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Cardiovascular Emergencies 

Cardiovascular Emergencies
Chapter:
Cardiovascular Emergencies
Author(s):

Ajoy Katari

and Benjamin Kohl

DOI:
10.1093/med/9780199377275.003.0004
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date: 21 September 2020

Arrhythmias: Asystole

Definition

Complete absence of electrical and mechanical cardiac activity.

Presentation

Usually preceded by other arrhythmias. Excessive vagal stimulation can sometimes be the initial trigger, for example, insufflation of the abdominal cavity for laparoscopic surgery or excessive intraocular pressure.

Pathophysiology

Primary asystole has a poor prognosis. Bradycardia is usually caused by conditions such as hypoxia, hyperkalemia or hypokalemia, acidosis, or myocardial infarction.

Immediate Management

  • Confirm asystole in >1 electrocariogram lead.

  • Begin cardiopulmonary resuscitation (CPR).

  • Establish an airway (endotracheal intubation preferred).

  • Administer epinephrine (1 mg every 3–5 minutes) OR

  • Administer vasopressin (40 U within the first 10 minutes of CPR).

  • Administer atropine (1 mg every 3–5 minutes for three doses showed earlier recovery to circulation, but no significant difference in 30-day survival or neurologic outcome).

Differential Diagnosis

  • Monitor lead disconnection

  • Severe bradycardia

  • Ventricular fibrillation

  • Low voltage electrocardiogram (ECG)

Diagnostic Studies

  • ECG

  • Echocardiogram

Subsequent Management

  • Employ reverse of underlying causes (e.g., hypoxia, acidosis).

  • Administer sodium bicarbonate to correct acidosis.

  • Consider temporary transcutaneous or transvenous cardiac pacing.

Risk Factors

  • Hypoxia

  • Electrolyte imbalances (e.g., hyperkalemia)

  • Hypovolemia

  • Hypothermia

  • Ocular surgery

  • Hypersensitive carotid sinus

  • Underlying cardiac conduction abnormalities

Prevention

Early identification of underlying conditions such as hypoxia, acidosis, and ensuing arrhythmias.

Special Considerations

  • Transcutaneous pacing has not been shown to favorably effect survival unless instituted early and is generally considered to be ineffective therapy.

  • Several factors need to be considered to terminate resuscitation efforts. The most commonly used parameters include

    • Duration of resuscitative effort >30 minutes without sustained return of spontaneous circulation (ROSC)

    • Asystole as initial rhythm

    • Advanced age with severe comorbid disease

  • Ensure normothermia before terminating resuscitation.

Further Reading

American Heart Association. Guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 7.2: Management of cardiac arrest. Circulation. 2005; 112: IV-58–IV-66. Atropine sulphate for patients with out-of-hospital cardiac arrest due to asystole and pulseless electrical activity. Circ J. 2011; 75(3): 580.Find this resource:

Arrhythmias: Atrial Fibrillation

Definition

An irregularly irregular heart rhythm with the absence of P waves on ECG. Most common cardiac arrhythmia.

Presentation

  • May be asymptomatic

  • Palpitations

  • Chest pain/angina

  • Congestive heart failure

  • Syncope

  • Transient ischemic attacks

Pathophysiology

Atrial fibrillation may often occur in patients with otherwise normal hearts, but is also associated with excessive alcohol consumption, hypertension, hyperthyroidism, and myocardial ischemia.

Atrial dilatation and fibrosis are the changes that occur most commonly in patients with atrial fibrillation.

Immediate Management

  • Administer synchronized DC cardioversion 150 J (may increase to 360 J) if the patient is unstable, including hypotension, chest pain, lightheadedness.

  • Consider DC cardioversion in stable patients if <48 hours after onset.

Pharmacologic Rate Control (Goal <110 bpm)

  • Beta-blockers (e.g., metoprolol 2.5 mg intravenously [IV] to initiate therapy)

  • Calcium channel blockers (diltiazem 0.25 mg/kg IV × 1 dose)

  • Amiodarone (IV dose of 150 mg × 1 over 10 minutes, follow 1 mg/min for 6 hours, and 0.5 mg/min for 18 hours)

  • Digoxin (only preferred when in heart failure or as second-line therapy)

Differential Diagnosis

  • Sinus tachycardia

  • Multifocal atrial tachycardia

  • Reentrant tachycardia

  • Junctional tachycardia

  • Atrial flutter

Diagnostic Studies

  • ECG

  • Electrophysiology study

  • Echocardiogram

  • Holter monitoring

Subsequent Management

  • Refer for electrophysiology study

  • If atrial fibrillation (AF) continues, request a cardiology consultation for antiarrhythmic therapy or DC cardioversion

  • Electrophysiology and cryoablation

  • Surgical ablation

  • If AF continues for >48 hours, initiate anticoagulation to decrease the risk of stroke

Risk Factors

  • Age (8% of people >80)

  • Recent cardiothoracic surgery (particularly valvular surgery)

  • Atrial dilatation

  • Hyperthyroidism

  • Males are at greater risk than females

  • Smoking

  • Alcohol consumption

  • Coronary artery disease

  • Stress

Prevention

  • Avoid discontinuing beta-blockers in the perioperative period

  • Maintain normal electrolyte values (particularly potassium and magnesium)

Special Considerations

  • Atrial fibrillation increases the risk of stroke by 700%.

  • Cardioversion is indicated for atrial fibrillation (<48 hours after onset) or if a transesophageal echocardiogram shows no evidence of thrombus.

  • Atrioventricular (AV) nodal blockers (Verapamil, Digoxin) are contraindicated in atrial fibrillation with pre-excitation rhythms (e.g., AV nodal re-entry or Wolff-Parkinson-White syndrome). Check for delta-wave on ECG.

Further Reading

American Heart Association. Guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 7.3: Management of symptomatic bradycardia and tachycardia. Circulation. 2005; 112: IV-67–IV-77.Find this resource:

Echahidi N. Mechanisms, prevention, and treatment of atrial fibrillation after cardiac surgery. J Am Coll Cardiol. 2008; 51: 793–801.Find this resource:

National Institute for Health and Clinical Excellence Guidelines for Atrial Fibrillation. http://www.nice.org.uk/nicemedia/pdf/CG036niceguideline.pdf Accessed August 9, 2009.

Arrhythmias: Bradycardia

Definition

A heart rate <60 beats per minute.

Presentation

  • Hypotension

  • Nausea

  • Altered mental status

  • Pulmonary edema

  • Chest pain

Pathophysiology

May be secondary to cardiac ischemia, atrioventricular node disease, hypoxemia, acidosis, or drugs (e.g., narcotics, beta-blockers).

A sick sinus node or conduction abnormalities may cause bradycardia. The preceding presentations are suggestive of organ malperfusion.

Immediate Management

  • If an iatrogenic cause is suspected (e.g., pressure on the globe, traction on a hernia sac), inform the surgeon and ask him or her to stop.

  • Administer atropine (0.5 mg IV, repeat every 5 minutes to a total dose of 3 mg).

  • If bradycardia is unremitting, begin transcutaneous pacing if there is evidence of tissue hypoperfusion (see page [link]).

