CRACKCast E199 – Adult Resuscitation

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This episode of CRACKCast focuses on adult resuscitation, reviewing core concepts from Chapter 8 of Rosen’s 9th edition.

Shownotes: PDF Here

[1] Describe your history and physical exam in the patient being actively resuscitated.

History:

  • Exact time of arrest
  • Witnessed vs unwitnessed arrest
  • Bystander CPR
  • CPR duration – crucial
  • ECG rhythm
  • Prehospital interventions
  • past medical/psychiatric history
  • drug ingestion or environmental exposures? do we need to give an antidote?
  • Allergies

Physical Exam:

TABLE 8.2 Physical Examination Findings (Rosen’s 9th Edition) 

PHYSICAL EXAMINATION ABNORMALITIES POTENTIAL CAUSES
General Pallor Hemorrhage
Cold Hypothermia
Airway Secretions, vomitus, or blood Aspiration
Airway obstruction
Resistance to positive-pressure ventilation Tension pneumothorax

Airway obstruction

Bronchospasm
Neck Jugular venous distention Tension pneumothorax
Cardiac tamponade
Pulmonary embolus
Tracheal deviation Tension pneumothorax
Chest Median sternotomy scar Underlying cardiac disease
Lungs Unilateral breath sounds Tension pneumothorax
Right mainstem intubation
Aspiration
Distant or no breath sounds or no chest expansion Esophageal intubation

Airway obstruction

Severe bronchospasm
Wheezing Aspiration
Bronchospasm
Pulmonary edema
Rales Aspiration
Pulmonary edema
Pneumonia
Heart Diminished heart tones Hypovolemia
Cardiac tamponade
Tension pneumothorax
Pulmonary embolus
Abdomen Distended and dull Ruptured abdominal aortic aneurysm or ruptured ectopic pregnancy
Distended, tympanitic Esophageal intubation
Gastric insufflation
Rectal Blood, melena GI Bleed
Extremities Asymmetrical pulses Aortic dissection
Arteriovenous shunt or fistula Hyperkalemia (think Renal Failure Pt)
Skin Needle tracks Intravenous drug abuse
Burns Smoke inhalation
Electrocution

[2] Discuss the process of deterioration to cardiac arrest with respiratory failure, cardiac obstruction, and hypovolemia.

 Respiratory Failure:

Primary respiratory failure leads to hypertension and tachycardia initially, followed by hypotension and bradycardia, progressing to PEA, VF, or asystole.

Cardiac Obstruction

Circulatory obstruction (eg, tension pneumothorax, pericardial tamponade) and hypovolemia lead to tachycardia and hypotension initially, progressing through bradycardia and then to PEA, but may deteriorate to VF or asystole as well.

 

[3] List 6 aspects of optimal CPR.

  1. Place two hands over lower half of sternum
  2. Compression rate (100–120 compressions/min)
  3. Compression depth (5–6 cm)
  4. Chest compression fraction ≥80%  (CPR performed 80 out of every 100 seconds) or limit interruptions to less than 10 seconds
  5. Full chest recoil
  6. Proper ventilation rate (10 breaths ventilations/min)

Throwing back to original episode:  P’s of high quality CPR: placement, pace, pressure, pauses, and puffs (don’t over-ventilate)

[4] What medications have been shown to improve outcomes in cardiac arrest?

From the book:

“Pharmacologic therapy during CPR improves the proportion of patients who achieve ROSC.17However, there is yet to be a randomized prospective placebo-controlled clinical trial that has been adequately powered to determine if pharmacologic therapy during CPR improves long-term survival or neurologic outcome.”

 

That trial has since been done – PARAMEDIC-2 showed an increased likelihood of ROSC in patients who received epi compared to those that didn’t. However, there was no increase in 30 day survival or survival to hospital discharge with favourable neurologic outcome. (Rebel EM Summary here).

Also in Rosen’s:

“For refractory VF or pVT, antidysrhythmics can be administered up to their maximum loading dose. Amiodarone (300 mg IV) is the only antidysrhythmic agent that has been shown to improve the rate of VF conversion to a perfusing rhythm.”

However, according to the 2018 AHA Focused Update on ACLS, both amiodarone and lidocaine can be considered to treat shock-refractory VF or VT.

 

[5] List 8 differential diagnoses for PEA arrest (See Table 8.4)

 

Based on Table 8.4 (Rosen’s 9th ed.)

CAUSE DIAGNOSIS PALLIATIVE THERAPY DEFINITIVE THERAPY
Hypovolemia Response to volume infusion Volume infusion Hemostasis if hemorrhage
Hypoxia Response to oxygenation Oxygenation, assisted ventilation Treat underlying cause
Hypothermia Rectal temperature Warm peritoneal or thoracic lavage, venoarterial ECMO
Hyperkalemia History of renal failure or elevated serum potassium level Calcium chloride, insulin and glucose, sodium bicarbonate Hemodialysis
Hypokalemia Serum Potassium, U waves/prolonged QTc on ECG, history of poor intake or losses Potassium supplementation
Acidosis Arterial blood gas Hyperventilation, sodium bicarbonate Treat underlying cause
Cardiac Tamponade Echocardiogram; jugular venous distention Pericardiocentesis Thoracotomy and pericardiotomy
Toxicity History of drug ingestion Drug-specific Drug-specific
Tension Pneumothorax Asymmetric breath sounds, tracheal deviation Needle thoracostomy Tube thoracostomy
 Thrombus Formation – PE Risk factors or evidence of deep venous thrombosis Venoarterial ECMO Lytic therapy, pulmonary embolectomy
Thrombus Formation – MI STEMI, Heart Block, or VF arrest DAPT +/- lytic depending on availability of cath lab Angiography and revascularization

 

[6] What is electromechanical dissociation (EMD) and how does it differ from pseudo electromechanical dissociation (pseudo EMD)?

