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Cardiology Exam III > Cardio 22,23:Acute MI and STEMI > Flashcards

Cardio 22,23:Acute MI and STEMI Flashcards

1
Q

According to D’Amico 99% of the time acute MI is caused by…

A

Destabilization of atherosclerotic plot with subsequent thrombus formation

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2
Q

The other 1% of Acute MI’s are caused by Embolic Phenomenon and Thoracic Aorta dissection. Which therapy is contraindicated in patients with these etiologies ?

A

Thrombolytic therapies

Side note: Thoracic aortic dissection cause AMI if it involved the rood of one of the coronary arteries

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3
Q

In Acute Coronary Syndrome you may see ST elevation but ACS may occur without ST elevation. What are the two diseases states seen in Non-ST Elevation associated ACS ?

A

Unstable Angina

NSTEMI (Non-ST Elevation Myocardial Infarction)

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4
Q

What is a more likely NSTEMI presentation: with Q wave or without Q wave on EKG ?

A

Most NSTEMI’s present without Q-wave on EKG (NQMI)

However, NSTEMI’s with Q waves sometimes do occur (QWMI)

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5
Q

What is is a more likely presentation of STEMI: With Q-wave or without ?

A

With Q-wave. Very few with ST elevation will develop without a Q wave.

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6
Q

Type I MI

A

Spontaneous thrombotic MI (vast majority)

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7
Q

Type II MI

A

Nonthrombotic MI

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8
Q

Type III MI

A

Sudden cardiac death with ischemic symptoms but no biomarkers

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9
Q

Type IV MI

A

MI in association with percutaneous coronary intervention (PCI)
(probs don’t need to know this)

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10
Q

Type V MI

A

MI in association with coronary artery bypass surgery (CABG)

Probs dont need to know this

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11
Q

Name the 3 major diagnostic indicators for acute MI

A

Symptoms: Chest pain (epigastric, jaw, shoulder)
EKG findings
Serum Markers : Usually have latent elevation and may not allow for instant diagnosis

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12
Q

List the two isotopes used in nuclear imaging of the heart

A

Technitium99: Pyrophosphate Scan

Detects MI as a “hot spot” on the nuclear scan between 24 hours and 5 days after symptom onset

Indium-111: Anti-myosin scan

Imaging is performed 24 hours after 111In-antimyosin injection
Positive scan (a “hot spot” on the nuclear scan) may be seen in:
Acute MI
Unstable angina pectoris
Active myocarditis
Cardiac transplantation rejection

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13
Q

What is used for enhancement of Cardiovascular Magnetic Resonance

A

Reveals a permanent record of both acute & chronic MI
“Bright is abnormal” shows you where ab
Newer technique
Expensive

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14
Q

Ddx of cardiovascular causes of chest pain

A 
Acuts MI 
Angina
Prinzmentals
Valvular 
Acute pericarditis
Aortic Dissection
Myocarditis
Hypertrophic cardiomyopathy
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15
Q

Ddx of pulmonary causes of chest pain

A 
Pleurisy
Embolism
Pneumothorax
Asthma
Pneumonia
Bronchitis
Pulm HTN
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16
Q

Ddx of GI causes for chest pain

A 
GERD
Esophagitis
Gastritis
Peptic Ulcer
Biliary colic
Pancreatitis
Mollory Weiss Tear.
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17
Q

Ddx of musculoskeletal causes for chest pain

A 
Costochondritis
Myositis
Somatic dysfunction
Chest of upper extremity trauma
Thoracic outlet syndrome
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18
Q

DDx of neurologic causes for chest pain

A

Herpes zoster
Exacerbation on touching patients skin
Intercostal neuralgia

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19
Q

DDx of psychologic causes of chest pain

A

Anxiety
Da Costa’s syndrome: Neurocirculatory asthenia.
Somatization disorder (Briquet’s syndrome)
External problems cause somatic pain
Converson disorder
Hypochondriasis
Munchausen syndrome

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20
Q

DDx for miscellaneous causes of chest pain

A

Splenic infarction
Subdiaphragmatic abscess
Hepatic distension

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21
Q

What is the first myocardial serum marker to be seen ? Why is it insignificant ?

A

Myoglobin: comes on quick but is very inspecific  will go up with chest trauma not very useful unless patient presents with typical MI problem.

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22
Q

When will CK-MB peak in serum concentration ?

A

CK-MB more unique for Heart Muscle ( peaks in first 24 hours )

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23
Q

Troponins will peak when ? Why do we use them instead of LDH ?

