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Cardiopulmonary > Pathology of the CV System > Flashcards

Pathology of the CV System Flashcards

1
Q

Coronary Artery Disease (CAD)

  • what is it
  • s/s
A

Obstruction to blood flow but DOES NOT affect heart function (atherosclerotic plaque build up)

Main coronary arteries = right coronary, left coronary and left circumflex

S/S: will vary based on severity of the obstruction and number/size of vessel involved

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2
Q

Atherosclerosis

  • defn
  • 2 step progression
A

narrowing of the arteries that cause obstruction to blood flow (endothelial dysfunction leading to subsequent inflammatory response)
- CAD (doesn’t affect function) vs. IHD (decreased function)

Lipid deposition is a fundamental part of this process

  1. Dev of fatty streaks (aka lipid deposits)
  2. Dev of fibrous plaques (can be stable or unstable)
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3
Q

Atherogenesis chain of effect

A
  1. Tear in endothelial wall
  2. LDL enters endothelial layer where it becomes oxidized
  3. Oxidation signals monocytes to enter where they become macrophages and eat the lipids, in which they become foam cells
    - this is the “fatty streak” development
  4. Hemodynamic stress and inflammation trigger platelet-derived growth factor (PDGF) to stimulate smooth muscle cells to drift to the fatty streak and form a fibrous cap
    - this decreases the lumen
    - eventually the center becomes necrotic and the plaque becomes stable

**this process is over a lifetime!

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4
Q

Clinical Presentations (3) of atherosclerotic plaque developments (usually middle-age to elderly)

A
  1. Aneurysm/rupture - due to weakening wall
  2. Occlusion by thrombus - due to plaque rupture, emobolus or thrombus
  3. Critical stenosis - progressive plaque growth and narrowing of artery
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5
Q

Ischemic Heart Disease (IHD)

  • what is it
  • presentations
A

occlusion or blockage of an artery that causes decreased myocardial blood flow, leading to tissue death and decreased function

Can present differently based on severity and rate of progression of atherosclerosis

  1. chronic stable angina
  2. unstable angina
  3. prinzmetal angina
  4. myocardial infarction
  5. silent ischemia
  6. arrhythmia
  7. sudden death
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6
Q

Chronic stable angina

  • what is it
  • symptoms
  • treatment
A

well-established onset, patient knows activity limitations and point at which angina present (Rate pressure product monitors myocardial O2 demand and point at which angina will present)

  • stable once it has remained unchanged > 60 days
  • Symptoms: chest pain that is brought on by transient hypoxia (usually due to physical activity) relieved w/ change in activity or nitrates
  • usually nitroglycerin given sublingual; should resolve after a max of 3 doses over 15 min period (every 5 min)
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7
Q

Unstable angina

  • what is it
  • due to (3 possibilities)
  • EKG stress test
A

chest pain due to inadequate blood supply to myocardium, that is not chronic and stable (S/S are changing)

Due to:

  • increased HR/BP for > 4 hours
  • increased platelet activation
  • change in atherosclerotic plaque

EKG during stress test will show a depressed ST segment

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8
Q

Myocardial infarction

  • what is it, due to
  • S/S for men and women
  • atypical S/S
A

when blood flow to the heart is extremely occluded or cut off completely, usually due to a ruptured plaque or blood clot obstructs flow

S/S for men: crushing chest pain, SOB, sweating, pain in left arm or jaw/neck, pale face, dizziness, cyanotic extremities

S/S for women: those above + unusual fatigue, sleep disturbances, indigestion, anxiety, chest discomfort

Atypical S/S: indigestion, LV dysfunction, arrhythmia, syncope, or silent

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9
Q

Precipitating factors for MI

A

cold weather, large meal, increased exertion, anxiety, tachycardia, hypoglycemia

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10
Q

Interventions w/ presentation at ER

A

MONA = morphine, oxygen, nitrates (usually beta blockers), and aspirin

EKG and blood draw for cardiac markers

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11
Q

Cardiac Markers w/ MI (4)

- onset, peak, return to normal

A
  1. Creatine Kinase (CK): onset 3-4 hours, peak 33 hours, normal 3 days
  2. Troponins: onset 3-12 hours, peak 18-24 hours, normal up to 10 days
    * *troponin I = gold standard
  3. Myoglobin: onset 1-4 hours, peak 3-15 hours
  4. Lactate dehydrogenase (LDH): onset 12-24 hours, peak 72 hours, normal 5-14 days
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12
Q

EKG findings w/ MI

  • STEMI
  • indication
  • requirements for elevation
A

STEMI = ST segment elevation in MI

Indicates an occlusion in a large vessel and a larger area at risk

ST will be elevated in at least 2 contiguous leads

  1. > 2mm in leads V1-V3
  2. > 1mm in all other leads
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13
Q

EKG findings w/ MI

  • NSTEMI
  • indication
A

Findings of an MI w/o ST elevation

Usually means it is a smaller area or a high grade lesion w/o total occlusion

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14
Q

Prinzmetal angina

  • what is it
  • EKG finding
  • treatment
A

unusual syndrome, chest pain not due to atherosclerosis but due to increased tone and vasospasms

  • will see after an MI
  • exclusively pain @ REST

EKG: ST segment will be elevated

Treatment: nitrates and Ca channel blockers

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15
Q

Sudden cardiac arrest

A

sudden death due to cardiac arrest
- 60-70% have CAD

Cardioprotection is the only way to prevent - AEROBIC exercise is only sustainable cardioprotection
- also education on risk factors, diet, etc.

