Alterations in Cardiovascular Function

Infective Endocarditis: Clinical manifestations

-Fever -New/changed cardiac murmur -Petechial lesions of the skin, conjunctiva, and oral mucosa -Osler nodes: Painful erythematous nodules on the pads of the fingers and toes -Janeway lesions: Nonpainful hemorrhagic lesions on the palms and soles

Peripheral Edema

Clinical Manifestations Jugular venous distension and hepatosplenomegaly Patho Inability of the heart to provide adequate blood flow into the pulmonary circulation at a normal central venous pressure

RA: Clinical Manifestations and Tx

Clinical manifestations -Carditis: Murmur -Polyarthritis: Large joints mainly affected -Chorea: Sudden, aimless, irregular, involuntary movements -Erythema marginatum: Truncal rash Tx: 10-day regimen of abx, NSAIDs, may need abx for 5 years

2 Major types of MI (was on Exam 1)

1. Subendocardial infarction -not associated with ST-segment elevations (non-STEMI) but suggest that additional myocardium is still at risk for recurrent ischemia and infarction. 2. Transmural infarction -Individuals at highest risk for complications -ST segment elevations (STEMI) on the ECG --requires immediate intervention. -Smaller infarctions are not associated with ST segment elevations (non-STEMI) -Suggest that additional myocardium is still at risk for recurrent ischemia and infarction

Clinical Manifestations and Tx of Atheroscerlosis

Clinical manifestations Depends on the organ affected. Symptoms and signs are the result of inadequate perfusion of tissues. Treatment Focuses on reducing risks factors, removing the initial causes of vessel damage, and preventing lesion progression. Exercising, smoking cessation, and controlling hypertension and diabetes when appropriate while reducing LDL cholesterol levels by diet or medications or both.

D/O of the Heart Wall: D/O of the pericardium: Pericardial Effusion

Accumulation of fluid in the pericardial cavity Tamponade Treatment: Pericardiocentesis

Systolic heart failure: Clinical manifestations and Tx

Clinical manifestations Dyspnea, orthopnea, cough of frothy sputum Fatigue Decreased urine output and edema Tx: O2 Administer nitrates, morphine, diuretics, ACE inhibitors, aldosterone blockers, and/or beta-blockers Increase contractility Reduce preload and afterload

A person with an MI is releasing angiotensin II. How should the nurse interpret this finding? Releasing angiotensin II is: 1. Beneficial; it helps the heart pump effectively. 2. Counterproductive; it causes the heart to work harder. 3. Beneficial; it decreases the release of catecholamines. 4. Counterproductive; it causes myocardial stunning.

ANSWER AND RATIONALE: 2. Counterproductive; it causes the heart to work harder. Angiotensin II is released during myocardial ischemia and contributes to the pathogenesis of MI in several ways. First, it results in the systemic effects of peripheral vasoconstriction and fluid retention. These homeostatic responses are counterproductive in that they increase myocardial work and thus exacerbate the effects of the loss of myocyte contractility. Angiotensin II is also released locally, where it is a growth factor for vascular smooth muscle cells, myocytes, and cardiac fibroblasts; promotes catecholamine release; and causes coronary artery spasm. 4. Stunning is caused by the alterations in electrolyte pumps, calcium homeostasis, and the release of toxic oxygen radicals. Angiotensin II is involved in remodeling, not stunning.

A person has a dx of valvular regurgitation. What pathophysiologic process is the person experiencing? The valves: 1. Are constricted and narrowed, impeding the forward flow of blood. 2. Fail to shut completely, permitting the backflow of blood to continue. 3. Have an inherited defect, such as thickening of the septal wall. 4. Cause acute pericarditis and filling of the pericardial sac.

ANSWER AND RATIONALE: 2. Fail to shut completely, permitting the backflow of blood to continue. In valvular regurgitation (also called insufficiency or incompetence) the valve leaflets, or cusps, fail to shut completely, permitting blood flow to continue even when the valve is supposed to be closed. 1. In valvular stenosis the valve orifice is constricted and narrowed, impeding the forward flow of blood and increasing the workload of the cardiac chamber proximal to the diseased valve. 3. Hypertrophic obstructive cardiomyopathy is the most common inherited heart defect, occurring in 1 of 500 individuals through autosomal dominant inheritance. It is characterized by thickening of the septal wall. 4.Acute pericarditis is acute inflammation of the pericardium. The etiology of acute pericarditis is most often idiopathic or caused by viral infection by coxackie, influenza, hepatitis, measles, mumps, or varicella viruses.

