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Cardio Block > CM- Acute Ischemic Heart Disease > Flashcards

CM- Acute Ischemic Heart Disease Flashcards

1
Q

What is the definition of an acute coronary syndrome? What are the 3 types?

A

It is an acute complication of ischemic heart disease.

  1. unstable angina
  2. non-ST segment elevation MI (NSTEMI)
  3. ST segment elevation MI (STEMI)
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2
Q

What is a myocardial infarction?

A

When heart muscle dies as a result of prolonged ischemia due to:

  1. obstructed blood flow
  2. increased myocardial demand
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3
Q

Does all myocardial ischemia result in cell death?
How much time for ischemia to cause CELL necrosis?
How much time to SEE necrosis on pathologic specimen?
How much time for ALL myocardium to be at risk of infarction?

A

No. The ischemia must exceed a threshold for an extended period of time to overwhelm myocardial repair mechanisms and allow necrosis to begin.

20 minutes of ischemia is necessary to cause cell necrosis.
Several hours to see necrosis on pathologic specimen.
6 or more hours for all the myocardium to be at risk of infarction.

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4
Q

How does the chest pain of a myocardial infarction differ from angina?
Where does the pain radiate?

A

It feels the same (pressure/pain) but is more severe and prolonged, lasting 20-30 minutes.

Radiates to neck, jaw, arm

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5
Q

What are EKG changes of ischemia?

What are the changes with myocardial injury?

A

Ischemia: T wave inversions, ST depression.

Myocardial injury: ST elevation

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6
Q

What are the EKG changes associated with NSTEMI?

A
  1. Inverted T waves, ST depression

2. no injury pattern

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7
Q

The EKG is diagnostic of STEMI if there is new _________ in _______________________.

As the infarct progresses, there is a loss of ____ and development of ______ in the affected leads.

A

new ST elevation in 2 or more contiguous leads

Loss of R wave voltage and Q waves develop

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8
Q

A new _____________________ in a patient presenting with chest pain suspicious of an MI is also treated as STEMI.

A

LBBB

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9
Q

IF there is ST elevation in II, III or avF, where is the infarction? What artery is likely occluded?

A

Inferior part of the heart- right coronary artery

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10
Q

If there is ST elevation in I, avL, V5, V6 where is the infarction?

A

lateral side of the heard- circumflex

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11
Q

If there is ST elevation in V1-V4, where is the infarction?

A

anterior part of the heart - LAD

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12
Q

In what type of acute coronary syndrome would the location of ST and T waves help determine the area of infarction?

A

The ST and T waves can help determine area of infarction for STEMI but NOT NSTEMI or unstable angina

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13
Q

What variation is seen on the EKG for :

  1. ischemia
  2. injury
  3. infarction (acute)
  4. Infarction (age uknown)
A
  1. tall or inverted T wave (infarct), ST depression (angina)
  2. Elevated ST, T wave inversion
  3. Q wave, ST elevation, T inversion
  4. Q wave, ST and T waves returned to normal
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14
Q

What cardiac enzymes are released when the myocytes become irreversibly injured?
Which is the preferred biomarker for diagnosing MI?

A

CK, CK-MB isoform

Troponin I or Troponin T (preferred for diagnosing MI)

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15
Q

What is the underlying pathology in most acute coronary syndromes?

A

A coronary arterial atherosclerotic plaque ruptures so the inner contents are exposed to circulating blood forming a compete or partial occlusion thrombus.

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16
Q

What increases a plaques propensity to rupture?

A

Multifactorial-

  1. cellular composition
  2. lipid composition
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17
Q

After a plaque ruptures, if there is sustained, full occlusion, what will the EKG show?
If there is partial occlusion, what will the EKG show?

A

Full occlusion-> transmural ischemia/injury->Infarction–> STEMI

Partial occlusion–> NSTEMI or unstable angina (differentiated by cardiac enzymes)

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18
Q

Unstable angina and NSTEMI both show inverted T waves and ST depression on EKG. How are they differentiated?

A

NSTEMI will have cardiac enzymes. Unstable angina will not.

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19
Q

When in the day is acute myocardial infarction most likely to occur? Why?

A

6am and noon with a peak incidence in the first 3 hours of waking because of increased arterial pressure, HR, adrenergic activity, vascular tone and or/platelet aggregation

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20
Q

What are the six things that must be done to treat an acute MI?

