Cardiovascular Disorders of the Human Body Pt. 2 Flashcards
Coronary Artery Disease
Any vascular disorder that narrows or occludes the coronary arteries
Atherosclerosis is the most common cause
Risk factors for CAD
Dyslipidemia Hypertension Cigarette smoking Diabetes mellitus & insulin resistance Obesity Sedentary lifestyle Atherogenic diet
Myocardial ischemia (Ischemic heart disease)
Local, temporary deprivation of the coronary blood supply
Leads to Anaerobic metabolism production of Lactic acid decrease in Myocardial pH Cell ischemia/death
Can lead to: Stable angina (decrease in O2, lactic acid buildup) Prinzmetal angina (vasospastic), when patient is resting Silent ischemia (asymptomatic, older diabetic women)
Acute coronary syndromes (ACS)
Atherosclerotic plaque ruptures and may form a clot Sudden coronary obstruction
Unstable angina
Plaque has ruptured, infarction may follow
Perfusion returns before necrosis
EKG changes (ST depression, T wave inversion)
Cardiac enzymes remain normal
Non-ST Elevation Myocardial Infarction
“Time = Muscle”
Subendocardial MI—only involving the layer beneath endocardium
ST depression, T wave inversion
Infarction can extend if thrombus lodges permanently into the vessel
Levine’s Sign: Fist over chest, heart pain
ST-Elevated Myocardial Infarction
Infarction through all layers of myocardium, endocardium to epicardium (transmural MI)
ST elevations
Elevated cardiac enzymes
Pain may radiate to jaw, left arm
Treatment: cardiac catheter to break up plaque
Stable Plaques
Have thick fibrous caps
Partially block vessels
Do not tend to form clots or emboli
Non Stable Plaques
Have thin fibrous caps over large lipid core
Plaque can rupture and cause a clot to form
May completely block the artery
The clot may break free and become an embolus
ACS: Clinical Manifestations
Chest pain Shortness of breath Feeling of impending doom Diaphoresis Nausea and vomiting Altered vital signs: going from hypertension to hypo Cyanosis
ACS Diagnosis
Electrocardiogram
Angiogram: cardiac catheter
Elevated CK-MB, Troponin I levels, Myoglobin
Dilated Cardiomyopathies
Cardiac hypertrophy & dilatation w/ impaired pumping
Ventricular wall thinning
S&S are r/t heart failure
Hypertrophic Cardiomyopathies
Excessive ventricular hypertrophy
Most common cause of sudden cardiac death in the young. Genetic
Disordered muscle fibers → uncoordinated contraction/relaxation→ arrhythmias→ premature death
Restrictive Cardiomyopathies
Least common in Western countries
Familial origin?? or r/t endocardial amyloid infiltrations
Excessive rigidity of ventricular walls restricts ventricular filling.
S&S resemble heart failure & constrictive pericarditis.
Risk Factors for Cardiomyopathies
Sustained high blood pressure
Valvular disease
Heart tissue damage from a previous heart attack
Chronic rapid heart rate
Metabolic disorders, such as thyroid disease or diabetes
Nutritional deficiencies
Pregnancy
Excessive use of alcohol over many years
Cocaine or certain medications
Viral infections
Cardiomyopathy Complications
Thrombosis (Blood clots)
Heart Murmurs (Turbulent blood flow)
Cardiac arrest
Cardiomyopathy Treatment
Manage symptoms Prevent further progression of the disease Reduce risk of complications Implantable defibrillator Heart transplantation Lifestyle changes
Stenosis
Failure of valve leaflets to open properly
Regurgitation
Failure of valve to close properly permitting backflow of blood
Murmurs
Characteristic sound of turbulent blood flow through a diseased valve
CHF
#1 reason to be admitted to the hospital Can be caused by: Cardiomyopathies - #1 cause Coronary insufficiency: CAD Myocardial infarction Valvular heart disease Regurgitant valvular disease Constrictive pericarditis
Manifestations of Heart Failure
Effects of impaired pumping
Compensatory responses to decreased CO
Effects of decreased renal blood flow RAA pathway
Effects of the sympathetic nervous system
Natriuretic peptides: inhibits renin, angiotensin, aldosterone
Left Heart Failure (CHF)
Impaired pumping of blood
Decrease in Cardiac Output:
Anxiety, Confusion, Impaired Memory, Fatigue & activity intolerance
Leads to congestion in pulmonary circulation
Dyspnea, orthopnea, paroxysmal nocturnal dyspnea
Pulmonary edema
Right heart failure
Can result from an increase in left ventricular filling pressure that is reflected back into the pulmonary circulation Impairs pulmonary circulation Systemic venous accumulation Peripheral edema Weight gain – weigh pt daily Visceral congestion (liver, spleen, GI tract) JVD Cor pulmonale
Treatment for CHF
Pharmacologic treatment Treatment of reversible causes Restriction of salt intake Cardiac rehabilitation Surgical repair of heart valves
John complains of severe shortness of breath, and has fluid in his lungs. He has tachycardia, increased diastolic blood pressure, pale moist skin, and says he feels weak, dizzy, and anxious all the time
Which are due to the sympathetic nervous system?
Which side of his heart do you think is failing?
(anxiety, increased BP, tachycardia)
Left (fluid in the lungs)
Pulmonary Edema
Capillary fluid moves into alveoli Lung becomes stiffer Harder to inhale…dyspnea/air hunger Less gas exchange in alveoli Crackles Frothy sputum Hemoglobin not completely oxygenated → cyanosis
Which of the following is the most dramatic symptom of left heart failure, can be life-threatening, and is characterized by capillary fluid moving into the alveoli?
Pulmonary edema
Varicose Veins
Veins in which blood has pooled with blood
Appear distended, tortuous, and can be palpable
Usually in the saphenous vein
Increased intra-abdominal pressure causes gradual venous distention
S/S:
Edema & aching of the lower extremities
Edema subsides w/ elevation of legs
Stretch calf muscles
Chronic venous insufficiency
Inadequate venous return cause by damage to the vein, valves leaflets, and muscle pumps
Causes: Varicose veins, Valvular incompetence, DVT’s
Leads to:
Tissue congestion
Edema
Impaired tissue nutrition
Brown pigmentation of skin (hemosiderin deposits)
Stasis dermatitis & Venous stasis ulcers – advanced venous insufficiency
Venous thrombosis (DVT)
Thrombus in a vein causing obstruction of venous flow causing an inflammatory response in the vessel wall.
Strongly associated with chronic venous insuff.
PREVENTION IS KEY!!!
Factors: Venous stasis, Venous endothelial damage, Trauma, surgery, SCI
Hypercoagulable states
Oral contraceptives
Hematological malignancy
Pregnancy/ Postpartum
Superior Vena Cava Syndrome
Progressive occlusion of the SVC that leads to venous distention in the upper extremities and head
Leading cause: Bronchogenic cancer
Treatment for SVC
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
