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01 CCRN Exam > Cardiac 04: Cardiomyopathy, ACS > Flashcards

Cardiac 04: Cardiomyopathy, ACS Flashcards

1
Q

Symptoms of Prinzmetal/Variant Angina

A

Pain that occurs at rest, during sleep or w/o evidence of provocation. Symptom thought to be caused by coronary vasospasm that may be DUE TO COCAINE

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2
Q

Unstable Angina symptoms

A

-Recent onset in last two months, limits activity.
- Differs from typical exertional angina. Occurs with less exertion, greater intensity or longer duration. Requires more intervention before obtaining relief.

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3
Q

What are the dangers of fibrinolytic therapy in thrombus occlusions?

A

Thrombuses are more platelet rich, where ANTI-platelets would be more effective. Fibrinolytic is not effectively and may paradoxically accelerate occlusion by releasing clot-bound thrombin, this then activates more platelets.

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4
Q

Delete

A
  1. Is it cardiac or not
  2. If cardiac, is it ischemic or not ischemic
  3. If ischemic, is it stable or not
  4. If unstable, what is it? Platelet? Blood clot?
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5
Q

What leads would indicate Anterior MI?
What coronary artery supplies that part of the heart?

A

Lead VI, V2, V3, V4.
LAD

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6
Q

What are major complications of anterior MI?

A
  1. Cardiogenic shock
  2. Bundle Branch Blocks
  3. Vent Dysrhythmia
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7
Q

What leads would indicate an inferior MI?
What coronary artery supplies the inferior heart?

A

Leads II, III, aVF.
RCA

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8
Q

What are major complications of inferior MIs?

A

Bradycardia, heart block

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9
Q

What leads would indicate a Lateral MI?
What coronary artery feeds that part of the heart?

A

Leads I, aVL, V5, V6. LAD

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10
Q

Major complications of lateral MI

A

Heart blocks in some

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11
Q

What are normal CK levels in females and males?

A

Female: 40-140 U/L
Male: 60-170 U/L

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12
Q

What does CK, Creatine Kinase do?

A

It’s an enzyme important in breaking down creatinine to creatine. Increases in the serum when muscle damage has occurred.

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13
Q

When does CK levels start to rise and when does it peak? When will it return to normal.

A

Rises 3-6 hours after chest pain
Peaks 12-24 hours
Normalizes after 2-3 days

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14
Q

Treatment of Angina

A

MONA
Loading dose of P2Y receptor Inhibitor: plavix, prasugrel, ticagrelor

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15
Q

If pt has acute MI and is adequately reperfused. What are post MI care?

A

Adjunct Therapy for ACS:
1. Calcium Channel Blocker: Vasodilate, decrease HR
2. ACE Inhibitor: decrease afterload and preload

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16
Q

Thrombolytics agents ARE given in MIs, vs being recommended against in angina. What are contraindications of thrombolytic agents?

A
  • active bleeding, hx ICH, recent (2 mo) surgery, cerebral vascular disease
17
Q

What are the BP, CO, PAOP like in from cardiogenic Shock.

A

Cardiogenic shock is the infarction of >40% of the L ventricle.
sBP<100 mmHg, Pulmonary edema PAOP>18mmHg, decreased contractility (low CO/CI), poor peripheral perfusion.
PCI is advocated.

18
Q

What exactly is cardiomyopathy?

A

Disease of the cardiac muscle and impacts the muscle globally.

19
Q

What are 3 kinds of cardiomyopathy?

A
  1. Dilated
  2. Hypertrophic
  3. Restrictive
20
Q

What’s the most common type of cardiomyopathy?

A

Dilated. This cardiomyopathy is mostly caused by env/external factors

21
Q

What is the pathophysiology of dilated cardiomyopathy?

A

Dilated ventricles, which leads to decreased contractility and systolic dysfunction. Drop in CO.

The heart muscle is stretched out!

22
Q

Dilated cardiomyopathy is in afib a lot so A/C should be done. It’s hard to be hypertensive with dilated cardiomyopathy as well.

A

–

23
Q

Hypertrophic and dilated cardiomyopathy is about the same size. What dx could be used to tell the difference?

A

ECHO

24
Q

Pathophysiology of hypertrophic cardiomyopathy?

A

Septum is enlarged, creating a narrow long cavity. The ventricle walls become rigid and the septum could obstruct outflow tract!
Backflow results into pulmonary congestion.

25
Q

What are the typical causes of hypertrophic cardiomyopathy?

A

Typically genetics. People die young. Type I dm. HTN

26
Q

What’s the pathophysiology of restrictive cardiomyopathy?

A

Stiff ventricles reduce ventircular filling, leading to drop in CO and bi atrial dilation. Note, septum isn’t enlarged.

Causes pulmonary edema and systemic congestion

27
Q

What are the causes of restrictive cardiomyopathy?

A
  • 90% from amyloidosis.
  • Other causes sarcoid, fibrosis, radiation tx.
28
Q

What medications should be used with caution in HCM?

A

To be careful of outflow tract obstruction.
- digitalis
- diuretics
- inotropic agents

29
Q

What are interventions that should be done on cardiomyopathies?

A
  • CONGESTION CONTROL: relieve pulmonary and systemic congestion
  • DYSRHYTHMIA CONTROL: prevent thromboemoblic event, tx w/pacer or meds
  • digitalis, diurectic, beta blockers, ace inhibitors, vasodilators, inotropic agents, antidyrhythmia
30
Q

Difference between ischemia, injury and infarction?

A

Severity from best to worse is ischemia (no O2 but reversible)/ST depression
, injury (non reversible)/ST elevation and infarction (necrosis)/Q wave form changes.

31
Q

LAD stands for?

A

Left ANTERIOR descending artery!!!

32
Q

What is stable angina?

A

More predictable and controllable, i.e occurs with exercise.

33
Q

What kind of drug could hypertophic cardiomyopathies use?

A

A negative inotrope, i.e diltiazem.

34
Q

**Evidence of coronary artery reperfusion? (Barron’s)

A
  • Chest Pain Relief
  • Resolution of ST segment deviations
  • Myocardial stunning, when vessels open. Elevated troponin/CK-MB.
  • Reperfusion arrhythmias (VT, VF,
35
Q

Goal of PCI for coronary artery reperfusion

A

90 minutes

36
Q

What should be monitored post PCI reperfusion? (5)

A
  • Signs of reocclusion: chest pain, ST elevation
  • Vasovagal reaction during sheath removal . Signs are pallor, nausea, yawning, diaphoresis
  • Monitor bleeding at sheath site.
  • Monitor for retroperitoneal bleeding. Lower back pain and hypotension
  • Vascular pulses
37
Q

** What exactly is Variant/ Prinzmetal’s angina?

A

Type of unstable angina associated with transient ST elevation
D/t coronary artery spasms
Occurs at rest and may be cyclic
Precipitated by nicotine, etoh, cocaine ingestion
trop negative
Nitro result in relief of chest pain and ST returns to normal

38
Q

MI Murmurs. Where are papillary muscle ruptures heard?

A

loudest at the apex. mid-clavicular 5th

39
Q

MI Murmur, Ventricular septal defect murmur heard at

A

Sternal border 5th ICS

01 CCRN Exam (17 decks)

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