A

Troponins peak in first 24 hrs and continue for about a week or so. Good if they present late to you.
Used because of their early onset, persistence and relative specificity for cardiac cells (not the most specific, however.)

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24
Q

What is the overall goal of management therapy for acute MI ?

A

Lower oxygen demand and increase oxygen supply

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25
Q

What can be done to decrease Myocardial oxygen demand ?

A

1.Bed Rest

2.NPO
(digestion uses a lot of O2, takes from heart)

3.Decrease the “Double Product”
I. Beta-Blockers
II. Additional Anti-hypertensives
(Avoid those that cause reflex tachycardia)
III. Digoxin
(if MI was caused by hypotension or CHF)
IV. Analgesics
(Morphine is a good preload reducer, but do not in RV infarction)

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26
Q

Who would you not want to give a Beta Blocker to when treating an acute MI ?

A

Patient with a history of Asthma
Patients who are diabetic
(unless BB is specific –> B2 blockers interfere with glycogenolysis leading to hypoglycemia)

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27
Q

Treating Acute MI with Na-Nitroprusside can help increase oxygen demand. What must be given with Na-NP to ensure its safety and why ?

A

A Beta Blocker

Decreases the risk of NaNP induced reflex tachycardia –> increased oxygen demand (bad news)

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28
Q

In treating Acute MI, how can you increase a patients O2 supply ? (more specifics on next few slides)

A
  1. Supplemental Oxygen
  2. Relieve pulmonary vascular congestion (if present)
  3. Acute revascularization
  4. Intra-aortic balloon pump (IABP)
29
Q

What is a reason for pulmonary vascular congestion ? What can you give to treat it ?

A

Edema in the lung due to Left sided infarction or CHF.

Prescribe: Diuretics, IV NTG, MSO4 (morphine sulfate)

30
Q

What are the two forms of therapy that can be given to allow for Acute Re-vascularization ? (of coronary arteries)

A

Thrombolytic Therapy

Mechanical Revascularization
     Catheter Based (PCI)
     Cabbage
31
Q

Explain how an Intra Aortic Balloon Pump works

A

It actively deflates in systole, increasing forward blood flow by reducing afterload through a vacuum effect. It actively inflates in diastole, increasing blood flow to the coronary arteries via retrograde flow.

If cardiogenic shock and if cath lab available this can be done.

32
Q

What are the Pro’s of Thrombolytic therapy ?

A
  1. Lyses occlusive coronary thrombus rapidly
  2. Improves LV function
  3. Reduces both short-term and long-term mortality
33
Q

What are the Risks involved in Thrombolytic

A

1.Bleeding
2.Anaphylaxis (SK and APSAC)
Streptokinase/APSAC are not used often
3.Hypotension
4. Arrhythmia (reperfusion)
Reactive Ox species during re-perfusion

34
Q

How are SK (streptokinase) and APSAC (anistreplase ) administered ?

A

IV infusion of SK with single bolus of APSAC

*not often used anymore due to their ability to cause anaphylaxis. SK was first thrombolytic on the market in the US.

35
Q

For Thrombolytics, what drug is considered the “standard of care” ? How is it administered ?

A

tPA (tissue plasminogen activator, Ateplase)

IV bolus and double infusion (accelerated dose)

36
Q

r-PA (reteplase) is administered in….

A

Double bolus, 30 minutes apart

37
Q

TNK-tPA (tenecteplase) is administered in…

A

Single bolus (over 5 to 10 seconds)

38
Q

n-PA (lanoteplase) is administered in …

A

Single bolus

39
Q

When is the use of thrombolytic therapy most beneficial to the patient ?

A

When give <6 hours from time of onset of symptoms

Between 6-12 hours it is still beneficial

After 12 it is of little use

40
Q

When would use of Thrombolytic therapy after 12 hrs actually be useful ?

A

ongoing chest discomfort or a “stuttering” course

Ask the patient if pain is still coming and going. If still persistent, go ahead and give it to them.

41
Q

Are there any age restrictions to Thrombolytic therapy ?

A

NOPE !

42
Q

T of F: Thrombolytic therapy can be administered with EKG finding of ST segment elevation > 1 mm in a single lead during Acute MI ?

A

False ! Must be seen in 2 or more CONTIGUOUS limb leads (ie. II, III, IV or V1 & V2)

43
Q

T or F: Thrombolytic therapy can be administered for New (or presumed new) LBBB in Acute MI ?

A

True !

