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Fast Facts
A brief refresher with useful tables, figures, and research summaries
Cardiopulmonary Emergencies
In this section, we cover the following cardiopulmonary emergencies:
Other topics related to cardiopulmonary emergencies are covered in the following rotation guides:
Acute Coronary Syndrome (STEMI/NSTEMI), Arrhythmias, Congestive Heart Failure, Pericardial Disease and Myocarditis, Valvular Disease, Atrial Fibrillation (Cardiology)
Asthma, Chronic Obstructive Pulmonary Disease (COPD), Interstitial Lung Disease, Pulmonary Hypertension (Pulmonology)
Anaphylaxis (Allergy/Immunology)
Cardiac Resuscitation and Advanced Cardiovascular Life Support (ACLS)
The American Heart Association (AHA) offers basic life support (BLS) and advanced cardiovascular life support (ACLS) training for providers or laypersons who could be involved in a resuscitation. The goal of ACLS is to improve outcomes for adult patients through early recognition and intervention in respiratory arrest, cardiac arrest, and life-threatening arrhythmias. Some related ACLS guidelines and links to algorithms are provided below. These guidelines are regularly updated to reflect new evidence and changes in practice.
High-Yield Summary Points:
Recognize respiratory arrest, cardiac arrest, and life-threatening arrhythmias.
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Know electrocardiogram (ECG) rhythms:
sinus rhythm
atrial fibrillation
atrial flutter
supraventricular tachycardia
atrioventricular blocks (first-degree, second-degree type I, second-degree type II, and third-degree)
asystole
pulseless electrical activity
ventricular tachycardia (VT)
ventricular fibrillation (VF)
Prioritize rapid, full-depth chest compressions.
Rapidly defibrillate appropriate rhythms.
Continuously assess the effects of interventions.
Identifying ACS and Stroke
Identifying acute coronary syndrome (ACS) and stroke is an important part of ACLS given that both conditions are associated with high risk of morbidity and mortality. The HEART Score is a commonly used decision aid to predict the risk of major adverse cardiac events. The NIH Stroke Scale quantifies stroke severity. (For more information on these rules, see the Clinical Rules and Guidance section in this rotation guide).
![[Image]](content_item_media_uploads/ACS_2015_f1.jpg)
(Reprinted with permission, 2010 & 2015 American Heart Association Guidelines for CPR & ECC, Part 9: Acute Coronary Syndromes ©2015 American Heart Association, Inc.)
Life-Threatening Arrhythmias
Become familiar with ECG changes associated with the following arrhythmias. These rhythms are unlikely to maintain adequate perfusion and can result in cardiac arrest.
![[Image]](content_item_media_uploads/Bradycardia_Pulse_2015.jpg)
(Reprinted with permission, 2010 & 2015 American Heart Association Guidelines for CPR & ECC, Part 7: Adult Advanced Cardiovascular Life Support ©2015 American Heart Association, Inc.)
![[Image]](content_item_media_uploads/Tachycardia_Pulse_2015.jpg)
(Reprinted with permission, 2010 & 2015 American Heart Association Guidelines for CPR & ECC, Part 7: Adult Advanced Cardiovascular Life Support ©2015 American Heart Association, Inc.)
Cardiopulmonary Arrest
Cardiac and pulmonary arrest go hand in hand. For airway management, please see the Common Procedures section in this rotation guide.
The most important interventions during cardiac arrest are high-quality chest compressions and early defibrillation when indicated.
During resuscitation, it is also important to consider reversible causes of arrest.
Hs and Ts Mnemonic for Common Causes of Arrest | |
---|---|
Hypovolemia | Toxins |
Hypoxia | Tamponade (pericardial) |
Hydrogen ions (acidosis) | Tension pneumothorax |
Hyperkalemia | Thrombosis (myocardial infarction or pulmonary embolism) |
Hypothermia | Trauma |
Preparation for ACLS
All teams have a leader and positions to ensure organization and efficiency. Closed-loop communication is pivotal to this group effort.
![[Image]](content_item_media_uploads/6_Person_High_Performance.jpg)
(Reprinted with permission, Advanced Cardiovascular Life Support Provider Manual ©2016 American Heart Association, Inc.)
![[Image]](content_item_media_uploads/Adult_Life_Support_2020.jpg)
(Reprinted with permission, 2020 American Heart Association Guidelines for CPR & ECC, Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. 2020 American Heart Association, Inc.)
Post-Cardiac Arrest Care
After return of spontaneous circulation (ROSC), focus on identifying the cause of arrest, preserving neurologic function, and treating complications of resuscitation efforts. The recently resuscitated patient has a proclivity to arrest again.