A person has atherosclerosis. Which pathophysiologic process has occurred? 1. Fatty streaks produce foam cells that accumulate and block the flow of blood in the vessel. 2. Macrophages release enzymes and toxic oxygen radicals that create oxidative stress. 3. Vasospasm in the small arteries from an imbalance between vasodilation and vasoconstriction produce fibrous plaque. 4. Significant T-cell activation and a lack of endothelial precursor cells affect blood vessel linings.

ANSWER AND RATIONALE: 2. Macrophages release enzymes and toxic oxygen radical that create oxidative stress. Macropages adhere to the injured vessels wall. These macrophages then release enzymes and toxic oxygen radicals that create oxidative stress, oxidize LDL, and further injure the vessel wall. 1. Foam cells produce a fatty streak; once lipid-laden foam cells accumulate in significant amounts, they form a lesion called a fatty streak. 3. Raynaud phenomenon and Raynaud disease are characterized by attacks of vasospasm in the small arteries and arterioles of the fingers and, less commonly, the toes. Blood vessels in affected individuals with Raynaud disease demonstrate endothelial dysfunction with an imbalance in endothelium-derived vasodilators (e.g., nitric oxide) and vasoconstrictors (e.g., endothelin-1). In atherosclerosis, fatty streaks produce more toxic oxygen radicals and cause immunologic and inflammatory changes, resulting in progressive damage to the vessel wall. At this point, smooth muscle cells proliferate, produce collagen, and migrate over the fatty streak forming a fibrous plaque. 4. There is evidence of significant T-cell activation and autoimmunity, as well as a lack of appropriate production of endothelial precursor cells in the bone marrow for people with Thromboangiitis obliterans (Buerger disease).

Systolic heart failure is associated with the activation of the: 1. Parasympathetic nervous system 2. Hypothalamic pituitary adrenal axis 3. Renin-angiotensin-aldosterone system (RAAS) 4. Antidiuretic hormone (ADH) vasopressin aldosterone system

ANSWER AND RATIONALE: 3. Renin-angiotensin-aldosterone system (RAAS). Activation of the RAAS causes not only increases in preload and afterload but also direct toxicity to the myocardium. Ang II mediates remodeling of the ventricular wall, contributing to sarcomere death, loss of the normal collagen matrix, and interstitial fibrosis. This leads to decreased contractility, changes in myocardial compliance, and ventricular dilation. 1. The sympathetic nervous system is chronically activated with heart failure. Secondary causes of decreased contractility, such as myocardial ischemia and increased myocardial workload, contribute to inflammatory, immune, and neurohumoral changes (activation of the SNS and RAAS) that mediate a process called ventricular remodeling. 2. The hypothalamic pituitary adrenal axis is not a component of heart failure. 4. There is no such system as the ADH vasopressin aldosterone system. However, ADH and aldosterone are components of systolic heart failure.

D/O of the Heart Wall: D/O of the pericardium: Acute pericarditis

Acute inflammation of the pericardium Clinical manifestations: Fever, myalgias, and malaise, followed by the sudden onset of severe chest pain Disturbing Sx's but not life threatening Treatment: Rest, salicylates and nonsteroidal antiinflammatory drugs; combined nonsteroidals and colchicine

Coronary Artery Disease

Any vascular disorder that narrows or occludes the coronary arteries Results in an imbalance between coronary supply of blood and myocardial demand for oxygen and nutrients Reversible myocardial ischemia or irreversible infarction may result. Most common cause: Atherosclerosis Nonmodifiable risk factors Advanced age; family history Male gender or women after menopause Results in an imbalance between coronary supply of blood and myocardial demand for oxygen and nutrients so that reversible myocardial ischemia or irreversible infarction may result.

Peripheral Artery Disease

Atherosclerotic disease of arteries that perfuse limbs, especially lower extremities Prevalent in people with diabetes or who smoke Intermittent claudication Obstruction of arterial blood flow in the iliofemoral vessels, resulting in pain with ambulation Often asymptomatic but can present with intermittent claudication (pain in leg on walking). Treatment Vasodilators, antiplatelet or antithrombotic medications (e.g., aspirin, cilostazol, ticlopidine, clopidogrel), cholesterol-lowering medications, and exercise rehabilitation

Chronic venous insufficiency

Chronic venous insufficiency Inadequate venous return over a long period as a result of varicose veins, valvular incompetence Venous stasis ulcers -Causes pathologic ischemic changes in the vasculature, skin, and supporting tissues.

