Common Clinical Conditions Flashcards
Aneurysm
Abnormal dilations of arteries caused by weakening of the arterial wall. Common causes: hypertension, atherosclerosis, infection, trauma, and hereditary or acquired connective tissue disorders. AUsually asymptomatic but can cause pain and lead to ischemia, thromboembolism, spontaneous dissection, and rupture, which may be fatal.
Diagnosis is by imaging tests (eg, ultrasonography, CT angiography, magnetic resonance angiography, aortography). Treatment of unruptured aneurysms is with risk factor modification (eg, strict BP control) plus surveillance imaging or with open or endovascular stent-graft surgery, depending on size and location of the aneurysm and presence of symptoms. Treatment of ruptured aneurysms: immediate repair with open surgical synthetic graft or an endovascular stent graft. Aneurysms, defined as a ≥ 50% increase in arterial diameter compared with normal segments, result from localized weakening of an arterial wall. True aneurysms involve all 3 layers of the artery (intima, media, and adventitia). Aneurysms may occur in any artery. Abdominal and thoracic aortic aneurysms are most common and significant.
Arrhythmia
The normal heart beats in a regular, coordinated way because electrical impulses generated and spread by myocytes with unique electrical properties trigger a sequence of organized myocardial contractions. Arrhythmias and conduction disorders are caused by abnormalities in the generation or conduction of these electrical impulses or both. Any heart disorder, including congenital abnormalities of structure (eg, accessory atrioventricular connection) or function (eg, hereditary ion channelopathies), can disturb rhythm. Systemic factors that can cause or contribute to a rhythm disturbance include electrolyte abnormalities, hypoxia, hormonal imbalances (eg, hypothyroidism, hyperthyroidism), and drugs and toxins (eg, alcohol, caffeine).
Cardiac Tamponade
Accumulation of blood in the pericardial sac of sufficient volume and pressure to impair cardiac filling. Patients typically have hypotension, muffled heart tones, and distended neck veins. Diagnosis is made clinically and often with bedside echocardiography. Treatment is immediate pericardiocentesis or pericardiotomy.
Cardiac Valve Diesease (Heart Murmurs)
2 types: stenosis and insufficiency. Sometimes combined
Valvular stenosis: results from a narrowing of the valve orifice that is usually caused by a thickening and increased rigidity of the valve leaflets, often accompanied by calcification–> the valve does not open completely –> high resistance to flow + a large pressure gradient across the valve when blood is flowing through the valve. In other words, pressure increases in the chamber proximal to the valve, decreases in the chamber or artery distal to the valve.
Valvular insufficiency: valve leaflets do not completely seal when the valve is closed–> regurgitation of blood (backward flow of blood) into the proximal chamber. Example: in aortic valve insufficiency blood regurgitates from the aorta into the left ventricle after ventricular ejection.
Coronary Artery Disease (CAD)
Impairment of blood flow through the coronary arteries, most commonly by atheromas.
Clinical presentations: silent ischemia, angina pectoris, acute coronary syndromes (unstable angina, MI), and sudden cardiac death.
Diagnosis: by symptoms, ECG, stress testing, and sometimes coronary angiography. Prevention: modifying reversible risk factors (eg, hypercholesterolemia, hypertension, physical inactivity, obesity, and smoking). Treatment: drugs and procedures to reduce ischemia and restore or improve coronary blood flow.
Coronary artery disease (CAD)–> changes in both structure and function of the blood vessels. Atherosclerotic processes cause an abnormal deposition of lipids in the vessel wall, leukocyte infiltration and vascular inflammation, plaque formation and thickening of the vessel wall. These changes lead to a narrowing of the lumen (i.e., stenosis), which restricts blood flow. There are also subtle, yet functionally important changes that can occur before overt changes in structure are observed. Early in the disease process, the endothelial cells that line the coronary arteries become dysfunctional. Because the endothelium produces important substances such as nitric oxide and prostacyclin that are required for normal coronary function, endothelial dysfunction can lead to coronary vasospasm, impaired relaxation, and formation of blood clots that can partially or completely occlude the vessel.
Deep Vein Thrombosis
Clotting of blood in a deep vein of an extremity (usually calf or thigh) or the pelvis. DVT is the primary cause of pulmonary embolism. DVT results from conditions that impair venous return, lead to endothelial injury or dysfunction, or cause hypercoagulability. DVT may be asymptomatic or cause pain and swelling in an extremity; pulmonary embolism is an immediate complication. Diagnosis is by history and physical examination and is confirmed by objective testing, typically with duplex ultrasonography. d -Dimer testing is used when DVT is suspected; a negative result helps to exclude DVT, whereas a positive result is nonspecific and requires additional testing to confirm DVT. Treatment is with anticoagulants. Prognosis is generally good with prompt, adequate treatment.
Edema
Edema is swelling of soft tissues due to increased interstitial fluid. The fluid is predominantly water, but protein and cell-rich fluid can accumulate if there is infection or lymphatic obstruction. Edema results from increased movement of fluid from the intravascular to the interstitial space or decreased movement of water from the interstitium into the capillaries or lymphatic vessels. Edema can be highly localized as occurs in a small region of the skin subjected to a bee sting. Edema, however, can also comprise an entire limb, specific organs such as the lungs (e.g., pulmonary edema) or the whole body.
