HMP2 Cardio-respiratory arrest

Sudden cardiac arrest (SCA) and sudden cardiac death (SCD) refer to the sudden cessation of cardiac activity with hemodynamic collapse, typically due to sustained ventricular tachycardia/ventricular fibrillation. These events mostly occur in patients with structural heart disease (that may not have been previously diagnosed), particularly coronary heart disease.

SCA most commonly results from hemodynamic collapse due to ventricular fibrillation (VF) in the setting of structural heart disease.

The outcome following SCA depends upon numerous factors including the underlying cause and the rapidity of resuscitation.

Most individuals suffering from SCA become unconscious within seconds to minutes as a result of insufficient cerebral blood flow. There are usually no premonitory symptoms. If symptoms are present, they are nonspecific and include chest discomfort, palpitations, shortness of breath, and weakness.

DEFINITIONS — Various criteria have been used to define SCA and SCD in the medical literature.

The following definitions of SCA and SCD were presented by American College of Cardiology/American Heart Association/Heart Rhythm Society (ACC/AHA/HRS) in 2006:

“[Sudden] cardiac arrest is the sudden cessation of cardiac activity so that the victim becomes unresponsive, with no normal breathing and no signs of circulation. If corrective measures are not taken rapidly, this condition progresses to sudden death. Cardiac arrest should be used to signify an event as described above, that is reversed, usually by CPR and/or defibrillation or cardioversion, or cardiac pacing. Sudden cardiac death should not be used to describe events that are not fatal.”

EPIDEMIOLOGY — The risk of experiencing SCA is increased by a number of factors. The incidence increases dramatically with age and with underlying cardiac disease. In addition, men are two to three times more likely to experience SCA than women.

The magnitude of the influence of underlying cardiac disease on the risk of SCA is illustrated by the following observations:

• The risk of SCA is increased six- to ten-fold in the presence of clinically recognised heart disease, and two- to four-fold in the presence of coronary heart disease (CHD) risk factors.


• SCD is the mechanism of death in over 60 percent of patients with known CHD.

ETIOLOGY — SCA usually occurs in people with some form of underlying structural heart disease, most notably CHD.
Coronary heart disease — As much as 70 percent of SCAs have been attributed to CHD. Among patients with CHD, SCA can occur both during an acute coronary syndrome (ACS) and in the setting of chronic, otherwise stable CHD.

Other structural heart disease — Other forms of structural heart disease, both acquired and hereditary, account for approximately 10 percent of cases of out-of-hospital SCA. Examples of such disorders include the following:

• Heart failure and cardiomyopathy in which SCD is responsible for approximately one-third of deaths.


• Left ventricular hypertrophy due to hypertension or other causes.


• Myocarditis.


• Hypertrophic cardiomyopathy.


• Arrhythmogenic right ventricular cardiomyopathy.


• Congenital coronary artery anomalies.


• Mitral valve prolapse.

Absence of structural heart disease — In different reports, approximately 10 to 12 percent of cases of SCA among subjects under age 45 occur in the absence of structural heart disease.

This can occur in a variety of settings:

• Brugada syndrome.


• Idiopathic VF, also called primary electrical disease.


• Congenital or acquired long QT syndrome


• Arrhythmogenic right ventricular cardiomyopathy.


• Familial polymorphic ventricular tachycardia, also called “catecholaminergic polymorphic VT”.


• Familial SCD of uncertain cause.


• Wolff-Parkinson-White syndrome.

Acute triggers — In addition to the presence of the above underlying disorders, superimposed triggers for SCA appear to play a major role in the pathogenesis of this disorder. These include ischemia, electrolyte disturbances (particularly hypokalemia and hypomagnesemia), the proarrhythmic effect of some antiarrhythmic drugs, autonomic nervous system activation, and psychosocial factors.

RISK FACTORS — A number of clinical characteristics and other factors are associated with an increased risk of SCA among persons without prior clinically recognized heart disease. Most risk factors for CHD are also risk factors for SCA.

Cigarette smoking — Current cigarette smoking and the number of cigarettes smoked per day among current smokers are strongly related to the risk of SCA in patients with CHD.

