Unrein Flashcards

1
Q

Various etiologies of IHD

A

o Atherosclerosis: western diets and lack of exercise
o Hyperthyroidism
o Anemia: decreased oxygen carry capacity
o Emotional stress: catecholamines and increased HR
o Variant angina: Prinzmetal’s - vasospasm in etiology, associated with other vasospastic phenomena, usually more common in females

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2
Q

RFs for IHD.
Which is the best to stop to improve overall health?
What is the most powerful modifiable risk factor for IHD?

A
  • Increasing age
  • Male
  • Smoking ** best thing to stop to improve health
  • Hypertension
  • Diabetes
  • High cholesterol/Dyslipidemia ***the most powerful modifiable risk factor for iIHD
  • Family history
  • Male
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3
Q

What is hsCRP useful for? What risk score does it influence?

A

Useful in assessing patients with intermediate Framingham risk scores, reclassifies up to 30% into either low or high risk

Reynolds Risk Score 2 → Sex specific tool that accounts for family history and high sensitivity C-reactive protein → he recommends this one

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4
Q

What is tako-tsubo CM caused by? Is it reversible?

A

Depression, anxiety, anger

Is reversible

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5
Q

What is the CIRT trial

A

a trial that started about a year ago to see whether the common anti-inflammatory drug low-dose methotrexate (LDM, target dose of 15 to 20 mg po weekly) will reduce rates of recurrent myocardial infarction, stroke, or cardiovascular death among patients with established coronary artery disease and either type 2 diabetes or metabolic syndrome
• Determine whether LDM will reduce the rate of new onset type 2 diabetes among those with metabolic syndrome at study entry

***not sure if this is important, but he said RVU is participating…

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6
Q

Serum markers for IHD. Which is “too” sensitive?

A

o CPK – MM, MB, BB
o Troponin → can leak with angina, but will not have CPK MB fraction, troponin might be too sensitive
o LDH (1-5)

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7
Q

3 kinds of stress tests? When do you do each?

A
  • Exercise stress test → Patients need to be stable as these are provocative tests.
  • Pharmacological → Induce stress on heart via drugs. Do this if a patient just cannot do normal
  • Imaging augmentation w/ nuclear and/or echo (do this when EKG is un-interpretable)
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8
Q

Gold standard for Dx’ing IHD?

A

• Angiography → gold standard → low dose radiation, squirt into left main and into right coronary

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9
Q

How is a CT determined coronary artery Ca score useful?

A

Maybe useful for patient with an intermediate risk for CAD, calcium helps if you see it to test more things, but does not give functional data and is not that useful.

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10
Q

Stable vs Unstable Angina vs MI

A

Unstable Angina –> Non-ST-elevation

  • New onset
  • At rest
  • Crescendo

MI – ST-elevation MI

Stratified based upon ECG and serum biomarkers (troponin and creatine kinase – CPK)

Come back to this ???

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11
Q

Typical Features of CP. What does this determine?

A

o Central substernal pain/discomfort – usually retrosternal +/- radiation to shoulder, arms, jaw or back. May be Visceral, which is assx w/ nausea, vomiting, diaphoresis and/or shortness of breath
o Exertional – Brought on or increased with activity/emotional stress
o Relieved by nitrates or rest

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12
Q

What is Baye’s Theorem? What do you do for the different risk classes?

A

A chart that tells you based on # of typical Sxs vs age & genger, how high their risk is, and how much of a workup you need to do

  • Low probability – no further work up
  • Intermediate + Normal EKG – stress test
  • Intermediate + Abnormal EKG – stress test w/ possible imaging augmentation, treatment based upon findings
  • High probability – medical therapy and coronary angiography, treatment based upon findings
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13
Q

When might you see atypical (silent) IHD (does not present with any of the classic clinical features)?

A

Woman, diabetics, elderly

atypical Sxs = Shortness of breath, palpitations, dizziness, and syncope

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14
Q

TIMI trial risk scores

A

Similar idea - it’s for risk stratification - but he calls these “narrow”

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15
Q

What are some mimickers of acute coronary syndromes? What are some key findings for each?