Differential Diagnosis

  • Excessive beta or calcium channel blocker therapy

  • Excessive vagal stimulation

  • High dose narcotic administration

  • Hypersensitivity of carotid sinus

  • Excessive intraocular pressure

  • Elevated systemic vascular resistance

  • Hypoxia

  • Acidosis

  • Cardiac tamponade

  • Electrolyte abnormalities

Diagnostic Studies

  • ECG

  • Echocardiogram

  • Angiogram (if acute myocardial infarction is suspected).

Subsequent Management

  • Begin transvenous pacing if transcutaneous pacing fails to capture (see page [link]).

  • Administer epinephrine (2 to 10 mcg/min) or Dopamine (2–10 mcg/kg/min) infusion.

  • Refer the patient for permanent pacemaker implantation.

Risk Factors

  • Obstructive sleep apnea

  • Pharmacologic (alpha-agonists, beta-blockers, calcium channel blockers, narcotics)

  • Ocular surgery

  • Surgery near carotid sinus (e.g., carotid endarterectomy)

  • Laparoscopic surgery

  • Age

  • Elevated blood pressure

  • Elevated cholesterol

  • Smoking

  • Heavy alcohol consumption

  • Use of recreational drugs

  • Psychological stress or anxiety

Prevention

  • Maintain normal electrolytes.

  • Ask the surgeon to inject the carotid sinus with lidocaine during carotid endarterectomy.

  • Use alpha-agonist agents cautiously.

Special Considerations

  • Atropine works at the AV node and is unlikely to be effective on bradycardia due to a block below the bundle of His. Glucagon 3 mg IV followed by a 3-mg/h drip can be used if bradycardia is attributed to beta-blocker therapy.

Further Reading

American Heart Association. Guidelines for cardiopulmonary resuscitation and emergency cardiovascular Care. Part 7.3: Management of symptomatic bradycardia and tachycardia. Circulation. 2005; 112: IV-67–IV-77.Find this resource:

Arrhythmias: Narrow Complex Tachycardia

Definition

Heart rate >100 beats per minute (bpm) (may be regular or irregular) with a narrow QRS complex (<120 msec)

Presentation

  • Hypotension

  • Palpitations

  • Altered mental status

  • Chest pain

  • Pulmonary edema

Pathophysiology

A narrow QRS complex implies rapid activation of the ventricles via the normal His-Purkinje system and suggests that the arrhythmia originates within or above the AV node (i.e., supraventricular). Narrow QRS complex tachycardia is most commonly either sinus or reentrant tachycardia (e.g., Wolff-Parkinson-White syndrome).

Immediate Management

  • Administer adenosine (6 mg rapid IV push, repeat 12 mg × 2).

  • Stable regular narrow complex tachycardia: Treat underlying cause (e.g., fever, anemia, shock, sepsis, pain).

  • Stable irregular narrow-complex tachycardias: Control heart rate with diltiazem (15 mg IV over 20 minutes) or metoprolol (5 mg IV).

  • Consider DC cardioversion if hemodynamically unstable.

  • Unstable non-sinus arrhythmias must be treated with DC cardioversion.

  • Unstable sinus arrhythmias can be treated with beta-blockers. (Consider a short-acting agent such as esmolol 1000 mcg/kg IV bolus for immediate or 500 mcg/kg bolus for more gradual control.)

Differential Diagnosis

  • Sinus tachycardia

  • Atrial tachycardia

  • Multifocal atrial tachycardia

  • Re-entrant tachycardia (e.g., Wolff-Parkinson-White syndrome)

  • Junctional tachycardia

  • Atrial fibrillation

  • Atrial flutter

Diagnostic Studies

  • ECG

  • Echocardiography

Subsequent Management

  • If adenosine fails, initiate rate control with either intravenous calcium-channel blockers or betablockers (diltiazem 0.25 mg/kg IV × 1, escalate to 0.35 mg/kg IV after 15 minutes if unsuccessful on first dose).

  • Chemical cardioversion: Administer procainamide (50 mg/min IV, up to a dose of 18–20 mg/kg) or amiodarone (5 mg/kg IV over 15 minutes).

  • Perform DC cardioversion for tachycardia resistant to pharmacologic interventions and/or in patients who are hemodynamically unstable.

  • Refer to the cardiology service for electrophysiology testing and possible ablation.

Risk Factors

  • Fever

  • Inadequate anesthesia

  • Hypovolemia

  • Myocardial ischemia

  • Hyperthyroid

  • Vagolytic drugs

Prevention

  • Maintain normothermia

  • Maintain normovolemia (adequate fluid resuscitation)

  • Avoid discontinuing beta-blockers in the perioperative period

  • Avoid using vagolytic drugs (e.g., atropine, pancuronium)

Special Considerations

  • Regular narrow complex tachycardia is most often sinus tachycardia.

  • Irregular narrow complex tachycardia may be atrial flutter, atrial fibrillation, or multifocal atrial tachycardia.

  • Transient chest discomfort, dyspnea, and flushing may occur when adenosine is administered.

  • Consider the risk of embolic stroke before cardioversion.

Further Reading

American Heart Association. Guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 7.3: Management of symptomatic bradycardia and tachycardia. Circulation 2005; 112: IV-67–IV-77.Find this resource:

Arrhythmias: Ventricular Fibrillation

Definition

A nonperfusing rhythm of the ventricles with disorganized and noncoordinated electrical activity.

Presentation

Either a witnessed cardiac arrest or noted on the ECG.

Pathophysiology

Usually secondary to myocardial ischemia or underlying conditions such as hypoxia and acidosis.

Immediate Management

  • Deliver a 360 J monophasic (200 J biphasic) cardioversion: may repeat every 2 minutes if necessary. (Avoid delay—administer shocks before airway management.)

  • If the airway is not secured, ventilate the patient with a self-inflating bag and mask. Intubate the trachea and ventilate with a self-inflating bag when feasible.

  • Begin cardiopulmonary resuscitation after shock to maintain 30:2 ratio for 2 minutes without pausing to check rhythm or pulse.

  • Administer epinephrine 1 mg IV (repeat every 3–5 minutes) OR 40 U IV vasopressin (single dose, replaces first or second dose of epinephrine).

Differential Diagnosis

  • Drug toxicity (cocaine, digitalis, antidepressants)

  • Pulmonary embolism

  • Hypoxia

  • Acidosis

  • Cardiac tamponade

  • Electrolyte abnormalities (hyperkalemia/hypokalemia)

  • Hypovolemia

  • Shivering

Diagnostic Studies

  • ECG

  • Serum electrolyte levels

  • Arterial blood gas

  • Cardiac enzymes

  • Echocardiogram

Subsequent Management

  • Airway management, secure endotracheal tube, and place on ventilator

  • ACLS secondary survey

  • Administer amiodarone 300 mg IV. (Repeat 150 mg in 3–5 minutes if VF/PVT persists.)

  • Administer lidocaine (if amiodarone unavailable) 1.0–1.5 mg/kg IV, may repeat to a 3 mg/kg max loading dose.

  • Administer magnesium sulfate 1–2 g IV diluted in 10 mL D5W for torsades de pointes or suspected/known hypomagnesemia.

Risk Factors

  • Cardiac comorbidities

  • Advanced disease states

Prevention

  • Early detection of precipitating underlying conditions and therapy.

Special Considerations

  • ACLS guidelines have been updated to emphasize the importance of early defibrillation, hence the recommendation to deliver 360 J instead of an escalating energy. Current guidelines recommend cardioversion before definitive airway management.