True EMD

  • Cause: abnormal automaticity and conduction. Associated with global myocardial depression and acidosis 2ndary to ischemia or hypoxia
  • Rhythm: bradycardia with wide QRS complex
  • This typically occurs after defib following prolonged VF.
  • Associated with: hyperkalemia, hypothermia, drug OD

Pseudo EMD

  • The step before true EMD…
  • Has all the same causes as true EMD. Additional causes of pseudo EMD include papillary mm rupture and myocardial wall rupture (ventricle contracting but forward flow severely reduced), hypovolemia, tension PTX, tamponade, massive PE.
  • Pseudo EMD of extracardiac origin is typically narrow and tachycardic, progressing to bradycardia and wide QRS

[7] What is echo-guided life support (EGLS) and how is it used?

5 clinical questions to be applied to patient in shock/extremis

At each stage – consider associated diagnoses and treatments

  1. Is there a pneumothorax? 
    1. US: lung slide, lung point
    2. Rx: needle decompression/finger thoracostomy, tube thoracostomy
  2. Is tamponade present?
    1. US: pericardial effusion, fixed dilated IVC, RA and RV diastolic collapse
    2. Rx: pericardiocentesis, thoracotomy, pericardotomy
  3. Is patient hypovolemic?
    1. US: no or few B lines, hyperdynamic LV, collapsible IVC
    2. Rx: volume infusion
  4. Is LV dysfunction main cause of shock? 
    1. US: Hypokinetic LV, B lines, fixed and dilated IVC
    2. Rx: pressors and inotropes
  5. Is there RV strain?
    1. US: RV dilation, D sign, paradoxical septal wall movement, fixed and dilated IVC
    2. Rx: consider thrombolysis, DVT search, further diagnostic workup for PE/MI, consider pulmonary hypertension

EGLS course site here.

[8] What are your targets during CPR for the following metrics? (See Table 8.3)

The following table has been adapted from Table 8.3 in Rosen’s Emergency Medicine, 9th Edition.

 

Monitoring Technique Indicator
Carotid or femoral pulse Present
CPP >15 mmHg
Arterial relaxation (diastolic) pressure > 20-25 mmHg
PETCO2 >10 mmHg
ScvO2 > 40%

WiseCRACKS

[1] What is cough CPR and when should it be used?

Cough CPR may sound like something you do to resuscitate your best friend that has just choked on that stray Dorito after seeing that hilarious meme you posted, but it is actually a resuscitation strategy that you can use to save a life.

As per Rosen’s, cough CPR is best used in the patient who enters into ventricular fibrillation or pulseless ventricular tachycardia while on cardiac monitors. The patient should be constructed to cough “vigorously” until a defibrillator is available. There is some evidence to suggest that this strategy can keep a patient conscious for up to a minute or longer.

 

[2] What is the only antidysrhythmic shown to improve rates of ventricular fibrillation conversion to a perfusing rhythm?

For all you guys thinking that the answer to this question was epinephrine, you are wrong. In cases of refractory ventricular fibrillation, amiodarone dosed at 300 mg IV is the ONLY antidysrhythmic to improve rates of conversion to a perfusing rhythm.

According to the 2018 AHA Focused Update on ACLS, both amiodarone and lidocaine can be considered to treat shock-refractory VF or VT.

 

[3] What is the minimum coronary perfusion pressure (CPP) is needed to achieve return of spontaneous circulation (ROSC)?

Some spaced repetition here, CRACKCast listeners. Remember, you want to target coronary perfusion pressure to 15 mmHg or more during resuscitation. This is the recommended value given the results of human and animal studies that identified a minimum CPP of at least 15 mm Hg to achieve return of spontaneous circulation.

 

[4] What is the triad of cardiopulmonary arrest?

The triad of cardiopulmonary is as follows: unconsciousness, apnea, and pulselessness.

If there is any suspicion that the patient is in cardiac arrest, CPR should be started immediately. Also, be sure to use a large artery to assess for pulselessness, as distal pulses become faint and undetectable at lower mean arterial pressures.

 

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Owen Scheirer

Owen Scheirer

Owen is a resident in the FRCPC Emergency Medicine program at the University of Saskatchewan. When he's not running around the emergency department, he's hanging out with his wife, new baby girl, and dog. Spare time = climbing and cycling!
Owen Scheirer

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Dillan Radomske

Dillan Radomske

Dillan Radomske is an Emergency Medicine resident at the University of Saskatchewan. He is passionate about technology-enhanced medical education, podcast creation and production, and Indigenous advocacy. He is one of the new CRACKCast hosts, and aspires to continue to contribute to the field of FOAMed in the future.
Dillan Radomske
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Dillan Radomske

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