Heart Failure
Heart failure (HF) is a syndrome of ventricular dysfunction. Left ventricular failure causes shortness of breath and fatigue, and right ventricular failure causes peripheral and abdominal fluid accumulation; the ventricles can be involved together or separately. Heart failure is the inability of the heart to supply adequate blood flow and therefore oxygen delivery to peripheral tissues and organs. Under-perfusion of organs leads to reduced exercise capacity, fatigue, and shortness of breath. It can also lead to organ dysfunction (e.g., renal failure) in some patients.
In HF, the heart may not provide tissues with adequate blood for metabolic needs, and cardiac-related elevation of pulmonary or systemic venous pressures may result in organ congestion. This condition can result from abnormalities of systolic or diastolic function or, commonly, both. Although a primary abnormality can be a change in myocyte function, there are also changes in collagen turnover of the extracellular matrix. Cardiac structural defects (eg, congenital defects, valvular disorders), rhythm abnormalities (including persistently high heart rate), and high metabolic demands can also cause HF.
Systolic dysfunction
In systolic dysfunction (also called HF with reduced EF), the ventricle contracts poorly and empties inadequately, leading initially to increased diastolic volume and pressure and decreased EF. Predominant systolic dysfunction is common in HF due to MI, myocarditis, and dilated cardiomyopathy. Systolic dysfunction may affect primarily the LV or the right ventricle (RV); LV failure often leads to RV failure.
Diastolic dysfunction
In diastolic dysfunction (also called HF with preserved EF), ventricular filling is impaired, resulting in reduced ventricular end-diastolic volume, increased end-diastolic pressure, or both. Contractility and hence EF remain normal; EF may even increase as the poorly filled LV empties more completely to maintain CO. Markedly reduced LV filling can cause low CO and systemic symptoms. Elevated left atrial pressures can cause pulmonary hypertension and pulmonary congestion. Diastolic dysfunction usually results from impaired ventricular relaxation (an active process), increased ventricular stiffness, valvular disease, or constrictive pericarditis. Acute myocardial ischemia is also a cause of diastolic dysfunction. Resistance to filling increases with age, probably reflecting myocyte loss and increased interstitial collagen deposition; thus, diastolic dysfunction is particularly common among the elderly. Diastolic dysfunction predominates in hypertrophic cardiomyopathy, disorders with ventricular hypertrophy (eg, hypertension, significant aortic stenosis), and amyloid infiltration of the myocardium. LV filling and function may also be impaired if marked increases in RV pressure shift the interventricular septum to the left. Diastolic dysfunction has increasingly been recognized as a cause of HF. Estimates vary, but about 50% of patients with HF have diastolic dysfunction and a normal EF; the prevalence increases with age and with diabetes.
LV failure
In failure due to LV dysfunction, CO decreases and pulmonary venous pressure increases. When pulmonary capillary pressure exceeds the oncotic pressure of plasma proteins (about 24 mm Hg), fluid extravasates from the capillaries into the interstitial space and alveoli, reducing pulmonary compliance and increasing the work of breathing. Lymphatic drainage increases but cannot compensate for the increase in pulmonary fluid. Marked fluid accumulation in alveoli (pulmonary edema) significantly alters ventilation/perfusion (V/Q) relationships: Deoxygenated pulmonary arterial blood passes through poorly ventilated alveoli, decreasing systemic arterial oxygenation and causing dyspnea. However, dyspnea may occur before V/Q abnormalities, probably because of elevated pulmonary venous pressure and increased work of breathing; the precise mechanism is unclear.
RV failure
Systemic venous pressure increases –> fluid extravasation and consequent edema, primarily in dependent tissues (feet and ankles of ambulatory patients) and abdominal viscera. The liver is most severely affected, but the stomach and intestine also become congested; fluid accumulation in the peritoneal cavity (ascites) can occur.
Hypertension
Hypertension is sustained elevation of resting systolic BP (≥ 140 mm Hg), diastolic BP (≥ 90 mm Hg), or both. Hypertension with no known cause (primary; formerly, essential hypertension) is most common. Hypertension with an identified cause (secondary hypertension) is usually due to chronic kidney disease or primary aldosteronism. Usually, no symptoms develop unless hypertension is severe or long-standing. Diagnosis is by sphygmomanometry. Tests may be done to determine cause, assess damage, and identify other cardiovascular risk factors. Treatment involves lifestyle changes and drugs, including diuretics, β - blockers, ACE inhibitors, angiotensin II receptor blockers, and Ca channel blockers.
Hypotension
Hypotension is a physiologic state in which the arterial blood pressure is abnormally low. For an adult, hypotension exists when the systolic pressure is less than 90 mmHg and the diastolic pressure is less than 60 mmHg. Because arterial pressure is determined by cardiac output, venous pressure and systemic vascular resistance (Click here for more details), a reduction in any of these variables can lead to hypotension.
Orthostatic hypotension
Orthostatic (postural) hypotension is an excessive fall in BP when an upright position is assumed. The consensus definition is a drop of > 20 mm Hg systolic, 10 mm Hg diastolic, or both. Symptoms of faintness, light-headedness, dizziness, confusion, or blurred vision occur within seconds to a few minutes of standing and resolve rapidly on lying down. Some patients experience falls, syncope (see Syncope), or even generalized seizures. Exercise or a heavy meal may exacerbate symptoms. Most other associated symptoms and signs relate to the cause. Orthostatic hypotension is a manifestation of abnormal BP regulation due to various conditions, not a specific disorder.
