Christopher Wray, MD
BASICS
DESCRIPTION
• Alcoholic cardiomyopathy (ACM) is classified as a non-ischemic, dilated cardiomyopathy (CM) that results from exposure to a myocardial toxin.
• ACM shares common characteristics with all dilated CMs (depending on the clinical stage of the disease progression):
– Dilated chambers
– Diastolic dysfunction (asymptomatic stage)
– Left ventricular dysfunction (symptomatic stage)
– Left ventricular hypertrophy (asymptomatic stage; followed by wall thinning in symptomatic stage)
• Diagnosis is clinically based upon a history of significant chronic alcohol exposure in conjunction with the exclusion of other causes of dilated CM.
PHYSIOLOGY PRINCIPLES
• Epidemiology of ACM:
– Second most common cause of dilated CM (4% of all CMs)
– Prevalence in Western countries is variable, but ranges from 20% to 40% of all non-ischemic dilated CMs.
– Significantly more prevalent in men (approximately 15% prevalence in women)
– The incidence of dilated CM is much higher in chronic alcoholics than in the total population.
– The 5-year incidence ranges from 20% to 26% in chronic alcoholics.
• Amount and duration of alcohol exposure:
– Studies have demonstrated variability and a lack of a specific linear relationship between the amount and duration of alcohol exposure and the development of asymptomatic and symptomatic ACM (1,2,3).
– Studies have shown changes in cardiac structure and function consistent with ACM in patients with a history of consuming >90 g/day of alcohol for >5 years (one drink contains approximately 12 g of alcohol). Studies in patients with symptomatic ACM have shown a history of longer durations of drinking (>10 years) (4,5).
– Despite the correlation between chronic heavy drinking and the development of ACM, not all heavy drinkers will progress to ACM.
– Although there may be other variables responsible for the occurrence of heart failure in alcoholics, the duration of heavy daily alcohol use is the most reliable predictor for the development of ACM.
PHYSIOLOGY
• Myocardial wall tension is closely related to myocardial oxygen consumption. of myocardial oxygen; it determines the number of times that tension needs to be generated.
• The left ventricle is ellipsoid and facilitates low wall tension DISEASE/PATHOPHYSIOLOGY
• The pathophysiology is not completely understood, despite a large number of studies.
Animal studies have demonstrated characteristic histologic and cellular changes associated
• Clinical presentation: ACM presents in stages and can progress from asymptomatic to symptomatic.
– Asymptomatic stage: Studies have demonstrated that in the early preclinical stage of ACM, LV remodeling occurs in the form of LV dilation (increased end-diastolic and systolic dimensions), increased LV mass, and LV hypertrophy (increased septal thickening).
Echocardiographic studies have demonstrated that diastolic dysfunction (impaired early diastolic filling of the LV) appears to be an early feature of asymptomatic ACM, regardless of LV mass and the presence of hypertension. Early ACM is often associated with a normal LV ejection fraction (EF) (3,4,5,6).
– Symptomatic stage: Characterized by progressive increases in LV dilation and LV mass, as well as the occurrence of systolic dysfunction with a decreased EF. Studies have demonstrated significantly greater LV end-diastolic and systolic dimensions in symptomatic ACM patients when compared to asymptomatic ACM patients (2,7).
• Tension: Dilated cardiomyopathy results in a more spherical left ventricle with subsequent increases in wall stress (radius is increased). In the asymptomatic stage, the myocardial wall hypertrophies and can decrease wall tension. However, in symptomatic stages, wall thickness decreases with resultant increases in wall tension (and myocardial oxygen demand).
• Diagnosis is clinically based upon having a history of significant alcohol consumption after ruling out other causes of dilated CM.
– History: After excluding other causes of dilated CM, the most important factor for
diagnosis is a chronic history of heavy alcohol use.
– Symptoms/physical exam: Signs and symptoms of heart failure may be noted in patients with symptomatic disease.
– EKG abnormalities are common and include nonspecific ST and T wave changes, QT prolongation, and atrial arrhythmias including atrial fibrillation.
