2. Cardiology

Coronary artery disease (CAD) refers to the narrowing of the coronary arteries that supply the myocardium with oxygen and nutrients.

Coronary disease in general remains an important focus for health care professionals of every specialty.

Using current guidelines and recommendations disease-modifying strategies should become part of everyday practice of medicine.

Common Causes to Remember

Cigarette smoking, diabetes mellitus (DM), hypertension (HTN), hyperlipidemia, obesity, and a family history of premature CAD are risk factors for CAD.

Many of the common symptoms such as chest pain, shortness of breath, diaphoresis, and nausea that physicians use in the outpatient setting to determine which patients are likely suffering an acute coronary event may not be routinely available to the intensivist when attempting to assess acute coronary syndrome (ACS) in the ICU patient.

Classic symptoms in an awake and alert patient often include chest pressure with radiation to the left arm/neck, diaphoresis, and nausea/vomiting. These symptoms may often be masked or altered in patients with diabetes mellitus and in female patients, with many of them presenting with little to no classic symptoms.

In an intubated patient under general anesthesia or an intensive care patient coming out of major surgery, the intensivist must look for other signs that ischemia is taking place, such as hemodynamic changes, difficulty weaning from the ventilator, and ECG changes. Other potential signs include new wall motion abnormalities on echocardiography, unexplained tachycardia, increasing vasopressor requirement, or a sudden increase in pulmonary artery pressure/central venous pressure.

Epidemiology

CAD continues to be the leading cause of death in the world and in the United States according to the World Health Organization and the American Health Association and American Stroke Association’s 2006 publication on heart disease.

It accounts for 7.25 million deaths a year worldwide.

Key Pathophysiology

CAD has been linked to the combination of several complex modifiable and nonmodifiable risk factors—most notably high levels of LDL cholesterol, low HDL cholesterol, HTN, DM, family history of CAD, and smoking. Other factors such as obesity and age also serve as additional risk factors for CAD. But bear in mind that these classic risk factors might not be present in all cases.

Many of these risk factors are at the front of a cascade of molecular mechanisms that work together to create disease.

Biochemical markers linked to vascular inflammation as well as the upregulation/downregulation of certain transcription pathways will likely play a key role in how we think about the process of coronary disease and the future of treatment options.

Familiarity with the anatomy of the coronary vessels is crucial to understanding the relationship between the path of each coronary vessel and the territory of the heart for which it is responsible for supplying blood, oxygen, and nutrients. This can be extremely useful when wall motion abnormalities are identified by the intensivist who utilizes point of care echocardiography.

Anatomy

The dominance of coronary circulation is determined by which vessel supplies the posterior descending artery.

Right dominance occurs in upward of 90% of individuals with the right coronary artery supplying the posterior descending artery.

The main stem of the left coronary artery divides into the left anterior descending artery and the circumflex artery.

The left anterior descending artery then branches into the diagonals that supply the anterior heart.

The circumflex artery also arises from the left main coronary artery and wraps around the left atrioventricular groove.

The branches of the left circumflex coronary artery include the left obtuse marginal.

The right coronary artery as previously mentioned typically supplies the posterior descending artery.

It also supplies the sinus node and is therefore responsible for dysrhythmias during ischemic events.

The right marginal branch comes off of the right coronary artery and supplies the right ventricle.

Management and Treatment

Cardiac troponin I is a regulatory protein frequently used as a marker for cardiac ischemia. While it has become the standard cardiac marker it is still not a perfect test.

The sensitivity of the test continues to increase without a clear understanding of how to interpret positive results.

For example, in the trauma patient anything from blunt chest trauma to demand ischemia can lead to a positive test.

Elevated troponins can occur in conditions other than cardiac ischemia including sepsis, congestive heart failure (CHF) renal failure, cardiac trauma/contusion, acute pulmonary embolism, acute pericarditis/myocarditis, and certain infiltrative cardiac disorders.

Elevated troponins are often used with the ECG/echo in addition to the overall clinical picture (vasopressor changes, dysrhythmias) to guide management rather than being used as a single test to make clinical decisions.

Management of CAD can be divided into prevention and acute management.

Prevention: lifestyle changes including weight loss and quitting smoking are some of the modifiable risk factors that can be achieved in the outpatient setting.

Acute management

Once an acute event is recognized, treatment should be aimed at reducing further injury and working to reperfuse the injured myocardium.

