Cardiology Class

CARDIOLOGY: SYNCOPE, FATIGUE & PERIPHERAL

EDEMADr. Sujay Iyer

I year PG, General Medicine

SYNCOPE FATIGUE PERIPHERAL EDEMA

TABLE OF CONTENT

Syncope is the abrupt and transient loss of consciousness associated with absence of postural tone, followed by complete and usually rapid spontaneous recovery.

Although, syncope can be a harbinger of a multitude of disease processes and can mimic cardiac arrest, it is most often benign and self-limting.

SYNCOPE: Introduction

Syncope is a common clinical problem. The Framingham Heart Study was one of the largest

epidemiological study that evaluated the incidence and prognosis of syncope.

822 of 7814 men and women (11%) were followed for an average 17 years.

Results:◦ Increased with age. Sharp rise at age 70 years.◦ Incidence, similar in men and women; with men more likely to

have a cardiac cause. Different studies suggest that one-third of individuals are

likely to have a syncopal episode during their lifetime. 3-5% of ER admissions are because of syncope.

SYNCOPE: Epidemiology

Cardiovascular disease is a major risk factor for syncope.

The incidence rate among participants of with cardiovascular disease was almost twice (10.6% vs 6.4%) that of participants without cardiovascular disease in the Framhingham cohort.

Other risk factors:◦ History of stroke◦ History of TIA◦ Hypertension

Additional risk factors are: low BMI, increased alcohol intake and diabetes.

SYNCOPE: Risk Factors

Determining the cause of syncope is important for both prognostic and therapeutic reasons.

In general, vasovagal attacks are the most common cause of syncope, followed by cardiac etiologies.

The cause is unknown in approximately, one-third of patients.

Patients with cardiac causes of syncope have higher rates of sudden cardiac death.

SYNCOPE: Etiology

REFLEX SYNCOPE (Neurally Mediated)VasovagalMediated by emotional distress (fear, pain, phobia, etc.)Mediated by orthostatic stressSituationalCough, sneezeGastrointestinal stimulation (swallowing, defecation, visceral pain)Post-MicturitionPost-PrandialPost-ExerciseOthers (laughter, weightlifting, etc.)Carotid sinus syncopeAtypical forms

SYNCOPE: Classification

CARDIOVASCULAR SYNCOPEArrhythmias Bradycardia:

• Sinus node dysfunction• Atrioventricular conduction system disease• Implanted device malfunction

Tachycardia:

• Supraventricular• Ventricular

Drug-induced bradycardia and tachyarrhythmiasStructural Disease

Cardiac: • Cardiac valvular disease• Myocardial infarction• Hypertrophic cardiomyopathy• Cardiac masses ( atrial myxomas, tumors, etc.)• Pericardial disease/ tamponade• Congenital anomalies

Others: Pulmonary embolus, aortic dissection, pulmonary hypertension

SYNCOPE: Classification

SYNCOPE DUE TO ORTHOSTATIC HYPOTENSIONPrimary Autonomic FailurePure autonomic failure, multiple system atrophy, Parkinson's disease with autonomic failure, Lewy body dementia.Secondary Autonomic FailureDiabetes, amyloidosis, uraemia, spinal cord injuriesDrug-induced Orthostatic HypotensionAlcohol, vasodilators, diuretics, phenothiazines, antidepressantsVolume DepletionHemorrhage, diarrhoea, vomiting, etc

SYNCOPE: Classification

Syncope occurs due to global cerebral hypoperfusion.

Brain parenchyma depends on adequate blood flow to provide a constant supply of glucose, the primary metabolic substrate.

Brain tissue cannot store energy in the form of high-energy phosphates found elsewhere in the body.

Cessation of cerebral perfusion lasting only 3-5 seconds can result in syncope.

SYNCOPE: Pathogenesis

Cerebral perfusion is maintained relatively constant by an intricate and complex feedback system involving:◦ Cardiac output, ◦ Systemic vascular resistance◦ Arterial pressure◦ Intravascular volume status◦ Cerebrovascular resistance◦ Metabolic regulation

Clinically significant defect in any of these may cause syncope.

SYNCOPE: Pathogenesis

Cardiac output can be diminished due to:◦ Mechanical outflow obstruction◦ Pump failure◦ Arrhythmias◦ Conduction defects

Systemic vascular resistance can drop due to:◦ Vasomotor instability◦ Autonomic failure◦ Vasovagal response

Mean arterial pressure can decrease due to all causes of hypovolemia.

Medications can affect CO, SVR or MAP.

SYNCOPE: Pathogenesis

Arrhythmias are the most common cardiac causes of syncope.