Further Reading

American Heart Association. Guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 7.2: Management of cardiac arrest. Circulation. 2005; 112: IV-58–IV-66.Find this resource:

Arrhythmias: Wide Complex Tachycardia

Definition

Heart rate >100 beats per minute (may be regular or irregular) with a wide QRS complex (>120 msec).

Presentation

  • Hypotension

  • Altered mental status

  • Palpitations

  • Chest pain

  • Pulmonary edema

Pathophysiology

A widened QRS complex implies slow ventricular activation. This arrhythmia commonly originates outside of the normal conduction system but may be ventricular or supraventricular. A regular, wide-complex tachycardia is most often ventricular tachycardia.

Immediate Management

  • Synchronized DC cardioversion if the patient is hemodynamically unstable (start at 100 J and escalate to 200 J, then 300 J, and 360 J)

Regular Rhythm

  • Administer amiodarone (150 mg IV given over 10 minutes, repeated as needed to a total of 2.2 g IV over the first 24 hours)

Irregular Rhythm

  • Administer procainamide (20 mg/min IV up to a total of 17 mg/kg)

  • Administer lidocaine (1 mg/kg IV, may repeat 0.5 mg/kg every 5 minutes as needed to total of 3 mg/kg)

Differential Diagnosis

Regular

  • Ventricular tachycardia

  • supraventricular tachycardia with aberrant conduction

  • Monitoring artifact (e.g., while scrubbing a surgical site)

  • Paced rhythm with atrial tachycardia (atrial sense, ventricular paced)

Irregular

  • Atrial fibrillation with aberrancy (bundle branch block),

  • Atrial fibrillation with pre-excitation (e.g., Wolff-Parkinson-White syndrome)

  • Polymorphic ventricular tachycardia

Diagnostic Studies

  • ECG

  • Echocardiogram

  • Electrophysiology testing

Subsequent Management

  • Perform DC cardioversion (start at 100 J and increase to 360 J) for regular tachycardia that is resistant to pharmacologic intervention or if the patient is hemodynamically unstable.

  • In a history of pre-excitation (e.g., Wolff-Parkinson-White syndrome), or evidence of pre-excitation on the ECG (e.g., delta wave), administer procainamide (20 mg/min continuous infusion until the arrhythmia is suppressed, the patient is hypotensive, the QRS widens 50% beyond baseline, or a maximum dose of 17 mg/kg is administered).

Risk Factors

  • Age >50 years

  • Myocardial ischemia or old myocardial infarction

  • Known re-entrant pathway

Prevention

  • Maintain normal electrolyte levels (particularly potassium and magnesium)

  • Anti-arrhythmic (Class I Na+ channel for recurrent cases, Class ll beta blockers reduce mortality from Myocardia Inforction, and class III K+ channel may be beneficial for diabetics) drugs

  • Refer for catheter ablation

  • Refer for implantable cardioverter defibrillator (ICD) implantation

  • Change pacemaker to VVI (or AAI) in at-risk patients

Special Considerations

  • AV nodal blockers are contraindicated in wide complex, irregular tachycardia, especially when the etiology is unknown because they may precipitate ventricular fibrillation. If the patient is stable, further diagnosis is warranted as AVNRT and AVRT (both are types of SVT) require different management and can present as wide complex tachycardia. Although amiodarone is used as an alternative treatment in wide complex tachycardia, it may cause irregular wide complex dysrhythmias due to pre-excitation. Converting to unstable ventricular tachycardia (VT) or ventricular fibrillation (VF).

Further Reading

American Heart Association. Guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 7.3: Management of symptomatic bradycardia and tachycardia. Circulation 2005; 112:IV-67–IV-77.Find this resource:

Cardiac Tamponade

Definition

Compression of the heart due to accumulation of fluid in the pericardial space. (The normal volume of fluid in the pericardial sac is 25–50 mL.) Gradual accumulation allows time for compensation and may not result in symptomatic tamponade; rapid accumulation may be life threatening.

Presentation

  • Dyspnea

  • Orthopnea

  • Tachycardia

  • Jugular venous distention

  • Distant heart sounds

  • Pulsus paradoxus (systolic blood pressure decreases by at least 10 mm Hg during inspiration)

  • Beck’s triad (small, quiet heart, rising venous pressure, and hypotension)

Pathophysiology

External pressure on the heart reduces the ventricular preload.

Immediate Management

  • In the setting of profound hypotension, emergency pericardiocentesis may be necessary.

  • Consider IV fluid administration to increase preload.

  • Maintain heart rate to maintain cardiac output.

  • Maintain normal sinus rhythm.

Differential Diagnosis

Note: Some of these conditions can cause tamponade.

  • Acute myocardial infarction

  • Postoperative bleeding

  • Aortic dissection

  • Iatrogenic (e.g., catheter insertion)

  • Connective tissue disorders

  • Uremia

  • Positive end expiratory pressure (auto-PEEP)

Diagnostic Studies

  • Electrical alternans on ECG (variation of R-wave axis with alternate beats)

  • Globular heart on chest radiography

  • Accumulation of fluid seen on echocardiography

  • Equalization of diastolic pressures in all four chambers of the heart

Subsequent Management

  • Consult a cardiac surgeon for pericardiectomy.

  • Consider using ketamine for induction of general anesthesia (may help to maintain heart rate and blood pressure).

  • Maintain spontaneous ventilation until the pericardial sac is opened.

  • If mechanical ventilation is necessary, use low tidal volume combined with a high rate to minimize intrathoracic pressure.

  • Keep the heart rate high.

  • Maintain adequate preload.

Risk Factors

  • Trauma

  • Myocardial infarction

  • Connective tissue disorders

  • Uremia

Prevention

  • Treat uremic patients early.

  • Ensure early recognition and control of cardiac surgical bleeding.

  • Maintain a high index of suspicion for cardiac injury during pacemaker electrode implantation or removal.

  • Early recognition and intervention are critical to successful management.

Special Considerations

  • Pneumothorax and cardiac perforation may occur during a cardiac window procedure.

  • Pulmonary edema and global systolic dysfunction may occur after drainage of pericardial fluid.

Further Reading

Grocott HP, Gulati H, Srinathan S, Mackensen GB. Anesthesia and the patient with pericardial disease. Can J Anaesth. 2011; 58(10): 952–966.Find this resource:

Soler-Soler J, et al. Management of pericardial effusion. Heart. 2001; 86: 235–240.Find this resource:

Cardiac Trauma

Definition

Penetrating or blunt injury to the myocardium.

Presentation

  • Dyspnea

  • Tachycardia

  • Chest pain

  • Flail chest

Pathophysiology

Severe blunt injury, usually caused by a high-impact force, that causes injury to thoracic organs.

Immediate Management

  • Assess airway, breathing, and circulation.

  • Provide supplemental O2 as required to maintain oxygenation.

  • Intubate the trachea and initiate mechanical ventilation if the patient is in respiratory distress. Note: Airway management may be complicated by concomitant injury to the trachea. Rule out tracheal injury if intubating the patient with direct laryngoscopy.

  • Request a surgical consultation for chest tube insertion and/or pericardiocentesis.

  • Emergency surgery, possibly requiring cardiopulmonary bypass, may be necessary.

  • Provide supportive management as required.

