Cardiovascular Flashcards

Question

Venous Thrombosis: Virchow's Triad and manifestations

Answer 1

Thrombus and inflammation of superficial and deep veins ``` Venous Stasis: Bed rest and immobility Spinal cord injury MI/CHF/Shock Venous Obstruction ``` ``` Vascular Trauma: Venous catheters Surgery Trauma or infection Hip fracture ``` ``` Hypercoaguability: Genetics Stress or trauma Pregnancy or childbirth Oral contraceptives or hormone replacement Dehydration and cancer ``` ``` Asymptomatic Pain Swelling Deep muscle tenderness Signs of inflammation ``` Pulmonary or cerebral edema

Answer 2

Heart disease caused by impaired coronary blood flow an cause a spectrum of disorders: Chronic Ischemic heart disease and acute coronary syndrome - MI, angina, conduction defects, HF, cardiac death Reason for being asymptomatic with CAD - development of collateral channels occurring in concert with atherosclerosis Aortic blood pressure is the main factor controlling perfusion pressure Contacting heart influence own blood supply by compressing vessels during systole Myocardial blood flow is regulated by myocardial men and auto regulating mechanisms Metabolic activity - adenosine Endothelial cells - transport of material sand substances that contract or relax tunica media Coronary blood flow is regulated by oxygen demand of the heart muscles Coronary uses 60-80% of o2 in blood; skeletal 25-30%

Answer 3

Atherosclerosis - predominate lt anterior descending and lt circumflex artery along the entire right coronary artery Vasospasm ``` Sex and gender Age Ethnicity - blacks Genetics HTN Hyperlipidema Tobacco use Diabetes Obesity Sedentary lifestyle and physical inactivity Ability to cope with stress ```

Answer 4

Chronic stable angina is associated with fixed coronary obstruction that produces an imbalance between coronary blood flow and metabolic demands Pain and pressure due to transient ischemia - upon exercise, exertion, cold, emotions Steady constricting, squeezing, or suffocating sensation - increasing intensity at the onset and end of episode Precordial/substernal - similar to MI with possible radiation and epigraphic discomfort Fixed coronary narrowing Relieved with rest and nitroglycerin

Answer 5

Due to spasm of coronary artery - cause is unclear Endothelial dysfunction, hyperactive sympathetic NS, defective calcium handling, altered NO Symptoms occur at rest or with minimal exercise Often occurs at night Transient ST elevation or depression T peaking inversion of U waves

Answer 6

MI in absense of angina pain Impaired blood flow from Atherosclerosis or vasospasm More common in the elderly Less myocardium involved in shorter episodes Defects in pain threshold or transmission Autonomic neuropathy with sensory denervation Hypotension, low body temp, vague complaints of discomfort, mild diaphoresis, stroke like symptoms, dizziness, sensorium changes

Answer 7

Classified on ECG changes - ST segment changes Unstable angina/NSTEMI - non ST segment elevation MI STEMI - ST segment elevation MI Classic ECG changes are ST elevation, T inversion, abnormal Q wave All changes are caused by an imbalance in myocardial oxygen supply and demand Biomarkers - determine if acute MI has occurred Troponin I and T: rise 2-3hr after MI onset; elevated for 7-10 days Myoglobin: within one hour after cell death; peak 4-8hr (not specific to cardiac tissue) Creatine Kinase: exceeds normal range 4-8hr; gone 2-3 days (cardiac tissue specific)

Answer 8

Unstable plaques rupturing to form a clot Thin fibrous cap with fatty core is most stable of them Coronary vasospasm Atherosclerotic narrowing Inflammation or infection Secondary - Anemia, fever, hypoxemia

Answer 9

Ranges from ischemia to true MI Prediagnosis of stable angina More severe pain or prolonged or frequent Frank pain of a new onset Occurs at rest or on minimal exertion Lasts more than 20min If biomarkers are elevated = NSTEMI and high risk of STEMI If no biomarkers are present = unstable angina

Answer 10

Irreversible myocardial cell death after 20-40 min of severe ischemia Substernal, transmural (Q wave), stunned myocardium MI = decreased contractile force (CO, coronary perfusion, increased pulmonary vasculature pressure),interruption of conduction (dysrhythmias) Abrupt or significant chest pain - crushing, constricting and suffocating, substernal radiation to left arm, jaw, neck ``` Women - atypical chest pain Elderly - SOB Fatigue, weakness of arms and legs Tachycardia palpitations Anxiety Restlessness Feeling of impeding doom Epigastic distress and nausea and vomiting Cool clammy skin ``` Prolonged and not relieved by rest or nitroglycerin

Answer 11

Persistence of fetal ductus beyond the prenatal period Blood shunts across the ductus from high pressure lt side to low pressure rt side after infants pulmonary vascular falls the ductus provides continuous runoff of aortic blood into the pulmonary artery Runoff increases pulmonary blood flow, pulmonary congestion increased resistance to the rt heart Increased pulmonary venous return, increased work demands may lead to lt ventricular heart failure

Answer 12

Most common cyanotic congenital defect 1. Ventricular septal defect - involving membranous septum and anterio portion of the muscular septum 2. Dextropositon (shifting to the right of the aorta) - overrides the rt Ventricular and is in communication with the septal defect 3. Obstruction and narrowing of the pulmonary outflow channel - including pulmonic valve stenosis, a decrease in the size of the pulmonary trunk or both 4. Hypertrophy of the right ventricle - due to increased work required to pump blood through the obstructed channels Display cyanosis: due to right to left shunt across the ventricular septal defect Right ventricular outflow obstruction causes deoxygenated blood from the right ventricle to shunt across the Ventricular septal defect and be ejected into systemic circulation Obstruction can increase in stress, crying, feeding, defecating, with a hypercyanotic spell Symptoms: Acutely cyanotic, hyperpneic, irritable, diaphoretic, limp, loss of consciousness, spontaneous squatting