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NURS617 Exam 5 Questions and Answers: Cardiovascular System, Exams of Pathophysiology

University of Southern Indiana (USI)Pathophysiology

A comprehensive set of questions and answers covering key concepts related to the cardiovascular system, particularly focusing on conditions like aortic aneurysms, aortic dissection, venous disorders, hypertension, and heart function. It includes explanations of various cardiovascular terms, mechanisms, and clinical manifestations, making it a valuable resource for students studying cardiovascular physiology and pathology.

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2024/2025

Available from 04/14/2025

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NURS617

NURS617 EXAM 5 QUESTIONS WITH CORRECT

VERIFIED SOLUTIONS 100% GUARANTEED PASS

(2025/2026)

Aortic aneurysms - ANS ✓-weakness in the wall of the aorta that makes it

susceptible to rupture

-involves any part of aorta; ascending, descending, and abdominal

-abdominal=most common

-usually asymptomatic; pulsing mass d/t calcification over time

-risk factors: HTN, atherosclerosis, male, smoker, 50+

Aortic dissection - ANS ✓-acute, life threatening haemorrhaged into blood

vessel wall w/ long tearing of vessel wall to form blood-filled channel

-causes: HTN, pregnancy, connective tissue disease (marfans)

-s/s: abrupt excrutiating pain, syncope, pulse unattainable in one or both arms,

paralysis of lower extremities

-occurs w/o evidence of previous vessel dilation; usually thoracic or ascending

aorta

Factors in developing venous dx - ANS ✓1. level of activity in lower extremities

- skeletal muscle contraction moves blood back to heart

2. # of valves in veins to prevent retrograde of blood - less=genetic

predisposition to varicose veins

3. changes in thoracic pressure when breathing - increase in pressure (ex-

HTN)=increase risk of varicose veins

Varicose veins - ANS ✓-abnormally swollen, twisted veins with defective valves;

most often seen in the legs

-most common cause=DVT

Partial preview of the text

Download NURS617 Exam 5 Questions and Answers: Cardiovascular System and more Exams Pathophysiology in PDF only on Docsity!

NURS617 EXAM 5 QUESTIONS WITH CORRECT

VERIFIED SOLUTIONS 100% GUARANTEED PASS

Aortic aneurysms - ANS ✓-weakness in the wall of the aorta that makes it susceptible to rupture

involves any part of aorta; ascending, descending, and abdominal
- abdominal=most common
usually asymptomatic; pulsing mass d/t calcification over time
risk factors: HTN, atherosclerosis, male, smoker, 50+ Aortic dissection - ANS ✓-acute, life threatening haemorrhaged into blood vessel wall w/ long tearing of vessel wall to form blood-filled channel
causes: HTN, pregnancy, connective tissue disease (marfans)
s/s: abrupt excrutiating pain, syncope, pulse unattainable in one or both arms, paralysis of lower extremities
occurs w/o evidence of previous vessel dilation; usually thoracic or ascending aorta Factors in developing venous dx - ANS ✓1. level of activity in lower extremities
skeletal muscle contraction moves blood back to heart

of valves in veins to prevent retrograde of blood - less=genetic

predisposition to varicose veins

changes in thoracic pressure when breathing - increase in pressure (ex- HTN)=increase risk of varicose veins Varicose veins - ANS ✓-abnormally swollen, twisted veins with defective valves; most often seen in the legs

most common cause=DVT

other causes: increase in abdominal pressure (HTN, obesity), prolonged standing w/o use of leg muscles to pump blood back to the heart - tx: compression stockings, calf pumps Chronic venous insufficiency - ANS ✓-venous circulation is inadequate due to partial vein blockage or leakage of venous valves (or both); muscle pumps ineffective
effective blood flow & emptying of deep veins cannot occur
s/s: edema, brown pigmented skin on LEs, necrosis, tissue congestion, stiffening of ankle joint & loss of muscle mass + strength
secondary lymphatic insufficiency occurs Venous thrombosis - ANS ✓-formation of blood clot in vein d/t stasis of blood, increase coagulability, vessel wall injury
causes: best rest/immobility, pregnancy, birth control, cancer, stress/trauma, hyperlipidemia, HTN, hip fracture, surgery
s/s: deep muscle tenderness, pain, hot to touch, fever, swelling
tests: doppler, d-dimer
tx: elevate legs 15-20 degrees, compression stockings, prophylactic anticoag (LD aspirin), heparin or warfarin 3-6mo after tx of thrombi to ensure dissolved Short vs long term BP regulation - ANS ✓-short=d/t exercise, stress, hemmorhage; regulated by medulla/reticular formation. SNS=increases HR and contractility of heart, constricts vessels. PNS=vagal nerve stimulated and decreases HR, dilates blood vessels
long=r/t kidney function; decrease in function=increase in BP/HR d/t retention of h2o + na+ Hypertension in children - ANS ✓-d/t renal disease, coarctation of the aorta, cystic disease, Wilm's tumor
causes left ventricle enlargement