– Echocardiography allows for a noninvasive delineation of the LV chamber size, diastolic function, and systolic function.
– There are no specific pathologic or immunologic tests for the diagnosis of ACM.
• Natural history and treatment
– Although the amount of alcohol required to cause progression of asymptomatic ACM to overt heart failure appears variable, studies clearly show that decreases in systolic function are significantly related to the amount and duration of alcohol consumption (1).
– Partial to complete regression of the pathologic cardiac changes associated with ACM may occur in some patients with abstinence alone.
– LV function in ACM patients may improve with standard medical therapy for dilated CM (diuretics, cardiac glycosides, ACE inhibitors, and beta blockade), although no therapies specific for ACM have been studied or described. Despite improvements in the LV function, survival is not improved in patients who continue to drink. The most important factor impacting survival in symptomatic patients receiving medical therapy is abstinence from further drinking.
PERIOPERATIVE RELEVANCE
• Chronic alcoholism results in a significantly higher incidence of postoperative cardiac complications, hypoxemia, and infections.
• The anesthesia provider should maintain an appropriate index of suspicion for the presence of ACM in patients with a history of chronic alcohol use. The presence of ACM can have worsened and even deleterious effects during the perioperative period. Even asymptomatic patients can have a limited cardiac reserve when exposed to severe perioperative stress that occurs with major surgery, trauma, or shock. Preoperative cardiac evaluation, including echocardiography, should be considered for risk-stratification and determination of the need for medical therapy for prospective surgical patients with a history of chronic alcohol use.
• Alcoholics presenting for emergency surgery may be acutely intoxicated or at risk for alcohol withdrawal syndrome, both of which can adversely affect a patient with ACM (8).
REFERENCES
1. Piano MR. Alcoholic cardiomyopathy: Incidence, clinical characteristics, and pathophysiology. Chest. 2002;121:1638–1650.
2. Fernandez-Sola J. Diastolic function impairment in alcoholics. Alcohol Clin Exp Med.
2000;24:1830–1835.
3. Fauchier L. Comparison of long-term outcome of alcoholic and idiopathic dilated cardiomyopathy. Eur Heart J. 2000;21:306–314.
4. Kupari M. Left ventricular filling impairment in asymptomatic chronic alcoholics. Am J Cardiol. 1990;66:1473–1477.
5. Lazarevic AM. Early changes in left ventricular function in chronic asymptomatic alcoholics: Relation to the duration of heavy drinking. J Am Coll Cardiol. 2000;35:1599–
1606.
6. McKenna CJ. Alcohol consumption idiopathic dilated cardiomyopathy: A case control study. Am Heart J. 1998;135:833–837.
7. Mathews EC. Echocardiogrphic abnormalities in chronic alcoholics with and without overt congestive heart failure. Am J Cardio. 1981;47:570–578.
8. Spies C. Perioperative morbidity and mortality in chronic alcoholic patients. Alcohol Clin Exp Res. 2001;25:164S–170S.
ADDITIONAL READING
• Laonigro I. Alcohol abuse and heart failure. Eur J Heart Failure. 2009;11:453–462.
• Spies CD. Effects of alcohol on the heart. Curr Opin Crit Care. 2001;7:337–343.
See Also (Topic, Algorithm, Electronic Media Element)
• Congestive heart failure
• Alcohol abuse
CODES
ICD9
425.5 Alcoholic cardiomyopathy ICD10
I42.6 Alcoholic cardiomyopathy
CLINICAL PEARLS
• ACM is a type of dilated CM that is diagnosed clinically, based on a history of significant chronic alcohol exposure in conjunction with the exclusion of other causes of dilated CM.
• The duration of heavy daily alcohol use is the most reliable predictor for the development of
• The most important factor impacting survival in ACM patients is abstinence from furtherACM.
drinking; medical therapy does not improve survival in patients who continue to drink alcohol.
• The presence of ACM in the surgical patient can have deleterious effects; the anesthesia provider should maintain an appropriate index of suspicion for the presence of ACM in patients with a history of chronic alcohol use.