Pharmacologic management

Aspirin should be considered and given as soon as possible, since it has a demonstrable benefit in ST-elevation myocardial infarctions (MIs) with a number-needed-to-treat for mortality of 1 in 42.

Consider nitroglycerin and opioids for pain control to decrease the sympathetic drive and the infarct size.

If safe, consider further therapy with anticoagulation and antiplatelet therapies (e.g., glycoprotein IIb/IIa inhibitors and thienopyridines).

Beta blocker should be considered for heart rate control, but care must be taken as it can worsen outcomes especially if given in the acute period among patients in heart failure, or at risk for heart failure. The largest study available on beta blockade on MIs, the COMMIT/CCS-2 study found that giving early beta blockade showed no difference in in-hospital mortality, with an increase in the risk of cardiogenic shock.

Revascularization

Communication with the cardiology and the surgical teams in postoperative patients should be timely as many of these patients could benefit from early revascularization. This is especially true among patients with ST-elevation MIs as the current guidelines recommend percutaneous angioplasty intervention within 90 minutes, with many centers trying to target a balloon time of less than 30 minutes.

However the clinical context must be taken into account, especially among patients that are immediately postoperative or actively bleeding, since all these interventions require immediate anticoagulation and possibly long-term anticoagulation.

Angioplasty often includes stent placement (bare-metal versus drug-eluting stents) and requires antiplatelet drugs throughout the perioperative period. Another possibility is for balloon dilatation without stenting in the acute period and return once the patient is stable for more definitive therapy.

Coronary artery bypass surgery continues, especially in diabetics with multivessel disease.

SUGGESTED READINGS

Annane D, Sébille V, Duboc D, et al. Incidence and prognosis of sustained arrhythmias in critically ill patients. Am J Respir Crit Care Med. 2008;178(1):20-25.

Chockalingam A, Mehra A, Dorairajan S, Dellsperger KC. Acute left ventricular dysfunction in the critically ill. Chest. 2010;138(1):198-207. Review.

Crawford TC, Oral H. Cardiac arrhythmias: management of atrial fibrillation in the critically ill patient. Crit Care Clin. 2007;23(4):855-872, vii. Review.

Falk RH, Knowlton AA, Bernard SA, et al. Digoxin for converting recent-onset atrial fibrillation to sinus rhythm: a randomized, double-blinded trial. Ann Intern Med. 1987;106:503–506.

Fuster V, Rydén LE, Cannom DS, et al. 2011 ACCF/AHA/HRS focused updates incorporated into the ACC/AHA/ESC 2006 Guidelines for the management of patients with atrial fibrillation: a report of the American College of Cardiology Foundation/American Heart Association Task Force on Practice Guidelines developed in partnership with the European Society of Cardiology and in collaboration with the European Heart Rhythm Association and the Heart Rhythm Society. J Am Coll Cardiol. 2011;57(11):e101-e198.

Lim HS, Hamaad A, Lip GY. Clinical review: clinical management of atrial fibrillation—rate control versus rhythm control. Crit Care. 2004;8(4):271-279. Epub 2004 Feb 19. Review.

Reinelt P, Karth GD, Geppert A, Heinz G. Incidence and type of cardiac arrhythmias in critically ill patients: a single center experience in a medical-cardiological ICU. Intensive Care Med. 2001;27(9): 1466-1473.

Roy D, Talajic M, Nattel S, et al. Atrial Fibrillation and Congestive Heart Failure Investigators. Rhythm control versus rate control for atrial fibrillation and heart failure. N Engl J Med. 2008;358(25):2667-2677.

Tsadok MA, Jackevicius CA, Essebag V, et al. Rhythm versus rate control therapy and subsequent stroke or transient ischemic attack in patients with atrial fibrillation. Circulation. 2012;126(23):2680-2687.

Walkey AJ, Wiener RS, Ghobrial JM, Curtis LH, Benjamin EJ. Incident stroke and mortality associated with new-onset atrial fibrillation in patients hospitalized with severe sepsis. JAMA. 2011;306(20):2248-2254.

2.3

Valvular Disorders

Nicholas C. Watson

Introduction

Valvular heart disease may be the primary cause of presentation, an exacerbating factor, or an incidental comorbidity in the critically ill patient.

The management of valvular heart disease grows increasingly complex as diagnostic and treatment options expand with the improvement of echocardiography and burgeoning percutaneous interventions.