Exercise — The risk of SCA is transiently increased during and up to 30 minutes after strenuous exercise compared to other

Regular exercise is associated with a lower resting heart rate and increased heart rate variability, characteristics associated with a reduced risk of SCA

Family history of SCA — A family history of SCA, either alone or with myocardial infarction, is associated with a 1.5 to 1.8-fold increased risk of

Serum CRP — Chronic inflammation, as manifested in part by higher serum concentrations of C-reactive protein (CRP), has been implicated as a risk factor for a variety of cardiovascular diseases (including acute coronary syndromes, stroke, and the efficacy of lipid lowering with statins). Elevated serum CRP is also associated with an increased risk of SCA

Excess alcohol intake — Moderate alcohol intake (eg, one to two drinks per day, and avoidance of binge drinking) may decrease the risk of SCD. In comparison, heavy alcohol consumption (six or more drinks per day) or binge drinking increases the risk for SCD

Psychosocial factors — Clinical observations have suggested a possible relation between acutely stressful situations and the risk of SCA

Fatty acids — Elevated plasma nonesterified fatty acid (free fatty acid) concentrations are associated with ventricular arrhythmias and SCD after a myocardial infarction and, after adjustment for confounding factors, in the general.

MANAGEMENT — The acute management of cardiac arrest is according to ALS Guidelines.

 

Management of cardiopulmonary arrest in pregnancy

Cardiopulmonary arrest during pregnancy presents a unique clinical scenario involving two patients: the mother and the foetus. Management of these patients demands a rapid multidisciplinary approach, including anesthesiology, medicine, obstetrics, neonatology and sometimes cardiothoracic surgery. Basic and advanced cardiac life support algorithms should be implemented; however, the physiological and anatomical changes of pregnancy require some modifications to these protocols.

This topic will focus on management of cardiopulmonary arrest during pregnancy.

PREVALENCE OF CARDIAC ARREST IN PREGNANCY — The prevalence of cardiac arrest in pregnant women varies from 1/20,000 to 1/50,000 ongoing pregnancies. The increasing prevalence and severity of maternal obesity, rising cesarean delivery rates, and advances in reproductive options for women with chronic illnesses and at older ages have elevated the medical acuity level of obstetrical practice and may be elevating the frequency of cardiac arrest in pregnant women.

AETIOLOGY — Cardiac arrest may be related to conditions unique to pregnancy or etiologies found in the nongravid state. In one review, the most common causes in pregnant women in the United States and United Kingdom were:

• Pulmonary embolism (29 percent),


• Haemorrhage (17 percent),


• Sepsis (13 percent),


• Peripartum cardiomyopathy (8 percent),


• Stroke (5 percent),


• Preeclampsia-eclampsia (2.8 percent),


• Complications related to anesthesia (eg, difficult or failed intubation, local anesthetic toxicity, aspiration) (2 percent),


• Amniotic fluid embolism,


• Myocardial infarction,


• Pre-existing cardiac disease (congenital, acquired, cardiomyopathy),


• Trauma.

Reversible causes of cardiac arrest should be treated promptly (eg, electrolyte abnormalities, tamponade, hypothermia, hypovolemia, hypoxia, hypomagnesemia, myocardial infarction, poisoning, pulmonary embolism, tension pneumothorax).

RESUSCITATION DURING PREGNANCY — Resuscitation of the pregnant women involves:

• In the USA they call for “maternal code blue”, but in the UK, usual cardiac arrest call (2222) and Gynae/Obs registrar fast bleep (Correct me if I am wrong.)


• If the uterus is above the umbilicus, displace the uterus laterally and to the left (ie, left uterine displacement)


• Initiate the ABCs using pregnancy modifications


• Estimate the gestational age of the fetus (See ‘Determining gestational age’ below.)


• If the uterine fundus is ≥4 fingerbreadths above the umbilicus, at four minutes, begin perimortem cesarean delivery and complete delivery by five minutes following cardiac arrest

At 15 minutes, if resuscitation remains unsuccessful, initiate direct cardiac massage if appropriate resources and personnel are available. Thoracotomy and open chest message would be particularly effective for patients with chest trauma, tension pneumothorax, massive pulmonary embolism, pericardial tamponade, and in patients with chest or spine deformities.

• Ongoing interventions: evaluate need to institute cardiopulmonary bypass therapy.


• Continue resuscitation measures until all resources and attempts have been exhausted. This will vary depending upon the clinical circumstances and resources of the facility.

ABCs — The ABCs (airway, breathing, circulation) of resuscitation are well-described.

In pregnant women with uterine fundal height at or beyond the umbilicus, the uterus should be displaced to the patient’s left to minimize aortocaval compression.