ALDOSTERONE
Joe C. Hong, MD
BASICS
DESCRIPTION
• Aldosterone is a steroid hormone in the mineralocorticoid family that plays a vital role in the maintenance of intravascular volume status and sodium balance.
• Aldosterone is synthesized and secreted by the zona glomerulosa of the adrenal cortex in response to low intravascular volume, decreased renal perfusion, hyperkalemia, and acidosis.
• Disease states include Addison disease (hypoaldosteronism) and Conn syndrome (hyperaldosteronism).
PHYSIOLOGY PRINCIPLES
• Aldosterone is synthesized from cholesterol within the adrenal cortex by a series of steroidogenic reactions catalyzed by enzymes of the cytochrome p450 family. It is a steroid hormone that exerts its action by binding to an intracellular cytoplasmic receptor. This bound complex enters the cell nucleus and stimulates DNA transcription, resulting in protein production that mediates the ultimate effects of aldosterone.
• Renin–angiotensin system (RAS) regulation: Aldosterone secretion is regulated primarily by RAS via the following mechanism:
– Intravascular volume depletion triggers a decrease in renal perfusion pressure.
– Renin is secreted by the juxtaglomerular cells of the afferent arteriole in response to this decrease in renal perfusion pressure.
– Renin catalyzes the conversion of angiotensinogen to angiotensin I in plasma.
– Angiotensin-converting enzyme (ACE) catalyzes the conversion of angiotensin I to angiotensin II, primarily in the lungs.
– Angiotensin II stimulates the synthesis and secretion of aldosterone.
• Adrenocorticotropic hormone (ACTH): Aldosterone is also under tonic control by ACTH (secreted by the anterior pituitary gland).
• Aldosterone hormone regulates volume and blood pressure via:
– Binding to mineralocorticoid receptors located in the principal cells of nephrons. This upregulates sodium/potassium pumps with resultant sodium and water reabsorption and potassium sercetion by the distal tubules and collecting ducts. The net effect is the restoration of intravascular volume and blood pressure.
– Acting on alpha-intercalated cells of the late distal tubule and collecting duct, resulting in increased renal hydrogen ion secretion.
ANATOMY
• Aldosterone is produced by cells within the zona glomerulosa of the adrenal cortex.
• The adrenal gland is composed of the inner medulla which produces catecholamines and the
outer cortex which is divided into 3 histologic zones. Going from outside and moving
– Characterized by elevated ACTH levels but decreased levels of glucocorticoids and mineralocorticoids
– Clinical features are related to the adrenocortical hormone deficiency. Hypoglycemia is caused by cortisol deficiency. Hypotension, hyperkalemia, metabolic acidosis, and volume contraction are caused by aldosterone deficiency. Hyperpigmentation is caused by elevated ACTH secretion. Other signs and symptoms include weakness, fatigue, lethargy, anorexia, nausea, abdominal pain, prerenal azotemia, hypercalcemia, convulsions, fever, and syncope.
– Treatment: Replacement of glucocorticoids (hydrocortisone, prednisone, methylprednisolone) and mineralocorticoids (fludrocortisone)
• Secondary adrenocortical insufficiency is caused by decreased ACTH secretion, resulting primarily in a glucocorticoid deficiency. Mineralocorticoid deficiency is also seen but to a lesser degree.
– Most common cause of secondary adrenocortical insufficiency is sudden withdrawal of long-term corticosteroid therapy (2). Other causes include pituitary tumor, pituitary surgery or radiation, postpartum hypopituitarism (Sheehan syndrome), and sarcoid infiltration of the pituitary gland.
– Chronic corticosteroid therapy suppresses the hypothalamus and anterior pituitary, resulting in decreased production of corticotropin-releasing hormone (CRH) and ACTH, respectively. Decreased levels of CRH and ACTH cause atrophy of the zona fasciculata, resulting in glucocorticoid deficiency. During times of physiologic stress, the patient is unable to acutely increase cortisol production, resulting in acute secondary adrenocortical deficiency.