Ejection fraction - ANS ✓-measurement of the volume percentage of left ventricular contents ejected with each contraction

SV/end-diastolic volume X 100
- normal=55-75%
55%>=heart failure Arteries vs veins - ANS ✓-arteries: carry blood away from heart; thick, elastic walls; have highest pressure, provide resistance to circulatory flow
veins: carry blood to heart; low pressure, thin walls to collect blood from capillaries (acts as reservoir to return blood to R side of heart); contains largest amount of blood Blood flow: normal vs abnormal - ANS ✓blood flow=laminar vessels, one directional flow abnormal=turbulent; causes whirlpool or backflow of blood, causes murmor/bruit upon auscultation **closed end system R vs L side of heart - ANS ✓R=pulmonary L=systemic
output of both must be the same; if R pumps less, blood accumulates in systemic circulation...if L pumps less, blood accumulates in lungs 3 factors governing blood flow - ANS ✓pressure, resistance, flow
increase in viscosity and decrease in temp=decrease in blood flow Compliance - ANS ✓-total quantity of blood that can be stored in a given portion of circulation for each mm HG increase in pressure
compliance=increase in volume/increase in pressure; ability to increase of decrease depending on BP
most distended=veins

Pre load vs after load vs inotropy - ANS ✓-pre-load: ventricular filling/end- diastolic pressure; volume of blood prior to systole, largely determined by venous return to heart

after-load: resistance of ejection of blood from the heart; pressure muscles are exerted to move blood into aorta and around body; aortic stenosis can increase afterload
inotropy: force of cardiac contractility; increase in inotropy=increase in ejection fraction + SV Heart Sounds S S S S4 - ans ✓S1 - normal; lub, produced by closure of the mitral valve S2 - norma; dub, produced by closure of the aortic valve S3 - abnormal; early diastole, occurs after the mitral valve opens; rapid ventricular fillingsyss S4 - abnormal; late diastole, occurs during atrial contraction **S3 + S4=indicative of resistance of ventricular filling Law of laplace - ANS ✓-pressure is directly proportional to surface tension and inversely proportional to radius of alveolus
wall tension increases as wall becomes thinner, wall tension decreases as wall becomes thicker Frank-starling mechanism - ans ✓-A mechanism by which the stroke volume of the heart is increased by increasing the venous return of the heart (thus stretching the ventricular muscle).
allows heart to adjust pumping ability to accommodate venous return

L atrium: receives oxygenated blood from lungs Fibrous skeleton of the heart - ANS ✓-4 interconnecting valve rings

separates artia and ventricles, forms rigid support for attachment of valves and insertion of cardiac muscle Digoxin - ANS ✓-increases force of contraction by increasing calcium, slows conduction through AV node L vs R side HF - ANS ✓L: pulmonary congestion R: venous pooling/edema Reactive hyperemia - ANS ✓-a bright red flush on the skin occurring after pressure is relieved
local increase in blood flow after temporary occlusion of blood flow; compensatory mechanism Albumin - ANS ✓-protein in blood; maintains the proper amount of water in the blood, major osmotic force
excessive fluid returned to circulation via lymphatic channels Systolic vs diastolic heart murmors - ANS ✓systolic: mitral regurgitation, aortia stenosis, mitral valve prolapse diastolic: mitral stenosis, aortic regurgitation HR effects on CO & SV - ANS ✓-increase in HR=decrease in SV & CO
time spent in diastole decreases, time spent in systole stays the same

