This episode of CRACKCast focuses on adult resuscitation, reviewing core concepts from Chapter 8 of Rosen’s 9th edition.
Shownotes: PDF Here[bg_faq_start]
 Describe your history and physical exam in the patient being actively resuscitated.
- 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?
TABLE 8.2 Physical Examination Findings (Rosen’s 9th Edition)
|PHYSICAL EXAMINATION||ABNORMALITIES||POTENTIAL CAUSES|
|Airway||Secretions, vomitus, or blood||Aspiration|
|Resistance to positive-pressure ventilation||Tension pneumothorax|
|Neck||Jugular venous distention||Tension pneumothorax|
|Tracheal deviation||Tension pneumothorax|
|Chest||Median sternotomy scar||Underlying cardiac disease|
|Lungs||Unilateral breath sounds||Tension pneumothorax|
|Right mainstem intubation|
|Distant or no breath sounds or no chest expansion||Esophageal intubation|
|Heart||Diminished heart tones||Hypovolemia|
|Abdomen||Distended and dull||Ruptured abdominal aortic aneurysm or ruptured ectopic pregnancy|
|Distended, tympanitic||Esophageal intubation|
|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|
 Discuss the process of deterioration to cardiac arrest with respiratory failure, cardiac obstruction, and hypovolemia.
Primary respiratory failure leads to hypertension and tachycardia initially, followed by hypotension and bradycardia, progressing to PEA, VF, or asystole.
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.
 List 6 aspects of optimal CPR.
- Place two hands over lower half of sternum
- Compression rate (100–120 compressions/min)
- Compression depth (5–6 cm)
- Chest compression fraction ≥80% (CPR performed 80 out of every 100 seconds) or limit interruptions to less than 10 seconds
- Full chest recoil
- 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)
 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.
 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|
 What is electromechanical dissociation (EMD) and how does it differ from pseudo electromechanical dissociation (pseudo 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
- 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
 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
- Is there a pneumothorax?
- US: lung slide, lung point
- Rx: needle decompression/finger thoracostomy, tube thoracostomy
- Is tamponade present?
- US: pericardial effusion, fixed dilated IVC, RA and RV diastolic collapse
- Rx: pericardiocentesis, thoracotomy, pericardotomy
- Is patient hypovolemic?
- US: no or few B lines, hyperdynamic LV, collapsible IVC
- Rx: volume infusion
- Is LV dysfunction main cause of shock?
- US: Hypokinetic LV, B lines, fixed and dilated IVC
- Rx: pressors and inotropes
- Is there RV strain?
- US: RV dilation, D sign, paradoxical septal wall movement, fixed and dilated IVC
- Rx: consider thrombolysis, DVT search, further diagnostic workup for PE/MI, consider pulmonary hypertension
EGLS course site here.
 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.
|Carotid or femoral pulse||Present|
|Arterial relaxation (diastolic) pressure||> 20-25 mmHg|
 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.
 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.
 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.
 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.[bg_faq_end]