Cardio 22,23:Acute MI and STEMI Flashcards
According to D’Amico 99% of the time acute MI is caused by…
Destabilization of atherosclerotic plot with subsequent thrombus formation
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 ?
Thrombolytic therapies
Side note: Thoracic aortic dissection cause AMI if it involved the rood of one of the coronary arteries
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 ?
Unstable Angina
NSTEMI (Non-ST Elevation Myocardial Infarction)
What is a more likely NSTEMI presentation: with Q wave or without Q wave on EKG ?
Most NSTEMI’s present without Q-wave on EKG (NQMI)
However, NSTEMI’s with Q waves sometimes do occur (QWMI)
What is is a more likely presentation of STEMI: With Q-wave or without ?
With Q-wave. Very few with ST elevation will develop without a Q wave.
Type I MI
Spontaneous thrombotic MI (vast majority)
Type II MI
Nonthrombotic MI
Type III MI
Sudden cardiac death with ischemic symptoms but no biomarkers
Type IV MI
MI in association with percutaneous coronary intervention (PCI)
(probs don’t need to know this)
Type V MI
MI in association with coronary artery bypass surgery (CABG)
Probs dont need to know this
Name the 3 major diagnostic indicators for acute MI
Symptoms: Chest pain (epigastric, jaw, shoulder)
EKG findings
Serum Markers : Usually have latent elevation and may not allow for instant diagnosis
List the two isotopes used in nuclear imaging of the heart
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
What is used for enhancement of Cardiovascular Magnetic Resonance
Reveals a permanent record of both acute & chronic MI
“Bright is abnormal” shows you where ab
Newer technique
Expensive
Ddx of cardiovascular causes of chest pain
Acuts MI Angina Prinzmentals Valvular Acute pericarditis Aortic Dissection Myocarditis Hypertrophic cardiomyopathy
Ddx of pulmonary causes of chest pain
Pleurisy Embolism Pneumothorax Asthma Pneumonia Bronchitis Pulm HTN
Ddx of GI causes for chest pain
GERD Esophagitis Gastritis Peptic Ulcer Biliary colic Pancreatitis Mollory Weiss Tear.
Ddx of musculoskeletal causes for chest pain
Costochondritis Myositis Somatic dysfunction Chest of upper extremity trauma Thoracic outlet syndrome
DDx of neurologic causes for chest pain
Herpes zoster
Exacerbation on touching patients skin
Intercostal neuralgia
DDx of psychologic causes of chest pain
Anxiety
Da Costa’s syndrome: Neurocirculatory asthenia.
Somatization disorder (Briquet’s syndrome)
External problems cause somatic pain
Converson disorder
Hypochondriasis
Munchausen syndrome
DDx for miscellaneous causes of chest pain
Splenic infarction
Subdiaphragmatic abscess
Hepatic distension
What is the first myocardial serum marker to be seen ? Why is it insignificant ?
Myoglobin: comes on quick but is very inspecific will go up with chest trauma not very useful unless patient presents with typical MI problem.
When will CK-MB peak in serum concentration ?
CK-MB more unique for Heart Muscle ( peaks in first 24 hours )
Troponins will peak when ? Why do we use them instead of LDH ?
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.)
What is the overall goal of management therapy for acute MI ?
Lower oxygen demand and increase oxygen supply
What can be done to decrease Myocardial oxygen demand ?
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)
Who would you not want to give a Beta Blocker to when treating an acute MI ?
Patient with a history of Asthma
Patients who are diabetic
(unless BB is specific –> B2 blockers interfere with glycogenolysis leading to hypoglycemia)
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 Beta Blocker
Decreases the risk of NaNP induced reflex tachycardia –> increased oxygen demand (bad news)
In treating Acute MI, how can you increase a patients O2 supply ? (more specifics on next few slides)
- Supplemental Oxygen
- Relieve pulmonary vascular congestion (if present)
- Acute revascularization
- Intra-aortic balloon pump (IABP)
What is a reason for pulmonary vascular congestion ? What can you give to treat it ?
Edema in the lung due to Left sided infarction or CHF.
Prescribe: Diuretics, IV NTG, MSO4 (morphine sulfate)
What are the two forms of therapy that can be given to allow for Acute Re-vascularization ? (of coronary arteries)
Thrombolytic Therapy
Mechanical Revascularization
Catheter Based (PCI)
Cabbage
Explain how an Intra Aortic Balloon Pump works
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.
What are the Pro’s of Thrombolytic therapy ?
- Lyses occlusive coronary thrombus rapidly
- Improves LV function
- Reduces both short-term and long-term mortality
What are the Risks involved in Thrombolytic
1.Bleeding
2.Anaphylaxis (SK and APSAC)
Streptokinase/APSAC are not used often
3.Hypotension
4. Arrhythmia (reperfusion)
Reactive Ox species during re-perfusion
How are SK (streptokinase) and APSAC (anistreplase ) administered ?