Stable vs unstable plaque - ANS ✓Unstable plaque - white/grey, platelet rich; large lipid core with a thin fibrous cap made of smooth muslce -- can easily rupture Stable plaque - red; small lipid core with a thick fibrous cap made of smooth muscle -- doesn't easily rupture Pericarditis - ANS ✓-inflammation of the sac surrounding the heart; associated w/ increased capillary permeability

can be acute (<2 weeks); d/t viral or bacterial infx, reoccurring=d/t autoimmune dx
fibrous exudate deposes scar tissue on pericardium; can lead to adhesions/thrombosis
causes increase in fluid and pain d/t fluid friction (high pitch/scratchy on systole), decreased CO
s/s: chest pain relieved by leaning forward, pericardial friction rub, increased ESR & CRP tx: NSAIDs, abx, corticosteroids, colchicine Pericardial Effusion and Cardiac Tamponade - ANS ✓-accumulation of fluid in the pericardial cavity
- extensive pericardial effusion leads to cardiac tamponade; excess fluid in the pericardial cavity limit the expansion of the heart during cardiac filling
s/s: pulsus paradoxus (weak pulse during inspiration, strong during exhalation; compressed L ventricle=less output & ventricle filling), cushing's triad (tachy, narrowed pulse pressure, jugular vein distention), shock
tx: pericardiocentesis, NSAIDs, corticosteroids, colchicine Constrictive pericarditis - ANS ✓-causes: tuberculosis (developing world); systemic lupus erythematosus (developed world)
- calcified scar tissue develops on pericardium, causes decrease in diastolic filling; causes equalization of end-diastolic pressures in all 4 chambers (R side filling pressures normally lower than L side)

ST-segment elevation MI: s/s + tx - ANS ✓-ischemic death of myocardial tissues; usually abrupt, or chronic is progressed from unstable angina/NSTEMI

s/s: substernal pain that radiates to L arm/neck/jaw, N/V, frothy pink mucous...eventually leads to shock d/t low CO
death d/t MI happens within 1h of s/s onset d/t arrythmias
results in scar tissue & decreased ability to contract heart
tx: thrombolytic agent within 60-90min, nitro, o2, nitrates, aspirin, pain (morphine), beta-blockers, reperfusion therapy (re-establish blood flow to heart to prevent necrosis, eg: CABG), fibrinolytic therapy (TPA) to dissolve unstable plaques Chronic ischemic heart disease: types of angina - ANS ✓-Chronic stable angina, silent myocardial ischemia, and variant or vasospastic angina
stable=fixed coronary obstruction; less blow flow=increased metabolic needs of myocardium
silent MI=no anginal pain, shorter episodes, less area effected; diabetes=increased risk d/t neuropathy
variant angina=d/t vasospasm; happens more @ night and w/ rest, EKG changes & arrythmias during attack
pectoris=pain precipitated by stress, cold, exercise *dx: EKG, stress test, echo; usually have high LDLs, low HDLs, insulin resistance Ischemic cardiomyopathy - ANS ✓-a weakness in the muscle of the heart due to coronary artery disease because of inadequate oxygen delivery to the myocardium
usually results in congestive heart failure, but ischemia can be reversed if treated in time Cardiomyopathy types - ANS ✓-Hypertrophic, Dilated, Restrictive
Due to: Ischemia, Genetic problems, Systemic Disease (primary d/t genetics or secondary d/t diabetes, cancer drugs, pregnancy, infection, HTN)

often leads to HF and death Infective endocarditis (ie) - ans ✓-an infection of the endocardial surface of the heart that leads to valve destruction; can lead to valve regurgitation, pericarditis, aneurysm, valve perforation
usually Staph A (IV drug users) or Staph E (prosthetic heart valve)
onset of s/s=2 weeks>; fever, N/V, spleen enlargement, lethargy, petechaie, flank/ABD pain
can lead to bacteremia and sepsis Rheumatic heart disease (RHD) - ANS ✓-valvular disease resulting from rheumatic fever, a syndrome that occurs after strep A bacterial infection
causes mitral valve stenosis
tx: penicillins, prophylactic penicillin during remission Mitral valve regurgitation - ANS ✓-backflow of blood caused by failure of the heart's mitral valve to close tightly
causes blood to move into L atrium during systole, leads to pulmonary congestion and R sided HF
associated w/ afib, RHD, IE Mitral valve prolapse - ANS ✓-Improper closure of the valve between the heart's upper and lower left chambers
associated w/ connective tissue dx (marfan's, osteogenesis imperfecta)
s3 & s4 present (late systolic murmor)
usually asymptomatic, but can lead to mitral valve regurgitation Aortic stenosis - ANS ✓-either d/t genetics or calcification of aortic valve cusps that increases resistance of ejection of blood from LV to aorta
causes measurable decrease in CO; eventually leads to HF

