Cardiopulmonary: Cardiovascular pathophysiology Flashcards

(44 cards)

1
Q

Functional classification of heart disease

A
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2
Q

Atherosclerotic heart disease

A
  • most common cause of CV disease
  • more common in men than women
  • characterized by irregular distributed lipid deposits in the intimal layer of medium and large Coronary arteries
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3
Q

Modifiable risk facors for atherosclerosis

A
  • elevated total cholesterol
  • high LDL/vLDLs
  • low HDL
  • high triglycerrides
  • obesity
  • HTN
  • smoking/tobacco
  • excessive alcohol
  • physcal inactivity
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4
Q

Non-modifiable risk factors for atherosclerosis

A
  • males
  • age
  • family history of CAD in male relative before 55 or female relative before 65
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5
Q

how does an atherosclerotic lesion occur

A
  • abnormal lipid metabolism and/or excessive intake of cholesterol and saturated fats
  • atherosclerotic plaque
  • fatty streak
  • fibrous plaque

  • atherosclerotic plaque: accumulation of intraellular anad extracellula lipids, connective tissue, smooth muscle cells, and glycosaminoglycans
  • fatty streak: first detectable lesion; consists of lipid-laden foam cells
  • foam cells: macropahges that have mirgated as monocytes from circulation into subendothelial layer of the intima
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6
Q

Describe the lipid hypothesis: pathogenesis

A
  • increased LDL levels result in penetration of LDL into the arterial wall
  • leads to lipid accumulation in smooth muscle
  • fatty streak evolves into fibrous plaque
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7
Q

Describe chronic endothelial injurry hypothesis

A
  • Endotheliam injury
  • over time the plaque becomes calcified
  • some plaques are stable but others may spontaneously fissue and ruptutre
  • ruptured plaques stimulate thrombosis

Endotheliam injury produces loss of endothelium, adhesions of plateletes to subendothelium, aggegation of plateletes to subendothelium, aggrergation of plateletes, chemotaxix of monocytes, and T-cell lymphocytes + release of platelet-derived and monocyte derived growth factors

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8
Q

What happens when a plaque ruptures

A
  1. may emobilize
  2. rapidly Occlude the lumen/cause MI or infarcation
  3. gradually becomes incorporated into the plaque
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9
Q

What is myocardial ischemia

A
  • results with an imbalane between O2 supple and demand
  • revesible
  • comforable at rest and symptoms during mild-moderate exercise
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10
Q

What is stable angina

A
  • classic symptom= angina pecoris (heaviness, pressure or tightness in chest)
  • may be precipitated by exertion, stess, emotion, heavy meals
  • lasts for several minutes
  • relieved by rest and nitroglycerin
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11
Q

What is unstable angina

A
  • change in angina pattern or angina at rest
  • may last longer ot not respond
  • typically caused by plaque rupture, ulceration or hemorrhage with subsequent thrombus forrmation
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12
Q

What is prinzmeta angina

A
  • unusual type of angina that occurs mostly at rest
  • hypothesized that it is the result of transient increase in vasomotor tone or due to vasospam
  • assoicated with ST elevation rather than depression on EKG
  • may be assoicated with acute MIs, severe arrhythmias (Ventricular tachycardia or fibrillation)
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13
Q

Asymptomatic/silent angina

A
  • Angina that is asymptomatic
  • factors include age, presence of CAD, or other disease process
  • pts with DM have a high incidence of painless MIs and definite silent ischemia
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14
Q

What are angina equivalents

A
  • dyspnea
  • fatigue
  • lightheaded
  • beltching brought on by exercise and relieved with rest or nitro
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15
Q

What is the pathogenesis of a MI

A
  • results from prolonged ischemia
  • almost always in the left ventricle
  • tissues become necrrotic in zone of infarction
  • formation of fibrous scar within 6-8 weeks (inelastic)
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16
Q

What is a transmural MI

A
  • full thickness necorsis
  • wall motion reduced (hypokinetic), abnormal (dsykinetic) or absent (akinetic)
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17
Q

What is the zone of hypoxic injury

A

area where tissue may be able to return to normal but may become necrotic if blood flow is not restored

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18
Q

How is an MI diagnosed

A

must have 2/3

  1. hx of ischemic type chest discomfort
  2. evolulationary changes on serially obtained ECG
  3. rise and fall in serum cardiac enzymes
19
Q

Clinical presentation of MI

A
  • crushing chest pain or pressure
  • may radiate to arms, neck, throat/jaw, and back
  • pain is constant and lasts >30 minutes
  • pallor/SOB
  • unrelieved pain w/ 3 doses of nitro
  • diaphoresis
  • nausea/vomitting
  • Denial
20
Q

Diagnosis of MI via ECG

A
  • peaked T-waves following
  • ST-segment elevation
  • q-wave development
  • and finally T-wave inversion
21
Q

