Same as idiojunctional rhythm.
Surgical intervention for preexcitation syndromes may involve cutting the accessory pathways.
Isolated right bundle branch block (RBBB) or left bundle branch block (LBBB) or hemiblock not treated, if acute and/or associated with acute anterior MI, treated with permanent pacer and vigorous pharmacology.
Systolic hypertension is the most significant factor in causing target organ damage.
The acute form of orthostatic hypotension is caused by a delay in the normal regulatory mechanisms.
Pharmacologic until pacemaker inserted, temporary pacing if caused by inferior MI because ischemia usually resolves.
Conduction of impulse through intercalated disks because conduction system transiently blocked because of hypoxia, electrolyte imbalances, digoxin toxicity, excessively rapid rates of discharge.
Chronic venous insufficiency is inadequate venous return over a long period that causes pathologic ischemic changes in the vasculature, skin, and supporting tissues.
These genes interact with diet, smoking, age, and the other risk factors to cause chronic changes in vasomotor tone and blood volume.
The treatment for aberrant conduction if ventricular rate abnormalities are present is to correct the underlying cause.
Inflammation of the pericardium (pericarditis).
Mitral valve prolapse.
A localized dilation of a vessel wall to which the aorta is particularly susceptible.
As systolic heart failure or diastolic heart failure.
Mainly trauma to the long bones, either through defective fat metabolism after trauma or through the release of fat globules from bone marrow exposed by fracture.
May result from third-degree block or accelerated junctional or ventricular rhythm, or be caused by sinus, atrial, and junctional bradycardias.
None.
DVT occurs in individuals who have venous stasis (immobility, age, left heart failure), spinal cord injury, vein wall damage (trauma, intravenous medications), or hypercoagulable states (pregnancy, oral contraceptives, malignancy, genetic coagulopathies).
Hypertension is managed pharmacologically using diuretics, adrenergic blockers, calcium channel blockers, ACE inhibitors, and Ang II receptor blockers.
In preexcitation syndromes, the PR interval is greater than 0.12 seconds and the QRS duration is greater than 0.11 seconds due to the presence of a delta wave in the PR interval.
Cardiac function may be severely impaired.
Infective endocarditis.
Antibiotic therapy.
A connection between the vascular compartment and a source of air.
Increased peripheral vascular resistance.
Abnormalities in the SNS, RAAS, arginine vasopressin, natriuretic peptides, inflammatory cytokines, and myocyte metabolism.
Advanced age, male gender (younger than age 60), hypertension, dyslipidemia, diabetes mellitus, smoking, obesity, sedentary lifestyle, psychosocial factors, elevated CRP, and possibly infectious agents.
Profound ischemia, hyperkalemia, acidosis.
P absent, QRS >300 and usually not observable.
Conservative, usually do not progress in severity, pharmacologic treatment includes vagolytics, sympathomimetics, pacing.
None.
Congenital presence of accessory pathways (bundle of Kent and fiber of Mahaim) that conduct very rapidly and bypass the AV node, causing early ventricular depolarization in relation to atrial depolarization, prone (reason unknown) to tachycardias and atrial fibrillation that can result in very rapid ventricular rates.
Hypertension is a sustained elevation of the systemic arterial blood pressure resulting from increases in cardiac output or total peripheral resistance, or both.
The compensatory vasoconstriction response to standing is altered by a marked vasodilation and blood pooling in the muscle vasculature.
The treatment goal for preexcitation syndromes is to line up refractory periods of the accessory pathway and AV node to prevent reentry.
Size of the cardiac muscle walls and chambers.
Rheumatic heart disease, a potentially disabling cardiovascular disorder.
Thrombi, air, amniotic fluid, bacteria, fat, and foreign matter.
Contractility, preload, and afterload.
A form of arteriosclerosis and the leading cause of coronary artery and cerebrovascular disease.
Increasing contractility and reducing preload and afterload.
Hypokalemia (<3.5 mEq/L), faulty cell metabolism low in bundle of His, MI, especially inferior wall, as nodal artery interrupted; results in ischemia of AV node.
None unless ventricular rate abnormalities present.
Varicosities may be caused by damaged valves as a result of trauma to the valve or by chronic venous distention involving gravity and venous constriction.
Primary hypertension is the result of extremely complicated interactions of genetics and the environment mediated by a host of neurohumoral effects.
The QRS duration in aberrant conduction is greater than 0.11 seconds.
Dysrhythmias, congestive heart failure, and sudden death.
A prosthetic heart valve.
Vegetations that collect on the valve leaflets.
The lower extremities, the brain, and the heart.
Myocardial ischemia.
Age, family history, gender, smoking, dyslipidemia, hypertension, and diabetes.
Risk factor reduction and antiplatelet therapy.
From occasional missed beats or rapid beats to disturbances that impair myocardial contractility and are life-threatening.
Myocyte necrosis occurs, which is called myocardial infarction (MI).
By measuring serum enzymes, such as creatinine kinase and troponins, as well as looking for characteristic changes in the ECG.
P waves present and independent of QRS, but not always because of block (e.g., ventricular tachycardia).
Correct underlying cause.