Active airway management is the initial consideration. Pregnant women are at increased risk of rapidly developing hypoxemia because of decreased functional residual capacity and increased oxygen consumption. Both intubation and bag mask ventilation can be more difficult in the late stages of pregnancy and back-up airway procedures, including cricothyrotomy, may be required in some cases. The increased risk of aspiration and narrowing of upper airways, particularly in the third trimester, require special consideration during pregnancy. Intubation via direct or video laryngoscopy using cricoid pressure and 100 percent oxygen is performed using a smaller sized endotracheal tube (0.5 mm to 1.0 mm less in internal diameter compared to that used for nonpregnant women). Endotracheal tube placement should be verified using capnography or an esophageal detector device.

For chest compressions, hand placement should be more cephalad than in nonpregnant women to accommodate the upward displacement of the diaphragm by the gravid uterus. Although specific landmarks have not been established, it is suggested that performing chest compressions slightly above the center of the sternum to adjust for the elevation of the diaphragm associated with the gravid uterus.

Intravenous access should be established above the groin area since drugs administered via the femoral vein may not reach the maternal heart until the fetus is delivered. Access to an antecubital vein with two 14-gauge catheters can be as effective as central line catheters for volume replacement, but do not allow hemodynamic monitoring.

Avoiding aortocaval compression — Supine positioning optimises the vectors required for effective chest compressions in the nonpregnant patient; however, left lateral uterine displacement is necessary in the pregnant patient with fundal height at, or above, the umbilicus, to minimise aortocaval compression (supine hypotensive syndrome), optimise venous return, and generate cardiac output during CPR.

Methods to achieve left lateral uterine displacement include:

• Manual uterine displacement


• Tilt of the operating room table, or


• Placement of pillows, a wood or foam resuscitation wedge (eg, Cardiff wedge) or rolled up towels or blankets

If a suitable wedge is not available, the patient can be tilted upon a rescuer (the rescuer sits on his/her heels and uses his/her thighs as a wedge under the patient). Manual uterine displacement  is preferred since it preserves the supine positioning of the upper torso for optimal chest compression vector forces. A hand is used to apply maximal leftward push to the right upper border of the uterus to achieve a displacement of about 1.5 inches from the midline.

Defibrillation — Management of ventricular arrhythmias may require defibrillation during maternal resuscitation. The physiological changes of pregnancy, including increases in blood volume and decreases in functional residual capacity, do not appear to alter transthoracic impedance or transmyocardial current. Therefore, current energy requirements for adult defibrillation are appropriate for use in pregnant women.

Determining gestational age — In pregnant women, determining gestational age is critical, as the likelihood of neonatal viability is a factor in decision-making. If the prenatal record is not available, physical examination can aid in establishing the gestational age. Uterine size correlates with gestational age, but can be misleading in some situations, such as when there is a multiple gestation, large fibroids, or severe oligohydramnios or polyhydramnios. The formula for estimating gestational age by physical examination is: distance from the top of the symphysis pubis to the top of the fundus (cm) = gestational age (weeks).

Foetal monitoring — In general, the status of the mother should guide management during the resuscitation process; if the status of the mother is poor and deteriorating, the status of the foetus will be further compromised. Therefore, foetal monitoring is not recommended during the resuscitation process.

Delivery as part of the resuscitation process — Despite implementation of maneuvers to ameliorate aortocaval compression, CPR may not restore spontaneous circulation or provide adequate cardiac output. Blood flow during CPR is produced by mechanical compression of the heart between the sternum and the spine and phasic fluctuations in intrathoracic pressure. Despite appropriate use of leftward uterine displacement, the mechanical effects of the gravid uterus can decrease venous return from the inferior vena cava, obstruct blood flow through the abdominal aorta, and diminish thoracic compliance, all of which contribute to unsuccessful CPR. Without restoration of cardiac output, both mother and fetus are at risk for hypoxia and eventually anoxia, especially when interruption of normal cardiac and respiratory function persists beyond four minutes. Although it may be counterintuitive to operate on a haemodynamically unstable patient, cesarean delivery may be life-saving for both mother and fetus in this situation. Delivery of the baby empties the uterus, relieving the aortocaval compression. This results in a 60 to 80 percent increase in cardiac output, thereby increasing the likelihood of maternal survival.

