Cardiac Arrest

1. Coronary artery disease – 70% of sudden cardiac arrests are due to CAD.
2. Other structural heart disease: 
   • Heart failure and cardiomyopathy
   • Left ventricular hypertrophy due to hypertension or other causes.
   • Myocarditis.
   • Hypertrophic cardiomyopathy.
   • Congenital coronary artery anomalies.
   • Mitral valve prolapse.
   • Cardiac tamponade
3. Absence of structural heart disease –  In around 10% of patients, sudden cardiac arrest can occur in the absence of structural heart disease. This can occur in a variety of settings:
   • Brugada syndrome (ST elevation in V1-V3 with incomplete RBBB)
   • Idiopathic VFib
   • Long QT syndrome
   • WPW syndrome.
   • Family history of sudden cardiac death
4. Pulmonary: Airway obstruction, angioedema, PE, pneumothorax, hypoxia, Severe hypercapnia
5. Acute triggers – Hypoglycemia, hypothermia, electrolyte disturbances (particularly hypokalemia and hypomagnesemia), medications that prolong QTc, proarrhythmic effect of some antiarrhythmic drugs, autonomic nervous system activation, and psychosocial factors. Electrolyte abnormalities by themselves are usually insufficient to cause cardiac arrest. Clinical settings that increase the proarrhythmic effect of hypokalemia and hypomagnesemia include acute myocardial infarction and long QT syndrome. 
6. Drug overdose
7. Shock: sepsis, anaphylaxis, tamponade, hemorrhage

1. ECG – acute myocardial infarction, cardiomyopathy, and primary arrhythmia are the most common causes for cardiac arrest.
2. ECHO– should be done in all patients to rule out structural heart disease.
3. Imaging: Obtain chest radiography to evaluate for pulmonary pathology and to confirm proper positioning of the endotracheal tube, if placed. Pulmonary edema and evidence of aspiration are common findings after CPR. CT of the chest is useful in cases of suspected pulmonary embolism (PE). Unenhanced computerized tomography (CT) of the brain can detect early cerebral edema or intracranial hemorrhage in the comatose post-cardiac arrest patient.
4. Labs 
   •  Arterial blood gas. When therapeutic hypothermia is used, arterial blood gas values can be interpreted with or without correction for the patient’s temperature. 
   • Serum glucose
   • Serum troponin is measured every 8 to 12 hours for 24 hours to detect myocardial injury. If initial measurements are elevated, testing continues until there is clear evidence they are decreasing. Cardiac arrest, CPR, and defibrillation often cause mild increases in the serum troponin, but rising or higher levels suggest acute coronary artery occlusion.
   • CBC to detect anemia and other hematologic abnormalities. Leukocytosis is common and may represent acute demargination of white blood cells and inflammation. Markedly elevated leukocytosis should prompt investigation of a cause other than cardiac arrest. 
   • Serum lactate:  Initial lactate concentrations and the rate of lactate clearance correlate with survival.
   • CMP, magnesium, phosphorus and PT/INR/PTT 
   • Serum toxicology should be screened for. 
   • Chest X ray.
   • CT chest / abdomen and pelvis, CT head if appropriate

