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Patho > Week 5 Cardiovascular System > Flashcards

Week 5 Cardiovascular System Flashcards

1
Q

What are the disorders of the endocardium

A
  • infective endocarditis
  • rheumatic fever
  • calcifications
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2
Q

Cardiac output is used to measure the efficiency of the heart as a pump. What is the equation used to express CO?

A. CO = HR X AV
B. CO = SV X HR
C. CO = AV X SV
D. CO = HR X EF

A

B. CO = SV x HR

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3
Q

What elements make up stroke volume? (select all that apply)

a. blood pressure
b. preload
c. afterload
d. rhythm
e. contractility
d. heart rate

A

b. preload
c. afterload
e. contractility

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4
Q

Which component of the blood pressure equation will be increased in a patient who is in a hypervolemic state

a. peripheral vascular resistance
b. heart rate
c. stroke volume
d. afterload

A

c. stroke volume

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5
Q

During an automobile accident where the client is bleeding heavily, which vascular component is the most distensible and can store large quantities of blood that can be returned to the circulation at this time of need?

A. liver and pancreas
B. capillary beds
C. veins
D. arteries

A

C. veins

tremendous amount of volume stored in the veins

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6
Q

What is hyperlipidemia? What are the two types and their causes?

A

elevation or all lipoproteins in the blood

Primary = genetics
Secondary results from many common diseases

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7
Q

Which elevated protein in the blood is strongly associated with atherosclerosis

A

hypercholesteremia

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8
Q

What is the difference between LDLs and HDLs? Which one is the most troublesome? What is the chemical makeup of each?

A
  • LDL = transports cholesterol from the liver to cells; most troublesome; 10% triglycerides, 50% cholesterol and 25% protein
  • HDL = transports cholesterol from cells to the liver; 5% triglycerides, 20% cholesterol, 50% protein
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9
Q

What is the leading cause of coronary artery disease, stroke, and peripheral artery disease?

A

atherosclerosis

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10
Q

What is the order of the 5 locations that atherosclerosis is likely to occur

A
  1. abdominal aorta and iliac arteries
  2. proximal coronary arteries
  3. thoracic aorta, femoral and popliteal arteries
  4. internal carotid arteries
  5. vertebral, basilar, and middle cerebral arteries
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11
Q

Explain the pathogenesis of atherosclerotic plaques

A
  1. occurs because of injury which begins an inflammatory process
  2. Inflammatory cells migrate and transform into activated macrophages and release ROS. the macrophages engulf oxidized LDL and become foam cells
  3. lipids accumulate and smooth muscle cells proliferate; SMC migrates into intima layer; foam cells die leaving necrotic debris and lipids
  4. plaque structure forms; plaques can rupture, ulcerate, or erode off the fibrous cap that the body has placed over it (out of sight out of mind) and may lead to bleeding into the plaque or blockage of vessel lumen
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12
Q

Explain thromboangiitis obliterans

A
  • inflammatory arterial disorder that causes thrombus formation
  • also called Brueger’s disease
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13
Q

Explain Raynaud’s disease and phenomenon

A
  • intense vasospasm of the arteries and arterioles in the finger and, less often, the toes and causes blockage of blood flow
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14
Q

What are the seven Ps of presentation for acute arterial occlusion

A
  • pistol shot (acute onset
  • pallor
  • polar (cold) (no blood flow)
  • pulselessness
  • pain (tissue is starved)
  • paresthesia (pins and needles)
  • paralysis (kill the nerve)
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15
Q

What is acute arterial occlusion and what does it typically result from

A
  • sudden event that interrupts arterial flow to the affected tissues or organ
  • result of emboli or thrombus
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16
Q

Explain peripheral artery disease and what it results from

A
  • occlusion that is the result of a chronic condition such as atherosclerosis
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17
Q

What are the symptoms of PAD? How much occlusion will occur before patients begin to experience symptoms?