Venous stasis ulcers follow the development of chronic venous insufficiency.
The most frequently cited theories of the pathogenesis of primary hypertension include overactivity of the SNS; overactivity of the RAAS; alterations in other neurohumoral mediators of blood volume and vasomotor tone such as ANP, BNP, and adrenomedullin; inflammation; a complex interaction involving insulin resistance and endothelial function; and obesity-related hormonal changes.
Aberrant conduction is caused by conduction of impulse through intercalated disks because the conduction system is transiently blocked due to hypoxia, electrolyte imbalances, digoxin toxicity, or excessively rapid rates of discharge.
Symptoms that are physically troublesome but not life-threatening.
They do not position themselves properly.
Severe valve abnormalities, chronic bacteremia, and systemic emboli.
Tissue death in lungs, kidneys, and mesentery.
It is increased.
Spasm or occlusion of the coronary arteries, most often the result of atherosclerotic lesions that limit the flow of blood to the heart.
Same as sinus bradycardia.
P absent or independent, QRS absent.
Same as junctional tachycardia.
Same as sinus block.
Treat according to cause, pacemaker or reducing rate of AV or ventricular discharge, or increasing rate of sinus or AV node discharge.
DVT is often asymptomatic but may lead to fatal pulmonary emboli.
Nonpharmacologic methods to manage hypertension include cessation of smoking, dietary modifications, and exercise.
Preexcitation syndromes are caused by the congenital presence of accessory pathways (bundle of Kent and fiber of Mahaim) that conduct very rapidly and bypass the AV node, causing early ventricular depolarization in relation to atrial depolarization.
A diverse group of primary myocardial disorders that are poorly understood.
An inflammatory disease that results from a delayed autoimmune response to a streptococcal infection.
A mobile aggregate of a variety of substances that occludes the vasculature.
The heart rate and stroke volume.
Raynaud disease, variant angina, and Buerger disease.
It can rupture, resulting in thrombosis and vasoconstriction that leads to obstruction of the lumen and inadequate perfusion of distal tissues.
The inability of the heart to adequately supply the body with blood-borne nutrients despite adequate volume and normal or elevated myocardial contractility.
The acute coronary syndromes result.
Subendocardial infarction and transmural infarction.
P absent or independent, QRS >0.11 and rate 20 or less.
Early beats with P waves, QRS occasionally opposite in deflection from usual QRS.
Same as PVCs.
None.
Decreased cardiac output from loss of atrial contribution to ventricular preload, variable effect on myocardial demand, depending on ventricular rate.
P present with QRS for each P, PR interval >0.12 and QRS >0.11 because of presence of delta wave in PR interval.
Venous stasis ulcers probably develop as a result of the borderline metabolic state of the cells in the affected extremities.
Clinical manifestations of hypertension result from damage of organs and tissues outside the vascular system, including heart disease, renal disease, CNS problems, and retinal changes.
Preexcitation syndromes include Wolff-Parkinson-White and Lown-Ganong-Levine.
Fluid (pericardial effusion).
Severe subjective symptoms or it may be completely asymptomatic.
A clot that remains attached to a vascular wall.
An inability of the heart to generate an adequate cardiac output to perfuse vital tissue.
Through trauma and in a hospital setting where intravenous and intra-arterial lines are being used.
Elevated CRP, increased serum fibrinogen, oxidative stress, infection, and periodontal disease.
Left heart failure and/or diffuse hypoxic pulmonary disease, such as COPD, cystic fibrosis, and ARDS.
Because of an abnormal rate of impulse generation or the abnormal conduction of impulses.
Same as accelerated junctional rhythm.
Same as PVCs, including electrical cardioversion.
Local hypoxia, scarring of intra-atrial conduction pathways, electrolyte imbalances, increased atrial preload.
Same as sinus block.
Always AV dissociation, same as idiojunctional rhythm.
QRS >0.11.
Varicosities are areas of veins in which blood has pooled, usually in the saphenous veins.
The risk factors for hypertension include a positive family history; male gender; advanced age; black race; obesity; high sodium intake; low potassium, calcium, and magnesium intake; diabetes mellitus; labile blood pressure; cigarette smoking; and heavy alcohol consumption.
The chronic forms of orthostatic hypotension are secondary to a specific disease or are idiopathic.
Characteristic heart sounds, cardiac murmurs, and systemic complaints.
Fainting, cardiovascular symptoms, impotence, and bowel and bladder dysfunction.
An inability of the heart to supply the metabolism with adequate circulatory volume and pressure.
Yes, they may be large enough to form an embolus.
The vicious cycle of decreasing contractility, increasing preload, and increasing afterload.
Singly or with systolic heart failure.
By noninvasive techniques of assessing coronary flow with or without exercise (stress ECG, thallium, or SPECT).
Aggressively with antithrombotic agents to prevent myocardial infarction (MI).
Same as sinus bradycardia.
Absent or barely present cardiac output and pulse, not compatible with life.
Pharmacology to change thresholds, refractory periods; reduce myocardial demand, increase supply, removal of cause.
Progressive prolongation of PR interval until one QRS is dropped, pattern of prolongation resumes.