Congestive (left) heart failure

Can be Systolic heart failure or diastolic heart failure CO: Depends on the heart rate and stroke volume Stroke volume: Contractility, preload, and afterload MI: Is the most common cause of decreased contractility. Preload: Increased when decreased contractility or excess plasma volume is present. Increased afterload: Is most commonly from increased peripheral vascular resistance. Management relies on increasing contractility and reducing preload and after load.

HTN Caused by

Caused by increases in cardiac output or total peripheral resistance, or both Cardiac output increased: Any condition that increases heart rate or stroke volume Peripheral resistance increased: Any factor that increases blood viscosity or reduces vessel diameter (vasoconstriction)

Unstable Angina

Causes reversible myocardial ischemia and a harbinger of impending infarction. Leads to MI when prolonged ischemia causes irreversible damage to the heart muscle. Transient episodes of thrombotic vessel occlusion and vasoconstriction occur at the site of plaque damage with a return of perfusion before significant myocardial necrosis occurs. Treatment Immediate hospitalization with the administration of oxygen, aspirin (if not contraindicated), nitrates, and morphine if pain is still present Antithrombotic agents

Pulmonary Edema

Clinical Manifestations Dyspnea, orthopnea, cough of frothy sputum Patho Inability of the heart to generate adequate cardiac output to perfuse vital tissues

HTN Clinical Manifestations

Clinical manifestations Early stages of hypertension have no clinical manifestations other than elevated blood pressure Called silent (lanthanic) disease Diagnosis Measurement of blood pressure on at least two separate occasions averaging two readings at least 2 minutes apart with the individual seated, the arm supported at heart level, after 5 minutes of rest, with no smoking or caffeine intake in the past 30 minutes

Hypertrophic obstructive cardiomyopathy

Common inherited heart defect of a thick septal wall Clinical manifestations: Angina, syncope, palpitations Treatment Beta blockers or verapamil to slow the heart rate Surgical resection of the hypertrophied myocardium Septal ablation Prophylactic placement of an implantable cardioverter-defibrillators in high-risk individuals

Heart Failure

Condition in which the heart is unable to generate adequate CO, resulting in an inadequate perfusion of tissues or an increased diastolic filling pressure of the left ventricle, or both. Is the inability of the heart to supply the metabolism with adequate circulatory volume and pressure. Risk factors include ischemic heart disease & HTN.

CAD: Myocardial Ischemia: Stable Angina Prinzmetal Angina Silent Angina Angina Pectoris

Develops if the supply of coronary blood cannot meet the demand of the myocardium for oxygen and nutrients. Stable angina: Causes predictable chest pain. Prinzmetal angina (variant): Causes unpredictable chest pain. Silent ischemia: Causes no detectable symptoms. Angina pectoris: Causes transient substernal chest discomfort.

Modifiable Risk Factors of CAD

Dyslipidemia Hypertension Endothelial injury, increase in myocardial demand Cigarette smoking Vasoconstriction and increase in LDL, decrease in high-density lipoproteins (HDL) Diabetes mellitus and insulin resistance Endothelial damage, thickening of the vessel wall Obesity and/or sedentary lifestyle Obesity, dyslipidemia, and hypertension: Metabolic syndrome Atherogenic diet

MI Complications

Dysrhythmias Cardiogenic shock Pericarditis Dressler (postinfarction) syndrome Organic brain syndrome

Atherosclerosis

Know slide 38 & 39

D/Os of the Myocardium: Cardiomyopathies

Effects of neurohumoral responses to ischemic heart disease or HTN on the heart muscle cause remodeling. Many cases of cardiomyopathy are idiopathic. A diverse group of primary myocardial disorders that are poorly understood. Categorized as dilated (congestive), restrictive (rigid and noncompliant), and hypertrophic (asymmetric). Size of the cardiac muscle walls and chambers may increase or decrease, depending on the type of cardiomyopathy, thereby altering contractile activity.