Recheck vital signs and ECG; consider bedside ultrasound to evaluate cardiac function, volume status, pulmonary edema, and to rule out pneumothorax or pericardial effusion.
If the patient is intubated, obtain chest radiograph to ensure endotracheal tube placement and double-check ventilator settings to avoid excessive ventilation, high tidal volume, or hypocapnia.
Administer intravenous (IV) fluids, blood, or vasopressors as needed to maintain a mean arterial pressure (MAP) of >65 mm Hg. Consider placing a central line and an arterial line.
Request cardiology consultation and consider extracorporeal membrane oxygenation (ECMO) for unstable patients.
Assess and document neurologic status.
Consider organ donation early in this population at high risk for mortality. Determine if the patient has an advance directive regarding donation and marshal resources as appropriate.
![[Image]](content_item_media_uploads/Adult_Post-Cardiac_2020.jpg)
(Reprinted with permission, 2020 American Heart Association Guidelines for CPR & ECC, Part 3: Adult Basic and Advanced Life Support: 2020 American Heart Association Guidelines for Cardiopulmonary Resuscitation and Emergency Cardiovascular Care. 2020 American Heart Association, Inc.)
Therapeutic Hypothermia
Targeted temperature management (TTM; therapeutic hypothermia) is artificially induced hypothermia. TTM is used in patients surviving out-of-hospital sudden cardiac arrest to improve rates of long-term neurologically intact survival. The rationale is that hypothermia reduces oxygen demand and the inflammation cascade.
Indications: The American Heart Association (AHA) and the European Resuscitation Council (ERC) recommend that comatose adult patients who experience return of spontaneous circulation (ROSC) after cardiac arrest should be treated with TTM and maintained at a constant temperature between 32°C and 36°C during TTM for at least 24 hours. However, the quality of evidence to support these recommendations is low and new data bring into question the benefit of TTM. The TTM2 study published in 2021 investigated the effects of TTM (goal 33°C) versus maintenance of normothermia (temperature <38°C) and found no differences in mortality, neurologic outcomes, or quality of life at 6 months.
In light of these new data, official guidelines may change.
Contraindications: There are few recognized contraindications to TTM. The ERC currently suggests that a higher temperature could be targeted in patients with severe cardiovascular impairment at 33°C.
Procedure
If TTM is used, patients should be cooled to 32°C-36°C (89.6°F-96.8°F) for at least 24 hours. Cooling should be initiated in the emergency department (ED) with cool IV fluids (30 mL/kg of 4°C sodium chloride via peripheral IV or femoral central line over 30 minutes) or external cooling devices (e.g., surface-cooling devices or cold packs).
![[Image]](content_item_media_uploads/phases_of_hypothermia.jpg)
Figure 2. Phases of hypothermia. BP indicates blood pressure; K+, serum potassium concentrations; O2 sat, oxygen saturation; and SBP, systolic blood pressure.(Source: Therapeutic Hypothermia After Cardiac Arrest, Circulation 2013.)
Note: Institutions usually have their own policies and procedures for therapeutic hypothermia. Be familiar with yours.
Management Considerations
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shivering: occurs in most patients; should be recognized early and treated aggressively with sedatives and analgesics
buspirone and meperidine may lower the shivering threshold; chemical paralysis with sedation is most effective
bradycardia: the most common arrhythmia; treat only if associated with hypotension
mechanical ventilation goal: arterial oxygen saturation of 94%-96%
blood glucose: hypothermia decreases insulin secretion and increases insulin resistance, leading to hyperglycemia, which typically does not require treatment until glucose levels exceed 200 mg/mL; measure it hourly to avoid hypoglycemia, especially with IV insulin treatment and during rewarming, when glucose levels can drop quickly
serum potassium levels: may decrease; serum electrolytes should be measured every 4-6 hours; potassium should be maintained at or above 3.5 mEq/L
Aortic Dissection
Aortic dissection is defined as a tear in the layers of the aorta (usually the intima) and results in the creation of a false lumen. Stanford classification type A involves the ascending aorta and is generally managed with surgery; type B involves the descending aorta and is generally managed medically or with endovascular intervention.
![[Image]](content_item_media_uploads/Stanford_Classification.jpg)
(Source: Surgery of the Thoracic Aorta. N Engl J Med 1997.)
Aortic dissection is a diagnostic challenge due to the broad differential diagnosis of chest pain. Untreated mortality is about 1% per hour during the first 2 days, primarily from type A dissections. About 40% of patients with type A dissection die before medical evaluation.