Differential Diagnosis

  • Pulmonary or myocardial contusion

  • Pneumothorax

  • Esophageal tear/rupture

  • Myocardial laceration

  • Cardiac tamponade (see page [link])

  • Thoracic aorta dissection

  • Coronary artery laceration

  • Diaphragmatic injury

Diagnostic Studies

  • Chest X-ray and CT scan

  • Bronchoscopy

  • Esophagoscopy

  • Transesophageal echocardiogram (TEE)

Subsequent Management

  • Request a surgical consultation for possible chest exploration.

  • Evaluate the tracheobronchial tree to rule out a concomitant lung injury.

  • Use lung isolation techniques as required to optimize ventilation.

Risk Factor

  • Trauma

Prevention

Although cardiac trauma is not truly a preventable phenomenon, early recognition and diagnosis of underlying pathology followed by timely intervention may reduce morbidity and mortality.

Special Considerations

  • The use of nitrous oxide should be avoided because an as-yet undiagnosed pneumothorax may exist. Be alert for impaired ventilation of the dependent lung during one-lung ventilation; it may be caused by a tension pneumothorax. Some degree of cardiac injury should be anticipated in patients with blunt chest injury. Monitor the ECG continuously in the postoperative period.

Further Reading

Bastos R, et al. Penetrating thoracic trauma. Semin Thorac Cardiovasc Surg. 2008; 20: 19–25.Find this resource:

Singh KE, Baum VC. The anesthetic management of cardiovascular trauma. Curr Opin Anaesthesiol. 2011; 24(1): 98–103.Find this resource:

Sybrandy KC, et al. Diagnosing cardiac contusion: old wisdom and new insights. Heart. 2003; 89: 485–489.Find this resource:

Congestive Heart Failure

Definition

A structural or a functional cardiac disorder with impaired ability of the ventricle to fill with (diastolic) or eject (systolic) blood.

New York Heart Association (NYHA) classification of severity:

  • Class I—symptoms of heart failure (HF) only at activity levels that would limit normal individuals

  • Class II—symptoms of HF with ordinary exertion

  • Class III—symptoms of HF with less than ordinary exertion

  • Class IV—symptoms of HF at rest

Presentation

  • Dyspnea

  • Fatigue

  • Edema

Pathophysiology

Systolic heart failure is idiopathic in approximately 50% of patients. Etiologies include myocarditis, ischemic heart disease, infiltrative disease (amyloidosis), peripartum cardiomyopathy, hypertension, human immunodeficiency virus (HIV) infection, connective tissue disease, substance abuse, and drugs (e.g., doxorubicin). Diastolic heart failure include all of these, and hypertrophic and restrictive cardiomyopathies.

Immediate Management

  • Increase FiO2 to maintain oxygenation.

  • Administer a loop diuretic (e.g., furosemide 20–40 mg IV).

  • Consider an ACE inhibitor (enalapril 2.5 mg IV every 6 hours).

  • Consider nitroglycerine (infusion starting at 0.5 mcg/kg/min, increase every 3–5 minutes to desired effect).

  • Consider nesiritide (2 mcg/kg IV bolus, then 0.01 mcg/kg/min to a maximum of 0.03 mcg/kg/min).

  • Consider beta-blockers (esmolol 500 mcg/kg over 1 minute, then 50 mcg/kg/min to a maximum of 300 mcg/kg/min).

  • If the patient is awake and can take oral medication, consider angiotensin II receptor blockers (candesartan).

  • Consider an aldosterone antagonist (i.e., spirinolactone).

Differential Diagnosis

  • Myocardial ischemia

  • Primary pulmonary pathology

  • Cardiomyopathy

Diagnostic Studies

  • Chest X-ray with cardiomegaly, Kerley B lines, pleural effusions

  • ECG to rule out ischemic or hypertrophic changes

  • Echocardiogram to evaluate cardiac function

  • Serum brain natriuretic peptide (BNP) level (elevated in heart failure)

Subsequent Management

  • Correction of contributing systemic disease

  • Lifestyle modification

  • Discontinue drugs implicated in HF

  • Specialized management for HF that is refractory to pharmacologic therapy:

    • Implantable cardioverter-defibrillator

    • Cardiac resynchronization therapy

    • Intra-aortic balloon pump (for life-threatening congestive heart failure [CHF])

    • Implantation of left ventricular assist device

    • Referral for heart transplantation

Risk Factors

  • Coronary artery disease

  • Smoking

  • Hypertension

  • Obesity

  • Valvular heart disease

Prevention

Careful fluid management in patient at risk for CHF.

Special Considerations

  • Implantable cardiac defibrillators detect and treat arrhythmias associated with heart failure, and may also be used for cardiac resynchronization therapy with biventricular pacing.

  • Cardiac wraps have been used to stop further dilation of the ventricles, preventing deterioration of heart function.

Further Reading

Hunt SA, et al. 2009 Focused update incorporated into the ACC/AHA 2005 guidelines for the diagnosis and management of heart failure in adults: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines developed in collaboration with the International Society for Heart and Lung Transplantation. J Am Coll Cardiol. 2009; 53(15): e1–e90.Find this resource:

Hypertension

Definition

A blood pressure >160/100 in a patient who is otherwise normotensive.

Presentation

  • Chest pain

  • Headache

  • Palpitations

  • Stroke

  • Pulmonary edema

Pathophysiology

The pathophysiology of hypertension is often multifactorial. Anything that increases preload, afterload, or contractility can cause hypertension.

Immediate Management

  • Increase depth of anesthesia.

  • Check for medication error.

  • Administer incremental doses of a beta-blocker (e.g., labetalol 5 mg IV) if the heart rate is >60. Note: Labetalol is preferred because it has both alpha- and beta-blocking properties.

  • If the heart rate is <60, administer hydralazine 5–10 mg IV in incremental doses.

  • Administer nicardipine: Start at 5 mg/h IV and increase by 2.5 mg/h every 5–15 minutes. Maximum dose is 15 mg/h.

  • Administer sodium nitroprusside for acute, life-threatening hypertension: Start at 0.3 mcg/kg/min and increase slowly. The maximum dose is 10 mcg/kg/min.

Differential Diagnosis

  • Inadequate anesthetic depth

  • Agitation

  • Vasopressor error (inadvertent administration or wrong dose)

  • Pheochromocytoma

  • Thyrotoxicosis

  • Aortic cross-clamp

  • Elevated intracranial pressure

  • Transection of the spinal cord at or above T5

  • Eclampsia in pregnancy

  • Electroconvulsive therapy

Diagnostic Studies

  • ECG

  • Echocardiogram

  • Intra-arterial catheter for continuous blood pressure monitoring

Subsequent Management

  • Request an internal medicine or cardiology consultation for workup and chronic treatment with long-acting beta-blockers, ACE inhibitors, angiotensin receptor blockers.

  • Administer anxiolytics if appropriate.

Risk Factors

  • Age >60 years

  • Males are at greater risk than are females.

  • Race

  • Weight

  • Stress

  • Alcohol

  • Smoking

  • Family history

  • Renal disease

  • Diabetes

  • Sleep apnea

Prevention

  • Maintain adequate depth of anesthesia.

  • Avoid rapid termination of antihypertensive medications.