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.
For Thrombolytics, what drug is considered the “standard of care” ? How is it administered ?
tPA (tissue plasminogen activator, Ateplase)
IV bolus and double infusion (accelerated dose)
r-PA (reteplase) is administered in….
Double bolus, 30 minutes apart
TNK-tPA (tenecteplase) is administered in…
Single bolus (over 5 to 10 seconds)
n-PA (lanoteplase) is administered in …
Single bolus
When is the use of thrombolytic therapy most beneficial to the patient ?
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
When would use of Thrombolytic therapy after 12 hrs actually be useful ?
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.
Are there any age restrictions to Thrombolytic therapy ?
NOPE !
T of F: Thrombolytic therapy can be administered with EKG finding of ST segment elevation > 1 mm in a single lead during Acute MI ?
False ! Must be seen in 2 or more CONTIGUOUS limb leads (ie. II, III, IV or V1 & V2)
T or F: Thrombolytic therapy can be administered for New (or presumed new) LBBB in Acute MI ?
True !
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 ?
That there is a posterior wall infarction rather than unstable angina
What must ALWAYS be done before administering Thrombolytic therapy to a patient >
Obtain a medical history
Vitals
220/110 not a candidate for lytic therapy.
Chest radiograph
EKG
Lab workList the contraindications for thrombolytic therapy
- Any prior intracranial hemorrhage
- Known structural cerebral vascular lesion (e.g., arteriovenous malformation)
- Known malignant intracranial neoplasm (primary or metastatic)
- Ischemic stroke within 3 months (except acute ischemic stroke within 3 hours)
- Significant closed-head or facial trauma within 3 months
- Suspected aortic dissection
- Active bleeding or bleeding diathesis
If you do not give TLT (Thrombolytic Therapy), you must state why since it is the “Standard of Care”
What is the best choice of mechanical intervention for a person who is contraindicated for TLT ?
Catheter based intervention aka Primary Percutaneous Intervention (PCI)
When would a person be referred for CABG placement ?
Not a candidate for Catheter based intervention (damage too extensive)
those with mechanical heart problems due to MI
What did the study relating the efficacy of PCI vs. Thrombolytics show ?
PCI improves mortality better than TLT in all categories except those including extensive bleeding
Every patient with ACS should receive 4 children’s chewable pills of which drug ? Why chewable ?
Asparin (ASA)
Because chewable = rapidly absorbable
Which anti-platelet drug is given to all ACS unless contraindicated ?
Clopidogrel (Plavix)
Morphine is standardly given to patients with ACS. Which patients would morphine be contraindicated in and why ?
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
What other common drug given to patients with ACS is contraindicated in RV infarction ?
Nitroglycerin
T or F: On top of the drugs listed previously, β-blocker ACE inhibitor and Statins are commonly given in treating ACS ?
True
List 3 Meds that should be avoided in Acute Myocardial Infarction unless directly indicated
Calcium Channel Blockers Especially Nifedipine Unless patient is currently on it. Lidocaine Can cause toxicity (used to be commonly used) IV Magnesium
When would an non-dihydropyridine CCB be indicated ?
In patients who are Tachycardic or have asthma Asthma –> NDHP blocker such as Diltiazem is great choice
Cannot give a BB to asthmatics.
When would it be alright to give IV magnesium ?
In a patient with Torsades de Pointes (as this is TOC for it)
List the 2 classes of complications associated with Acute MI
Electrical
Mechnical
List Mechanical Complications to Acute MI
Acute mitral regurgitation Papillary muscle dysfunction Ventricular septal rupture Must be fixed via surgery (serious) Ventricular pseudoaneurysm Ventricular free wall rupture
List the electrical complications associated with Acute MI
Tachyarrhythmia
Bradyarrhythmia
Most mechanical complications can be diagnosed with…
EKG
Most mechanical complications can be treated by
Most are treated by IABP insertion followed by emergent open-heart surgery
What is the time period for seeing most mechanical disturbances due to MI ?
3-5 days post MI ***
I V. tach or V.fib occur during the first 48 hrs post MI, is EPS indicated ?
NO
What is done if an unstable patient goes into A. fib or A. flutter
Cardioversion
If patient is stable but goes into A.fib or A.flutter, what is done ?
control ventricular rate with medical therapy (beta-bockade, digoxin) and anticoagulate
List 3 kinds of bradyarrythmias
Sinus bradycardia
AV block
Asystole
List the treatment modalities for treating a patient with a bradyarrhythmia
1.Observation only
2.Atropine
3.Temporary pacemaker (external or transvenous)
If external, patient must be sedated
4.Permanent cardiac pacemaker