A
  1. reperfuse immediately for STEMI
  2. Limit infarct size
  3. stabilize ruptured plaque with antithrombotics
  4. relieve pain
  5. prevent electrical/mechanical complications
  6. prevent reinfarction, recurrent ischemia, heart failure
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21
Q

If the person has STEMI, the goal is to achieve reperfusion within ________, optimally _____.
What are the 2 options for reperfusion?

A

Within 120 minutes (optimally 60)

  1. Primary coronary intervention (PCI)
  2. Intravenous Thrombolytic therapy
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22
Q

PCI should be performed with optimal “door to balloon time” of ________________. It can restore perfusion in _________ % of cases.

Intravenous thrombolytic therapy should be “door to needle” in ________________.

A

90 minutes, 90-95% of cases

30 minutes

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23
Q

What are the 5 ABSOLUTE contraindications for thrombolytic therapy?

A
  1. active internal bleeding
  2. less than 2 months since cerebrovascular insult or neurosurgery
  3. less than 2 weeks since major surgery, organ biopsy
  4. less than 1 month since GI bleed
  5. Recent serious trauma including prolonged CPR
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24
Q

What are the 5 RELATIVE contraindications for throbolytic therapy?

A
  1. severe hypertension (200/110)
  2. recent minor trauma
  3. hemostatic defect
  4. hepatic/renal disease
  5. diabetic hemorrhagic retinopathy
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25
Q

What is the difference between PCI “bleeding risk” and thrombolytic therapy “bleeding risk”?

A

PCI- bleeding at the site of access (groin from the femoral entrance)

Thrombolytic- potential brain bleeds

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26
Q

In patients who present at a hospital without capacity to perform PCI, what is the course of action?

A
  1. Transfer to a hospital with PCI

2. Give thrombolytic therapy and THEN transfer to a hospital with PCI

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27
Q

Why is aspirin given for MI?

A

It interferes with cyclooxygenase and inhibits formation of TXA2.
It interferes with platelet activation and adhesion.
It is used in unstable angina, NSTEMI and STEMI to decrease mortality and decrease risk of reinfarction

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28
Q

What is “dual anti-platelet therapy”? What 2 drugs are involved and when is it used?

A

Aspirin and clopidogril and is used to decrease risk of stent thrombosis

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29
Q

What 8 drugs are given as acute therapies for MI?

A
  1. Aspirin
  2. Clopidogril
  3. Heparin
  4. Nitrates
  5. B-blocker ***
  6. ACE-inhibitor ***
  7. STatin
  8. Oxygen
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30
Q

What are nitrates given when a patients has acute coronary syndrome?

A

To relieve chest pain by relaxing vascular smooth muscle and dilating arteries and veins

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31
Q

In what situation would B-blocker used be contraindicated for a person with an acute coronary syndrome? Why?

A

Tachycardia, HF or a large infarct because it could precipitate cardiogenic shock

32
Q

ACE inhibitors are initiated for a person with acute coronary syndrome if they have normal ________ and are not ______________.

What specific situations call for ACE inhibitors?

A

Normal creatinine (no renal damage) and are not hypotensive

Ace inhibitors block angiotensin conversion which decreased blood volume and BP.

USed when LVEF <40, diabetes, hypertension

33
Q

What are the two functions of STatins?

A
  1. lower cholesterol

2. stabilize plaques

34
Q

What is “platelet-mediated coronary arterial vasoconstriction”?

A

When a plaque ruptures, as platelets aggregate, they may release alpha granule contents (TXA2 and serotonin) which vasoconstrict, so in addition to the platelet plugging, you also have vasoconstriction further narrowing the vessel and decreasing 02/nutrient supply to tissue

35
Q

How does treatment differ for stable angina and unstable angina?

A

Unstable is poorly controlled by nitroglycerin where stable angina is controlled by nitro

36
Q

Reperfusion therapy and thrombolytic therapy is NOT beneficial in patients with ___________________.

A

Unstable angina or NSTEMI

37
Q

Coronary intervention is usually not required for unstable angina or NSTEMI except for what 3 scenarios?
Why?

A
  1. > 65 years old
  2. ST and T wave alterations
  3. enzymatic evidence of myocyte necrosis (NSTEMI)

Intervention will NOT decrease mortality but will decrease morbidity (likelihood of recurrent ACS)

38
Q

In addition to possible coronary revascularization, what 4 drugs are used in therapy for NSTEMI and unstable angina?