Arrhythmias lead to abrupt change in heart rate and the blood pressure may precipitously decline, especially in an upright position, causing transient loss of consciousness.

They usually cannot be diagnosed as they are paroxysmal and infrequent.

In contrast to vasovagal or other causes of syncope, arrhythmic syncope often occurs without warning.

Tachycardias are usually more hemodynamically unstable and are less well tolerated than bradycardias.

Common arrhythmic causes of syncope: sinus bradycardia, AV nodal block, sustained VT and SVT.

SYNCOPE: Pathogenesis

Edema is defined as a palpable swelling produced by expansion of interstitial fluid volume.

A variety of conditions are associated with the development of edema, including heart failure, cirrhosis and nephrotic syndrome.

EDEMA: Introduction

There are two basic steps involved in edema formation:◦ An alteration in capillary hemodynamics that

favors the movement of fluid from vascular space into interstitium.

◦ The retention of dietary or intravenously administered sodium and water by the kidneys.

Edema doesnt become apparent until the interstitial volume has increased by atleast 2.5 to 3 litres.

EDEMA: Pathophysiology

Capillary Hemodynamics The exchange of fluid between plasma and interstitium is

is determined by the hydraulic and oncotic pressures. The relationship between the two has been described by

Starling’s Law:◦ Net Flitration = Lps x (Delta Hydraulic pressure – Delta Oncotic

Pressure)◦ ‘Lp’ is the unit of permeability of the capillary wall and ‘s’ is the

surface area available for fluid movement. Edema formation occurs when there is alteration of

capillary dynamics:◦ Elevation in capillary hydraulic pressure◦ Increased capillary permeability◦ Lower plasma oncotic pressure.

EDEMA: Pathophysiology

Heart failure can be produced by a variety of disorders, including coronary artery disease, hypertension, cardiomyopathies, valvular disease and cor pulmonale.

Edema in the different causes is due to:◦ An increase in venous pressure (augmentation of

blood volume) that produces a parallel rise in capillary hydraulic pressure.

◦ Renal sodium retention due to reduced perfusion of kidneys.

Site of edema accumulation is variable and dependent upon nature of cardiac disease.

EDEMA: Pathophysiology

Coronary artery disease, hypertensive heart disease and left-sided valvular disease tend to preferentially impair left ventricular function. As a result, these disorders typically present with pulmonary but not peripheral edema.

Cor pulmonale is initially associated with pure right ventricular failure, resulting in prominent edema of lower extremities, and perhaps, ascites.

Cardiomyopathies tend to produce equivalent invovlement of both right and left ventricles, leading to simultaneous onset of pulmonary and peripheral edema.

Peripheral edema is usually pitting (5 seconds), as it reflects movement of interstitial fluid in response to pressure.

EDEMA: Pathophysiology

Fatigue is a subjective feeling of tiredness which is distinct from weakness, and has a gradual onset.

Fatigue can be alleviated by periods of rest. Fatigue can have physical or mental causes. Prolonged fatigue is self-reported, persistent

fatigue lasting for at least one month, whereas chronic fatigue lasts for six months.

Chronic fatigue is a symptom of heart disease.

FATIGUE: Introduction

It is defined as extreme generalized edema characterised by widespread swelling of the skin due to effusion of fluid into the extracellular space.

It is usually caused by liver failure, renal failure, right heart failure and severe malnutrition.

ANASARCA

Increasing fatigue is a symptom of cardiovascular disease.

It occurs because less blood reaches the muscles and the tissues due to reducing pumping ability of the heart.

The body diverts blood away from the less vital organs.

Causes:◦ Congestive heart failure◦ Coronary artery disease◦ Valvular heart disease◦ Cor pulmonale

FATIGUE: Etiology

Autoimmune diseases (Celiac, Lupus, MS, Myasthenia Gravis, Sjorgen’s etc.) Blood disorders (Anemia & Hemochromatosis) Chronic Fatigue Syndrome Drug abuse including alcohol abuse Depression Eating disorders Endocrine diseases (Diabetes, Hypothyroidism) Fibromyalgia HIV Gulf war syndrome Infection diseases (Infectious Mononucleosis) IBS Leukemia or Lymphoma Physical Trauma Liver Failure Neurological disorders (Narcolepsy, Parkinson’s, Post-concussion syndrome) Stroke Sleep Disorders Uremia Medications (Lithium salts, Ciprofloxacin, Beta Blockers)

FATIGUE: Etiology

Harrison’s Principles of Internal Medicine www.uptodate.com www.medscape.com

REFERENCES

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