Aortic Stenosis

Common Causes to Remember

Calcific degeneration is the most common cause; Other causes include congenital bicuspid or unicuspid aortic valve, rheumatic heart disease, and radiation.

Epidemiology

Prevalence increases with age, 2% of people >65 years old have calcific aortic stenosis (AS).

Congenital bicuspid valve is found in approximately 2% live births, 4:1 male predominance.

Rheumatic AS is invariably associated with rheumatic change of the mitral valve.

Key Pathophysiology

Regardless of the initial cause, the advancing pathophysiology of AS is similar.

Gradual worsening of obstruction leads to compensatory left ventricular hypertrophy (LVH) that reduces ventricular wall stress and preserves ejection fraction (EF).

LVH reduces the compliance of the LV, raising LV diastolic pressure and leading to adaptive left atrial (LA) hypertrophy that augments filling of the stiff LV.

High LA pressures eventually lead to pulmonary congestion.

Decompensation occurs under several possible conditions.

Depressed LV contractility occurs independent of AS sequelae.

Rising LV afterload that outpaces compensatory LVH leads to a critical decrease in EF, and exertional syncope ensues.

Atrial fibrillation (AF) prevents adequate LV preload.

An increased oxygen demand (e.g., exercise, tachyarrhythmia) leads to subendocardial ischemia because hypertrophied heart muscle requires more oxygen than its vasculature can support under stress, and angina ensues.

Reduced systemic vascular resistance (e.g., systemic inflammatory response syndrome, heavy analgesia, or sedation) leads to hypotension as the stroke volume (SV) cannot be raised by the LV against a fixed stenotic aortic valve.

Differential Diagnosis

Severe AS: dyspnea, angina, syncope, low amplitude and slow rise of pulse, reduced pulse pressure, crescendo-decrescendo systolic murmur, LVH on electrocardiogram (EKG), AV calcification on chest x-ray (CXR), on echocardiography (echo) gradient >40 mmHg, or AV area (AVA) <1 cm² is critical.

Pseudo AS: inadequate leaflet opening due to poor ventricular function; echo finding of low aortic transvalvular gradient is present in pseudo AS and severe AS with depressed LV function, differentiated by dobutamine stress echo.

Aortic sclerosis: focal thickening and calcification of AV leaflets, no AV obstruction to flow, ejection murmur that mimics that of AS, differentiate on echo by jet velocity <2.5 m/s in aortic sclerosis and higher in AS.

AS must also be differentiated from supravalvular stenosis, subvalvular stenosis, and hypertrophic cardiomyopathy (HCM).

Management and Treatment

There is no medical management for progressive disease.

For patients with rheumatic AS, antibiotics are indicated for prevention of recurrent rheumatic fever.

Statins have not been shown to slow rate of AS progression.

Treatment of acutely decompensated AS (LV dysfunction, shock): invasive hemodynamic monitoring, prompt inotropic support, percutaneous aortic balloon valvuloplasty (PABV) as a bridge to valve replacement in patients with cardiogenic shock

Hemodynamic goals during acute management: preload augmentation, HR <90, maintain sinus rhythm, maintain contractility (avoid beta blockade), maintain or augment systemic vascular resistance

Aortic valve replacement (AVR) indications: symptomatic severe AS, asymptomatic AS with LVEF <0.5, moderate AS in patients undergoing coronary artery bypass grafting or aortic aneurysm repair

Post-AVR care: expect SV to increase and LV end-diastolic pressure (LVEDP) to decrease, LVH persists for an extended period and may require preload augmentation.

Outcomes

Once moderate stenosis has developed, progression is almost certain.

Without intervention survival is 2 to 3 years after onset of symptoms.

PABV has no long-term benefit in acutely decompensated AS.

Transcatheter AVR and surgical AVR may have equivalent perioperative mortality in high-risk patients.

AVR improves symptoms and survival.

AVR perioperative mortality is 3% to 4%, higher when combined with bypass grafting.

Aortic Regurgitation

Common Causes to Remember

Causes of acute aortic regurgitation (AR): infective endocarditis (IE), aortic dissection, blunt chest trauma, acute-on-chronic decompensation of AR

Many causes of chronic AR: bicuspid valve, calcific degeneration, rheumatic heart disease, aortic aneurysm, degenerative aortic dilation

Epidemiology

Calcific AR is present to some extent in many older patients.

Aortic root disease is most common cause of isolated AR.