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16
Q

Hypertension

  • what is it
  • etiology
  • values
A

chronic elevation of BP, most powerful contributor to CV disease

Etiology:

  • primary/essential: occurs in absence of disease
  • secondary/nonessential: occurs in presence of disease
  • labile: no rhyme or reason, comes and goes

Norm = 120/80
Prehypertension = 120-139 and/or 80-89
Stage 1 HTN = 140-159 and/or 90-99
Stage 2 = >160 and/or > 100

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17
Q

PT implications w/ HTN

  • medical clearance
  • termination criteria
  • aerobic exercise prescription
A

Require medical clearance IF:
resting systolic BP > 200 or diastolic > 105

Terminate exercise IF:
SBP > 250 or DBP > 115
or a decrease in BP w/ increased exercise intensity

Aerobic exercise:
4-7days/week, 30-45 min, 60-85% of MHR, RPE 12-16

18
Q

SE of BP medications during exercise

- terminate if…

A

orthostatic hypotension, may have blunted HR and BP response to exercise

Terminate IF:
systolic drops > 20 mmHg
OR
systolic drops > 10 AND diastolic drops > 10

19
Q

CV disease Risk factors

- modifiable and nonmodifiable

A

nonmodifiable = hereditary/fam history, age

Modifiable = smoking, sedentary lifestyle, BMI/obesity, hypercholesterolemia, HTN, diabetes

20
Q

Cardiac output and VO2 & CV disease

- why does this happen

A

Normal VO2 is 35-70 mL/kg/min, those w/ CAD have a VO2 of 20 or lower due to decreased O2 delivery

Cardiac output decreases which causes the decrease in VO2… why?

  1. chronotropic incompentance (HR/BP doesn’t respond to exercise)
  2. LV dysfunction due to MI
  3. transient ischemia (decreased squeeze)
  4. cardiomyopathy

**can try to increase exercise tolerance by increasing efficienty of the periphery since central system is affected

21
Q

HR and CV disease

- response to exercise and return to normal

A

chronotropic incompentence = failure to reach 85% of MHR (in absence of beta blockers or other meds)

Abnormal return to resting HR if:
less than 12bpm after 1 min of ACTIVE recovery OR
less than 22bpm after 2 min of SUPINE recovery

22
Q

Blood pressure and CV disease

A

chronotropic incompetence = failure of SBP to rise in proportion of exercise intensity

23
Q

Cardiac Muscle Dysfunction (CMD)

- what is it

A

abnormality of the structure or function that impairs the heart’s ability to pump (systole) or receive (diastole) blood
- exercise tolerance & functional abilities are min/mod reduced depending on cause and severity

24
Q

CMD Characteristics (6)

A
  1. Ejection fraction 30-40%
  2. Angina
  3. Arrhythmias –> timing is off which will not allow for proper filling, decreasing the stretch and the squeeze
  4. MI –> most common cause of CMD
  5. HTN –> LV hypertrophy, dec stretch & squeeze, over time will lead to CHF
  6. Renal insufficiency causing fluid overload
25
Q

Cardiomyopathy

  • what is it
  • 2 categories
A

abnormality/disorder affecting the heart muscle’s abilty to contract and relax
- inadequate pumping leads to enlargening of the heart to compensate for its weakened condition

will see a “cardiac silhouette” on X-ray

2 categories:

  • ischemic: result from CAD
  • nonischemic: disease of the heart muscle itself (cardiomyocytes)
26
Q

Dilated cardiomyopathy

  • what is it (3 cardinal things)
  • cause
  • who does it affect
  • treatment
A

most common cause of CHF

  1. dilated LA and LV chambers (cavity size) leading to thin walls
    - the LV fills w/ blood w/o the walls stretching since the chamber is already dilated, leading to a decreased ability to squeeze
  2. bulging IV septum from L –> R
  3. myocardial mitochondrial dysfunction (increased energy usage required)

Inefficient and ineffective pump which will severely decrease cardiac output, making ADL’s difficult

Cause: idiopathic
Affects: middle-aged, men > women (2.5:1)

Treatment = transplant

27
Q

Hypertrophic cardiomyopathy

  • what is it (3 main things)
  • cause
  • who does it affect
A
  1. severe thickening of IV septum and LV wall, decreasing the LV chamber size
  2. Diastolic dysfunction; poor relaxation which leads to poor filling
  3. Hypercontractile LV systolic dysfunction
    - Increased LV diastolic pressure, causing blood to back up into atria and pulmonary system, since there is less blood filling the ventricle it will try to compensate by hypercontracting