Special Considerations

  • An acute rise is of more significance than the actual numbers, but systolic values >220 mm Hg and diastolic values >120 mm Hg must be treated promptly.

  • Elevated blood pressure in patients with chronic hypertension should be decreased by no more than 20%–30% of baseline to compensate for a rightward shift of the autoregulation curve.

Further Reading

Laslett L. Hypertension-preoperative assessment and perioperative management. West J Med. 1995; 162: 215–219.Find this resource:

Varon J. The diagnosis and treatment of hypertensive crisis. Postgrad Med. 2009; 121: 5–13.Find this resource:

Hypotension

Definition

Low systemic blood pressure that may be insufficient to maintain end-organ perfusion. Criteria vary with the patient and surgical setting, but commonly accepted definitions include:

  • Systolic blood pressure <80 mm Hg

  • Mean arterial blood pressure <60 mm Hg

  • Decline of systolic blood pressure (SBP) or mean arterial pressure (MAP) by 20% from baseline

Presentation

  • Chest pain

  • Short of breath

  • Nausea

  • Altered mental status

  • Oliguria

Pathophysiology

The pathophysiology is often multifactorial. Anything that decreases preload, afterload, or contractility can cause hypotension.

Immediate Management

  • Administer IV fluid.

  • Check for medication error (e.g., drug overdose or swapped syringe).

  • Administer ephedrine 5 mg IV bolus (may repeat as necessary).

  • Administer phenylephrine 100 mcg IV bolus (may repeat as necessary).

  • Epinephrine 5–10 mcg IV bolus (may repeat as necessary).

Differential Diagnosis

  • Deep level of anesthesia

  • Hypovolemia

  • Vasodilation caused by spinal or epidural anesthesia

  • Anaphylaxis

  • Pericardial tamponade

  • Pnuemothorax

  • Acute heart failure

  • Endocrine dysfunction

Diagnostic Studies

  • ECG

  • Echocardiogram

  • Intra-arterial catheter for continuous blood pressure (BP) monitoring

Subsequent Management

  • Treat the underlying cause (e.g., fluid resuscitation, discontinue vasodilating drugs)

  • If unresponsive to catecholamines, consider vasopressin 40-µ IV bolus

  • Administer corticosteroids if adrenal insufficiency is suspected: hydrocortisone 100 mg IV in adults.

Risk Factors

  • Dehydration

  • Age >65 years

  • Beta-blocker or calcium channel blocker therapy

  • Neuraxial analgesia

  • Cardiac disease

  • Medications

Prevention

  • Maintain normovolemia: Provide adequate fluid resuscitation during surgery.

  • Monitor the level of spinal and epidural anesthetics.

  • Administer vasodilating medications slowly (e.g., protamine, vancomycin).

Special Considerations

  • Hypotension can be caused by a myriad of abnormalities. Rapid differential diagnosis can narrow the therapeutic options and improve patient outcome.

Further Reading

American Heart Association. Guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 7.4: Monitoring and medications. Circulation. 2005; 112: IV-78–IV-83.Find this resource:

Myocardial Ischemia

Definition

Oxygen supply inadequate to meet myocardial demand.

Presentation

  • Chest pain, pressure, or tightness often localized behind the sternum

  • Radiates to either arm, neck, jaw, back or abdomen

  • Usually associated with increase in either physical or emotional activity

  • Dysrhythmias, ST segment changes, or hypotension may be the only findings in an anesthetized patient.

Pathophysiology

Myocardial ischemia may be caused by coronary obstruction (physical obstruction from plaque and/or thrombus, or physiologic from coronary spasms), decreased oxygen carrying capacity, or decreased coronary perfusion pressure.

Immediate Management

  • Administer supplemental O2 to maintain SpO2 >90%.

  • Administer oral nitroglycerine 0.4 mg sublingual or 0.5 mcg/kg/min IV (starting dose). Note: Nitroglycerine is contraindicated in patients with systolic pressure <90 mm Hg, diastolic pressure <30 mm Hg, or severe bradycardia.

  • Administer morphine 1- to 2-mg IV boluses to control pain if the patient is awake.

  • Administer beta-blockers (e.g., labetalol 5-mg IV bolus, esmolol 50 mcg/kg/min) to decrease heart rate and blood pressure. (Decrease myocardial oxygen demand.)

  • Request an emergency cardiology consult for possible thrombolysis or stenting.

  • Discuss anticoagulation with the surgical service. If safe:

    • Administer aspirin 325 mg chewed and swallowed.

    • Begin a heparin infusion or (60 U/kg bolus, 12 U/kg/h).

    • Administer a loading dose of clopidogrel 600 mg PO if possible.

    • Manage arrhythmias aggressively.

    • Consider fibrinolysis (tenecteplase within 30 minutes, only for ST segment elevation myocardial infarction [STEMI]).

Differential Diagnosis

  • Heartburn/dyspepsia

  • Myopathic pain

  • Thoracic (bone and cartilage) or pleuritic pain

Diagnostic Studies

  • ECG

  • Echocardiogram

Subsequent Management

  • Refer the patient for primary percutaneous coronary intervention (coronary angioplasty and/or stents).

  • Percutaneous cardiopulmonary support (pacemaker, intra-aortic balloon pump) if the patient is hemodynamically stable.

  • Prepare for emergency coronary artery bypass grafting (CABG) to preserve myocardium if the patient is unstable or percutaneous therapy is contraindicated or unavailable.

  • Long-term care should include antiplatelet therapy (e.g., clopidogrel) to reduce mortality.

Risk Factors

  • Age >50 years

  • Males are at greater risk than females.

  • Pre-existing hypertension

  • Pre-existing diabetes mellitus

  • Hyperlipidemia

  • History of smoking

  • Family history

  • Illicit drug use (cocaine)

Prevention

Maintain normal hemodynamics and monitor at-risk patients carefully.

Special Considerations

  • Mortality for emergency CABG for acute coronary syndrome (due to left main coronary) is approximately 9%.

  • Although outcomes of emergency CABG intervention remain unclear for acute myocardial infarction (MI), cardiogenic shock prior to CABG intervention has been identified as a significant predictor of mortality.

  • Despite concerns of excessive bleeding during CABG, clopidogrel is recommended as an early intervention (on admission), even for those who ultimately undergo CABG.

Further Reading

American Heart Association. Guidelines for cardiopulmonary resuscitation and emergency cardiovascular care. Part 8: Stabilization of the patient with acute coronary syndromes. Circulation 2005; 112: IV-89–IV-110.Find this resource:

American Heart Association Task Force on Guidelines. 2013 ACCF/AHA guideline for the management of ST-elevation myocardial infarction: executive summary. J Am Coll Cardiol. 2013; 61(4): 485–510.Find this resource:

Rao AK, Pratt C, Berke A, Jaffe A, Ockene I, Schreiber TL, Bell WR, Knatterud G, Robertson TL, Terrin ML Thrombolysis in Myocardial Infarction (TIMI) Trial—phase I: hemorrhagic manifestations. J Am Coll Cardiol. 1988; 11(1): 1–11.Find this resource:

Postoperative Hemorrhage

Definition

Excessive bleeding in the postoperative period (>300 mL/h in the first few hours after surgery).