A
  • intermittent claudication (painful to walk)
  • atrophic changes and thinning of skin and subcutaneous tissues
  • you can lose 50% of vessel before symptoms occur
  • cool, weak or absent pulses
  • limb color blanches with leg elevation
  • arterial ulcers (punched out appearance)
  • pain at night
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18
Q

List and explain the different types of aneurysms

A
  1. berry aneurysm: often found in circle of Willis (feeds the brain) in the brain circulation; consists of a small, spherical vessel dilation; normally at bifurcation
  2. fusiform and saccular aneurysms: often found in thoracic and abdominal aorta; characterized by gradual and progressive enlargement of the aorta; accepts more volume than it should
  3. dissecting aneurysm: acute, life threatening condition; tearing sensation; involves hemorrhage into the vessel wall with longitudinal tearing (dissection) of the vessel wall to form a blood-filled channel
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19
Q

Explain a venous thrombosis. Where is most likely seen? What are the causes?

A

definition: presence of a blood clot in the veins of the body (can be in superficial or deep veins

Often seen in the great saphenous vein

Causes; virchow’s triad

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20
Q

What are the labs that you would draw for a venous thrombosis and why?

A
  1. D-dimer: this is a breakdown products of a clot. If your D-dimer is high, it probably means you have a clot somewhere that your body is trying to get rid of
  2. CBC: looking at platelets and everything else to see what is going on (increase platelets could increase chances of a clot)
  3. PT, PTT, INR (international normalizing ratio): values that tell us how fast is your blood clotting; once you get in the way of the clotting process, the INR will go up (normally at 1
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21
Q

Explain varicose veins and list the causes

What can help prevent these

A
  • dilated veins in the lower body that result from incompetent valves or blockage
  • causes: long periods of standing, increased intra-abdominal pressure, DVTs, heavy lifting
  • compression devices can help prevent this by limiting the amount of fluid that the vein can collect so it doesn’t stretch
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22
Q

Explain Peripheral vascular disease and what it results from

A
  • chronic venous disease of the lower extremities that results in venous hypertension
  • results/causes: incompetent valves, prolonged standing, blockage of the venous system
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23
Q

What are the manifestation of PVD

A
  • edema (exacerbated by long periods of standing)
  • ulcers
  • calf pain or tenderness
  • warmth in the lower extremity
  • varicose veins
  • stasis dermatitis (thin, shiny, strange looking skin)
  • lower extremities weeping
  • can lead to ulcer formation, DVT leads to PE
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24
Q

Why do patients who suffer from PAD have pain at the affected areas?

a. the tissue is permanently inflamed
b. the tissue is getting too much oxygen
c. the tissue is dead
d. the tissue is not getting enough oxygen

A

d. the tissue is not getting enough oxygen

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25
Q

You are caring for a patient who is sedentary and who has peripheral ulcerations that are weeping. Which of the following disorders are most likely affecting this individual?

a. PAD
b. venous insufficiency
c. aneurysm
d. chronic hypertension

A

B. venous insufficiency

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26
Q

What are the consequences of low and high blood pressure?

A

low - tissues don’t receive sufficient blood flow to ensure delivery of nutrients and oxygen and removal of cellular wastes

high - can damage endothelial tissue, increasing the likelihood of both atherosclerotic vascular disease and vascular rupture

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27
Q

Explain primary hypertension

A
  • sustained condition of elevation of the blood pressure within the arterial circuit
  • modifiable / non modifiable
  • lack of dilators / too much constrictors
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28
Q

Explain secondary hypertension

A
  • elevation of blood pressure that results from some other disorders such as:
  1. renal disease (holding onto volume)
  2. primary hyperaldosteronism
  3. Cushing disease or syndrome (increase in aldosterone/cortisol)
  4. pheochromocytoma (tumor and releasing too much epinephrine and norepinephrine which causes vasoconstriction)
  5. oral contraceptive drugs
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29
Q

What are the places that hypertension can cause damage to and what damage can occur to each of those locations?

A
  • heart = hypertrophy
  • brain = dementia and cognitive impairment
  • peripheral vascular = atherosclerosis
  • kidney = nephrosclerosis
  • retinal complications
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30
Q

What is the difference between hypertensive urgency and emergency

A
  • urgency = rapid markedly elevated blood pressure without target organ damage (acute)
  • emergency = elevated blood pressure with end organ damage which can cause mental changes, intracranial hemorrhage, retinopathy, aortic dissection, cardiac ischemia or CHF or acute renal failure
31
Q

What do baroreceptors respond to

A

pressure

32
Q

How would each of the following affect blood pressure and why?