• Maintaining end-organ perfusion – an adequate blood pressure must be maintained in the post-cardiac arrest patient. Episodes of hypotension can cause secondary injury, in addition to any initial insult incurred during the arrest by the brain and other organs. Mean arterial blood pressure (MAP) should be above 65 mmHg to reverse the acute shock state, and to optimize cerebral perfusion. Hypotonic fluids, which can exacerbate cerebral edema, should be avoided. 
• Coronary revascularization – Emergent coronary catheterization or reperfusion therapy is indicated for patients with findings on the electrocardiogram (ECG) of ST segment elevation myocardial infarction (STEMI) or new left bundle branch block (LBBB). Regardless of ECG findings, emergent coronary catheterization may be needed for patients with ongoing hemodynamic instability, which may be due to cardiogenic shock or associated with rising troponin levels, or evidence of focal wall-motion abnormalities on echocardiogram. 
• Preventing arrhythmia – Antiarrhythmic drugs should be reserved for patients with recurrent or ongoing unstable arrhythmias. No data support the routine or prophylactic use of antiarrhythmic drugs after the return of spontaneous circulation following cardiac arrest, even if such medications were employed during the resuscitation. 
• Antiarrhythmic Therapy – Pharmacologic therapy, in the form of beta blockers and antiarrhythmic medications, can be helpful in controlling arrhythmias in survivors of sudden cardiac arrest (SCA). However, due to the efficacy of the implantable cardioverter-defibrillator (ICD) in treating sustained ventricular tachyarrhythmias and improving mortality, antiarrhythmic drugs are generally reserved for use in select patients as adjunctive therapy, or as primary therapy when an ICD is not indicated or refused by the patient. 
• Empiric pharmacologic therapy – Empiric antiarrhythmic drug therapy, primarily with amiodarone or beta blockers, is an effective approach for survivors of sudden cardiac arrest who have refused ICD placement or are not candidates for an ICD. 
  • Amiodarone – Amiodarone is the most effective for preventing recurrent ventricular tachyarrhythmias. Empiric therapy with amiodarone is an effective approach to the management of survivors of sudden cardiac arrest. Upon return of spontaneous circulation, follow with an infusion of 1 mg/minute for 6 hours, then 0.5 mg/minute for 18 hours. The total dose is 10gm during first week.
  • Beta blockers – Beta blockers reduce the incidence of sudden death and total mortality in patients with a recent myocardial infarction and in those with symptomatic heart failure or congenital long QT syndrome. 
• ICD Placement: Among survivors of sudden cardiac arrest, prevention of recurrent arrest is a primary goal of long-term management. An implantable cardioverter-defibrillator (ICD) is indicated in almost every survivor of sudden cardiac arrest. Although the ICD does not prevent malignant ventricular arrhythmias, it treats them promptly when they occur. 
• Vasopressors: Following ROSC, many patients experience a sepsis-like vasoplegic state due to a surge in pro-inflammatory cytokines and vasodilation. Also, some patients have post cardiac arrest myocardial stunning which could result in severe LV dysfunction, and needs inotropes.
• Steroids: Cardiac arrest also impairs the function of the adrenal axis, leaving patients especially vulnerable to post-arrest shock. ESICM guidelines recommend giving stress dose steroids routinely, post cardiac arrest. Steroids improve hemodynamic stability, decrease vasopressor requirements, and its antipyretic effect could help with fever control and shivering suppression. Cardiovasc Drugs Ther. 2014; 28(5): 477–488
• Sedation: If sedation is required, preferable drugs are Precedex and propofol. Propofol has the advantage of shorter-life,which facilitates neurological exam after stopping it for a few hours. Pain dose ketamine has the dual advantage of managing both analgesia and sedation at the same time. Also, ketamine has a very short half-life. Long acting drugs including fentanyl should be avoided, if possible.
• Mechanical ventilation – Maintain the carbon dioxide tension (PaCO2) no lower than 40 to 45 mmHg. Targeting this slightly higher PaCO2 range prevents hypocapnia-induced cerebral vasoconstriction and partly accounts for the temperature correction when induced hypothermia is used. Avoid hyperoxia as it can lead to worse mortality. JAMA. 2010 Jun 2;303(21):2165-71 , Resuscitation. 2014 Sep;85(9):1142-8 
• Enteral feeding can resumed once therapeutic hypothermia is completed, because bowel motility is usually suppressed during hypothermia. 
• Maintain serum glucose between 140 and 180 mg/dL during the period following cardiac arrest

1. Asystole – when the initial rhythm is asystole, the likelihood of successful resuscitation is low. Only 10% of patients with out-of-hospital arrests and initial asystole survive until hospital admission and only 0-2% until hospital discharge
2. Pulseless electrical activity – Patients who have sudden cardiac arrest due to pulseless electrical activity (PEA) have a poor outcome. 23% were resuscitated and survived to hospital admission; only 11% survived until hospital discharge.
3. Ventricular tachyarrhythmia – the outcome is much better when the initial rhythm is a sustained ventricular tachyarrhythmia. Approximately 25-40% with sudden cardiac arrest caused by VF survive until hospital discharge. Mayo Clin Proc. 2004 May;79(5):613-9 . Survival is approximately 65-70% in patients who present with hemodynamically unstable ventricular tachycardia (VT).
4. An end-tidal carbon dioxide level of less than 10 measured 20 minutes after the initiation of ACLS accurately predicts death in patients with cardiac arrest associated with electrical activity but no pulse. N Engl J Med. 1997 Jul 31;337(5):301-6

• Indications and contraindications – Patients not following commands or showing purposeful movements following resuscitation from cardiac arrest are eligible for therapeutic hypothermia. Absolute contraindications include active noncompressible bleeding and a do-not-resuscitate order. 
• Timing and duration of therapeutic hypothermia – The goal is to achieve target temperature (core temperature less than 36°C) within 6 hours and maintaining it for 28 hours. After 28 hours, gradual rewarming to 37°C in hourly increments of 0.5°C was recommended. Its also beneficial to have some sort of temperature monitoring with an aim of keeping temperature less than 37.5C from 36 to 72 hours. The sooner we cool the patient, the better is the outcome. Cooling a patient for 48 hrs didn't improve functional outcomes compared with cooling for 24 hours. JAMA. 2017 Jul 25;318(4):341-350 
• Methods for implementing therapeutic hypothermia – Clinicians can use cool intravascular ( Zoll catheter) or surface cooling methods. Rapid infusion of cold saline to achieve the core temperature is strongly discouraged. Shivering is very common, especially when aiming for 33C. Patients with more severe neurologic injury and an inability to autoregulate body temperature may achieve the goal temperature more rapidly when treated with therapeutic hypothermia.
• Sedation and suppression of shivering – Shivering raises body temperature and must be suppressed in patients being treated with therapeutic hypothermia. Failure to suppress shivering is a common reason for inability to achieve goal temperatures. Therefore, sedation should be titrated to shivering suppression, rather than using standard sedation scales. High doses of sedatives are frequently necessary to accomplish this.  A continuous infusion of propofol and fentanyl, with or without intermittent treatment with benzodiazepines (eg, midazolam), is one effective approach to sedation. If shivering doesn't stop with sedatives/analgesia alone, Meperidine (Demerol) can be a useful drug to use except when there is a renal failure. Neuromuscular blockers can be used if other measures fail to achieve target temperature. 
• Temperature monitoring and rewarming – Core body temperature should be monitored continuously during therapeutic hypothermia. The gold standard for core temperature measurement is central venous temperature, but several surrogates are available. In order of preference, surrogate monitoring methods include esophageal, bladder, or rectal probes.

