatively brief periods of hypoxia.
IN-WATER BASIC LIFE SUPPORT AND RESCUE
the decision when to do basic water life support is based on
the victim’s level of consciousness.
If the victim is conscious, rescue to land without any further
medical care is the protocol.
For an unconscious victim, rescuers should check ventilation
and, if possible and if indicated, attempt to provide mouth-tomouth ventilation while still in the water.
In-water resuscitation (ventilation only) provides the victim a
3.15 times better chance of surviving without sequelae.
Routine cervical spine immobilization in water rescues is not
recommended.
ON – LAND BASIC DROWNING LIFE SUPPORT
- how the victim is removed from the water
- how the victim is placed on the land
the abdominal thrust (Heimlich) maneuver is ineffective and
carries significant
If vomiting occurs, turn the victim mouth to the side and
remove the vomitus with a finger sweep, a cloth, or suction.
ADVANCED DROWNING LIFE SUPPORT ON SITE
*Dead Body: (submersion time >1h ) do not start resuscitation
*Grade 6 : (Cardiopulmonary Arest )
- The first priority is adequate oxygenation and ventilation.
- Continue cardiac compressions
- Suctioning the airways
- The Sellick maneuver should be used
- Venous access to give drugs
- Dose of epinephrine 0.01 mg/kg after 3 min. And 0.1 mg/kg
each 3-5 min.
*Grade 5 (Respiratory Arrest) :
continue ventilation using 15 liters of o₂ at 12 to 20
breaths/min. Until restoration of normal breathing.
*Grade 4 (Acute Pulmonary Edema With Hypotension):
- O₂ 15 l/min. by face mask until OTT be inserted (100% of
cases)
- Rapid crystalloid infusion (colloid solutions only for refractory
hypovolemia)
- Inotropic or vasopressor drugs rarely needed
Mechanical Ventilation With:
- TV at least 5 ml/kg
- FiO₂ start at 1.0 then reduced to 0.45 or less
- PEEP start at 5 cm H₂O and then increased 2 to 3 cm H₂O
until shunt of 20% or less or PaO₂ / FiO₂ of 250 or more
sedative, analgesics, and MR needed to tolerate intubation
*Grade 3 (Acute Pulmonary Edema Without Hypotension):
- O₂ 15 l/min. by face mask or OTT
(only 27.6% of cases have SaO₂ > 90% and tolerate
noninvasive ventilation)
- Recovery Position
- Restore pH to normal
*Grade 2 (Abnormal Auscultation With Rales in Some Pulmonary Fields):
- oxygen by nasal cannula
*Grade 1 (Coughing With Normal Lung Auscultation):
- do not need any O₂ or respiratory assistance
*Rescue (No Coughing, Foamy Secretions, or Difficulty Breathing):
- released from the accident site
Other Interventions
Nasogastric tube.
orogastric tube.
Bronchoscopy.
Surfactant therapy.
Echocardiography.
Other Treatment Considerations
Initiation of appropriate management of hypoglycemia and other
electrolyte imbalances, seizures, bronchospasm and cold-induced
bronchorrhea, dysrhythmias, and hypotension may be necessary in
the drowning patient.
Treatment of metabolic acidosis (PH<7.2, bicarbonate <12 mEq/I)
Early coronary interventions that re-establish coronary
blood flow improve myocardial recovery and electrical and
hemodynamic stability.
Fibrinolytic therapy in survivors of out-of-hospital cardiac
arrest has not been shown to have favorable outcomes,
particularly compared with PCI.
early PCI in survivors of cardiac arrest as part of an
advanced postcardiac arrest protocol, including those
patients remaining comatose after resuscitation
TARGETED TEMPERATURE MANAGEMENT
The median survival rate from out-of-hospital cardiac
arrest is 8.4% Only one-third of individuals in out-of-hospital
cardiac arrest survive to hospital admission, and two-thirds of
these die before hospital discharge.
The majority of patients dying after successful ROSC die from
ischemic neurologic injury.
In normothermia, cerebral blood flow less than 125 mL
per minute
persisting for longer than 7 minutes is associated with
permanent neurologic damage
Cerebral ischemia induces an inflammatory response
of platelet aggregation and degranulation, protein and
enzyme denaturalization, and neutrophil and
complement activation, all of which increase
permeability and/
or blood-brain barrier disruptions demonstrated by
neuronal damage biomarkers.