Presentation

  • Increased output from chest tubes or other drains

  • Hemodynamic instability

Pathophysiology

Coagulopathy after cardiothoracic surgery may be a result of anticoagulation therapy, resulting in chest wall bleeding. Inadequate surgical hemostasis resulting in suture line bleeds and elevated blood pressure causing generalized bleeding, are also contributory.

Immediate Management

  • Immediately notify the surgical team if bleeding is >300 mL/h over the first few hours. The patient may require emergency surgery.

  • Send blood for laboratory coagulation studies (e.g., prothrombin time [PT], international normalized ratio [INR], platelet count, fibrinogen level). Transfuse factors or platelets as necessary to correct.

  • Correct hypothermia (may interfere with coagulation)

  • Fluid resuscitate with crystalloid or blood products as necessary. Note: If the patient is rapidly bleeding, it may be necessary to activate the rapid transfusion protocol.

Differential Diagnosis

  • Hypovolemia

  • Cardiac dysfunction

  • Pericardial tamponade

Diagnostic Studies

  • Coagulation studies

  • Temperature

Subsequent Management

  • Blood component therapy

  • Antifibrinolytic therapy

Risk Factors

  • Elevated blood pressure

  • Inadequate surgical hemostasis

  • Coagulopathies

  • Hypothermia

Prevention

  • Adequate surgical hemostasis is the best prevention.

  • Adequate reversal of heparin (with protamine) confirmed with activated clotting time (ACT) is mandatory. Adjuncts like fibrin glue at specific surgical sites can be useful.

Special Considerations

  • If chest tube output decreases suddenly, carefully examine them for clots. Occluded chest tubes may cause cardiac tamponade. If the patient is requiring massive transfusion, follow the ionized calcium level and correct as necessary. Avoid hypothermia by warming all infusions. Consider using scopalamine, midazolam, or ketamine to sedate patients who are hypovolemic and hemodynamically unstable.

Further Reading

Despotis G, et al. Prediction and management of bleeding in cardiac surgery. J Thromb Haemost. 2009; 7(Suppl 1): 111–117.Find this resource:

Pulmonary Embolism

Definition

Material (e.g., thrombus, air, fat) that travels from a primary site (e.g., deep veins of the lower extremities for thrombus) and eventually becomes lodged in the pulmonary artery or its branches.

Presentation

  • Minor pulmonary emboli may be undetected.

  • Massive pulmonary emboli usually cause sudden, severe pulmonary and hemodynamic compromise, which most commonly includes tachycardia, tachypnea, and rales.

  • Classic triad is dyspnea, hemoptysis. and chest pain (in an awake patient).

  • Increased central venous pressure, coupled hypoxia, hypocapnea, and respiratory acidosis on ABG, especially when coupled with a sudden decrease in end-tidal CO2.

  • Cyanosis

Pathophysiology

More than 95% of pulmonary thrombi are from lower extremity deep vein system. Sluggish blood flow combined with vein wall pathology and a hypercoagulable state are the usual etiologies.

Immediate Management

  • If possible, begin anticoagulation (e.g., begin a heparin infusion. Administer heparin 5000 units IV bolus followed by an infusion of 1000 U/h).

  • Thrombolytic therapy

  • Hemodynamic support and resuscitation

Differential Diagnosis

  • Acute myocardial infarction

  • Severe bronchospasm

  • Anaphylaxis

  • Pneumothorax

Diagnostic Studies

  • D-dimer assays (negative predictive value)

  • Helical CT scan

  • Echocardiography (to evaluate right ventricular dilation and strain)

  • Evidence of right ventricular strain or right bundle branch block on ECG

  • Ventilation perfusion scan

  • Pulmonary angiogram

Subsequent Management

  • Femoral-femoral bypass may be required for cardiopulmonary support

  • Surgical embolectomy

  • Inferior vena cava filter implantation

Risk Factors

  • Virchow’s triad:

    • Coagulation anomalies

    • Venous stasis of blood

    • Vein wall pathology

Prevention

  • Deep venous thrombosis prophylaxis with anticoagulation and compressive stockings

  • IVC filter

Special Considerations

  • Surgical embolectomy has a high mortality.

  • Brain natriuretic peptide elevation predicts right ventricular dysfunction and mortality.

  • Elevated troponins are similarly associated with higher mortality.

Further Reading

DeLoughery TG. Venous thrombotic emergencies. Emerg Med Clin North Am. 2009; 27(3): 445–458.Find this resource:

Thoracic Aortic Dissection

Definition

Dissection of the intimal and medial layers of the thoracic aortic wall by penetrating blood. Type A dissections involve the ascending aorta, whereas Type B dissections involve the descending aorta.

Presentation

  • Chest pain

  • Back pain (often described as “ripping”)

  • Congestive heart failure with aortic insufficiency

  • Pericardial tamponade

  • Elevated blood pressure

  • Dyspnea and hoarseness caused by compression of the recurrent laryngeal nerve compression or trachea

  • Hemoptysis caused by tracheal erosion

  • Myocardial ischemia

Pathophysiology

Blood most commonly penetrates an intimal tear and separates the intima and media. This differs from an aneurysm, in which all three layers of the vessel wall are dilated. Tears in the ascending aorta and aortic arch make up 70% of all dissections. Vasa vasorum rupture has been implicated in a minority of cases without intimal tear.

Immediate Management

  • Administer vasodilators to maintain systolic BP 105–115 mm Hg (e.g., nicardipine infusion starting at 5 mg/h or nitroprusside infusion starting at 0.25 mcg/kg/min).

  • Administer beta-blockers (e.g., labetalol or esmolol infusion) to control heart rate. Goal is 60–80 bpm.

  • Transfuse packed red cells and/or coagulation factors as necessary.

  • Refer the patient to a cardiothoracic surgeon for emergency repair.

Differential Diagnosis

  • Acute myocardial infarction

  • Cardiogenic shock

  • Pancreatitis

  • Thoracic outlet syndrome

Diagnostic Studies

  • Chest X-ray (mediastinal width >8 cm, look for >5-mm space between aortic arch and the calcified aortic intima)

  • Computed tomography scan of the chest

  • Transesophageal echocardiography

  • Angiogram

Subsequent Management

Continuous assessment of organ function is important. Neurologic changes, deteriorating kidney function, and gastrointestinal perfusion (which may manifest as metabolic acidosis) are all indications for acute surgical intervention.

Risk Factors

  • Hypertension

  • Age >60 years

  • Males are at greater risk than females.

  • Marfan syndrome and other connective tissue disorders

  • Pregnancy

Prevention

Aggressive control of blood pressure prevents further injury.

Special Considerations

  • Surgical mortality is >30%. Untreated 2-day mortality is 50% and 6-month mortality is as high as 90%.

  • Preoperative pain medication should be used judiciously to permit evaluation of the patient’s neurologic status. Neurologic deterioration may be the first sign of propagation of dissection into the neck.

  • A balance between full-stomach precautions requiring rapid sequence induction and slow, controlled induction to maintain hemodynamic stability is required.

  • Femoral artery cannulation may be required if the entire ascending aorta is involved, so as to allow for perfusion of the major vessels.

  • Left radial artery is preferred for insertion of an intra-arterial catheter in patients with ascending aortic dissections because the right subclavian artery may be involved.