Cause: autosomal dominant
Affects: 10-25 yr old - principle cause of sudden death in healthy individuals and athletes

28
Q

Restrictive cardiomyopathy

  • what is it
  • 3 forms
A

rarest form, worst prognosis

  1. Diastolic dysfunction - stiffened walls of R and L ventricles with lost flexibility due to infiltration of abnormal tissue

3 forms:

  1. amyloidosis - abnormal protein fibers (amyloid) accumulate in heart muscle
  2. Sarcoidosis - inflammatory disease that causes formation of small lumps in organs (lungs)
  3. Hemochromatosis - iron overload of the body, usually due to a genetic disease
29
Q

Congestive Heart failure (CHF)

  • what is the number one cause
  • pathophysiology
A

1 cause = cardiac muscle dysfunction

usually manifested as pulmonary edema or congestion, which causes RV hypertrophy, which will cause a back up of blood in the periphery, increasing pressure, and will cause LV hypertrophy…

Can be due to a problem in the heart itself (infarction, valve defect) or increased demand on the heart (HTN, lung disease) or combo of both

30
Q

Forward effect of CHF

A

less blood reaches the periphery (SV and/or Q is decreased)

31
Q

Backup effect of CHF

- left vs. right

A

output from the ventricle is less than the inflow, causing blood to accumulate behind it

Left sided back-up leads to –> pulmonary congestion/edema
- cough, dyspnea, orthopnea, paroxysmal nocturnal dyspnea

Right sided back-up leads to –> peripheral edema
- edema in legs/periphery, distention of veins, cerebral edema (flushed face, headaches), disgestive tract issues, ascites

32
Q

Signs of CHF (11)

- what to look for

A
  1. Ejection fraction less than 30%
  2. Enlarged cardiac silhouette
  3. Abnormal heart sounds **hallmark sign of CHF
  4. Sinus tachycardia (compensating w/ increased SNS activity)
  5. Abnormal breathing patterns
  6. Peripheral edema
  7. Crackles/rales
  8. SBP does not change w/ controlled expiratory maneuver
  9. Jugular vein distention
  10. Decreased exercise tolerance
  11. Decreased QOL
33
Q

Symptoms of CHF (3)

- what patients will complain of

A
  1. Dyspnea - difficult or labored breathing
    - due to pulmonary edema, abdominal ascites, or ventilator muscle weakness
  2. Paroxysmal nocturnal dyspnea - sudden awakening due to SOB
  3. Orthopnea - difficulty breathing in supine
    - supine increases venous return, overloads poorly functioning heart, increases pulmonary edema
34
Q

O2 sat/PaO2 and associated S/S

A

O2sat > 95 (PaO2 80-100) = none

O2 sat 90 (PaO2 60) = tachycardia, tachypnea, restlessness

O2 sat 85 (PaO2 50) = incoordination, impaired judgement, labored respirations, confusion

O2sat 80 and below (PaO2 45 and below) = all of the above

35
Q

Pathophysiological effects of CHF (4)

  • can be considered chronic when these things happen…
  • they all lead contribute to eachother
A
  1. Increased SNS activity (inc HR and cutaneous and visceral vasoconstriction)
  2. Muscle wasting (sedentary)
  3. Pulmonary edema
  4. Renal insufficiency: water retention due to decreased Q and oliguria (low urine output)
36
Q

Medical Interventions for CHF

- what medications to avoid

A

treat the cause:

  • improve heart’s pumping ability: beta blockers
  • control Na intake: diet (low cholesterol & fat)
  • water retention: diuretics

Can implant a device

  • ICD for EF less than 35%
  • L-VAD (last hope, bridge to transplantation)

Avoid: anti-arrhythmias, Ca channel blockers, NSAIDS

37
Q

Class I Heart failure

A

cardiac disease w/o limitations

38
Q

Class II Heart failure

A

cardiac disease w/ slight limitations
- they are OK at rest, but an increase in physical activity like going for a brisk walk will result in fatigue, palpitations, dyspnea and angina

39
Q

Class III Heart failure

A

cardiac disease w/ marked limitations

  • they are OK at rest, but symptoms are brought on w/ less than ordinary activities (ADL’s)
  • fatigue, palpitations, dyspnea, angina
40
Q

Class IV heart failure

A

cardiac disease w/ severe limitations; inability to perform physical activity w/o discomfort

  • symptoms are at rest and intensified w/ physical activity
  • fatigue, palpitations, dyspnea, angina
41
Q

Criteria for modification/termination of exercise for those w/ CHF (6)

A
  1. marked dyspnea or fatigue
  2. RR > 40
  3. development of S3 heart sound
  4. increase in pulmonary crackes/rales
  5. decrease in HR or BP > 10 mmHg during steady state or progressive exercise
  6. Diaphoresis (sweating), pallor or confusion

Cardiopulmonary (10 decks)

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