In this issue:

Special Edition - Part Four: Our e-newsletter continues a look at the just-released guidelines and recommendations for Advanced Cardiac Life Support ---in this issue, we look at post-resuscitation and the acute coronary and acute stroke recommendations reviewed in the August 22, 2000 issue of Circulation.

Post-Resuscitation Care

Optimal Approach to Treatment, Post-resuscitation

Acute Coronary Syndromes

Acute Stroke-Identification and Intervention

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Please refer to the previous newsletters for an explanation of the classification system referred to in the following. Newsletter medical information is archived at www.acutecare.com/narchive.htm

Post-Resuscitation Care

Four phases of post-resuscitation

1. "Almost one-half of post-resuscitation syndrome deaths take place with 24 hours of the event." Included here are "microcirculatory dysfunction" from hypoxia and release of 'toxic enzymes and free radicals into the cerebrospinal fluid and blood."


2. Over 1-3 days cardiac function improves, but "intestinal permeability increases," predisposing to sepsis syndrome. Progressive challenges are presented by liver, pancreas and kidneys (multiple organ dysfunction syndrome-MODS);

3. in subsequent days, infection becomes serious and the patient's condition deteriorates rapidly;

4. Death

Reviewing these phases gives greater appreciation to strategies that go beyond simple restoration of blood pressure and gas exchange, and into aggressively monitoring of gastric, hepatic and renal perfusion with appropriate interventions "The splanchnic circulation and gut are assuming increased importance for targeted therapy in long-term outcome and survival."

Optimal Approach to Treatment, Post-resuscitation

Initially, replace lines established without proper aseptic technique (peripheral and central);

Give glucose only for documented hypoglycemia;

If patient had VF or VT corrected without antiarrhythmic treatment, and now has adequate cardiac rhythm and perfusion, consider lidocaine bolus and infusion continued for several hours while correctable underlying contributors to arrest are corrected. If another antiarrhythmic was used successfully during the resuscitation, then that agent should be established as the infusion (instead of lidocaine);

Complete ongoing patient assessment including battery of labs, ECG, vital signs, and continuous monitoring;

Temperature regulation-cerebral metabolism increases approximately 4% per degree Fahrenheit---treat fever "aggressively" controversy surrounds use of deliberate hypothermia, with "mild levels" around 93F appearing to be effective without "detrimental side effects"-----and metabolic decreases of 7% per every degree centigrade (2 degrees Fahrenheit) noted. If a patient is hemodynamically stable and experiences spontaneous hypothermia no lower than 91.5F, active rewarming is not recommended. Not intervening in spontaneous occurrence is Class IIb, deliberate induction of hypothermia is Class Indeterminate, and treating fever aggressively is Class IIa.

Respiratory

Evidence supports concept that hypocapnia may worsen cerebral ischemia. Hyperventilation after cardiac arrest should be avoided. Ventilate to normocarbia (Class IIa); routine hyperventilation is Class III, hyperventilation for cerebral herniation syndrome and pulmonary 
hypertension are Class IIa.

Cardiovascular

Avoid "even mild hypotension" (for cerebral recovery); ideal pulmonary occlusive pressure higher than normal-18mmHg, though may need to vary depending on specific conditions. In patients with low cardiac output, peripheral vasoconstriction may render noninvasive blood pressure assessments inaccurate---some suggest monitoring with femoral artery catheter vs. radial when vasoconstriction is "severe." 

Complete exam includes serial vitals, urine output, 12-lead ECG, chest x-ray, serum electrolytes (including magnesium and calcium), cardiac markers.

Renal

Outputs include urine, suctioned vomitus and gastric secretions, diarrhea---monitor for rising serum creatine, urea nitrogen, and hyperkalemia. Consider dialysis.

CNS

Because of damage to microvasculature during cardiac arrest, cerebral perfusion pressure may be normal and yet cerebral perfusion can still be in a reduced state. Post-arrest treatment includes normal to slightly elevated mean arterial pressure and keeping intracranial 
pressure normal. Aggressively manage elevated temperatures, seizures, and elevate head to about 30 degrees and keep in midline to avoid challenges to cerebral venous drainage. Caution with suctioning as this dramatically increases ICP during procedure.

Gastrointestinal

Insert NG tube if reduced bowels sounds or mechanical ventilator is used.

Systemic Inflamatory Response Syndrome (SIRS) and Septic Shock

Treatment goal: normal tissue oxygen uptake---

• Volume replacement, consider adding inotrope/vasopressin; 

• dobutamine/norepinephrine in severe septic shock; 

• Empirical antibiotic therapy in septic shock; 

• Glucocorticoid therapy---no evidence they improve survival rates; 

• supraphysiological (lower than normal) doses may benefit patients with "persistent vasopressor-resistant shock maximally treated with broad-spectrum or organism-specific antimicrobial." (Class IIb).

Post-Resuscitation Concerns Summary

Assess and consider multiple organ injury due to hypoxic injury; "Splanchnic circulation and gut are assuming increased importance for targeted therapy in long-term outcome and survival. Physicians should be skilled and knowledgeable in all aspects of care in these complicated survivors of cardiac arrest and shock syndromes."