44
Q

What must also be assumed true in order to give thrombolytic therapy on finding ST segment depression with prominent R waves in leads V1 and V2 ?

A

That there is a posterior wall infarction rather than unstable angina

45
Q

What must ALWAYS be done before administering Thrombolytic therapy to a patient >

A 
Obtain a medical history
Vitals
    220/110 not a candidate for lytic therapy.
Chest radiograph
EKG 
Lab work
46
Q

List the contraindications for thrombolytic therapy

A
  1. Any prior intracranial hemorrhage
  2. Known structural cerebral vascular lesion (e.g., arteriovenous malformation)
  3. Known malignant intracranial neoplasm (primary or metastatic)
  4. Ischemic stroke within 3 months (except acute ischemic stroke within 3 hours)
  5. Significant closed-head or facial trauma within 3 months
  6. Suspected aortic dissection
  7. Active bleeding or bleeding diathesis

If you do not give TLT (Thrombolytic Therapy), you must state why since it is the “Standard of Care”

47
Q

What is the best choice of mechanical intervention for a person who is contraindicated for TLT ?

A

Catheter based intervention aka Primary Percutaneous Intervention (PCI)

48
Q

When would a person be referred for CABG placement ?

A

Not a candidate for Catheter based intervention (damage too extensive)

those with mechanical heart problems due to MI

49
Q

What did the study relating the efficacy of PCI vs. Thrombolytics show ?

A

PCI improves mortality better than TLT in all categories except those including extensive bleeding

50
Q

Every patient with ACS should receive 4 children’s chewable pills of which drug ? Why chewable ?

A

Asparin (ASA)

Because chewable = rapidly absorbable

51
Q

Which anti-platelet drug is given to all ACS unless contraindicated ?

A

Clopidogrel (Plavix)

52
Q

Morphine is standardly given to patients with ACS. Which patients would morphine be contraindicated in and why ?

A

RV infarction. Morphine is a pre-load reducer. This is not good for RV infarction patients seeing as pre-load is a major determiner of Force of Contraction which may be compromised in ischemic tissues of the RV

53
Q

What other common drug given to patients with ACS is contraindicated in RV infarction ?

A

Nitroglycerin

54
Q

T or F: On top of the drugs listed previously, β-blocker ACE inhibitor and Statins are commonly given in treating ACS ?

A

True

55
Q

List 3 Meds that should be avoided in Acute Myocardial Infarction unless directly indicated

A 
Calcium Channel Blockers 
   Especially Nifedipine
   Unless patient is currently on it.
Lidocaine
   Can cause toxicity (used to be commonly used)
IV Magnesium
56
Q

When would an non-dihydropyridine CCB be indicated ?

A

In patients who are Tachycardic or have asthma Asthma –> NDHP blocker such as Diltiazem is great choice
Cannot give a BB to asthmatics.

57
Q

When would it be alright to give IV magnesium ?

A

In a patient with Torsades de Pointes (as this is TOC for it)

58
Q

List the 2 classes of complications associated with Acute MI

A

Electrical

Mechnical

59
Q

List Mechanical Complications to Acute MI

A 
Acute mitral regurgitation
  Papillary muscle dysfunction 
Ventricular septal rupture
   Must be fixed via surgery (serious)
Ventricular pseudoaneurysm
Ventricular free wall rupture
60
Q

List the electrical complications associated with Acute MI

A

Tachyarrhythmia

Bradyarrhythmia

61
Q

Most mechanical complications can be diagnosed with…

A

EKG

62
Q

Most mechanical complications can be treated by

A

Most are treated by IABP insertion followed by emergent open-heart surgery

63
Q

What is the time period for seeing most mechanical disturbances due to MI ?

A

3-5 days post MI ***

64
Q

I V. tach or V.fib occur during the first 48 hrs post MI, is EPS indicated ?

A

NO

65
Q

What is done if an unstable patient goes into A. fib or A. flutter

A

Cardioversion

66
Q

If patient is stable but goes into A.fib or A.flutter, what is done ?

A

control ventricular rate with medical therapy (beta-bockade, digoxin) and anticoagulate

67
Q

List 3 kinds of bradyarrythmias

A

Sinus bradycardia
AV block
Asystole

68
Q

List the treatment modalities for treating a patient with a bradyarrhythmia

A

1.Observation only
2.Atropine
3.Temporary pacemaker (external or transvenous)
If external, patient must be sedated
4.Permanent cardiac pacemaker

Cardiology Exam III (12 decks)

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