Classic History
Aortic dissection most often presents as a sudden-onset tearing or ripping sensation to the chest or back. Other presentations include neck or jaw pain, altered mental status, stroke symptoms, and flank pain.
Risk Factors
Risk factors for aortic dissection include the following:
hypertension
advanced age
aortic-valve pathology
connective-tissue disease
substance abuse
smoking
history of tuberculosis
syphilis
vasculitis
third-trimester pregnancy
blunt trauma
cardiac surgery
family history of dissection
Physical Exam
Aortic dissection can be associated with the following symptoms:
aortic regurgitation
tamponade
pulse deficit
hemodynamic instability
focal neurologic deficit
Diagnosis
Labs are not very helpful, but obtain blood type and cross-matching for 6 units if suspicion is high; consider D-dimer testing (associated with a high negative predictive value, although the American College of Emergency Physicians (ACEP) does not recommend its use alone for ruling out aortic dissection).
ECG is neither sensitive nor specific; acute myocardial infarction with ST elevation can occur if dissection is very proximal and involves one or more coronary arteries.
Chest radiograph can show a widened aortic knob or mediastinum, pleural effusion, left apical pleural cap, indistinct or irregular aortic contour, or tracheal deviation (these findings are not specific).
Computed tomography with contrast is highly sensitive and specific.
Ultrasound is also useful to evaluate pericardial effusion and tamponade.
The type of dissection is important to know since it will determine management.
Management
Place on cardiac monitor and obtain IV access.
-
To reduce aortic wall stress, the heart rate should be reduced to around 60 beats per minute with the use of IV beta-blockade.
Esmolol is the first-line medication because it is easily titratable and fast-acting.
Calcium-channel blockers (e.g., diltiazem) may also be used if beta-blockers are contraindicated.
Benzodiazepines are first-line treatment for acute cocaine toxicity-related dissection. Theoretically, unopposed alpha stimulation is a concern if beta-blockers are used.
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Follow with other IV vasodilators to achieve a target systolic blood pressure (BP) <120 mm Hg.
Nicardipine or nitroprusside are the ideal agents.
Do not attempt to lower BP before controlling heart rate because it may induce a reflex tachycardia and worsen aortic injury.
Do not send an unstable patient to the scanner!
Be certain to treat pain.
Consult vascular surgery immediately. Cardiac surgery may be needed if injury is proximal and involves the coronary arteries or aortic valve.
Type A (involves ascending aorta) is associated with aortic rupture, tamponade, acute myocardial infarction (AMI), aortic regurgitation, hemorrhage, and stroke. Surgical intervention is usually indicated.
Type B (does not involve ascending aorta) is associated with limb/organ ischemia and is usually treated medically or with endovascular intervention (31%).
Pulmonary Embolism
Occlusion of part of the pulmonary arterial tree can cause acute hypoxemia and cardiac strain. Pulmonary embolism (PE) is a pulmonary artery occlusion caused by a clot that traveled from another part of the body, most often the legs. Other sources include upper-extremity deep-vein thrombosis (DVT), indwelling catheter, and right-sided heart-chamber thrombus.
Risk Factors
previous PE/DVT
hypercoagulable state
oral contraception use
cancer
recent surgery or immobilization
indwelling vascular catheter
acute medical illness
Classic Symptoms
dyspnea (acute or subacute)
pleuritic chest pain
palpitations
cough
hemoptysis
lower-extremity pain
syncope
severe hemodynamic instability
Clinical Signs
tachypnea (96%)
rales (59%)
tachycardia (45%)
fever (43%)
lower-extremity edema (25%)
Workup
Clinical decision rules can guide workup using evidence-based decision-making. Wells Criteria for PE probability and Pulmonary Embolism Rule-Out Criteria (PERC) can be used to guide your workup. For more on these rules, see Clinical Rules and Guidance in this rotation guide and Venous Thromboembolism (VTE) and Anticoagulation in the Hematology rotation guide.
Management
Manage PE based on clinical presentation. Current efforts in PE management focus on identifying a stable population eligible for discharge on direct oral anticoagulant (DOAC) therapy or parenteral low-molecular-weight (LMW) heparin compounds versus unstable or potentially unstable patients who would benefit from thrombolytic therapy or embolectomy. For more on PE management see Management of Venous Thromboembolism in the Hematology rotation guide.
Syncope
Syncope is a transient loss of consciousness with an inability to maintain postural tone with self-limited recovery. For a small subset of patients this sign can serve as a life-threatening presage, although most causes of syncope are benign.