Key Pathophysiology

Acute Aortic Regurgitation

Sudden regurgitant flow through the aortic orifice causes an abrupt rise in LV diastolic pressure, subsequent elevation of LA and pulmonary vascular pressures, pulmonary edema and dyspnea follow.

Forward SV drops as the LV cannot undergo immediate compensatory dilation, hypotension ensues

Chronic Aortic Regurgitation

Chronic AR progresses from mild (asymptomatic with compensation) to moderate (symptomatic) to severe (failure).

Regurgitant flow through the aortic orifice over a prolonged period leads to LV compensatory dilation, large regurgitant volume increases SV resulting in elevated systolic blood pressure (SBP) while lowering diastolic blood pressure (DBP).

Reduced DBP lowers coronary perfusion pressure, LV dilation increases wall tension, oxygen demand can outstrip supply.

With time the LV remodels, preload reserve is exhausted, systolic performance declines, pulmonary vascular pressures rise, congestive heart failure (CHF) symptoms appear.

Differential Diagnosis

Acute severe AR: sudden onset, weakness, dyspnea, presyncope, hypotension, tachycardia, bounding pulse, early and short diastolic murmur, possible pulmonary edema on CXR

Using echo to evaluate the regurgitant aortic valve jet, severity can be quantified.

Chronic AR: symptoms may be absent/mild/severe, elevated SBP and low DBP, bounding pulse, long diastolic murmur, LVH on EKG, cardiomegaly, and possibly pulmonary edema on CXR

Pulmonary edema unrelated to aortic valve disease

CHF unrelated to aortic valve disease

Management and Treatment

Acute Hemodynamic Management of Mild/Moderate Aortic Regurgitation

Increase LV preload, increase HR, maintain contractility, decrease SVR, maintain pulmonary vascular resistance (PVR)

Acute Severe Aortic Regurgitation

Surgical intervention (AVR) takes precedence over medical management in urgent and emergent severe AR.

CHF and cardiogenic shock therapies: vasodilation and diuresis as tolerated, inotropes as needed, intraaortic balloon pump (IABP) contraindicated

Antibiotics for infectious endocarditis

Type A acute aortic dissection: beta blockade with caution (compensatory tachycardia should not be prevented)

Post-AVR care: LVEDP decreases while LVH and LV dilation persist, may require augmentation of LV preload; if LV function declines, inotropes or IABP may be necessary.

Outcomes

Acute severe AR leads to death without rapid intervention.

AVR perioperative mortality is 3% to 4%, higher when combined with bypass grafting.

Mitral Stenosis

Common Causes to Remember

Rheumatic heart disease is the most common cause.

Less common causes are leaflet calcification, congenital disease, systemic lupus erythematosus, and rheumatoid arthritis.

Epidemiology

40% of rheumatic heart disease patients have isolated mitral stenosis (MS).

Male to female ratio of rheumatic MS is 1:2.

Key Pathophysiology

Severe MS may take 20 to 40 years to develop following acute rheumatic fever.

Incomplete LA emptying leads to increased LA pressure (LAP) and reactive pulmonary hypertension; CHF symptoms can follow if reactive pulmonary hypertension fails to adequately compensate for elevated LAP.

Atrial fibrillation can result from chronic enlargement of LA due to sustained elevated LAP.

Low flow in the LA predisposes to thrombus formation while turbulent flow across the mitral valve (MV) increases risk for infectious endocarditis.

Differential Diagnosis

Mild to moderate MS is typically asymptomatic at rest.

Severe MS: AF or systemic embolus commonly leads to acute decompensation; presents with dyspnea, orthopnea, paroxysmal nocturnal dyspnea (PND), fatigue; exam shows signs of CHF, diastolic “rumbling” murmur is a classic finding but may be absent in AF or low output states; LA enlargement +/– RVH on EKG and CXR, pulmonary edema on CXR in advanced disease; on echo valve area <1 cm² is critical.

Known MS without typical pulmonary congestion symptoms should raise concern for concomitant tricuspid stenosis (TS).

Management and Treatment

Acute management: address precipitating factor(s), increase LV preload, decrease HR, maintain contractility, maintain SVR, decrease PVR

Anticoagulation for MS with AF or MS with prior embolic event

Surgical treatment

Percutaneous balloon mitral valvuloplasty (PBMV)—for severe MS with certain valve anatomy and absence of LA thrombus

MV commissurotomy—for severe, symptomatic MS when valve anatomy not acceptable for PBMV

MV replacement (MVR)—for moderate to severe MS with abnormal valve anatomy

Intervention of coexisting TS should be considered at time of MV operation

Management after surgical intervention: the chronically deprived LV may fail in the setting of acute increase in volume across the open MV, inotropic support may be necessary, maintaining preload and reducing SVR may also be beneficial.