Acute Coronary Syndromes

Prehospital Guideline Recommendations

• 12-lead ECG diagnostic programs in urban and suburban paramedic systems (Class I).

• Studies show that this may take from 0-4 minutes of additional scene/transport time, but typically saves 20-55 minutes.

• Out-of-hospital thrombolytic administration if transport time is > one hour or physician is present.

• "When possible," triage patient to appropriate facility (capable of cardiac catheterization or bypass surgery) for severe left ventricular compromise with signs of shock, pulmonary congestion HR>100, systolic BP < 100mmHg, < 75 years of age, and high risk of mortality. (Class I).
  

Therapies

Early thrombolytic intervention for AMI with ST-segment elevation (< 75 years of age is Class I; >75 years of age is Class IIa);

If thrombolysis is contraindicated (Class IIA), as well as with acute coronary patients less than 75 years of age experiencing signs of shock (Class I), consider transfer to facility with interventional capacity (angioplasty, angioplasty with stent, etc.) if chance of reperfusion exists;

Heparin is recommended for patients receiving tPA and reteplase. New dosing is 60 U/kg bolus followed by infusion of 12 U/kg/hr (maximum of 4000-Unit bolus and 1000 Units per hour). Activated PTT should be between 50-70 seconds for initial 48 hours.

GP IIb/IIIa inhibitors are Class IIa recommendations for experiencing high-risk unstable angina or MI without ST segment elevation. GP IIb/IIIa inhibitors provide additional benefit when used in conjunction with aspirin and unfractionated heparin (Class IIa).

When treating unstable angina/non-Q wave MI, low molecular weight heparin is an acceptable alternative to unfractionated heparin.

"Troponin-postive patients are at risk for major adverse cardiac events and should be considered for aggressive therapy."

Initial Management

Targeted history (AMI, thombolytics), vitals, focused physical exam, 12-lead ECG, chest x-ray, continuous ECG monitoring;

MONA-Morphine, Oxygen, Nitroglycerin (sublingual tablet/spray followed by infusion), Aspirin (160-325mg) chewed and swallowed;

Specific Interventions

Aim for fibrinolytic therapy (if not contraindicated) door-to-needle time of less than 30 minutes (include simultaneous administration of heparin and aspirin);

Target time for cardiac catheterization, door-to-dilation, in 90 minutes (plus or minus 30 minutes);

Adjunctive (if no contraindications)

Beta-blockers (anti-ischemic and reduces pain); IV nitroglycerin (especially heart failure, large anterior MI, hypertension, recurrent ischemia);

ACE inhibitors (history of previous MI, evidence of large anterior MI, heart failure with systolic pressure greater than 100mmHg) after patient is stabilized.

Other notes

"There is no routine indication" for the use of magnesium-however, maintain magnesium levels at greater than 2 mEq/L is recommended to avoid ventricular rhythm disturbances;

Glucose-Insulin-Potassium-"metabolic manipulation" of an infarct "may be helpful; it is easily administered and associated with few adverse effects." Larger clinical trial are necessary, presently it is Class Indeterminate.

Acute Stroke-Identification and Intervention

7 Ds of Stroke Management--Detection, Dispatch, Delivery, Door,Data, Decision, Drug

Detection, Dispatch, Delivery ---Rapid identification of signs andsymptoms and transportation of eligible patients (half of patients currently use EMS80 percent of strokes occur at home) to a facility able to provide intervention within one hour of arrival to Door;

Data (noncontrast CAT scan), Decision (eligibility for fibrinolytic therapy), Drug (treating eligible patients).

Assessment and Treatment

Out-of-hospital stroke assessment---evaluate using validated tools such as Los Angeles Prehospital Stroke Screen or Cinncinati Prehospital Stroke Scale (both explained in Guidelines).

Initial treatment-IV NS or LR, correct hyperglycemia and hyperthermia (Class IIa);

DO NOT routinely administer supplemental oxygen to mild and moderate strokes if oxygen saturation is greater than 90 percent. (Data regarding the need for supplemental oxygen for severe strokes with similarly high SaO2 is currently lacking);

Management of hypertension is controversial;

Treatment of seizures and intracranial pressure (less than 10-20 percent of stroke patients need clinical management of this) follow conventional guidelines;

Fibrinolytic therapy, if indicated must be initiated within 3 hours of onset of stroke signs/symptoms in patients with ischemic strokes that meet eligibility criteria. (Class I); this can be extended to six hours if there is a capability to administer fibrinolytic agents such as prourokinase intraarterially to patients with occlusion of the middle cerebral artery. Based on current evidence, streptokinase should not be used in treating stroke patients.

"The efficacy of anticoagulants in acute stroke has not been established. Heparin is frequently administered to patients with acute ischemic stroke, but its value is unproved. Routine use of any type of anticoagulant in acute ischemic stroke is not recommended. "Low 
molecular weight heparin has advantages over conventional heparin and is currently being investigated. Aspirin is a useful adjunct if administered within 48 hours of onset in patients that are not eligible for fibrinolytic therapy.

Anticoagulants are effective when administered in patients with TIAs to reduce the risk of a stroke.