R side; prolongs closure of pulmonary valve and produces separation of aortic + pulmonary components

there is a hole between the atria; oxygenated blood from the left atrium is shunted to the right atrium and lungs
do not compromise children seriously; surgical closure is recommended before school age; can lead to congestive heart failure or atrial dysrhythmias later in life if not corrected Tetralogy of Fallot (TOF) - ANS ✓-set of 4 congenital heart defects occurring together; blood shunted from R to L
ventricular septal defect, dextroposition of the aorta, R ventricular outflow obstruction, R ventricular hypertrophy
s/s: hypercyanotic "tet" spells (d/t crying, feeding, pooping d/t increased pulmonary resistance causing decreased pulmonary blood flow)
tx: surgery, knee to chest position Transposition of the great vessels - ANS ✓-a congenital abnormality where the aorta is attached to the right ventricle and the pulmonary artery to the left ventricle (this is backwards and leads to two separate blood routes)
surgery needed Coarctation of the aorta (coa) - ANS ✓-severe congenital narrowing of the aorta
s/s: weak distal lower extremity pulses, bounding proximal (ex: carotid and brachial), BP higher in arms than in legs (normally higher in legs by 10-20 mm Hg)
surgery needed; risk for HTN post-op Kawasaki disease - ANS ✓-immune response causes inflammation of blood vessels (hence the strawberry tongue) & coronary artery aneurysms
effects skin, brain, eyes, heart, liver, and lymph nodes
acute phase=4-8 weeks; abrupt fever, conjuctivitis, rash, swelling/edema, unresponsiveness to abx

can lead to pericarditis, mitral regurgitation, myocarditis
- subacute=8 weeks-4y; peeling skin, s/s slowly disappear Pathophysiology of shock - ANS ✓Decreased Blood Volume Decreased Venous Return Decreased Stroke Volume Decreased Cardiac Output Decreased Tissue Perfusion Impaired cellular metabolism/death Cardiogenic shock - ANS ✓-not enough oxygen is delivered to the tissues of the body d/t low CO/hypotension/hypoxia
severe complication of a large acute myocardial infarction or DVT Hypovolemic shock - ANS ✓shock resulting from blood or fluid loss, most common Obstructive shock - ANS ✓-Shock that occurs when there is a block to blood flow in the heart or great vessels, causing an insufficient blood supply to the body's tissues
ex: DVT, atherosclerosis Distributive shock - ANS ✓-Shock due to a shift of fluid from blood to tissues; results in low BP, loss of blood vessel tone, or enlarged vascular compartment
ex: serious burns, hypothermia Complications of shock - ANS ✓Acute renal failure Shock lung, acute lung injury, or adult respiratory distress syndrome Hepatic failure Paralytic ileus, stress or hemorrhagic ulcers

Extends from the terminal portion of phase 3 until the beginning of phase 4 Cardiac arrhythmias develop EKG: what each segment represents - ANS ✓P: SA node P-Q: delay in AV node tranmission QRS: ventricular contraction/purkinje S-T: repolarization of ventricles

EKG detects early ischemia and prevents early MI complications
- improper lead placement can change QRS Mechanisms of arrhythmias and conduction dx - ANS ✓1. automaticity: specific cells spontaneously initiating an impulse

excitability: cells ability to respond to an impulse
conductivity: cells ability to conduct impulses
refractoriness: extent of cells to respond to stimulus *cardiac scar tissue slowens conduction, increases chance of unilateral block & arrythmias Respiratory sinus arrythmia - ANS ✓-normal P, QRS and T waves but the heart rate varies with respiration - the rate increases on inspiration and decreases on expiration

more common in kids Sinus bradycardia - ANS ✓< normal sinus rhythm, origin=SA node can be d/t rx, athletes Sinus tachycardia - ans ✓>100 bpm

normal sinus rhythm, origin=SA node can be d/t fever, blood loss, anxiety, exercise, SNS stimulation, loss of vagal tone Supraventricular vs ventricular arrythmias - ANS ✓-supraventricular=dx of atrial rhythm or conduction above the ventricles (ex: afib, a flutter, PAC)

