Cor pulmonale consists of right ventricular (RV) impairment or failure in the absence of left ventricular (LV) disease. It is secondary to acute or chronic abnormalities of the pulmonary circulation, lungs, or thorax and is sometimes referred to as "pulmonary" heart failure.
It can be diagnosed by noninvasive assessment of RV function using EKG and invasively via pulmonary artery catheterization; however, for both of these modalities, diagnostic criteria are not standardized.
Epidemiology
Incidence
Unknown; poorly studied in the population of patients undergoing general anesthesia.
RV failure occurs in ~30% of patients after left ventricular assist device placement (LVAD).
Prevalence
Greater in patients with underlying pulmonary disease that contributes to chronic hypoxic states
Morbidity
Cor pulmonale and pulmonary hypertension (PH) are associated with a 13.1-fold increase in perioperative morbidity and mortality when undergoing noncardiac surgery compared to cross-matched patients without PH (1).
More likely to develop congestive heart failure (OR = 11.9)
Susceptible to more hemodynamic instability and respiratory failure
Patients were shown to need longer ventilator support, stay longer in the intensive care unit (ICU), and have higher readmission to the hospital within 30 days of surgery.
Mortality
Despite equivalently smooth operative courses, PH patients had increased in-hospital deaths compared to matched controls (9.7% vs 0%); systolic pulmonary artery pressure (PAP) served as an independent predictor of mortality (2).
These patients also had significantly more frequent postoperative heart failure and delayed extubation.
Etiology/Risk Factors
Cor pulmonale and RV failure can be either acute or chronic.
Acute etiologies include thromboembolic disease, cardiac tamponade, RV ischemia, and acute chest syndrome with sickle cell disease
Chronic etiologies include chronic obstructive pulmonary disease, obstructive sleep apnea, valvular disease, congenital heart disease, PH, and collagen-vascular disease
Physiology/Pathophysiology
Similar to the LV, the RV stroke volume is affected by preload (central venous pressures), afterload (pulmonary artery pressures and pulmonary vascular resistance), and contractility.
In contrast to the LV, the RV has ~1/6th the muscle mass, decreasing its ability to pump effectively against an increased afterload. It functions more as a volume pump than a pressure pump.
Elevations in RV afterload can result in
Acute: Dilation of the RV
Chronic: Hypertrophic response to improve contractile forces against the increased tension; recall LaPlace's law. This results in decreased compliance and impaired diastolic filling.
In low cardiac states, compensation is primarily with a tachycardic response due the the RV's limited ability to respond with greater contractile force. The RV is more prone to overt failure when faced with decreased preload (vasodilatory states), increased afterload (hypoxia, hypercarbia, coughing, bucking), or decreased contractility (ischemia, anesthetics).
Hypoxemia. The degree of hypoxemia and inability to maintain arterial oxygenation is directly associated with the development of PH and RV failure. Hypoxia induces pulmonary vasoconstriction (increased PVR), which in turn increases the risk of RV strain and failure.
Arrhythmias
Atrial (more common) or ventricular arrhythmias can develop.
Inhaled beta-agonists may induce tachycardias.
Systemic beta antagonists may worsen bronchospastic status, thus creating further complications.
Hepatic congestion secondary to venous congestion is common, usually evident by elevations in transaminases and INR. This may partially subside with optimization of cor pulmonale.
Anesthetic GOALS/GUIDING Principles
Patients should be optimized prior to elective surgery. Control infections and bronchospastic diseases prior to administering anesthesia.
Pulmonary hygiene should be focused on the clearance of secretions and recruiting poorly ventilated units of lung in order to optimize oxygenation and ventilation.
Avoid acute increases in the PAP (hypoxia, hypercarbia, acidosis, increased sympathetic states), or decreases in contractility.
Volume optimization must be carefully assessed and addressed. Hypovolemia will decrease preload and RV output; whereas fluid overload may exacerbate arrhythmias and RV strain.
Diagnosis⬆⬇
Symptoms
Peripheral edema and ascites, often presenting as ankle edema and congestive hepatomegaly
Distress during mild exertion or rest, not relieved by sitting upright (in contrast to orthopnea present in patients with LV failure)
Nonproductive cough
Other classically associated symptoms of heart failure
History
Dyspnea and tachypnea often overlap with underlying pulmonary disease.
Severity of underlying disease: Exercise tolerance, need for bronchodilators, or supplemental oxygen
Exacerbations: Fatigue, worsening dyspnea, and increased oxygen requirements
Signs/Physical Exam
Cardiac examination: A right-heave may be palpated along the left sternal border or in the epigastrium; an augmented pulmonic component of the second heart sound; and associated murmurs due to incompetence of the tricuspid valve (during systole) and/or pulmonic valve exist (during diastole). Both murmurs are augmented by inspiration.
Peripheral edema, jugular venous engorgement, and positive hepatojugular reflex
Treatment History
Options are focused primarily on maintaining and restoring oxygenation and ventilation to decrease PVR, volume status, and RV workload.
Supportive therapy of oxygen is important to maintain a PaO2 >60 mm Hg or SpO2 >90%.
Lung transplantation in severe disease
Medications
Anticoagulation for thromboembolic disease
Heart failure regimens (diuretic therapy) may be needed to manage peripheral edema but can also impair RV function (decreased preload and metabolic alkalosis).
Calcium channel blockers (CCBs) are a first-line outpatient treatment, although many are not candidates or responders to these. These agents can exacerbate perioperative hypotension and can increase mortality risk in patients with systolic dysfunction.