Diagnosis of MI with cardiac enzymes

A
  • creatine kinase (MB specific to myocardium)
  • myoglobin
  • cardiac specific troponin
  • lactic dehydrogenase
  • serum glutamic-oxaloacetic transaminase

CK-MB will increase with 4-8 hours and retunr to normal withiin 2-3days

22
Q

Treatments of MI

A

Medical: pharmocologic agents to

  • decrease O2 demand
  • increase O2 supply
  • improve or maintain myocadial function

Surgical:

  • thrombolysis
  • intra-aortic ballon pump
  • angioplasty and stent placement

some drugs that dissolve a thrombus (lysis) may be delievered surgically via catheter

23
Q

What determines systolic dysfunction

A
  • end-diastolic volume/preload
  • afterload
  • contracile state of myocardium (contractility)
  • heart rate (chronotrophy)

heart function may be impaired as a esult in alterations of any four of these

24
Q

What is predominant distolic dysfunction

A
  • filling of ventricle is impaired due to hypetrophy or changes in myocardium composition
25
What are some cardia adaptations that occur with heart failure
- stroke volume is decreased = pressure/end diastolic pressure is increased - condition is chronic can cause ventricular dilation
26
What are some common causes of left sided heart failure
- ASHD - cardiomyopathy - HTN - valve disease - congential defects
27
What happens with left sided heart failure
- systolic dysfunction => decrease SV and increase end-diastolic volume and reduced ejecion fraction - atrial volume will begin to expand => atrial dilation due to higher EDP - blood will be reflected back to lungs
28
Clinical manifestations of left sided heart failure
- progressive dyspnea - orthopnea - PND - fatigue and weakness - pulmonary rales - S3 gallop - enlarged heart
29
Causes of right sided heart failure
**increased pulmonary artery pressure** caused by - left ventricle failure - mitral valve regurgitation - chronic/acute pulmonary disease | *may undergo cardiac hypertrophy or not*
30
clinical manifestations of right sided heart failure
- dependent edema - hepatomegaly - ascites - fatigue - anorexia - nausea/bloating - rright sided S3 or S4 - accentuated P2 - murmurs w/ pulmonary or tricuspid insufficiency - jugularr venous distension - weight gain - cyanosis
31
what is primary dilated cardiomyopathy
- increased cardiac mass - dilation of chambes - little to no systolic function - results from infections or non-infectious inflammatory processes, toxins, pregnancy, and metabolic disorders
32
How does primary dilated cardiomyopathy affect normal heart function
- decreased stroke volume - compensated at rest by increased heart rate - reduced exercise tolerance
33
Signs and symptoms of pimary dilated cardiomyopathy
- similar to heart failure
34
Hypertrophic cardiomyopathy
- increased cardiac mass that can be symmetrical or asymmetrical without dilation - normal or increased systolic function
35
Hypertrophic obstructive cardiomyopathy
- left ventricular outflow is obstructed - results in diastolic dysfunction - type of hypertrophic cardiomyopathy
36
Restrictive cardiomyopathy
- restricted ventricular filling due to endocardial or myocardial disease - ventricle walls lose compliancce and become excessively rigid - causes a reduced ventricular filling => creates back up pressure in the atria causing atrial enlargement
37
# Other cardiac disorders: Acute myocarditis: | what is it/signs and symptoms
- inflamation of myocardium often caused by streptococcal infections - can also be caused by bacterial, rickettsial, fungi, or parasites/other inflammatory processes - signs and symptoms: fatigue, palpitations, dyspnea, pericardial discomfort ## Footnote - often accompanied by pericarditis
38
# Other cardiac disorders: pericarditis
- inflammation of the pericaardium - caused by viral infections typically
39
# Other cardiac disorders: pericarditis: signs and symptoms
- wide range - progress simplease inflammation with no cardiovascular compromise to pulmonary effesions and cardiac temponade - initiall no symtpoms - chest pain - elevated temp - dyspnea - higher resting HR - pain is relieved by leaning forward, kneeling on all fours or sitting upright
40
# Other cardiac disorders: pericardial effusion
- fluid accumulation within pericadial sac - painful and result from acute inflammation - pericardial friction rub may occur
41
# Other cardiac disorders: pericardial effusion: signs and symptoms
- large effusions that develop slowly may cause no symptoms - small effusions that develop rapidly may cause tamponade - painful - dyspnea/cought
42
# Other cardiac disorders: pericardial effusion: cardiac tamponade
- elevated intrapericardial pressure that restricts venous return and ventricular filling - stroke volume and pulse pressure fall - heart rate/venous pressure rise
43
# Other cardiac disorders: rheumatic heart disease
- systemic immune process that may result from a throat infection - leads to an infection of the endocardium/valves
44
# Other cardiac disorders: Infective endocarditis
- bacterial/fungal infection of the heart valves - interferes with normal opening and closing - any abnormality of the heart valves or blood flow through the valves increase ones risk - clinical manifestations = flulike symptoms