Cardiovascular Flashcards
Hyperlipidemia: Causes
Primary - genetically based
Secondary- diabetes, thyroid disease, renal disorder, liver disorders, cushings, obesity, high calorie diet, alcohol, drugs (beta blocker, protease inhibitors, estrogen)
Hyperlipidemia: types of lipoproteins
Chylomicrons
Very low density lipoprotein (VLDL) - high amounts of triglycerides
Intermediate density lipoprotein (IDL
Low density lipoprotein (LDL) - carrier of cholesterol; deposits for uptake in arterial wall
High density lipoprotein (HDL) - 50% protein carrying less cholesterol and little triglyceride; carries cholesterol from tissues to liver for disposal
Risk Factors for Atherosclerosis
Increasing age Male Postmenopausal women Family history Genetics
Smoking Obesity Hypertension Hyperlipidemia Diabetes
Systemic inflammation marked by elevated C reactive protein
Hyperhomocysteinemia
Increased lipoprotein a levels
Infectious agents
Types of Plaques
Stable - thick fibrous caps that partially block vessels; dont tend to form clots
Unstable - thin fibrous caps that completely block artery; clot may rupture and break free
Fatty Streaks - thin yellow lines running along major arteries
Smooth muscle cells filled with cholesterol and macrophages can develop into fibrous
Fibrous atheromatous plaques - basic lesion of clinical atherosclerosis
Accumulation of lipids and proliferation of vascular smooth muscle, formation of scar tissue and calcification
May eventually occlude vessel or predispose to thrombus formation
Complicated atherosclerotic lesion - fibrous plaque breaks open producing hemorrhage, ulceration, and scar tissue deposits
Development of Atherosclerosis
- Injury to endothelium - inflammation is key
- LDL accumulates and undergoes chemical changes in arterial wall signaling endothelial cells to latch onto WBC in the blood
- WBC penetrate intimate and trigger inflammatory response and devour LDL creating foam cells
Growth factors contribute to migration and proliferation of smooth muscle and elaborations of Extracellular matrix - Formation of fatty streak
- Plaque continues to grow and forms fibrous cap
- Substances released by foam cells can eventually destabilize and rupture creating clots
Peripheral Artery Disease: risk factors
Atherosclerosis distal to the aortic arch
Male
Greater than 60yrs old
Smokers
Diabetes Mellitus
Peripheral Artery Disease: manifestations
Intermittent claudication Thinning of skin and subcutaneous tissue Gradual atrophy of muscles Decreased blood supply Absent or weak pulses Cool extremities Brittle nails and hair loss Pallor Dependent rubor
Ischemic pain
Ulceration
Gangrene
Raynaud Phenomenon: causes
Intense episode vasospsatic disorder of the arteries and arterioles
Primary - symmetrical vasospasm precipitated by cold or strong emotions; minimal pain
Secondary - non symmetrical association with previous vessel injury
Frostbite, occupational trauma, temp extremes; very painful
Raynaud Phenomenon: manifestations
Ischemic - pallor to cyanosis, cold, numbness and tingling
Hyperemia- intense redness, throbbing, paresthesia
Return to normal colour
True Aneurysms
Bounded by a complete vessel wall - blood remains within the vascular compartment
Berry - small spherical dilation at a bifurcation
Circle of Willis
Fusiform - entire circumference of vessel; gradual progressive dilation of the vessel varying in diameter and length
Ascending and transverse thoracic and abdominal aorta
Saccular - extends over part of the circumference of the vessel and appears saclike
False Aneurysms
Localized dissection or tear in the inner wall of the artery with formation of extravascular hematoma that causes vessel enlargement
Bounded by outer layers of the vessel or supporting tissue
Dissecting - tear of the intima allowing blood to enter the vessel wall dissecting into layers to create a blood filled cavity
Aortic Aneurysm
Age and atherosclerosis are risk factors
Abdominal Aortic:
Asymptomatic pulsating mass if large can cause abdominal and back pain; commonly located below the renal artery
Thoracic Aorta
Due to Atherosclerosis
Often asymptomatic
Substernal, back, or neck pain
Pressure on trachea = stridor, cough, dyspnea
Laryngeal nerve = hoarseness
Esophagus = difficulty swallowing
Superior vena cava = facial and neck edema
Define: Arterial Blood Pressure Systolic Blood Pressure Diastolic Blood Pressure Pulse Pressure Mean Arterial Blood Pressure
Arterial Blood Pressure - ejection of blood from lt ventricle