Outcomes

Asymptomatic patients with MS have >80% 10-year survival

10-year survival is 0% to 15% after onset of symptoms.

Natural history of untreated MS is death by heart failure, systemic or pulmonary embolism, or infection.

Outcomes for surgical intervention are dependent on institutional experience, patient comorbidities, and valve morphology.

Perioperative mortality for MVR is 5.7%, 1.6% for MV repair; mortality increases for both when combined with bypass grafting.

Mitral Regurgitation

Common Causes to Remember

Acute mitral regurgitation (MR) can result from a rapid precipitating factor affecting a normal valve or by decompensation of chronic MR.

MV prolapse, pathologic dilation of LV, rheumatic heart disease, infectious endocarditis, ischemic heart disease, trauma, intracardiac tumor

Epidemiology

Exact incidence and prevalence is unknown.

Key Pathophysiology

Acute Mitral Regurgitation

Sudden regurgitation of LV SV into the LA decreases forward CO, raises LA volume, and increases the LVEDV as regurgitant and normal pulmonic blood enter the LV during diastole.

Decreased forward CO leads to hypotension.

The minimally compliant LA cannot adapt to sudden increased volume, leading to increased LAP, pulmonary congestion, and subsequent dyspnea and pulmonary edema.

Increased LVEDV may stretch the myocardium beyond optimal length on Starling curve, reducing contractility and further impairing forward CO.

Chronic Mitral Regurgitation

Gradually worsening regurgitation causes chronic stretching and compensatory increased compliance of the LA which prevents pulmonary congestion.

As the LA dilates with time the LAP drops and an increasing portion of the LV SV becomes regurgitant, leading to diminishing forward CO and ultimately symptoms of low CO.

Chronically increased LVEDV leads to LV dilation and eventual poor contractility, contributing to low CO.

Chronically dilated LA predisposes to AF

Differential Diagnosis

Acute severe MR: dyspnea, cough, chest pain, ±hypotension, tachycardia, tachypnea, crackles, variable murmur, possible AF or atrial flutter, pulmonary edema on CXR; echo can identify specific leaflet morphologic abnormality, regurgitant jet, and quantify severity.

Decompensated chronic MR: symptoms of CHF, early soft systolic murmur, cardiomegaly on EKG and CXR, pulmonary edema on CXR; echo can show LA and LV dilation, identify specific leaflet morphologic abnormality, regurgitant jet, and quantify severity.

Pulmonary edema unrelated to MR

Murmur of AS can be confused with that of posterior MV leaflet prolapse or flail.

Management and Treatment

Mild/Moderate Mitral Regurgitation

Preload based on clinical response, maintain or increase HR, maintain contractility, decrease SVR, decrease PVR

Interventions for nonacute MR include percutaneous MV repair and cardiac resynchronization therapy for select populations.

Acute severe Mitral Regurgitation

Medical management of CHF and cardiogenic shock: vasodilation and diuresis as tolerated, inotropes, IABP as needed; antibiotics for IE

It is frequently possible to medically stabilize/optimize a patient with acute severe MR prior to operative intervention (unlike acute severe AR).

MV repair preferred if adequate MV structure remains

MV replacement if native tissue is inadequate for repair.

Management after surgical intervention: inotropic support or IABP may be needed as LV contracts against a new elevated afterload, AF must be aggressively treated.

Outcomes

Without surgical intervention, prognosis for patients with MR and heart failure is poor.

Perioperative mortality for MVR is 5.7%, 1.6% for MV repair; mortality increases for each when combined with bypass grafting.

Percutaneous MitraClip procedure may be a feasible option in patients at high risk for surgical mortality, more data are needed.

Hypertrophic Cardiomyopathy

HCM is marked by a thickened, nondilated LV in the absence of other cardiac or systemic conditions that could induce such LVH.

Because LV outflow tract (LVOT) obstruction is not ubiquitous in HCM, several terms have been abandoned in favor of HCM: idiopathic hypertrophic subaortic stenosis (IHSS), hypertrophic obstructive cardiomyopathy (HOCM), muscular subaortic stenosis