Progression of Atherosclerosis

Endothelium injury Inflammation of endothelium Cytokines released Cellular proliferation Macrophage migration Low-density lipoproteins (LDL) oxidation (foam cell formation) with oxidative stress Fatty streak Fibrous plaque Complicated plaque

Primary HTN

Extremely complicated interactions of genetics and the environment mediated by neurohumoral effects Genetics interact with diet, smoking, age, and other risk factors to cause chronic changes in vasomotor tone and blood volume. Overactivity of sympathetic nervous system and renin-angiotensin-aldosterone system (RAAS), and alterations in natriuretic peptides Inflammation, endothelial dysfunction, obesity-related hormones, and insulin resistance

Constrictive (restrictive) pericarditis

Fibrous scarring with occasional calcification of the pericardium causes the visceral and parietal pericardial layers to adhere. Clinical manifestations: Exercise intolerance, dyspnea on exertion, fatigue, and anorexia. Tx: Dietary Na restriction, digitalis glycosides, and diuretics improve CO. If these treatments are not successful, then surgical excision is performed.

Cardiovascular Disease Overview

Leading cause of death in US and World Genetic, neurohumoral, and inflammatory mechanisms Underlying tissue and cellular processes: Endothelial injury Remodeling Stunning Reperfusion injury Autoimmune disease

Tricuspid regurgitation

Leads to volume overload in the right atrium and ventricle, increased systemic venous blood pressure, and right heart failure

Atherosclerosis

Form of arteriosclerosis Thickening and hardening caused by the accumulation of lipid-laden macrophages in the arterial wall Plaque development Process that occurs throughout the body Leading cause of coronary artery and cerebrovascular disease

Diastolic heart failure: Clinical Manifestations and Tx

Heart failure with preserved ejection fraction Decreased compliance of the left ventricle and abnormal diastolic relaxation (lusitropy) Can occur singly or with systolic heart failure. The major causes include HTN-induced myocardial hypertrophy and ischemia, with resultant ventricular remodeling. Clinical manifestations: Dyspnea on exertion and fatigue Treatment Physical training (aerobic and weight training): Improves endurance and quality of life Beta-blockers, ACE inhibitors, ARBs, and aldosterone blockers

MI Tx

Hospitalization Immediate admin of O2 and aspirin Morphine Bed rest Cardiac medications: Thrombolytic, antithrombotic, vasodilators Percutaneous coronary intervention (PCI) Surgery

Diseases of the Arteries

Hypertension Orthostatic (postural) hypotension Aneurysm Thrombus formation Embolism Peripheral arterial diseases Atherosclerosis Peripheral artery disease Coronary artery disease Myocardial ischemia Acute coronary syndromes

Treatment for varicose veins and chronic venous insufficiency

Leg elevation, compression stockings, and physical exercise Endovenous ablation (radiofrequency and laser) and ultrasound-guided foam sclerotherapy Surgical ligation and vein stripping

DVT Tests and Tx

Prevention is crucial Mobilization/ambulation soon after surgery, illness, bed rest, injury Prophylactic low-molecular-weight heparin, antithrombin agents, warfarin, or pneumatic devices Inferior vena cava filter Tests: d-dimer, computed tomography (CT), magnetic resonance imaging (MRI) Treatment Low-molecular-weight heparin, unfractionated intravenous heparin, antithrombin agents, or adjusted-dose subcutaneous heparin Thrombolytic therapy Aspirin

Hypertensive or valvular hypertrophic cardiomyopathy

Hypertrophy of the myocytes: Attempts to compensate for increased myocardial workload. Clinical manifestations: Asymptomatic or may complain of angina, syncope, dyspnea on exertion, and palpitations.

Dilated (congestive) cardiomyopathy

Impaired systolic function, leading to increases in intracardiac volume, ventricular dilation, and systolic heart failure Causes: MI; diabetes; alcohol; deficiencies of niacin, vitamin D, and selenium; hyperthyroidism Clinical manifestations: Dyspnea and fatigue Treatment: Salt restriction, vasodilators, diuretics, inotropic agents, anticoagulants, pacemakers

Mitral stenosis

Impairment of blood flow from the left atrium to the left ventricle Most common cause: Acute rheumatic fever Clinical manifestation: Opening snap Treatment: Surgical repair; may require valve replacement