The American Heart Association recommends cesarean delivery if maternal resuscitative efforts have not been successful within four minutes. The rationale for this approach is that:

• Irreversible brain damage can occur in nonpregnant individuals after four to six minutes of anoxia


• Pregnant women become anoxic sooner than nonpregnant women because of decreased functional residual capacity


• If the uterine fundus is ≥4 fingerbreadths above the umbilicus, ineffective resuscitation efforts may become effective when the uterus is no longer gravid and potentially causing aortocaval compression


• Intact fetal survival diminishes as the time between maternal death and delivery lengthens

“Five minute rule” — Although there have been no controlled clinical trials in this area, a review of case reports of perimortem cesarean delivery from 1900 to 1985 suggested that normal neonatal neurological outcome was most likely when delivery occurred within five minutes of maternal cardiac arrest. In this series, 42 of 42 infants delivered within five minutes had a normal neurological outcome compared with 7 of 8 infants delivered within 6 to 10 minutes, 6 of 7 infants delivered within 11 to 15 minutes, 0 of 1 infant delivered between 16 and 20 minutes, and 1 of 3 infants delivered within 21 to 25 minutes.

Minimum gestational age — The minimum gestational age for perimortem cesarean delivery is controversial. Although physiologically aortocaval compression begins as early as 20 weeks, there is some imprecision within the range of 20 to 24 weeks. Neonatal viability is also an imprecise assessment, as it is uncertain which extremely preterm infants, particularly those born at 23 and 24 weeks of gestation, have a reasonable chance of survival without severe deficits. Most centers would provide full neonatal support to infants at least 24 weeks of gestation and some centers provide this level of care to infants greater than 22 weeks of gestation.

Delivery issues — As discussed above, perimortem cesarean should be performed within five minutes after cardiac arrest, thus transporting the patient to an operating room is not a priority. An emergency cesarean delivery kit should be part of the resuscitation cart in patient care areas that commonly serve pregnant women or transported to the location of the pregnant patient who has arrested.

Chest compressions should be continued without interruption until return of spontaneous circulation and broad spectrum antibiotics should be administered to decrease the risk of postpartum infection.

We suggest a vertical skin incision to provide fast entry, adequate uterine exposure, and access to the diaphragm, which may be useful for further resuscitative interventions. Bleeding may be minimal during the procedure due to hypoperfusion. Extraction of the placenta and closure of the hysterotomy are important steps to prevent subsequent hemorrhage when hemodynamic stability is eventually restored.

Medications use for CPR during pregnancy — Given the lethality of cardiopulmonary arrest, the benefits from use of potentially life-saving drugs outweigh any known or possible feral risks. All medications for treatment of cardiopulmonary arrest in the nonpregnant patient are used for the pregnant patient.

If magnesium toxicity (following treatment of pre-eclempsia/eclempsia) is suspected, magnesium sulfate infusion should be discontinued and calcium gluconate (10 mL of a 10 percent solution)

Sodium bicarbonate is not routinely given during CPR, but it may be useful in life-threatening hyperkalemia or tricyclic antidepressant overdose.

Arryhthmias are difficult to control, especially those resulting from bupivacaine toxicity. Amiodarone is the favored treatment for severe bupivacaine-induced arrhythmias. Early administration of lipid emulsion (eg, 20 percent intralipid) is becoming a significant component in resuscitation of bupivacaine-induced cardiotoxicity.

ADDITIONAL INTERVENTIONS — After 15 minutes of unsuccessful closed chest CPR, direct cardiac massage via thoracotomy or through the diaphragm (if the abdomen is open) can be implemented. Direct cardiac massage results in near normal systemic perfusion throughout the compression cycle and with higher cranial and myocardial flow than achieved with external chest compressions of conventional CPR.

For pregnant women with ST elevation myocardial infarction, percutaneous coronary intervention is the preferred reperfusion strategy since fibrinolytics are relatively contraindicated in pregnancy.

Successful fibrinolysis has been reported for massive pulmonary embolism and for ischemic stroke during pregnancy.

MATERNAL OUTCOME — A multicenter study reported outcomes of 55 women with a cardiac arrest during pregnancy, including 12 women who underwent perimortem cesarean delivery. In total, only 15 percent (8 of 55) of the women survived. Perimortem cesarean delivery was not associated with a higher survival rate (17 versus 14 percent). However, none of the perimortem cesarean deliveries were performed within the recommended five minutes. Cardiac output was regained in 67 percent (8 of 12) of women after perimortem cesarean delivery; two women (17 percent) and five infants (42 percent) survived.

SUMMARY 

• The most common causes of cardiopulmonary arrest in pregnant women are pulmonary embolism, amniotic fluid embolism, hemorrhage, sepsis, cardiomyopathy, stroke, preeclampsia-eclampsia, and complications related to anesthesia (eg, difficult or failed intubation, local anesthetic toxicity, aspiration).