  • vasodilation
  • decreased stretching of baroreceptors
  • hypoxemia
  • inhibiting angiotensin converting enzyme
  • beta blockers
  • a2 agonists
  • calcium channel blockers
A
  • vasodilation: down; reduced resistance
  • decreased stretching of baroreceptors: up; signal for body to kick in
  • hypoxemia: up; vasoconstriction trying to get blood to core
  • inhibiting angiotensin converting enzyme:
  • beta blockers - lower
33
Q

A client is immobilized following a hip injury. The client has developed lower leg discoloration with edema, pain, and tenderness in the midcalf area. How should the nurse document these clinical findings?

a. stasis ulcerations
b. arterial insufficiency
c. primary varicose veins
d. deep vein thrombosis

A

d. deep vein thrombosis

34
Q

Explain pericarditis and its common causes

A
  • inflammation of the heart-normally leaves an exudate can form scar tissue in the heart
  • viral infections common cause; also connective tissue diseases, surgery, radiation therapy, trauma, drug toxicity
35
Q

What are the manifestations of pericarditis

A
  • friction rub
  • ECG changes
  • exercise intolerance
  • pain
36
Q

What are the complications of pericarditis

A
  • pericardial effusion
  • cardiac tamponade
  • dysrhythmias
  • cardiac arrest
  • death
37
Q

What is constrictive pericarditis

A
  • fibrous, calcifies scar tissue develops between the visceral and parietal layers of the serous pericardium
38
Q

What can pericardial effusion result from? What are the complications and SERIOUS complications of it?

A
  1. result of pericarditis, cancer, surgery, trauma
  2. complications: cardiac tamponade, dysrhythmias, cardiac arrest, death
  3. SERIOUS: cardiac tamponade, increased intracardiac pressure, muffled heart sounds and signs of circulatory shock due to accumulation of fluid
39
Q

Explain cardiac tamponade

A

the compression of the heart caused by the accumulation of fluid, pus, or blood in the pericardial sac

40
Q

Explain the characteristics of cardiomyopathies and the clinical manifestations

A
  1. Restrictive; myocardium becomes rigid and noncompliant; manifested by right heart failure due to systemic venous congestion
  2. Hypertrophic; common inherited heart defect of a thick septal wall and enlarged left ventricle; need more oxygen and perform less efficiently, so the person is prone to heart failure and may suffer sudden death during exertion (phoebe heart example)
  3. Dilated: impaired systolic function (contraction/squeeze) leading to intracardiac volume, ventricular dilation and systolic heart failure, heart gets more volume than it should; causes by Mi, diabetes, alcohol, vit D, hyperthyroidism
41
Q

What are the two types of coronary artery disease and their subtypes

A
  1. Chronic ischemic heart disease: chronic stable angina, silent myocardial ischemia, and variant or vasospastic angina
  2. acute coronary syndromes: represent the spectrum of ischemic coronary disease ranging from unstable angina through myocardial infarction
42
Q

List and explain the different types of chronic ischemic heart disease

A
  1. stable: predictable, associated with exertion
  2. unstable: unpredictable, during rest or with minimal activity; may evolve into a myocardial infarction
  3. Prinzmetal / Variant: nothing wrong with lumen; occurs during rest or with minimal exercise, frequently between midnight and 8 am
43
Q

ischemic heart disease is nearly always a consequence of

a. atherosclerosis
b. dysrhythmias
c. primary cardiomyopathies
d. carditis

A

a. atherosclerosis

44
Q

Explain the two types of myocardial infarction

A
  1. STEMI: ST elevation MI; look like tombstones on ECG; highly indicative of injury; transmural injury (damaging through entire depth of heart; all the layers)
  2. Non STEMI: still having a heart attack but it does not cause a ST elevation; typically they have thrown a clot and clogged the vessels and then the clot has moved on; it was there long enough to damage the myocardial wall and cause pain, but it has moved on; occasionally depression of ST segment
45
Q