Aortic regurgitation

Inability of the aortic valve leaflets to close properly during diastole Clinical manifestations: Widened pulse pressure as a result of increased stroke volume and diastolic backflow Tx: Valve replacement may be delayed for many years with the use of vasodilators and inotropic agents

Systolic Heart Failure

Inability of the heart to generate adequate CO to perfuse tissues Catecholamines RAAS: Angiotensin II and aldosterone Arginine vasopressin (antidiuretic hormone) Natriuretic peptides Inflammatory cytokines: Endothelial hormones, tumor necrosis factor-alpha (TNF-α) and interleukin 6 (IL-6) Myocyte calcium transport Insulin resistance and diabetes

High Output Failure

Inability of the heart to supply the body with bloodborne nutrients, despite adequate blood volume and normal or elevated myocardial contractility. Common causes Anemia, septicemia, hyperthyroidism, and beriberi

Clinical manifestations of MI

Infarcted myocardium is surrounded by a zone of hypoxic injury, which may progress to necrosis or return to normal; adjacent to this zone is a zone of reversible ischemia. Sudden severe chest pain ECG changes Troponin I: Most specific Elevates in 2 to 4 hours Creatine phosphokinase-MB (CPK-MB), LDH Hyperglycemia slide 58

Infective Endocarditis

Inflammation of the endocardium from infectious agents Most common: Bacteria, especially streptococci, staphylococci, and enterococci Pathogenesis Endocardial damage Bloodborne microorganism adherence Formation of infective endocardial vegetations

Rheumatic fever

Is a diffuse, inflammatory disease caused by a delayed immune response to infection by the group A beta-hemolytic streptococci. Is a febrile illness. Inflammation of the joints, skin, nervous system, and heart Resolves without sequelae if treated early If left untreated, rheumatic fever causes rheumatic heart disease. (It may have a genetic component.) Abnormal immune response to the M proteins that cross react with normal tissues Fibrinoid necrotic deposits: Aschoff bodies

Right heart failure

Is the inability of the right ventricle to provide adequate blood flow into the pulmonary circulation. Can result from an increase in left ventricular filling pressure that is reflected back into the pulmonary circulation. Can result from left heart failure and/or diffuse hypoxic pulmonary disease, such as COPD, cystic fibrosis, and ARDS Can result from diffuse hypoxic pulmonary disease. Clinical manifestations Jugular venous distension, peripheral edema, hepatosplenomegaly Treatment: Is the same as left heart failure.

Mitral valve prolapse syndrome

Mitral valve prolapse syndrome Anterior and posterior cusps of the mitral valve billow upward (prolapse) into the atrium during systole Clinical manifestations: Asymptomatic Treatment: None needed or beta blockers

Mitral regurgitation

Most common causes: Mitral valve prolapse and rheumatic heart disease Permits backflow of blood from the left ventricle into the left atrium Treatment: Surgical repair or valve replacement

Cardiac Complications of Acquired Immunodeficiency Syndrome

Most common: Pericardial effusion and left heart failure Myocarditis Endocarditis Cardiomyopathy AIDS tx with combo antiretroviral therapy (cART): Causes hyperlipidemia and atherosclerotic disease

Increased Afterload

Most commonly the result of increased peripheral vascular resistance. This increase in resistance decreases ventricular emptying and makes more workload for the left ventricle, resulting in hypertrophy and ventricular remodeling. The vicious cycle of decreasing contractility, increasing preload, and increasing afterload causes progressive worsening.

Restrictive cardiomyopathy

Myocardium becomes rigid and noncompliant, impeding ventricular filling and raising filling pressures during diastole. Clinical manifestations: Right heart failure occurs with systemic venous congestion. Treatment: Correct the underlying cause.

HTN

Prehypertension: 120 to 139 mm Hg systolic; 80 to 90 mm Hg diastolic Isolated systolic hypertension: Elevated systolic blood pressure accompanied by normal diastolic blood pressure Hypertension Consistent elevation of systemic arterial blood pressure Sustained elevation of 140 mm Hg systolic or higher OR 90 mm Hg diastolic or higher

Tx of Myocardial Ischemia

Nitrates, β-adrenergic-receptor blockers, calcium channel blockers Percutaneous coronary intervention Coronary artery bypass graft (CABG) Minimally invasive direct coronary artery bypass (MIDCAB) Transmyocardial laser revascularization (TMR) Gene therapy for myocardial angiogenesis Spinal cord stimulation Laser revascularization, percutaneous in situ coronary venous arterialization