P waves present and independent of QRS with no observed relationship between P and QRS.
QRS >0.11, R-S-R' in V1, V2, V5, V6.
Prevention and careful assessment in individuals at risk are crucial in managing DVT.
Orthostatic hypotension is a drop in blood pressure that occurs on standing.
Individuals with preexcitation syndromes are prone to tachycardias and atrial fibrillation that can result in very rapid ventricular rates.
As dilated (congestive), restrictive (rigid and noncompliant), and hypertrophic (asymmetric).
The disorder usually resolves without sequelae.
Myocarditis, endocarditis, pericarditis, and cardiomyopathy.
Ischemia and necrosis.
Ventricular emptying.
Pulmonary vascular congestion and inadequate systemic perfusion.
An imbalance between coronary supply of blood and myocardial demand for oxygen and nutrients, leading to reversible myocardial ischemia or irreversible infarction.
Reversible myocardial ischemia and is a harbinger of impending infarction.
P absent or independent, QRS >0.11 and rate 60-21.
Same as agonal rhythm, including electrical defibrillation.
PR interval >0.2.
More aggressively than Mobitz I because block can progress to type III, pacemaker after pharmacologic treatment.
Faulty cell metabolism in right and left bundle branches, RBBB more common than LBBB because of dual blood supply to left bundle branch, congestive heart failure, mitral regurgitation, especially anterior MI, because of infarct of fascicles, left anterior hemiblock more common than left posterior hemiblock, since posterior fascicles have dual blood supply.
Aimed at lining up refractory periods of accessory pathway and AV node to prevent reentry, may slow rate with pharmacology, may surgically cut pathways.
Hypertension can be primary (without known cause) or secondary (caused by disease or drugs).
Orthostatic hypotension may be acute or chronic.
The rate in preexcitation syndromes can be slowed with pharmacology.
Properly functioning cardiac valves.
A general term for infection and inflammation of the endocardium, especially the cardiac valves.
Left heart failure.
Amniotic fluid may be forced into the bloodstream during the labor and delivery of pregnancy.
The left ventricle, resulting in hypertrophy and ventricular remodeling.
Atherosclerosis of arteries that perfuse the limbs, especially the lower extremities.
Chronic coronary obstruction results in recurrent predictable chest pain called stable angina. Abnormal vasospasm of coronary vessels results in unpredictable chest pain called Prinzmetal angina. Myocardial ischemia that does not cause detectable symptoms is called silent ischemia.
Sudden cardiac death.
Depolarization and contraction not coupled: electrical activity present with little or no mechanical activity, usually caused by profound hypoxia.
P absent or independent, QRS >0.11 and rate 41-99.
Same as PVCs.
Rapid infusion of potassium, same as PVCs including electrical defibrillation.
Same as sinus block.
Congenital or acquired disorders that result in stenosis or incompetence or both.
A wide range of conditions.
Mitral and aortic valvular disease and atrial fibrillation.
Myocardial infarction (MI).
It begins with endothelial injury and progresses through several stages to become a fibrotic plaque.
It is often asymptomatic but can present with intermittent claudication (pain in leg on walking).
A disturbance of heart rhythm.
Because of transient episodes of thrombotic vessel occlusion and vasoconstriction at the site of plaque damage, with return of perfusion before significant myocardial necrosis occurs.
No cardiac output, not compatible with life.
Same as PVCs.
Occasional decrease in cardiac output, increase in preload for the following beat.
Same as sinus block.
Hypertension-induced myocardial hypertrophy and ischemia with resultant ventricular remodeling.
Lifestyle changes, vasodilators, antithrombotics, PCI, or CABG surgery.
ST-segment elevations on the ECG (STEMI).
Thrombolytic drugs, antithrombotic drugs, vasodilators, PCI, or immediate surgery.
Vigorous pharmacology aimed at restoring rate and force, usually ineffective, may attempt to pace.
P absent or independent, QRS >0.11 and rate 100 or more.
Occasionally absent P, with loss of QRS for that beat.
Hypokalemia (<3.5 mEq/L), faulty cell metabolism in atrioventricular (AV) node, severity increases as heart rate increases, supports theory that AV node is fatiguing, digoxin toxicity, beta-blockade, coronary artery disease (CAD), myocardial infarction (MI), hypoxia, increased preload, valvular surgery and disease, diabetes.
Anemia, septicemia, hyperthyroidism, and beriberi.
Myocardial infarction (MI).
Hibernating, stunning, and remodeling of the myocardium.
That additional myocardium is still at risk for recurrent ischemia and infarction.
Impulse originates in cell outside normal conduction system and spreads through intercalated disks.
Same as PVCs.
Conservative, discovery and correction of cause.
Same as PJCs.
Same as ventricular standstill.
Hyperkalemia (>7 mEq/L), hypokalemia (<3.5 mEq/L), formation of myocardial abscesses in endocarditis.
Hypokalemia (<3.5 mEq/L), faulty cell metabolism below AV node, antidysrhythmics, cyclic antidepressants, CAD, MI, hypoxia, increased preload, valvular surgery and disease, diabetes.
