Diseases Of Cardiovascular System

Diseases of Cardiovascular system

Chest Pain • Chest pain” is an imprecise term • It is often used to describe any pain, pressure, squeezing, choking, numbness or any other discomfort in the chest, neck, or upper abdomen, and is often associated with pain in the jaw, head, or arms • It can last from less than a second to days or weeks, can occur frequently or rarely, and can occur sporadically or predictably.

• Chest pain is merely a symptom, not a diagnosis • Many medical problems can cause chest pain, and before the chest pain can be adequately treated, the actual underlying cause needs to be identified

Differential Diagnosis of Chest Pain Cardiovascular

Typical angina pectoris Prinzmetal’s or variant angina Unstable or accelerating angina Acute myocardial infarction Aortic dissection Mitral valve prolapse Pericarditis Dressler’s syndrome Postpericardiotomy syndrome

Pulmonary

Pleuritic chest pain Pneumonia Pulmonary embolism Pulmonary hypertension Spontaneous pneumothorax

Gastrointestinal Reflux esophagitis Esophageal spasm/angina Peptic ulcer Pancreatitis Cholecystitis

Miscellaneous Herpes zoster Anxiety/depressive disorder Panic disorder Cocaine use Post coronary artery bypass pain

Musculoskeletal disorders Costochondritis Tietze’s syndrome Rib fracture or trauma Cancer metastasis Sternoclavicular arthritis Painful xiphoid syndrome Fibromyalgia Traumatic muscle pain Shoulder arthritis/bursitis Cervicothoracic nerve root compression Thoracic spine arthritis Throracic outlet syndrome

Differential Diagnosis of Chest Pain Myocardial ischemia • • Pain is described as dull, aching, or as a sensation of "pressure," "tightness," "squeezing," or "gas," rather than as sharp or spasmodic • Ischemic symptoms usually subside within 5–20 minutes but may last longer • Progressive symptoms or symptoms at rest may represent unstable angina due to coronary plaque rupture and thrombosis • One clue that the pain may be ischemic is other symptoms associated with the pain, such as shortness of breath, dizziness, a feeling of impending doom, and vagal symptoms, such as nausea and diaphoresis

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Myocardial infarction

• Pain is commonly accompanied by a sense of anxiety or uneasiness • The location is usually retrosternal or left precordial • Because there are no appropriate sensory nerves on the heart, the central nervous system (CNS) interpretation of pain location often results in pressure or “heaviness” being referred to the throat, lower jaw, shoulders, inner arms, upper abdomen, or back • Ischemic pain may be precipitated by exertion, cold temperature, meals, stress, or combinations of these factors and is usually relieved by rest, but many episodes do not conform to these patterns • It is not related to position or respiration and is usually not elicited by chest palpation • In myocardial infarction, a precipitating factor is frequently not apparent.

• Hypertrophy of either ventricle or stenotic aortic valvular disease may also give rise to ischemic pain or pain with less typical features • Myocarditis, pulmonary hypertension, and mitral valve prolapse are also associated with chest pain atypical for angina pectoris

• Reflux oesophagitis or Oesophageal spasm • The most common cause of chest pain • Heartburn • Worse in recumbent position, but also while straining, like angina pectoris • No ECG changes

• Aortic dissection • Classically produces an abrupt onset of tearing pain of great intensity that often radiates to the back • Pulses may be asymmetrical • Type A dissection sometimes obstructs the origin of a coronary artery (usually the right) with signs of impending inferoposterior infarction • Sometimes broad mediastinum on chest x-ray • New aortic valve regurgitation

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• Pericarditis Pericarditis may produce pain that is greater supine than upright Change of posture and breathing or swallowing influence the pain A friction sound may be heard ST-elevation but no reciprocal ST depression

• Pleuritis • A stabbing pain when breathing • The most common cause of stabbing pain is, however, caused by prolonged cough

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Pulmonary embolism

• Pain is not often marked • Tachypnoea, hypoxaemia, hypocarbia • No pulmonary congestion on chest x-ray • Clinical presentation may resemble hyperventilation. • Both arterial oxygen pressure (PaO2) and partial arterial pressure of carbon dioxide (PaCO2) decreased. • D-dimer assay positive

• Musculoskeletal Chest Pain • Pain on palpation • Cholecystitis • Character of pain; RUQ tenderness with + Murphy’s sign; age; gender; obesity; relationship to eating fatty foods • • Psychogenic • Unexplained chest pain and hyperventilation;

DIAGNOSTIC STUDIES • An immediate diagnostic study would include a 12 lead electrocardiogram (ECG) • Examine the ECG for Q waves and ST segment elevation greater than 1 mm in two contiguous leads which would indicate injury and/or myocardial infarction • ST segment depression greater than 0.5 mm is suggestive of myocardial ischemia • Further evaluation would include cardiac enzymes including CK-MB and a chest x-ray

Palpitations • Awareness of the heartbeat • It may be a normal phenomenon • It may reflect increased cardiac or stroke output in patients with many noncardiac conditions (eg, exercise, thyrotoxicosis, anemia, anxiety • It may also be due to cardiac abnormalities that increase stroke volume (regurgitant valvular disease, bradycardia)

• It may be a manifestation of cardiac dysrhythmia • Ventricular premature beats may be sensed as extra or "skipped" beats • Supraventricular or ventricular tachycardia may be felt as rapid, regular or irregular palpitations or "fluttering”

• If the abnormal rhythm is associated with a sufficient decline in arterial pressure or cardiac output, it may—especially in the upright position—impair cerebral blood flow, causing lightheadedness, blurring of vision, loss of consciousness (syncope), or other symptoms • Dizziness in particular is nonspecific and is an uncommon symptom of cardiac disease or dysrhythmia