Further Reading

Kohl BA, McGarvey ML. Anesthesia and neurocerebral monitoring for aortic dissection. Semin Thorac Cardiovasc Surg. 2005; 17(3): 236–246.Find this resource:

Subramanian S, Roselli EE. Thoracic aortic dissection: long-term results of endovascular and open repair. Semin Vasc Surg. 2009; 22(2): 61–68.Find this resource:

Valvular Disease: Aortic Regurgitation

Definition

Abnormalities in the leaflets or supporting structures of the aortic valve, resulting in retrograde flow into the left ventricle during diastole.

Presentation

  • Dyspnea

  • Fatigue

  • Palpitations

  • Angina

Pathophysiology

Aortic insufficiency leads to increased LV systolic and diastolic volumes. A regurgitant fraction of <40% is well tolerated with minimal symptoms. As regurgitation approaches 60%, LV end-diastolic pressure (LVEDP) increases. LVEDP gradually increases indicating worsening dilation and hypertrophy of the LV and eventually leads to pulmonary edema.

Immediate Management

  • Mildly vasodilate the patient to minimize afterload and promote

  • forward flow (e.g., Begin a nicardipine infusion, start at 5 mg/h)

  • Avoid anesthetic induction with ketamine (may increase afterload).

  • Administer fluid to maintain preload.

  • Increase heart rate (goal 90 bpm) to minimize diastolic time.

Differential Diagnosis

  • Other causes of diastolic murmurs (e.g., mitral stenosis)

  • Pulmonary edema

  • Coronary artery disease

  • Congestive heart failure

Diagnostic Studies

  • ECG

  • Echocardiogram

  • Refer for coronary angiography.

Subsequent Management

  • Decreased afterload with by administering vasodilators

  • Refer for aortic valve repair or replacement.

Risk Factors

  • Marfan syndrome

  • Bacterial endocarditis

  • Cystic medionecrosis

  • Trauma

  • Aortic dissection

  • Bicuspid aortic valve

Prevention

Early detection and medical management of symptoms.

Special Considerations

Regurgitant fraction is calculated as

Regurgitant Fraction=Backward flowTotal Flow

Total flow = (End diastolic volume – End systolic volume) × HR

Forward flow = Cardiac output

Backward flow = Total flow – forward flow

An intra-aortic balloon pump is contraindicated in patients with significant aortic insufficiency.

Further Reading

Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP 3rd, Guyton RA, O’Gara PT, Ruiz CE, Skubas NJ, Sorajja P, Sundt TM 3rd, Thomas JD; American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014; 63(22): 2438–2488.Find this resource:

Valvular Disease: Aortic Stenosis (AS)

Definition

Narrowing of the aortic valve diameter at the valvular, subvalvular or suprvalvular level. Normal valve area is 2.6–3.5 cm2. Aortic stenosis is graded as mild (1.5–2.5 cm2), moderate (1.0–1.4 cm2), severe (0.6–0.9 cm2), or critical (<0.6 cm2).

Presentation

  • Angina

  • Syncope

  • Dyspnea

Pathophysiology

A congenital bicuspid valve is the major predisposing factor (>75% of cases) followed by rheumatic fever and senile calcific degeneration.

Mild aortic stenosis leads to left ventricular hypertrophy and increased left ventricular systolic and end-diastolic pressures to compensate for increased resistance to flow. Progression of left ventricular dilation and hypertrophy further increases left ventricular end diastolic volume and increase workload. This eventually leads to pulmonary edema and increases the risk of sudden death.

Immediate Management

  • Treat hypotension immediately with a vasoconstrictor (e.g., phenylephrine 100-mcg IV bolus).

  • Maintain normovolemia.

  • Avoid drugs that decrease systemic vascular resistance.

  • If necessary, begin a phenylephrine infusion to augment preload and maintain afterload (starting dose 0.5 mcg/kg/min).

  • Decrease heart rate (goal is 50–70 bpm)

  • Preserve sinus rhythm: Immediate cardioversion for supraventricular dysrhythmias

Differential Diagnosis

  • Pulmonary hypertension

  • Coronary artery disease

  • Congestive heart failure

  • Systolic murmurs (mitral regurgitation)

Diagnostic Studies

  • ECG

  • Echocardiogram

  • Chest radiograph

Subsequent Management

  • Afterload reduction is not helpful because the stenotic valve resists forward flow.

  • Administer alpha-adrenergic agents to treat hypotension because they maintain systemic vascular resistance (SVR). A high SVR ensures that diastolic pressure is sufficient to perfuse the hypertrophied myocardium.

  • Patients with aortic stenosis do not usually tolerate beta-blockade well because beta-blockers decrease myocardial contractility. They may be beneficial in a patient with idiopathic hypertrophic subaortic stenosis (which is a dynamic stenosis).

  • Patients with critical AS should be monitored intraoperatively with with transesophageal echocardiography.

Risk Factors

  • Bicuspid aortic valve

  • History of rheumatic fever

  • Age >70 years

  • Males are at greater risk than females.

Prevention

Early detection and medical management of symptoms.

Special Considerations

  • LV dysfunction (i.e., CHF) in patients with aortic stenosis is associated with high risk for sudden death.

  • Myocardial hypertrophy is a risk factor for subendocardial ischemia. Myocardial ischemia may be difficult to detect because ECG signs of left ventricular hypertrophy may mask ischemic changes.

Further Reading

Frogel J, Galusca D. Anesthetic considerations for patients with advanced valvular heart disease undergoing noncardiac surgery. Anesthesiol Clin. 2010; 28(1): 67–85.Find this resource:

Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP 3rd, Guyton RA, O’Gara PT, Ruiz CE, Skubas NJ, Sorajja P, Sundt TM 3rd, Thomas JD; American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014; 63(22): 2438–2488.Find this resource:

Valvular Disease: Mitral Regurgitation (MR)

Definition

  • Blood flowing backward from the left ventricle into the left atrium during systole. Regurgitant fraction = regurgitant volume/LV stroke volume

  • Mild MR: Regurgitant fraction <30%

  • Moderate MR: Regurgitant fraction 30%–60%

  • Severe MR: Regurgitant fraction >60%

Presentation

  • Fatigue

  • Dypnea

  • Orthopnea

Pathophysiology

  • Mitral regurgitation (MR) can be primary (due to a defective valve) or secondary (due to LV dilation). The most common cause of MR is mitral valve prolapse. Myocardial infarction with papillary muscle dysfunction may also present as acute onset MR.

  • Acute MR leads to increased left atrial volumes and pressures, which are transmitted to the pulmonary circuit. Compensatory tachycardia maintains cardiac output at the expense of increased myocardial oxygen demand.

  • Chronic, slow onset MR causes compensatory left ventricular hypertrophy and left atrial dilation. This maintains forward flow and normal pressures to the pulmonary circuit, and is responsible for the relative absence of symptoms. When the regurgitant fraction increases to 60%, the hypertrophic and dilated LV is unable to compensate and heart failure ensues.

Immediate Management

To ensure forward flow:

  • Maintain preload

  • Avoid bradycardia (increases LV and regurgitant volume)

  • Decrease afterload (e.g., vasodilator such as hydralazine 10 mg IV)

  • Avoid further increases in pulmonary vascular resistance (hypoxia, hypercapnea, acidosis)

Differential Diagnosis

  • Primary pulmonary hypertension

  • Myocardial ischemia

  • Cardiomyopathy

Diagnostic Studies

  • Echocardiogram

  • Giant V wave on pulmonary artery occlusion pressure tracing

Subsequent Management

  • Consider nitric oxide is a pulmonary vasodilator

  • Consider prostaglandin E1

  • Refer for surgical intervention

Risk Factors

  • Mitral valve prolapse

  • Myocardial ischemia with papillary muscle dysfunction

  • Bacterial endocarditis

Prevention

Once LV dysfunction has become established, it may be irreversible; early intervention offers the best chance of a good outcome.