• Primary hyperaldosteronism is caused by aldosterone-secreting tumors.
– Conn syndrome (aldosterone-secreting adrenocortical adenoma) is the most common cause. Bilateral adrenal hyperplasia occurs less commonly.
PERIOPERATIVE RELEVANCE
• Hypoaldosterone states:
– Patients with adrenocortical insufficiency should continue their mineralocorticoid and glucocorticoid replacement therapy up until their time of surgery. Clinical features of overt hypoaldosteronism include hyperkalemia, hyponatremia, acidosis, and myocardial conduction defects. Administration of mineralocorticoids (fludrocortisone 0.05–0.1 mg/d) should occur preoperatively (1). Doses must be carefully titrated to avoid hypertension.
– Additional perioperative stress dose of glucocorticoids may be necessary since these patients may not be able to mount an adequate stress response. The traditional recommendation is 200 mg hydrocortisone per 70 kg body weight per day. However, smaller doses of 100 mg per 70 kg body weight per day have been used with success (2).
– The amount of perioperative hydrocortisone is based on the anticipated stress of the procedure. The relative degree of trauma and depth of anesthesia should be considered.
• Hyperaldosterone states:
– Patients presenting for elective surgery should be medically optimized in terms of their adrenocortical disorder. Preoperative EKG, glucose, and serum electrolytes (particularly sodium and potassium) should be checked. Volume status and blood pressure should be optimized.
– Primary aldosteronism (Conn syndrome) should be suspected in patients who present with concurrent hypertension and hypokalemia, severe refractory hypertension, adrenal incidentaloma and hypertension, or onset of hypertension at a young age.
– Antihypertensive medications (e.g., spironolactone) should be maintained up to the time of surgery. Careful cardiac assessment is necessary because these patients have increased cardiac comorbidity. Serum sodium and especially serum potassium should be checked prior to surgery. Hypokalemia is common. Severely hypokalemic patients should have their potassium replaced preoperatively.
REFERENCES
1. Dorin RI, Qualis CR, Crapo LM. Diagnosis of adrenal insufficiency. Ann Intern Med.
2003;139:194–204.
2. Symreng T, Karlberg BE, Kagedal B, et al. Physiological cortisol substitution of long-term steroid-treated patients undergoing major surgery. Br J Anaesth. 1981;53:949–954.
3. Young WF Jr. Adrenal causes of hypertension: Pheochromocytoma and primary aldosteronism. Rev Endocr Metab Disord. 2007;8:309–320.
ADDITIONAL READING
• Graham GW, Unger BP, Coursin DB. Perioperative management of selected endocrine disorders. Int Anesthesiol Clin. 2000;38:31–67.
• Lampe GH, Roizen MF. Anesthesia for patients with abnormal function of the adrenal cortex.
Anesthesiol Clin North Am. 1987;5:245–268.
• Udelsman R, Ramp J, Gallucci WT, et al. Adaptation during surgical stress: A reevaluation of the role of glucocorticoids. J Clin Invest. 1986;77:1377–1381.
See Also (Topic, Algorithm, Electronic Media Element)
• Cortisol
• Acute adrenal insufficiency
CLINICAL PEARLS
• Patients with adrenocortical insufficiency have deficiencies in both mineralocorticoids and glucocorticoids. Hydrocortisone has both glucocorticoid and mineralocorticoid activity.
Therefore, it is an ideal agent to use for the management of adrenocortical insufficiency.
• Patients with aldosterone deficiency should continue their fludrocortisone up until the time of surgery. Hypokalemic acidosis or hypovolemia must be treated preoperatively.
Supplementation of mineralocorticoids (fludrocortisone 0.05–0.1 mg/d) should occur preoperatively. Doses must be carefully titrated to avoid hypertension.
• Primary hyperaldosteronism (Conn syndrome) should be suspected in patients who present with concurrent hypertension and hypokalemia, severe refractory hypertension, adrenal incidentaloma and hypertension, or onset of hypertension at a young age.