Cardiogenic syncope Most commonly results from: • Bradyarrhythmias (sinus node arrest or exit block, atrioventricular [AV] conduction block) • Very rapid supraventricular rhythms • Ventricular tachycardia or fibrillation • The absence of premonitory symptoms helps distinguish cardiogenic syncope from vasovagal faints, postural hypotension, or seizure but is not a reliable screening tool • Although recovery is often immediate, some patients may exhibit seizure-like movements

• Aortic stenosis and hypertrophic obstructive cardiomyopathy may also cause syncope, which is usually exertional or postexertional

Neurocardiogenic syncope • Commonly known as vasovagal syncope • There is an inappropriate increase in vagal efferent activity, often resulting from a precedent increase in sympathetic cardiac stimulation • Syncope may follow presyncopal symptoms and may accompany a brief period of nausea and/or diaphoresis, or it may be abrupt in onset, mimicking arrhythmia-induced syncope

• Autonomic dysfunction due to venous insufficiency or peripheral neuropathy can result in a positional fall in blood pressure (BP), and supine and upright BPs should be checked in all patients with syncope • Carotid sinus hypersensitivity may also result in syncope that is related to stimulation of the baroreceptors in the carotid sinus • Gentle carotid massage while monitoring the BP and cardiac rhythm usually can elicit the response

Edema General Concepts • Edema is defined as soft tissue swelling due to expansion of the interstitial volume • Edema can be localized or generalized. 

• Generalized edema involves an increase in extracellular fluid only • Generalized edema is due to increases in both total body water and sodium • Generalized edema can occur with low, normal, or high serum sodium concentration. 

Mechanisms maintaining interstitial fluid volume • The volume of interstitial fluid is determined by Starling's Law: • Hydrostatic Pressure (capillary - tissue) - Oncotic pressure (capillary - tissue) = net fluid movement out of capillary into interstitium. • Oncotic pressure = osmotic pressure created by plasma protein molecules that are impermeable across the capillary membrane.

Causes of generalized edema I. Decreased oncotic pressure

•             Nephrotic syndrome •             Cirrhosis •             Malnutrition

II. Increased vascular permeability to proteins •             Angioneurotic edema (usually allergic)

III. Increased hydrostatic pressure •             Congestive heart failure •             Cirrhosis

IV. Obstruction of lymph flow •             Congestive heart failure

V. Inappropriate renal sodium and water retention •             Renal failure •             Nephrotic syndrome

Edema formation in congestive heart failure (CHF) • CHF implies a primary failure of the pumping ability of the heart • When the heart begins to fail, blood backs up in the venous system, while arterial volume is initially reduced • This reduction in arterial filling is detected by arterial volume receptors, triggering sympathetic nervemediated vasoconstriction in an attempt to restore the ratio of cardiac output to vascular capacitance • The net result of this vasoconstriction is that the brain, heart and lungs continue to receive as much blood flow as possible • In contrast, blood flow to the kidney and other organs is reduced, having been shunted to the organs necessary for immediate survival.  • Thus, blood flow to the kidney is reduced and the kidney begins to retain sodium and water.

• In more severe degrees of CHF, the patients can become hyponatremic • This occurs because more water is retained by the kidney than is sodium • In this setting, serum ADH levels are markedly elevated, resulting in a very concentrated urine • Additionally, proximal tubule sodium and water reabsorption are very high, permitting relatively little water to reach the urine • Finally, ADH stimulates thirst, resulting in increased water intake. 

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Edema formation in cirrhosis Cirrhosis of the liver is defined as increased

fibrous tissue in the liver associated with regeneration of focal areas of damaged liver parenchyma • If severe, scarring and distortion of normal liver architecture can lead to marked hepatic dysfunction. • This can cause sodium retention and edema formation by the following mechanisms: 1. Decreased total peripheral resistance: Damaged liver fails to degrade or overproduces vasodilating factors 2. Increased portal pressure (portal hypertension) 3. Decreased hepatic albumin synthesis

Edema formation in nephrotic syndrome • The nephrotic syndrome is defined as a glomerular disease which results in proteinuria (urinary protein losses of ≥ 3.5 gm/day), hypoproteinemia, edema, and hyperlipidemia • Most patients with nephrotic syndrome have an expanded plasma volume due to an intrinsic, as yet unidentified, defect in renal sodium and water excretion • Hypoalbuminemia due to urinary protein losses favors fluid movement from the intravascular to the interstitial compartment and exacerbates edema formation in the nephrotic syndrome • In some patients, urinary protein loss and hypoalbuminemia can be so severe that plasma volume becomes reduced, leading to renal hypoperfusion and further stimulating sodium and water retention

Rationale for treatment • Edema of the skin, particularly in the lower extremities can be painful, interferes with normal blood circulation, impairs wound healing, increases the likelihood of infection, and is unattractive • Ascites can impair normal respiration, decrease venous blood return to the heart, and promotes intraperitoneal infection • Pulmonary edema interferes with respiratory gas exchange and is a major cause of morbidity and mortality • Most importantly, edema is a sign of an underlying disease process which needs to be treated.

Treatment of edema • The basic approaches to treatment are as follows.   • 1. First, treat the underlying disease. • 2. Decrease sodium and water intake, either dietary or intravenous.  • 3. Increase excretion of sodium and water             a. Diuretics - remember, these are palliative, not curative.             b. Bed rest, local pressure • 4. Do not make the disease worse.  Other than treatment of severe pulmonary edema, treatment of edema is not usually an emergency.  The use of all diuretics entails one major risk: excessive diuresis • Overdiuresis causes volume depletion, hypotension, inadequate organ perfusion and a host of complications