A
  1. aspirin with clopidogril (platelet inhibition)
  2. Heparin (thrombin inhibition)
  3. B-blockers (decrease O2 demand)
  4. Nitroglycerin (prevent coronary vasoconstriction)
39
Q

Upon discharge from the hospital for NSTEMI or unstable angina, the patient is sent home with what 5 drug cocktail?

A
  1. Aspirin
  2. clopidodril
  3. b-blocker
  4. ACEI
  5. Statin

(an usually a nitrate for emergencies)

40
Q

Long term prognosis following acute MI is determined by what 3 factors?

A
  1. patient age
  2. residual LV function (systolic)
  3. severity of coronary artery disease
41
Q

What are the 3 issues used to determine whether PCI or thrombolytic therapy is in the patients best interest?

A
  1. Availability
  2. Bleeding risk
  3. experience of the operator duing the PCI
42
Q

What are the most common electrical complications of acute MI?

A
  1. Ventricular fibrillation

2. AV block

43
Q

What are the most common mechanical complications of acute MI?

A
  1. CHF
  2. Mitral regurgitation
  3. Ventricular Septal Defect
44
Q

What is commonly seen on the EKG in the first 2-3 days after the onset of an acute MI?
What is the therapy?

A

VPB (ventricular premature beats) which generally do not require therapy.

However, they are put on telemetry to monitor for Vtach and Vfib. No prophylactic anti-arrhythmias are used

45
Q

What is the prognosis of someone who has VT/VF within 24 hours of their acute MI?

A

they are NOT at increased risk for recurrence. It is NOT associated with adverse prognosis

46
Q

What are the characteristics of a first degree AV block?
Patients with an MI in what area may have it? Why?

What is the therapy?
How long does the block last?

A

Prolonged PR interval (>.2) in patients with inferior MI.
Cardiac vagal receptors in the inferior/posterior LV cause the first degree block.
There is no therapy, but the patients are monitored closely for the appearance of 2nd or 3rd degree blocks. First degree usually lasts only 1-2 days

47
Q

What is type I second degree AV block?
Patients with an MI in what area usually have it? Why?
What is therapy?

A

Wenchebach type in patients with inferior MI (due to increased vagal tone like type I AV block). The PR interval gets longer and longer and then a QRS is dropped.
After the dropped beat, P is normal and the PR interval is shortest in sequence.

Therapy is unnecessary unless the ventricular rate is so slow it causes syncope or hypotension, or chest pain in which case they get atropine.

It lasts 2to3 days

48
Q

What is Mobitz II AV block?
Patients with an MI in what area usually have it?
What is the therapy?

A

Multiple unconducted QRS waves. Consistently long PR interval with many dropped waves.
It occurs in patients with anterior MI usually due to necrosis so it is PERMANENT..
Therapy is a pacemaker

49
Q

What is third degree AV block?
Patients with an MI in what area are likely to get it?
What is the therapy?

A

It is when P and QRS waves conduct completely independent of each other.
It usually occurs in inferior MI (similar to 1 and 2(type 1))–> transient so no pacemaker
If it does occur with anterior MI, it reflects infarction and requires a pacemaker

50
Q

What are the 3 ways LV failure can occur after an acute MI?

A
  1. Systolic failure- impaired contraction
  2. Diastolic failure- reduced LV compliance
  3. Combo of both
51
Q

What is the pathogenesis in :

  1. Killip 1
  2. Killip class II
  3. Killip class III
  4. Killip class IV
A
  1. no evidence of heart failure
  2. mild heart failure
  3. substantial heart failure
  4. cardiogenic shock - hypotension with hypoperfusion of kidneys, and pulmonary congestion
52
Q

What is the most serious form of LV pump failure?

What are the 3 associated presentations of this?

A

Cardiogenic shock- cardiac function inadequate to meet the metabolic needs of the body.

  1. hypotension (sys <90)
  2. hypoperfusion of critical organs
  3. deranged hemodynamics at catheterization
53
Q

Why does LV pump failure cause a “downward spiral”?

A

Hypotension and high LV filling pressure (which increases LA pressure, which increases pulmonary venous pressure, which increased pulmonary edema) will decrease perfusion of coronary arteries which will worsen ischemia and worsen ventricular function

54
Q

What are the risk factors for developing cardiogenic shock?