Phosphodiesterase inhibitors and endothelin antagonists
While not FDA approved for this use, inhaled nitric oxide (iNO) and inhaled epoprostenol have been used to treat acute crises (RV failure, hypoxemia, and PH).
Diagnostic Tests & Interpretation
Labs/Studies
Arterial blood gas: Objectively assess the degree of respiratory insufficiency.
Liver function tests: Dysfunction and coexisting coagulopathy
EKG: Findings include RV enlargement, ventricular septal flattening "D-sign," ventricular dysmotility, and evidence of elevated estimated RV systolic pressure.
Chest x-ray: A decrease in the retrosternal space on lateral films indicates RV hypertrophy. A prominent main pulmonary artery and decreased vascular markings may be consistent with PH.
Echocardiogram: Right atrial and RV hypertrophy (peaked P waves in leads II, III, and aVF). Right axis deviation and right bundle branch blocks can also be seen.
Pulmonary function tests: Assess the response to bronchodilator therapy.
Right atrial pressure tracing: Predominant A wave due to enhanced right atrial contraction with decreased ventricular compliance.
Right heart catheterization: Elevated PAP with normal pulmonary artery occlusion pressures (representing normal left ventricular end-diastolic pressure, LVEDP).
Cardiac MRI: While not widely available, can provide accurate information on RV function.
Treatment⬆⬇
PREOPERATIVE PREPARATION
Premedications
Maintaining oxygenation and ventilation is imperative; thus, medications that may depress ventilation (i.e., opioids) should be used judiciously.
Inhaled beta-agonists may be needed to optimize pulmonary disease.
Special Concerns for Informed Consent
Increased risk of perioperative complications, morbidity, and mortality
INTRAOPERATIVE CARE
Choice of Anesthesia
Dependent on the procedure. As a sole technique, regional anesthesia has the benefit of avoiding anesthetic induction, airway instrumentation, mechanical ventilation, and extubation, as well as minimizing systemic opioids. However, supplemental sedation, failed blocks, or complications of the block (e.g., high spinal and local anesthetic toxicity) need to also be considered. Additionally, patients may not be able to lie flat during a procedure.
Supplementing the general anesthetic with a regional technique has the benefit of decreasing the need for systemic opioids.
Caution should be exercised when performing regional techniques that can affect respiratory parameters. Interscalene blocks can cause phrenic nerve palsies (C3, C4, C5); neuraxial techniques to the T6 level can affect accessory muscles of respiration.
Monitors
Standard ASA monitors
Invasive monitoring is dependent on the degree of patient dysfunction and the operative procedure.
Arterial line. Monitoring arterial line BP helps identify rapid changes in hemodynamics and allows frequent blood gas measurements of PaO2 and PaCO2 (can aid with decision to extubate).
Central lines can assess RV pressures.
Pulmonary artery catheters. May be used to assess the degree of patient illness, effect of fluid shifts and changes in acid/base status from hypercarbia, laparoscopy, etc. by monitoring the PAPs.
An alternative to invasive monitoring includes transesophageal echocardiogram; however, this monitor requires expertise and is usually employed only while the patient is intubated
Induction/Airway Management
To minimize increases in PVR, patients should have an adequate depth of anesthesia prior to instrumenting the airway.
Supraglottic devices (i.e., LMA) may decrease airway stimulation; however, adequate ventilation must be ensured to prevent respiratory acidosis.
The RV can also be preload dependent against the fixed afterload of PH. Anesthetic selection must avoid sympathetic spikes without dropping systemic vascular resistance.
Maintenance
N2O is controversial with conflicting evidence on its effects on PVR. Monitoring the right atrial or PAP can allow early identification of intolerance and allow discontinuation.
Neuromuscular blockade (and other anesthetic drugs) should avoid histamine release.
Fluids should be titrated judiciously; patients can be sensitive to hypovolemia and require a sufficient preload to maintain the RV output. However, hypervolemia can overload the Frank–Starling curve of the RV and lead to strain or failure and worsening venous congestion.
Extubation/Emergence
Extubation. Standard criteria apply; however, patients may be less capable of meeting them. If adequate ventilation and oxygenation cannot be ensured, consider delaying extubation. Deep extubation can result in inadequate ventilation and hypercarbia.
A smooth emergence with minimal coughing is desired to prevent increased intrathoracic pressure, RV afterload, and sympathetic input.
Tracheal application of lidocaine may be helpful to minimize the response to airway instrumentation.
References⬆⬇
KawR, PasupuletiV, DeshpandeA, et al.Pulmonary hypertension: An important predictor of outcomes in patients undergoing non-cardiac surgery. Respir Med. 2001;105:619–624.
LaiHC, LaiHC, WangKY, et al.Severe pulmonary hypertension complicates postoperative outcome of non-cardiac surgery. Br J Anaesth. 2007;99(2):184–190.
LahmT, McCaslinCA, WozniakTC, et al.Medical and surgical treatment of acute right ventricular failure. J Am Coll Cardiol. 2010;56(18):1435–1446.
Veillard-BaronA, JardinF.Why protect the right ventricle in patients with acute respiratory distress syndrome? Curr Opin Crit Care. 2003;9(1):15–21.
Additional Reading⬆⬇
HaddadF, CoutureP, TousignantC, et al.The right ventricle in cardiac surgery, a perioperative perspective: I. Anatomy, physiology, and assessment. Anesth Analg. 2009;108(2):407–421.
HaddadF, CoutureP, TousignantC, et al.The right ventricle in cardiac surgery, a perioperative perspective: II. Pathophysiology, clinical importance, and management. Anesth Analg. 2009;108(2):422–433.
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