Coronary artery disease can lead to further complications by

A. forming new blood vessels
B. changing the tissue distribution of the heart
C. Decreasing the amount of oxygen the myocardium receives
D. interfering with the blood flow through the chamber of the heart

A

C. Decreasing the amount of oxygen the myocardium receives

46
Q

What are the clinical manifestations of acute myocardial infarction

A
  • chest pain (severe, crushing, constrictive or like heartburn)
  • sympathetic nervous system response (GI distress, nausea, vomiting; tachycardia and vasoconstriction; anxiety, restlessness, feeling of impeding doom)
  • hypotension and shock (weakness in the arms and legs)
47
Q

A client is experiencing impaired circulation secondary to increased systemic arterial pressure. Which statement is the most relevant phenomenon?

A. Increased preload due to vascular resistance
B. High afterload because of back pressure against the left ventricle
C. impaired contractility due to the aortic resistance
D. systolic impairment because of arterial stenosis

A

B. high afterload because of back pressure against the left ventricle

afterload = things that influence the heart after the heart (arterial); pressure play a large role; icing hardening around cake decorator tip, not enough pressure coming out

48
Q

Explain infective endocarditis and its causes

A
  • infection of the inner portion of the heart, result in vegetation and tissue death if untreated; the valve is affected; vegetation acts like blood clot and could potentially cause PE (r side) or stroke (left side)
  • Causes: bloodstream infection (commonly staph), surgical procedure, IV drug use, underlying valve disease
48
Q

Explain infective endocarditis and its causes

A
  • infection of the inner portion of the heart, result in vegetation and tissue death if untreated; the valve is affected; vegetation acts like blood clot and could potentially cause PE (r side) or stroke (left side)
  • Causes: bloodstream infection (commonly staph), surgical procedure, IV drug use, underlying valve disease
49
Q

What are the manifestations of infective endocarditis

A
  • fever
  • new heart murmur
  • change in existing murmur
  • petechial hemorrhages
  • cough
50
Q

Name and explain the two types of valve defects

A
  1. Stenosis: the valve will not open all the way; stiff; harder to force blood through it; you will hear a murmur of blood shooting through the narrow opening when the valve is open
  2. Regurgitation: the valve will not close all the way; it leaks when ‘closed’; will hear a murmur of blood leaking back through when the valve should be closed
51
Q

Explain rheumatic heart disease and some of the complications

A
  • immune-mediated disease that results in cardiac inflammation at all three layers and valve damage
  • complications: heart failure, valvular heart disease, recurrent throat infections
52
Q

What are the clinical manifestations of rheumatic heart disease

A
  • lesions on trunk and arm
  • friction rubs
  • arrhythmias
  • murmur (mitral and aortic valves affected)
  • polyarthritis
  • chorea
53
Q

What are the labs that we would draw for rheumatic heart disease

A
  • CBC
  • BNP (brain naturetic peptides; promotes diuresis; they cause kidneys to get rid of water; if this is high it means your body is working to get rid of fluid)
  • blood culture
  • throat culture
54
Q

A client has a history of intravenous drug use and has been told that he has vegetation on his mitral valve. Which of the following is the most likely cause of this issue?

A. rheumatic heart disease
B. pericarditis
C. myocardial infarction
D. infective endocarditis

A

D. infective endocarditis

55
Q

What are the three classifications of heart failure?

A
  1. systolic (is the heart failing to pump out enough blood?) or diastolic (failing to accept enough blood from body/lungs)
  2. right sided or left sided failure
  3. high output versus low output failure (CO high or low?)
56
Q

What are the two different kinds of left sided heart failure

A
  • diastolic: LV does not accept enough blood from lungs

- systolic: LV does not pump enough blood to body

57
Q

What are the manifestations of heart failure and explain examples of each

A
  1. fluid retention and edema: result of increased hydrostatic pressure; nocturia, oliguria, pleural effusion
  2. respiratory manifestations; congestion of pulmonary circulation causing orthopnea and paroxysmal nocturnal dyspnea
  3. fatigue, cachexia, malnutrition, cyanosis, arrhythmias, and sudden cardiac death
58
Q

A client has presented with left sided heart failure. Which of the following assessment data are consistent with this diagnosis?