Differential Diagnosis
The following table describes some of the many conditions that can cause syncope:
Organ System | Conditions |
---|---|
Vasomotor/vascular | Hemorrhage (gastrointestinal bleed, ruptured ectopic pregnancy); dehydration/hypovolemia; diabetic neuropathy; diuresis; drug-induced orthostasis (e.g., olanzapine, antihypertensives); dysautonomia/postural hypotension; hypotension; multisystem atrophy; peripheral polyneuropathy; sepsis; subclavian steal; vasomotor insufficiency |
Cardiac | Aortic dissection; aortic stenosis; bradyarrhythmia (e.g., sick sinus syndrome, sinoatrial block/atrioventricular block/conduction block, sinus pause >3 seconds); tachyarrhythmia (e.g., ventricular tachycardia, torsades de pointes, paroxysmal supraventricular tachycardia, Wolff-Parkinson-White syndrome); Brugada syndrome; cardiac myxoma; cardiac outflow obstruction; hypertrophic subaortic stenosis; pacemaker malfunction; primary pulmonary hypertension; prolonged QT syndrome; pulmonary embolism; stress-induced (takotsubo) cardiomyopathy; tricuspid stenosis |
Situational (vasovagal) | Carotid sinus syncope; cough (post-tussive) syncope; defecation syncope; micturition syncope; postprandial syncope; swallow syncope |
Metabolic/endocrine | Hypothyroidism; hypoxemia; pheochromocytoma |
Central nervous system | Intracranial hemorrhage (subarachnoid hemorrhage, hemorrhagic stroke); hyperventilation syndrome; hydrocephalus; migraine headache; narcolepsy; panic attack; seizure disorder; stroke; transient ischemic attack; vertebrobasilar insufficiency; vertebral dissection; drug use |
High-Yield History
It is important to elicit the following details of the syncope event:
triggers
prodromal symptoms
duration of loss of consciousness
present symptomatology
infection symptoms
antecedent trauma
family history of sudden death and risk factors for coagulation problems
acute coronary syndrome and stroke
Exam
Orthostatic vital signs are useful for drug-induced and vasomotor causes; they correlate poorly with volume status.
Listen for murmur.
Seek neurological abnormality regarding intracranial pathology.
Consider pulmonary embolism and look for signs of DVT.
Check for pulse asymmetry, which can suggest dissection.
Workup
Consider obtaining complete blood count (CBC), basic metabolic panel (BMP), D-dimer (if Wells score is high), prothrombin time/international normalized ratio (PT/INR), B-type natriuretic peptide (BNP), troponin, toxicology screen, urinalysis, and pregnancy test in women.
Look for ECG evidence to suggest an underlying cardiac arrhythmia disorder, which can be subtle (e.g., Wolff-Parkinson-White syndrome, Brugada syndrome, prolonged QT interval, conduction block, left ventricle [LV] hypertrophy, and arrhythmia).
Obtain chest radiograph to evaluate for infectious disease, wide mediastinum, or a finding suggestive of PE.
Consider cardiac ultrasound to assess valves and appropriate contraction or strain.
Consider lung ultrasound to evaluate for pulmonary edema.
Consider pelvic ultrasound if there is concern for ectopic pregnancy.
Consider CT/MRI of the head to rule out stroke or hemorrhage.
Patients with syncope can have concomitant trauma and may need additional imaging.
Management and Disposition
Numerous clinical decision aids can help guide the appropriate disposition of patients with syncope, including the Canadian Syncope Risk Score, the Boston Syncope Rule, and the San Francisco Syncope Rule. (For more on these rules, see the Clinical Rules and Guidance section in this rotation guide.)
Treat suspected etiology. Address airway, breathing, and circulation (ABCs) and emergent situations.
Young patients with a reassuring clinical history, ECG, and physical exam do not need labs and may be discharged home with appropriate return instructions.
Admit high-risk patients for observation and further syncope workup.
Research
Landmark clinical trials and other important studies
Dankiewicz J et al. N Eng J Med 2021.
In this international, multicenter, randomized control trial, investigating the effect of TTM on patients who suffered out-of-hospital cardiac arrest and remained unconscious, there were no differences in all-cause mortality, neurologic outcomes, and quality of life at 6 months between patients who received TTM to 33°C and patients who received targeted normothermia.
![[Image]](content_item_media_uploads/nejmoa2100591_f3.jpg)
Szarpak L et al. Am J Emerg Med 2021.