1. Cardiac: Hypothermia slows cardiac conduction and can provoke arrhythmias, including bradycardia and QT interval prolongation. Also, can cause hypotension and myocardial shunning. A heart rate in the 40’s is common at 33ºC, but does not require intervention if the blood pressure is acceptable. 
2. Increased mortality in presence of shock: There was a trend towards increased mortality among patients who were cooled to 33C in the presence of shock. Intensive Care Med. 2014 Sep;40(9):1210-9
3. Bleeding: Hypothermia induces a mild coagulopathy. With temperatures below 35ºC, clotting enzymes operate more slowly and platelets function less effectively. As a result, some bleeding is seen in up to 20% of patients treated with therapeutic hypothermia. In the event of significant bleeding (eg, significant decrease in hemoglobin, hemodynamic instability, intracranial hemorrhage, noncompressible site), therapeutic hypothermia should be stopped and the patient rewarmed to a core temperature >35°C.
4. Infections: Hypothermia impairs leukocyte function and suppress immune function. The incidence of significant infections is likely to increase if hypothermia is maintained longer than 24 hours.
5. Hyperglycemia: Elevated sugars due to insulin resistance has been noted during therapeutic hypothermia. Large doses of insulin may be needed in severely hyperglycemic patients.
6. Metabolic derangements: Hypothermia leads to a “cold diuresis,” which in turn can cause hypovolemia, hypokalemia, hypomagnesaemia, and hypophosphatemia. In addition, temperature fluctuations during the induction of therapeutic hypothermia and rewarming cause potassium to move between the extracellular and intracellular compartments. Therefore, careful monitoring of volume status and measurement of basic electrolytes approximately every three to four hours during temperature manipulation is prudent.
7. Ileus: Bowel motility is suppressed but early feeding should be resumed once therapeutic hypothermia is finished.
8. Therapeutic hypothermia slows the metabolism and excretion of many drugs and thus the duration of effect may be prolonged.
9. Appropriately sedate the patients. If there is a need for more sedation, add sedative with a different mechanism of action. 
10. Avoid calcium infusions as calcium is toxic to neurons.
11. Recent trials found no difference in mortality or neurological outcomes between 33c and 36c.  TTM Trial- N Engl J Med 2013; 369:2197-2206 , Resuscitation. 2015 Jun;91:8-18
12. Therapeutic hypothermia delays neuro prognostication.

1. ​ As we don't have to induce therapeutic hypothermia, we don't need to do serial labs and replace electrolytes as aggressively.
2. There is absolutely no contraindications for normothermia protocol. 
3.  No need for deep sedation or paralytics. This helps in minimizing any sedatives or analgesics, which might delay neuro prognostication. Sometimes, these sedatives can take more than 72 hours to wear off and there is a real danger of misdiagnosing thse people with severe anoxic brain damage, when they may be still recovering from the sedative effect. 
4. No wasting of time on mechanical ventilation trying to cool the patient for 24 hours and wasting another 24 hours to rewarm. We can start planning for extubation soon after reversal of respiratory failure and improvement in mental status. 
5. Also, sometimes we see that families want to withdraw care in the middle of a hypothermia/rewarming phase. It's unethical to start and therapy, and withdraw care, without even finishing it. It's almost like stopping in the middle of a asurgery, due to family's wishes.

• Instead of trying to achieve hypothermia ( 32-34C), the current evidence support targeted temperature management, whose primary goal is to avoid temperatures in excess of 36C for the first 48 hours. 
• Involuntary movements that are observed after brain death may include triple flexion (Stimulation of the feet causes flexion at the ankles, knees, and hips ) and Myokymia ( localized quivering of  facial or ocular muscles ). These are purely spinal reflexes buy may induce anxiety in familes.
• Other mimics of brian death inlcude prolonged sedation, hypothermia, urecognised drug intoxication/overdose, locked-in syndrome or high c-spine injury. 
• ABG Correction in hypothermia: Oxygen and CO2 solubility increases as temperature goes down and hence, partial pressures go down as well. Blood is rewarmed to room temperature and ABG results are given. PO2 is 5 mmHg lower for each degree below 37C. PCO2 is 2mmHg lover for each degree below 37C. Change in pH = 0.015 pH units higher per degree C change in temperature