A. peripheral edema
B. jugular vein distention
C. liver congestion
D. crackles in the lungs

A

D. crackles in the lungs

59
Q

What are the four types of shock

A
  • hypovolemic
  • cardiogenic
  • distributive
  • obstructive
60
Q

Explain how hypovolemic shock occurs. What are the complications

A
  • loss of blood (hemorrhage), dehydration, excessive fluid shifts out of ECF
  • complications: cell injury due to hypoxia, cellular dysfunction, metabolic acidosis, cell death, organ failure, cardiovascular collapse, death
61
Q

What are the manifestations of hypovolemic shock

A
  • thirst, confusion
  • SNS activation: tachycardia, tachypnea, cool skin, decreased blood pressure
  • baroreceptors: ADH release, oliguria, thirst
  • inadequate O2: decreased level of consciousness, possible loss of consciousness
62
Q

What are the causes and complications of cardiogenic shock

A

The pump is broken

  • Causes: acute MI, myocardial contusion, valvular heart disease, severe heart failure, cardiac surgery
  • complications: cell injury due to hypoxia, metabolic acidosis, cellular dysfunction, cell death, organ failure, cardiovascular collapse, death
63
Q

What are the manifestations of cardiogenic shock and what labs would be useful to determine this?

A
  • confusion, restlessness, cyanosis, hypotension, tachycardia, tachypnea, decreased urine output, altered LOC, LOC, elevated preload and afterload
  • labs: CBC, chemistry ABG, lactate, BNP, cardiac enzymes
64
Q

Explain causes and complications of distributive or vasodilatory shock

A
  • causes: spinal cord injury, anesthesia, anaphylaxis, sepsis (blood vessels dilate, inadequate blood to fill vasculature, blood flow decreases)
  • complications: cell injury due to hypoxia, metabolic acidosis, cellular dysfunction, cell death, organ failure cardiovascular collapse, death
65
Q

What are the manifestations of distributive or vasodilatory shock and what are the labs to determine this

A
  • confusion, restlessness (hypoxemia); tachycardia (sepsis and anaphylaxis), bradycardia (neurogenic), warm, flushed skin, hypotension, weak, thready pulse, oliguria
  • labs: CBC, chemistry, ABG, lactate, blood culture, wound cultures, urine cultures, PT, PTT, INR
66
Q

Explain the causes and complications of obstructive shock

A

You have disrupted the blood flow in some way

  • cause: dissecting aortic aneurysm, cardiac tamponade, pneumothorax, PE
  • complications: cell injury due to hypoxia, metabolic acidosis, cellular dysfunction, cell death, organ failure, cardiovascular collapse, death
67
Q

What are the manifestations of obstructive shock

A
  • lethargy
  • confusion
  • possible pain
  • tachycardia
  • tachypnea
  • JVD
  • hypotension
  • altered level of consciousness
68
Q

What are the resting conditions for SA node, AV node, purkinje fibers

A

SA = 60-100 bpm
AV = 45-50 bpm
Purkinje fibers: 15-40 bpm

69
Q

Explain atrial fibrillation

A
  • you lose your atrial kick
  • the pocket in the left ventricle allows for turbulent blood flow
  • afib leads to stroke, heart attack
70
Q

What are the two categories of arrhythmias

A
  1. impulse generation disorders (altered rate and premature beats)
  2. conduction disorders (pathway is broken; disrupt the flow of impulses through the conduction system; typically end with “blocks”)
71
Q

Explain preload and afterload

A

preload: amount of tension applied to the muscle before contraction
afterload: load against which a muscle exerts its force

72
Q

Explain pulsus paradoxus

A

on inhalation, the right ventricle fills with extra blood. Because the heart cannot expand fully when the right ventricle is overfilled, the left ventricle is compressed and cannot accept much blood

On the next heartbeat, the left ventricle does not send out much blood and your systolic blood pressure drops

Patho (10 decks)

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