Nontraditional Risk Factors of CAD

Nontraditional risk factors Markers of inflammation and thrombosis C-reactive protein Troponin I Hyperhomocysteinemia Adipokines Adiponectin and leptin Infection Microorganisms and periodontal disease Air pollution Coronary artery calcification, carotid wall thickness

Aortic stenosis

Orifice of the aortic semilunar valve narrows, causing diminished blood flow from the left ventricle into the aorta Clinical manifestations: Angina, syncope, and heart failure Treatment Most require valve repair or replacement with a prosthetic valve, followed by long-term anticoagulation therapy Transcatheter aortic valve implantation

HTN Risk Factors

Positive family history Advancing age Gender: Female >70 years of age; male <55 years of age Race: Black Sodium (Na+) intake Glucose intolerance (diabetes mellitus) Heavy alcohol use Obesity Cigarettes Potassium (K+), magnesium (Mg++), calcium (Ca++)

Primary and Secondary HTN

Primary (essential) hypertension No known cause; is 95% of those with hypertension. - the result of extremely complicated interactions of genetics and the environment mediated by a host of neurohumoral effects. These genes interact with diet, smoking, age, and other risk factors to cause chronic changes in vasomotor tone and blood volume. Secondary hypertension Is caused by altered hemodynamics from an underlying primary disease or drugs.(motrin) Affects the entire cardiovascular system Systolic hypertension: Most significant factor in causing target organ damage Increases the risk for myocardial infarction (MI), kidney disease, and stroke

Superior vena cava (SVC) syndrome

Progressive occlusion of the SVC that leads to venous distention in the upper extremities and head Leading cause: Bronchogenic cancer Treatment Malignant disorders Radiation therapy; surgery; chemotherapy; administration of diuretic, steroidal, and anticoagulant agents Nonmalignant causes Bypass surgery using various grafts, thrombolysis (both locally and systemically), balloon angioplasty, and placement of intravascular stents

Myocardial Infarction

Prolonged ischemia causes irreversible damage to the heart muscle (myocyte necrosis). -Cellular injury, leading to cellular death -Structural and functional changes 1. Myocardial stunning: Is the temporary loss of contractile function that persists for hours to days after perfusion has been restored. 2.Hibernating myocardium: Tissue that is persistently ischemic undergoes metabolic adaptation to prolong myocyte survival. 3. Remodeling: Process that occurs in the myocardium after an MI. 4. Repair

HTN Tx

Reducing or eliminating risk factors Restricting sodium intake to 2.4 g/day, increasing potassium intake, restricting saturated fat intake, and adjusting calorie intake as required to maintain optimal weight Dietary approaches to stop hypertension (DASH) Cessation of smoking Exercise program that promotes endurance and relaxation slide 18

ECG changes with MI

STEMI ST- depression T wave inversion See slide 54

Secondary HTN

Secondary hypertension Caused by systemic disease that raises peripheral vascular resistance and/or cardiac output Complicated hypertension Hypertrophy and hyperplasia with associated fibrosis of the tunica intima and media in a process called vascular remodeling Malignant hypertension Rapidly progressive hypertension Diastolic pressure is usually >140 mm Hg Can lead to encephalopathy

More D/Os of conduction

Sinus block -Occasionally absent P wave associated with a loss of QRS complex for that beat First-degree block -PR interval >0.2 Second-degree block, Mobitz I, or Wenckebach -Progressive prolongation of PR interval until one QRS complex is dropped; pattern of prolongation resumes Second-degree block or Mobitz II -Same as sinus block

Dysrhythmias: Disorders of impulse generation

Sinus bradycardia -Pulse 60 beats per minute (bpm) or less Simple sinus tachycardia -Pulse rate 100 to 150 bpm Premature atrial contractions Early P waves Atrial flutter P rate 251 to 300 bpm Atrial fibrillation P rate over 300 bpm

Valvular dysfunction

Stimulates chamber dilation and/or myocardial hypertrophy. Treatment Careful fluid management Valvular repair or valve replacement with a prosthetic valve, followed by long-term anticoagulation therapy and life-long antibiotic prophylaxis before invasive procedures

Dyslipidemia in CAD

Strong link between lipoproteins and CAD Abnormal concentrations of serum lipoproteins Dietary fat packaged into chylomicrons for absorption in the small intestine Chylomicrons: Function by transporting exogenous lipid from the intestine to the liver and peripheral cells. Primarily contains triglyceride; triglycerides may be removed and either stored by adipose tissue or used by muscle as an energy source. Remnant contains cholesterol, which is taken up by the liver.