Although prehospital therapeutic hypothermia may improve patient outcomes after out-of-hospital cardiac arrest, data on efficacy and safety are lacking. In this analysis, therapeutic hypothermia did not improve survival at discharge or neurologic outcome in patients with out-of-hospital cardiac arrest.
![[Image]](content_item_thumbnails/47167.jpg)
Lascarrou J-B et al. N Engl J Med 2019.
In an open-label randomized trial, moderate therapeutic hypothermia (33°C for 24 hours) resulted in a higher percentage of patients who survived with a favorable neurologic outcome using the Cerebral Performance Category scale as compared with targeted normothermia (37°C) for patients with coma admitted to the ICU after resuscitation from cardiac arrest with a nonshockable rhythm. There was no difference in 90-day mortality.
![[Image]](content_item_thumbnails/23931.jpg)
Kearon C et al. N Engl J Med 2019.
This prospective study found that a combination of low clinical pretest probability (C-PTP) and a D-dimer level of <1000 ng/mL identified a group of patients at a low risk for pulmonary embolism during follow-up.
![[Image]](content_item_thumbnails/23930.jpg)
Bledsoe JR et al. Chest 2018.
This prospective cohort study found that outpatient treatment of low-risk patients with PE as assessed by the Pulmonary Embolism Severity Index score was safe and acceptable to patients.
![[Image]](content_item_thumbnails/23932.jpg)
Schenone AL et al. Resuscitation 2016.
This study pooled and compared hypothermic and normothermic outcomes and found increased survival and neuroprotective benefit on patients who underwent therapeutic hypothermia, including nonshockable rhythms, unwitnessed arrest, or persistent shock.
![[Image]](content_item_thumbnails/3990.png)
Watanabe H et al. Sci Rep 2016.
This analysis is based on 22 articles where the D-dimer test showed good accuracy to predict the possibility of acute aortic dissection. The strongest utility was negative predictive value.
![[Image]](content_item_thumbnails/3992.png)
Costantino G et al. Am J Med 2014.
This meta-analysis retrieved relevant articles that used clinical guidelines versus judgment in syncope patients. Results found that prediction tools did not show better sensitivity, specificity, or prognostic yield compared to clinical judgment in predicting short-term serious outcome after syncope.
![[Image]](content_item_thumbnails/3996.png)
Nielsen N et al. N Engl J Med 2013.
In an international trial, authors randomly assigned 950 unconscious adults after out-of-hospital cardiac arrest of presumed cardiac cause to targeted temperature management at either 33°C or 36°C. Results showed that hypothermia at a targeted temperature of 33°C did not confer a benefit as compared with a targeted temperature of 36°C.
![[Image]](content_item_thumbnails/4003.jpg)
Wells PS et al. Ann Intern Med 2001.
This is the original prospective cohort study that determined the Wells PE criteria. This clinical model is used to determine the patient’s pretest probability of pulmonary embolism, then adding the D-dimer assay, it recommends the appropriate workup, thus decreasing the need for diagnostic imaging.
![[Image]](content_item_thumbnails/4004.png)
Reviews
The best overviews of the literature on this topic
Hepburn-Brown M et al. Intern Med J 2019.
![[Image]](content_item_thumbnails/43040.jpg)
Polderman KH and Varon J. Circulation 2018.
![[Image]](content_item_thumbnails/46438.jpg)
Saklani P et al. Circulation 2013.
![[Image]](content_item_thumbnails/23933.jpg)
Upadhye S and Schiff K. Emerg Med Clin North Am 2012.
![[Image]](content_item_thumbnails/3993.png)
Stub D et al. Circulation 2011.
![[Image]](content_item_thumbnails/3991.jpg)
Tapson VF. N Engl J Med 2008.
![[Image]](content_item_thumbnails/3994.jpg)
Guidelines
The current guidelines from the major specialty associations in the field
Nolan JP et al. Intensive Care Med 2021.
![[Image]](content_item_thumbnails/46503.jpg)
Ortel TL et al. Blood Adv 2020.
![[Image]](content_item_thumbnails/43041.jpg)
Callaway CW et al. Circulation 2015.
![[Image]](content_item_thumbnails/31012.jpg)
Raja AS et al. Ann Intern Med 2015.
![[Image]](content_item_thumbnails/4000.png)
Scirica BM. Circulation 2013.
![[Image]](content_item_thumbnails/3998.png)
Peberdy MA et al. Circulation 2010.
![[Image]](content_item_thumbnails/3999.png)
Huff JS et al. Ann Emerg Med 2007.
![[Image]](content_item_thumbnails/4001.png)