Special Considerations

  • Atrial fibrillation occurs in approximately 75% of cases of MR.

Further Reading

Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP 3rd, Guyton RA, O’Gara PT, Ruiz CE, Skubas NJ, Sorajja P, Sundt TM 3rd, Thomas JD; American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014; 63(22): 2438–2488.Find this resource:

Valvular Disease: Mitral Stenosis (MS)

Definition

  • Normal valve area 4–6 cm2 (valve index 4–4.5 cm2/m2)

  • Symptomatic at 1.5–2.5 cm2 (valve index 1–2 cm2/m2)

  • Critical <1 cm2

  • Incompatible with life <0.3 cm2

Presentation

  • Dyspnea

  • Fatigue

  • Palpitations

  • Paroxysmal nocturnal dyspnea

  • Hemoptysis

  • Angina

Pathophysiology

  • Usually secondary to rheumatic heart disease, which causes fusion of valvular commissures and progressive scarring.

  • Mild disease can be asymptomatic if physiologic compensation is adequate. Increased filling pressure in the left atrium with mild mitral stenosis is not usually transmitted to the pulmonary circulation. Gradually progression of stenosis increases pulmonary vascular resistance and right ventricle pressure. Hypertrophy and dilation of the RV further compromise LV function by shifting the interventricular septum toward the LV, decreasing LV volumes.

Immediate Management

  • Maintain preload (increases can precipitate pulmonary edema)

  • Slow heart rate (maximize time spent in diastole)

  • Maintain pulmonary vascular resistance (avoid increases in pulmonary vascular resistance caused by by hypoxia, hypercarbia, and acidosis)

  • Maintain sinus rhythm: Treat arrhythmias immediately with DC cardioversion.

Differential Diagnosis

  • Primary pulmonary hypertension

  • Other causes of diastolic murmurs (e.g., aortic regurgitation)

  • Myocardial ischemia

Diagnostic Studies

  • Transesophageal echocardiogram

  • Pulmonary artery catheter—large A wave on PA tracing

Subsequent Management

  • Afterload reduction is not helpful because the proximal stenosis at the mitral valve is the limiting factor.

  • AV pacing with long PR intervals (to allow adequate filling) may be necessary.

  • Begin treatment with beta-blockers.

  • Maintain sinus rhythm.

  • Refer the patient for surgical intervention.

Risk Factors

  • Females are at greater risk than males.

  • History of rheumatic fever

Prevention

Early detection and medical management of symptoms and early intervention to avoid irreversible ventricular dysfunction.

Special Considerations

  • Atrial contraction contributes to the LV stroke volume and is extremely important because it could be as high as 30% of the stroke volume.

  • Even though mitral commisurotomy results in a restonosis rate of 30% in 5 years, early morbidity is lower than that of valve replacement.

Further Reading

Nishimura RA, Otto CM, Bonow RO, Carabello BA, Erwin JP 3rd, Guyton RA, O’Gara PT, Ruiz CE, Skubas NJ, Sorajja P, Sundt TM 3rd, Thomas JD; American College of Cardiology/American Heart Association Task Force on Practice Guidelines. 2014 AHA/ACC guideline for the management of patients with valvular heart disease: executive summary: a report of the American College of Cardiology/American Heart Association Task Force on Practice Guidelines. J Am Coll Cardiol. 2014; 63(22): 2438–2488.Find this resource:

Venous Gas Embolism

Definition

Gas bubbles in the blood stream (usually in the venous system) that interrupt blood flow.

Presentation

  • In an awake patient, the earliest signs include coughing and chest pain.

  • Arterial desaturation

  • Decreased end-tidal CO2

  • If systemic embolization occurs, ischemic changes may be seen on the ECG.

  • In awake patients, acute neurologic deficits may be noted.

  • The surgeon may note bubbles in arterial blood.

  • If a large volume of gas is rapidly entrained, cardiovascular collapse will occur.

Pathophysiology

Two components are required for a gas embolism to occur: an interface between the vascular system and air, and a pressure gradient between air and the vascular system. Gas bubbles move to the pulmonary circulation and cause progressive right heart failure. They may also accumulate in the right ventricular outflow tract, decreasing cardiac output. Gas emboli can also cause ischemic injury in end organs if the bubbles pass into the arterial circulation through a right-to-left shunt.

Immediate Management

  • Immediately alert the surgeon. Ask him or her to flood the field with irrigation fluid or cover it with wet sponges. He or she should also find and occlude the point of gas entrainment using bone wax and/or electrocautery.

  • Call for help.

  • Increase FiO2 to 100%.

  • If possible, position the OR table flat or head-down to place the surgical wound below the level of the right atrium.

  • Support the blood pressure: Administer vasoactive drugs to maintain a normal systolic blood pressure (e.g., phenylephrine 100 mcg IV bolus).

  • Volume resuscitate with isotonic crystalloid or colloid solutions to support systemic blood pressure and increase right atrial pressure.

  • If a central venous catheter is in place, it may be possible to remove air in the right atrium by aspirating from the most distal port.

  • If cardiovascular collapse occurs, perform cardiopulmonary resuscitation with the patient in head-down and rolled-to-the-left lateral decubitus position.

Differential Diagnosis

  • Pulmonary thromboembolism

  • Stroke

  • Myocardial ischemia

  • Cardiogenic shock

Diagnostic Studies

  • Sudden decrease in end-tidal CO2

  • Echocardiogram (most sensitive) shows gas bubbles in the right atrium.

  • Precordial Doppler (sensitive but not specific for clinically significant emboli)

  • Arterial blood gas reveals respiratory acidosis, increased PaCO2, hypoxia.

Subsequent Management

  • In the case of massive embolism, or if gas has migrated to the arterial circulation, consider hyperbaric therapy.

Risk Factors

  • Lung barotrauma

  • Craniotomy in the sitting position (classic risk factor)

  • Any surgical procedure in which the operative site is located above the level of the heart, including caesarean section, arthroscopic surgery of the shoulder, and total hip arthroplasty

  • Laparoscopic surgery: Direct injection of CO2 into the circulation through a trocar that is placed into a vein, or gas that enters veins at the operative site. Carbon dioxide bubbles are more soluble and disappear more quickly than nitrogen or oxygen, but can cause a symptomatic gas embolus.

Prevention

Maintain normovolemia. Low venous pressure is a risk factor for venous air embolism (VAE). Position the patient in such a way as to to reduce the pressure gradient between operative site and the right atrium during surgery and also when inserting or removing a central venous catheter.

Special Considerations

  • Twenty to thirty percent of the population have an asymptomatic patent foramen ovale, which allows gas bubbles in the venous circulation to move into the arterial circulation. This can result in stroke, myocardial ischemia, and other life-threatening complications.

Further Reading

Mirski M, et al. Diagnosis and treatment of vascular air embolism. Anesthesiology. 2007; 106(1): 164–177.Find this resource: