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Flashcards in Cardiovascular Deck (36)
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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

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
Postmenopausal women
Family history


Systemic inflammation marked by elevated C reactive protein
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

1. Injury to endothelium - inflammation is key
2. LDL accumulates and undergoes chemical changes in arterial wall signaling endothelial cells to latch onto WBC in the blood
3. 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
4. Formation of fatty streak
5. Plaque continues to grow and forms fibrous cap
6. Substances released by foam cells can eventually destabilize and rupture creating clots


Peripheral Artery Disease: risk factors

Atherosclerosis distal to the aortic arch

Greater than 60yrs old
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
Dependent rubor

Ischemic pain


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


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



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
Diabetes - insulin resistance


Hypertension: Secondary

High blood pressure as the result of another disorder

Kidney disease
Adrenocortical disorder
Coarctation of the aorta


Hypertension: risk factors

Oral contraceptives
Illicit drugs
Sympathomimetic agents


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
Brain - dementia, cognitive impairments, narrowing and sclerosis of vessels leading to demyelination, stroke, hemorrhage
Kidney - nepherosclerosis leading to chronic kidney disease
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
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
Venous Obstruction

Vascular Trauma:
Venous catheters
Trauma or infection
Hip fracture

Stress or trauma
Pregnancy or childbirth
Oral contraceptives or hormone replacement
Dehydration and cancer

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

Sex and gender
Ethnicity - blacks
Tobacco use
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
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

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

Acutely cyanotic, hyperpneic, irritable, diaphoretic, limp, loss of consciousness, spontaneous squatting