Systolic Blood Pressure - highest pressure on contraction
Diastolic Blood Pressure - lowest pressure on relaxation
Pulse Pressure - systolic and diastolic difference
Mean Arterial Blood Pressure - average pressure in the arterial system during contraction and relaxation indicates tissue perfusion
Cardiac output and peripheral resistance
CO = product of stroke volume and heart rate
Peripheral resistance reflects changes in radius of the arterioles and viscosity of the blood
BP = COXPR
Blood Pressure Regulation
Neural - reticular formation of the medulla and pons; integration and modulation of ANS
Parasympathetic slow HR
Sympathetic accelerate HR and vasoconstriction
Baroreceptors and chemoreceptors detect
Extrinsic reflexes mediate response to stimuli originating outside the CV system
Humoral - RAAS, epinephrine
Hypertension: Primary
High blood pressure consistency over 140 or diastolic 90
Chronic elevation of blood pressure without evidence of other disease conditions
Risk factors: Family history Race (blacks) Older age Lifestyle - high salt, fat, calorie diets, chronic alcohol consumption, smoking, stress Obesity Diabetes - insulin resistance
Hypertension: Secondary
High blood pressure as the result of another disorder
Kidney disease
Adrenocortical disorder
Pheochromocytoma
Coarctation of the aorta
Hypertension: risk factors
Oral contraceptives Illicit drugs Erythropoietin Sympathomimetic agents Licorice OSA
Target Organ Damage
HTN is asymptomatic until long term effects are seen in organs
Heart - lt ventricular hypertrophy leading to coronary heart disease, cardiac arrhythmias, sudden death, CHF
Angina or prior MI
Prior coronary revascularization
HF
Lungs
Brain - dementia, cognitive impairments, narrowing and sclerosis of vessels leading to demyelination, stroke, hemorrhage
Kidney - nepherosclerosis leading to chronic kidney disease
Liver
Eye - retinopathy
Hypertensive Crisis
Accelerated or severe form of HTN Systolic above 180 or diastolic above 110 Emergency diastolic 120 Impending target organ damage Vascular damage and symptoms
Orthostatic Hypotension: causes
Reduced blood volume Pharmaceuticals - antihypertensive drugs Aging - diminished ability to adequately increase HR, ventricular stroke volume, muscle pumps, impaired cerebral circulation, decreased blood volume Bed rest and immobility Disorders of the ANS
Orthostatic Hypotension: manifestations
Visual changes
Dizziness
Syncope
Drop in systolic of 20 and diastolic of 10
Venous Blood Return
Low pressure system with thin walls
Skeletal muscle pumps - increase flow to deep venous channels and return to the heart
Changes in abdominal and intrathoracic pressure
Valves prevent retrograde flow of blood
Blood from skin and subdue collects in superficial veins
Transported across communicating veins
Deeper venous channels for return to the heart
Venous Thrombosis: Virchow’s Triad and manifestations
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
Coronary Artery Disease
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%
Coronary artery disease: risk factors
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
Chronic Ischemic Coronary Artery Disease: Stable Angina Pectoris
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
Chronic Ischemic Coronary Artery Disease: Variant/Prinzmental Angina
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
Chronic Ischemic Coronary Artery Disease: Silent MI
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
Acute Coronary Syndrome: diagnostic measures
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)
Acute Coronary Syndrome: pathology
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
ACS: unstable angina (NSTEMI) - symptamology
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
ACS: ST Elevation MI (STEMI): symptamology
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
Patent Ductus Arteriosus
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
Tetralogy of Fallot
Most common cyanotic congenital defect
- Ventricular septal defect - involving membranous septum and anterio portion of the muscular septum
- Dextropositon (shifting to the right of the aorta) - overrides the rt Ventricular and is in communication with the septal defect
- Obstruction and narrowing of the pulmonary outflow channel - including pulmonic valve stenosis, a decrease in the size of the pulmonary trunk or both
- 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
