Exam 3 part 3 Flashcards

1
Q

Main threat of DVT

A

pulmonary embolism

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2
Q

treating DVT

A

TPA: dissolve the clot with tissue plasminogen activator (thromoblytic agent)

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3
Q

preventing DVT

A
  • anticoagulants/blood thinners
  • Pneumatic compression devices on for prolonged bed rest so blood doesn’t pool in the extremities
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4
Q

etiology DVT

A

Stasis of blood
- Bed rest
- Immobility
- CHF
Increased blood coagulation
- Dehydration
- Pregnancy
- Genetic factors
Vessel wall injury
- Indwelling venous catheters
- Surgery
- Trauma/infection

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5
Q

s/s DVT

A
  • inflammation pain, swelling, deep muscle tenderness
  • Elevated WBC count, fever
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6
Q

acute coronary syndrome

A

A spectrum of acute ischemic heart disease ranging from unstable ischemia to acute MI based on the presence of ECG changes

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7
Q

characteristics of acute coronary syndrome

A

ECG changes
- ST-segment elevation
- Serum cardiac markers
- Proteins released from necrotic heart cells
–Myoglobin, creatine kinase, troponin

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8
Q

types of acute coronary syndrome

A

Unstable angina (heart cells are not dying), non-ST segment elevation MI (no q waves), ST segment elevation MI (q waves)

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9
Q

s/s acute coronary syndrome

A

chest pain or pressure, shortness of breath, sweating, nausea, and pain radiating to the back, neck, jaw, or arms.

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10
Q

Stable plaque

A

thick fibrous cap, less likely to rupture

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11
Q

Unstable plaque

A

thin fibrous cap, likely to rupture and cause clot or embolism

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12
Q

Chronic stable angina

A

fixed coronary obstruction
- Imbalance between blood flow and metabolic demand
- Pain when the heart’s oxygen demand increases. occurs during:
– Physical exertion
– Emotional stress
** relieved by nitroglycerin - dilates coronary vessels

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13
Q

Unstable angina

A
  • unexpected chest pain
  • usually occurs while resting
  • reduced blood flow to the heart muscle because the coronary arteries are narrowed by fatty buildups
  • increased intensity and duration - MI
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14
Q

Variant/vasospastic angina

A
  • Pain when coronary arteries spasm
  • Occurs at rest or with minimal activity
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15
Q

Silent myocardial ischemia

A
  • Myocardial ischemia without pain
  • Factors associated are same as those responsible for angina
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16
Q

main cause of death associated with an MI

A

cardiac arrhythmias

17
Q

complications of an MI

A
  • Heart failure
  • Cardiogenic shock
  • Pericarditis
  • Thromboemboli
  • Rupture of the heart
  • Ventricular aneurysms
18
Q

Hypertrophic cardiomyopathy

A
  • Defects in contractile proteins make cells too weak.
  • Cells hypertrophy to do the same amount of work as normal cells.
  • Need more oxygen and perform less efficiently, so the person is prone to heart failure and may suffer sudden death during exertion.
    most common cause of sudden cardiac death (athletes)
  • Genetic - heart cells don’t have enough actin and myosin - each heart cell is working harder, it
    hypertrophies - heart enlarges
    –Enlargement of septum and left ventricle wall
19
Q

dilated cardiomyopathy

A

progressive cardiac dilation - the heart is enlarged 2-3x normal.
- Easy for blood to get into chambers but hard for it to leave
- Heart loses contractile function - walls are thin like a stretched balloon
All - 4 chambers involved, thinning walls

20
Q

dilated cardiomyopathy s/s

A

dyspnea, orthopnea, exercise intolerance

21
Q

dilated cardiomyopathy treatment

A

relieving symptoms of heart failure
- Beta blockers, diuretics, ACE inhibitors
- Heart transplant

22
Q

Restricted cardiomyopathy

A

Restricted cardiac filling - heart is “stiff” so it can’t fill properly
- can’t get blood into the heart because it is not expanding when blood is entering

23
Q

Restricted cardiomyopathy s/s

A
  • Dyspnea
  • PND
  • Orthopnea
  • Peripheral edema
  • Neck vein distension
24
Q

Post partum cardiomyopathy

A
  • Dilated cardiomyopathy that occurs in the last month of pregnancy or within 5 months after delivery
  • Half of the women recover with no loss of cardiac function
  • Heart weakens after childbirth, chance is higher after each child
25
Q

pathophysiology of an MI

A
  • complete obstruction of coronary artery infarction
  • area affected becomes necrotic death of myocardium replaced by fibrous tissue
26
Q

How is an MI diagnosed

A

Blood work including raised levels of troponin (also myoglobin and creatine-kinase)

27
Q

s/s of MI

A

Chest pain: radiating to left arm/neck
- Severe, crushing, constrictive OR like heartburn
Sympathetic nervous system response
- GI distress, nausea, vomiting
- Tachycardia and vasoconstriction (pallor)
- Anxiety, restlessness, feeling of impending doom
Hypotension and shock
- Dizziness, weakness in the arms and legs
- Women may also experience - SOB, nausea and vomiting, back and jaw pain

28
Q

In what type of patient do you see ST wave elevation, ST wave depression?

A
  • Elevation - MI
  • Depression - ischemia
29
Q

30) What does non-ST wave elevation MI and ST wave elevation MI have in common?

A

Necrosis of heart cells, release of cardiac markers (myoglobin, CK, troponin)

30
Q

signs and symptoms of an anaphylaxis reaction

A
  • general, sudden vasodilation resulting in a rapid drop in blood pressure
  • edema of the mucosa
  • constriction of the bronchioles occurs obstructing airflow.
  • hives
  • Itching
  • skin erythema
  • Vomiting
  • Abdominal cramping
31
Q

anaphylaxis treatment

A

epinephrine: stabilizes the cardiovascular system; Causes vasoconstriction , increases heart rate, increases stroke volume, bring blood pressure back up, Bronchodilation