ventricular=dx of ventricular rhythm or conduction; can be life threatening (ex: vtach, vfib) Premature arterial contraction (PAC) - ANS ✓-arrhythmia in which atria contract earlier than they should; SA node does not reach AV
additional P wave Atrial tachycardia - ans ✓Rate: 150 - 250 beats per minute Regularity: regular P-waves: may be upright or inverted will appear different from underlying rhythm; up to 3 P waves QRS-complex: Normal PR interval- may be normal, shortened, or prolonged Atrial flutter - ANS ✓-irregular beating of the atria (240-450 bpm); re-entry of rhythm in R atria
sawtooth pattern; no observable p wave Atrial fibrillation (a-fib) - ans ✓-an irregular and often very fast heart rate originating from abnormal conduction in the atria; atrial cells cannot repolarize in time for next stimulus
atria=400-600bpm, ventricles=80-180bpm
can occur w and w/o cardiac disease
absent p wave, widened QRS
pulse deficit: difference in apical rate and peripheral pulses

Third degree AV block - ANS ✓-atria and ventricles function independently

QRSs and the P waves have no relation to each other
- permanent pacemaker required PNS vs SNS impact on respiratory system - ANS ✓PNS=airway constriction, increase in secretions SNS=airway dilation, decrease in secretions Structure of lung - ANS ✓- trachea
splits into 2 bronchi - one to each lung
bronchi split into smaller tubes - bronchioles
bronchioles end in alveoli where gas exchange occurs
R lung=3 lobes, L lung=2 lobes
mediastinum holds lungs in place Conducting airways - ANS ✓-nasal cavity, oral cavity, pharynx, larynx, trachea, right and left pulmonary bronchi, bronchioles
"conditions" inspired air; warms, filters, and moisturizes air as it passes through; mucous membranes moistened, blood flow warms, and mucociliary blanket removes foreign materials
impairment of mucociliary blanket=increased debris in lungs; causes=tobacco, dust; results in chronic bronchitis, emphysema Fever: effect on resp system - ANS ✓-increase in water vapor=loss of water from mucosa=thicker mucous
^ why you need to increase h2o intake when sick Nasopharyngeal - ANS ✓-pertaining to nose and throat
help protect against obstruction

Larynx - ANS ✓voice box; passageway for air moving from pharynx to trachea; contains vocal cords Tracheobronchial tree - ANS ✓branching structures of the respiratory system that resemble an upside-down tree trunk and its branches; includes trachea, bronchi, and bronchioles. Function of lungs vs lobules vs alveoli - ANS ✓-lungs: gas exchange, inactive vasoactive substances (bradykinin), convert angiotensin I to II. reservoir for blood storage.

lobules: gas exchange
alveoli: terminal air space for resp tract; gas exchange between air and blood. contains brush cells (monitor air quality of lungs) and macrophages (remove debris from lungs) Alveoli: type I vs II pneumocytes - ANS ✓I: 95% of cells; create barrier between air and alveoli wall, cannot divide II: 5%; synthesize surfacant, which decreases surface tension of alveoli to aid in expansion/inflation; starts maturing at 26-27 weeks, betamethasone used for pre-term babies to prevent ARDs Pulmonary vs bronchial circulation - ANS ✓Pulmonary Circulation=deoxygenated blood that flows from the right ventricle to the alveoli to be oxygenated. It returns to the heart via the pulmonary vein. Bronchial Circulation=oxygenated blood that flows from the left ventricle (via the thoracic aorta) to supply the tissues of the lungs and tracheobronchial tree; some of the now-deoxygenated blood returns to the heart via the pulmonary vein, some by the bronchial veins, and some by the bronchopulmonary veins.
can undergo angiogenesis (formation of new vessels) Lymphatic circulation: resp system - ANS ✓-superficial vessels: drains surface of the lungs, travels through connective tissue of visceral pleura

NURS617 Exam 5 Questions and Answers: Cardiovascular System, Exams of Pathophysiology

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Partial preview of the text

Download NURS617 Exam 5 Questions and Answers: Cardiovascular System and more Exams Pathophysiology in PDF only on Docsity!

NURS617 EXAM 5 QUESTIONS WITH CORRECT

VERIFIED SOLUTIONS 100% GUARANTEED PASS

of valves in veins to prevent retrograde of blood - less=genetic