Acute coronary Syndromes

Sudden coronary obstruction because of thrombosis formation over a ruptured atherosclerotic plaque When there is sudden coronary obstruction because of thrombosis formation over a ruptured atherosclerotic plaque Sudden cardiac death can occur Examples Unstable angina MI Most common complications Dysrhythmias, congestive heart failure, and sudden death

MI: Angiotensin II Effects

Systemic effects: -Peripheral vasoconstriction and fluid retention -Myocardial work increases; thus the effects of the -loss of myocyte contractility are exacerbated. Local effects: -Growth factor for vascular smooth muscle cells, myocytes, and cardiac fibroblasts; promotes catecholamine release; causes coronary artery spasms -Involved in myocardial remodeling -Causes myocyte hypertrophy, scarring, and loss of contractile function in the areas of the heart distant from the site of the infarction.

Third- Degree Block and Preexcitation Syndromes

Third-degree block -P waves are present and independent of the QRS complex; no relationship between P waves and QRS complex is observed; atrioventricular (AV) dissociation is always present. Preexcitation syndromes (Wolff-Parkinson-White and Lown-Ganong-Levine) -Congenital presence of accessory pathways (bundle of Kent and Mahaim fibers) conducts very rapidly and bypasses the AV node. -Cause early ventricular depolarization in relation to atrial depolarization.

Deep venous thrombosis (DVT)

Usually asymptomatic Thrombosis: Clot Detached thrombus: Thromboembolus; can lead to pulmonary emboli Clot in a large vein Obstruction of venous flow leading to increased venous pressure Factors: Virchow triad Venous stasis Venous endothelial damage Hypercoagulable states Postthrombotic syndrome occurs in individuals who have venous stasis (e.g., immobility, age, left heart failure), spinal cord injury, vein wall damage (e.g., trauma, intravenous medications), or hypercoagulable states (e.g., pregnancy, oral contraceptives, malignancy, genetic coagulopathies).

Valvular Stenosis vs. Valvular Regurgitation

VS: Valve orifice is constricted and narrowed. -Aortic Mitral VR: Valve fails to shut completely. Is also called insufficiency or incompetence. -Aortic Mitral Tricuspid Both: Characteristic heart sounds, cardiac murmurs, and systemic complaints: Assist in determining which valve is abnormal Mitral valve prolapse syndrome

Disease of the Veins Varicose veins

Vein in which blood has pooled Usually in the saphenous vein Distended, tortuous, and palpable veins Cause: Trauma or gradual venous distention, rendering valves incompetent Altered connective tissue proteins, increased proteolytic enzyme activity, and decreased transforming growth factor B in vein walls

Disorders of impulse generation

Ventricular standstill or asystole Is not compatible with life. Premature ventricular contractions (PVCs) or depolarizations -Originates outside the normal conduction system. Ventricular tachycardia QRS complex is >0.11 ms, with a rate of 100 bpm or more. Ventricular fibrillation QRS complex is characterized by a heart rate of >300 bpm and is usually not observable; is not compatible with life.

Serum cholesterol (Dyslipidemia) in CAD

Very low-density lipoproteins (VLDL): Mainly triglycerides plus a carrier protein. - LDL: Mainly cholesterol plus a carrier protein Are responsible for the delivery of cholesterol to the tissues. - Inc levels: Play a role in endothelial injury, inflammation, and immune responses that are important in atherogenesis. HDL: Mainly phospholipids plus a carrier protein Are responsible for "reverse cholesterol transport," which returns excess cholesterol from tissues to the liver, where it is eliminated as bile or converted to cholesterol-containing steroids. Can remove excess cholesterol from arterial walls. -Low levels are bad

Infective Endocarditis: Tx

Was once a lethal disease, but morbidity and mortality have significantly diminished with abx and improved dx techniques. Abx for 4-6 weeks. Begin with IV and end with PO. May use a combination. Other drugs are administered to treat left heart failure, secondary to valvular dysfunction. Surgery to repair or replace the valve, as prescribed.