A
  1. severe coronary atherosclerosis
  2. prior MI
  3. Increased age
  4. Females
  5. diabetes
  6. STEMI
  7. Anterior infarct
55
Q

How do we measure LA pressure?

A

A wedge catheter in the pulmonary veins so no blood perfuses and you can read pulmonary venous pressure which should be the same as LA pressure

56
Q

What are the treatment options for cardiogenic shock?

A
  1. pharmacologic agents to support BP and augment ventricular function
  2. intraaortic balloon pump (deflates in systole to vacuum the blood out to perfuse body and inflates in diastole to increase coronary artery perfusion)
  3. Coronary revascularization- PCI or bypass
57
Q

What are the 3 locations of rupture of infarcted myocardium?

A
  1. ventricular septal rupture
  2. papillary muscle rupture (MR)
  3. free wall rupture (pericardial effusion)
58
Q

Infarctions of what heart areas would leave to a ventral septal rupture?

A

Anterior- upper half of septum is supplied by LAD

Inferior - lower half of septum is supplied by RCA

59
Q

What symptoms develop 1-5 days after a ventricular septal rupture?

A

dyspnea and orthopnea related to pulmonary congestion 1-5 days after the rupture

60
Q

What are the audible characteristics of a VSD?

A

Harsh systolic murmur at left sternal border.

A palpable thrill is present.

61
Q

What will echo with color flow Doppler show for VSD?

A

left-to-right intracardiac shunting

62
Q

If there is a VSD, what will blood samples from the RV and pulmonary arteries show?

A

Increase in O2 saturation caused by shunted oxygenated blood from the left heart

63
Q

What 3 drugs, and 3 other therapies are used when the patient has a VSD?

A
  1. diuretics - lower cardiac filling pressures and decongest lungs
  2. inotropes - lower filling pressures and decongest lungs
  3. vasodilators to reduce LtoR shunting
  4. Intraaortic balloon pump
  5. Cardiac cath
  6. Surgical closure of VSD
64
Q

Where is the primary MI usually located when there is a papillary muscle rupture?
Which papillary muscle is most likely to rupture? Why?

A

Inferior location because the posteromedial papillary is more likely to rupture than the anterolateral.
PM is only supplied by RCA
AL is supplied by LAD and L circumflex

65
Q

What is seen on the EKG with:

  1. acute VSD rupture
  2. Acute MR
  3. Acute Free wall rupture
A
  1. Q waves anteroseptal or inferior
  2. Q wave or non-Q wave MI
  3. Q wave infarction
66
Q

Which acute ruptures are associated with a thrill?

A

VSD

67
Q

What symptoms develop with an acute papillary rupture 1-5 days after the event?

A

Pulmonary congestion on X-ray with dyspnea and orthopnea due to mitral regurgitation and increased LA pressure

68
Q

What do you hear on physical exam with an acute papillary rupture?

A

a holosystolic murmur at the cardiac apex (mitral regurgitation) with NO thrill

69
Q

What is the treatment for papillary muscle rupture?

A
  1. Ionotropes and diuretics to lowe intracardiac filling pressure and decongest lungs
  2. vasodilator to reduce regurgitation into LA
  3. Cardiac cath
  4. Mitral valve replacement
70
Q

What is the result of a free wall rupture due to MI?

A

Sudden cardiac death. It does NOT cause pulmonary congestion.
Blood rapidly enters the pericardial splace and causes hemodynamic collapse

71
Q

What is the intervention for free wall rupture?

A

If you can temporarily seal off the blood entering the pericardial space, you can do:

  1. pericardiocentesis- drain fluid
  2. emergency surgery
72
Q

In addition to the inferior wall of the LV, where else does the RCA supply? What problem does this raise?

A

It supplies RV so inferior myocardial infarct could cause RV dysfunction in addition to LV dysfunction.

73
Q

What are the associated symptoms of a patient with RV infarct?

A
  1. hypotension
  2. elevated neck veins
  3. peripheral edema with clear lungs
74
Q

What drugs are definitely contraindicated in patients with RV infarction?

A

nitrates, morphine and diuretics reduce preload and exacerbate the hypotension

75
Q

What is a right-sided EKG?

What lead and what EKG change would be indicative of RV infarction?

A

When the leads are placed on the right side of the chest.

0.5mm or higher ST elevation in V4R is indicative of RV infarction

Cardio Block (25 decks)

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