Resuscitation of the pregnant women

• Cardiac arrest call, which, ideally, activates a multi-disciplinary team


• Place firm support under the patient


• Modify the ABCs for pregnancy:

• Remove fetal and uterine monitoring devices, if present


• Displace the uterus laterally and to the left using a wedge or rolled towels/blankets while leaving the upper body supine rather than tilting the entire patient.


• Secure the airway using 100 percent oxygen, cricoid pressure, and a slightly smaller endotracheal tube (0.5 mm to 1.0 mm less in internal diameter compared to that used for nonpregnant women).

• For chest compressions, hand placement is more cephalad than that used for nonpregnant women. Perform chest compressions slightly above the center of the sternum.


• Estimate the gestational age of the fetus (using prenatal record, physical examination, or ultrasound), as it is a factor in the decision making process.

Study suggests perimortem cesarean delivery with delivery of the infant within five minutes of maternal cardiac arrest. Maternal and neonatal outcomes are best when delivery occurs within five minutes of maternal cardiac arrest: normal neurological outcome is possible for both mother and child.

The youtube video below summarises the above topic.

UK Resus Council have their own guidance on their manual. It is under “Cardiac arrest under special circumstances”

Cardiac arrest in pregnancy: Poster for your department  Cardiac Arrest in Pregnancy Poster

Hypothermic Cardiac Arrest: “no one is dead until warm and dead”

Death from exposure and accidental hypothermia occurs throughout the world and can present significant management problems. Even with modern supportive care, the in-hospital mortality of patients with moderate or severe accidental hypothermia approaches 40 percent.

DEFINITIONS — Hypothermia is defined as a core temperature below 35ºC (95ºF). The stage of hypothermia, defined by core temperature, has a large impact on both recognition and treatment. The most commonly used definitions found in the literature are as follows:

• Mild hypothermia – Core temperature 32 to 35ºC (90 to 95ºF)


• Moderate hypothermia – Core temperature 28 to 32ºC (82 to 90ºF)


• Severe hypothermia – Core temperature below 28ºC (82ºF)

The Swiss staging system is based on clinical signs can be used by rescuers at the scene to describe victims:

• Stage I – clearly conscious and shivering;


• Stage II – impaired consciousness without shivering;


• Stage III – unconscious;


• Stage IV – no breathing; and


• Stage V – death due to irreversible hypothermia.

MANAGEMENT

For detail management of hypothermic cardiac arrest from European Resus Council, click here

Summary from that guidance:

• The risk of hypothermia is increased by drug or alcohol ingestion, exhaustion, illness, injury or neglect especially when there is a decrease in the level of consciousness.


• Beware of diagnosing death in a hypothermic patient because cold alone may produce a very slow, small-volume, irregular pulse and unrecordable blood pressure. Dilated pupils can be caused by a variety of insults and must not be regarded as a sign of death.


• In the pre-hospital setting, resuscitation should be withheld only if the cause of a cardiac arrest is clearly attributable to a lethal injury, fatal illness, prolonged asphyxia, or if the chest is incompressible.


• ABC as usual. Palpate a central artery, look at the ECG (if available), and look for signs of life for up to 1 min before concluding that there is no cardiac output.


• Drug metabolism is slowed, leading to potentially toxic plasma concentrations of any drugs given repeatedly. For these reasons, withhold adrenaline and other CPR drugs until the patient has been warmed to a temperature higher than approximately 30 °C. Once 30 °C has been reached, the intervals between drug doses should be doubled when compared with normothermia intervals. As normothermia is approached (over 35 °C), standard drug protocols should be used.


• As the body core temperature decreases, sinus bradycardia tends to give way to atrial fibrillation followed by VF and finally asystole.


• Arrhythmias other than VF tend to revert spontaneously as the core temperature increases, and usually do not require immediate treatment.


• If VF is detected, give a shock at the maximum energy setting; if VF/VT persists after three shocks, delay further defibrillation attempts until the core temperature is above 30 °C.


• Rewarming may be passive, active external, or active internal.


• In a hypothermic patient with apnoea and cardiac arrest, extracorporeal (ECMO) rewarming is the preferred method of active internal rewarming because it provides sufficient circulation and oxygenation while the core body temperature is increased by 8–12 °C h−1

HMP2 Cardio-respiratory arrest