Ischemic neurons become
progressively acidotic in low-flow or no-flow states,
leading to intracellular lactic acidosis and carbon dioxide
Intracellular acidosis inhibits enzymatic function, impairing
neurotransmitter reuptake and depleting
adenosine triphosphate (ATP) and adenosine diphosphate
(ADP) stores
adenosine accumulates, vasodilatation and neuronal edema
energy stores are depleted, sodium-potassium-ATPase
dysfunction
extracellular hyperkalemia and intracellular hypercalcemia.
Elevated intracellular calcium activates proteolytic and
lipolytic Enzymes
glutamate is the most neurotoxic influx of calcium into the
neuron, resulting in neuronal death
Induced hypothermia might reduce cerebral metabolic rate
and oxygen consumption
Since 2005, the AHA has endorsed targeted temperature
management (i.e., induced core body temperatures 32° to
34° C) over 12 to 24 hours for patients who are
hemodynamically stable and resuscitated from out-ofhospital VF or pulseless VT but remain comatose.
The entire body must be
cooled for improved neurologic recovery after resuscitation
from cardiac arrest, not only the patient’s head
fluid-filled cooling blankets, ice packs, forced air blankets, cold
IV fluids, and/or invasive devices or catheters for managing
controlled cooling and rewarming of patients.
Sepsis is more frequent when intravascular devices are used
to induce hypothermia, making this approach unfavorable
2010 AHA GuideLinessuggesting the benefit of targeted
temperature management only to shockable cardiac
arrhythmias.
At this time, for all survivors of nontraumatic cardiac arrest,
particularly those with inhospital cardiac arrests, although
clinical evidence benefits for shockable arrhythmias
Sedation, neuromuscular blockade, and mechanical
ventilation are required for patient management during
the period of inducing, maintaining, and rewarming
from hypothermia.
During the time period of targeted temperature
management, hemodynamic instability, arrhythmias,
elecrolyte
abnormalities,
seizures,
bleeding,
hyperglycemia and infections are not uncommon.
Pneumonia occurred in nearly one-half of patients (with
or without hypothermia therapy) but had no inlfuence on
mortality.
Only seizures requiring anticonvulsant therapy and
sustained hyperglycemia (>144 mg/dL) were associated
with increased mortality.
hypoglycemia was also associated with increased
mortality as well.
Benzodiazepines, neuromuscular blocking agents, IV
sedatives,
and narcotics used in the period during which
hypothermia is induced after resuscitation from cardiac
Arrest. –
A neurologist’s clinical evaluation assessing neurologic
recovery after resuscitation from cardiac arrest
includes pupillary light response, corneal reflexes, and
motor responses to painful stimuli.
In those patients treated with hypothermia,
recovery of motor function within 24 hours of
discontinuing sedation for induced hypothermia
predicts good neurologic outcome with 100%
specificity.
The EEG is useful even during hypothermia since
the waveforms should not be significantly affected
by hypothermia
Sedatives and hypnotic drugs induce extremely low
voltage EEG patterns
The AHA 2010 Guidelines for CPR and ECC
recommend a “spot” EEG as early as possible or
continuous EEG monitoring
BOX 108-5 Glasgow-Pittsburgh Cerebral
Performance Category Scale and Functional
Outcome
CPC 1 Full neurologic recovery
CPC 2 Moderate neurologic disability
CPC 3 Severe neurologic disability but preserved
consciousness
CPC 4 Coma or persistent vegetative state
CPC 5 Death
C, Cerebral performance category.
Seizures noted on EEG monitoring should be aggressively
treated, but the effect that anticonvulsants have on
neurologic outcomes is not known.
POSTRESUSCITATION OXYGEN THERAPY
during normothermic hypoperfusion (circulatory arrest)
cellular energy (ATP) production converts from aerobic to
anaerobic
metabolism (glycolysis)oxygen free radicals, particularly
superoxide produced in the mitochondria and
through(NADPH)
Superoxide dismutase is a cellular enzyme responsible
for oxygen free radical detoxification but becomes
persists, as well as when large amounts of oxygen free
radical species are generated during reperfusion.
Bellomo and associates, in a retrospective analysis of 12,108
patients resuscitated from nontraumatic cardiac arrest,
reported that hyperoxia (arterial partial pressure of oxygen
[PaO2] greater than 300 mm Hg) had no independent
association with negative outcomes with respect to in-hospital
mortality.
They also reported that hypoxia after cardiac arrest had the
lowest
hospital discharge rates.
hyperoxia probably offers no additional benefit, hypoxia is clearly
harmful to these patients and must be avoided.
2010 AHA Guidelines for CPR and ECC recommend an approach
for managing survivors of cardiac arrest that titrates oxygen
therapies to attain oxygen saturations of 94% to 98% as soon as
reliable continuous pulse oximetry is available.