A

Recent med use may mimik
Aortic dissection - Widened mediastinum on CXR
PE - New onset of Atrial fibrillation
CHF – SOB, orthopnea

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16
Q

MGMT of ST-elevation MI

A

Early reperfusion is indicated – time is muscle!
Needto get to cath lab w/in 90 minutes. If can’t meet that timeline, give t-PA (Thrombolytic therapy)

• Most significant determining factor is “Door to Balloon” time (

17
Q

Absolute C-I’s to thrombolytic therapy

A
  • Intracranial Hemorrhage
  • Ischemic CVA in the last 3 months
  • Facial trauma in the last 3 months
  • Bleeding diathesis
  • History of closed head trauma 2 months ago (CIS example)
18
Q

MGMT of IWMI?

A

always think about RV infarct with inferior wall MI, and RV infarcts are volume dependent *** → treat volume

19
Q

MGMT of AWMI?

A

Intra-aortic balloon pump synchronous counterpulsation → very invasive device, deflates during systole and allows heart to pump with very little resistance, in diastole, it inflates and helps push the blood distally and increase perfusion. Some backflow into coronary arteries as well. Used in times of desperation

20
Q

EARLY complications of MIs that you may see post thrombolytics?

A
o	Bleeding (2-3 times higher incidence of hemorrhagic CVA in women)
o	Reperfusion arrhythmias → rapid tachycardic idoventricular rhythms common, it will calm down
21
Q

LATE complications of MIs (24-48 hrs)

A

• Cardiogenic shock → Pump function loss and thought to have an inflammatory component
• VSD → New systolic murmur and thrill on left sternal border
• Papillary muscle rupture and MR → New systolic murmur, pulmonary edema, thrill and cardiogenic shock → important to have a baseline before this happens so you can recognize something new
• Free wall rupture → usually not compatible with life
o Electromechanical dissociation → Electrical activity still working but not pumping b/c pericardium full of fluid that creates pressure against heart
o First infarction, anterior infarctions, females, elderly
• Left ventricular thrombus → strokes
o Blood stasis, endocardial injury and possible inflammation leading to a hypercoagulable state
o Most often located in the left ventricular apex

22
Q

Indications for Angiography (revascularization in cath lab) for high-risk patients

A

o 3 vessel disease and left main disease
o
o EF

23
Q

What has been shown to decrease mortality in post acute coronary artery syndrome (ACS) Pts?

A

• Beta-blockers 20%
• Anti-Plt drugs (ASA or clopidogrel) 33%
• Angiotensin-Converting Enzyme Inhibitors (ACE-Is)
• HMG-CoA Reductase Inhibitors 25-30% (Statins)
o Proportional to the reduction in LDL levels
o LDL goal

24
Q

Why do we worry about IHD in diabetics?

A

Might not have ANY CP b/c of neuropathy (silent ischemia)!
• 2-8x more likely to suffer from and die from CVD
• Patients typically have more advanced and higher grade disease and less collateralization at presentation
• Need Glycemic control & BP control to reduce risk
• Fatigue, dyspnea, nausea and vomiting may predominate the presentation
• Some care with angiography, but not an absolute contraindication – contrast nephropathy → can hurt kidneys if not monitored

25
Q

How should you handle a 60 y/o male who presents for cardio eval before hernia repair. EKG was normal, no other RFs identified or presenting Sxs?

A

Recommend him for surgery without any further cardiovascular evaluation

26
Q

55 y/o female c/o 2 episodes of 20+ minute retrosternal chest pain over the last 4 hours. Has a third episode of chest pain that is associated with ST depression and relieved with nitroglycerin right in front of you. Normal BP & HR

A

Admission to the hospital and treatment with anti-anginal agents and stress test evaluation

27
Q

The patient’s anti-anginal medications are adjusted as discussed and she is placed on an exercise treadmill with a standard Bruce protocol and reaches her maximum heart rate and has no ST changes. Your clinical approach should be to:

A

Discharge her from the hospital with a follow up in two weeks.

28
Q

Drugs for Angina Prophylaxis

A

Cardioselective beta blockers
E.g., atenolol, metoprolol
Nonselective agents also frequently used
Calcium channel blockers
Long-acting DHPs (amlodipine or felodipine)
Non-DHPs (verapamil or diltiazem)
Long-acting nitrates
Oral: isosorbide dinitrate or nitroglycerin (NTG)
Sublingual (tablet or spray): NTG as needed
*** Don’t combine B-blockers w/ non-DHP CCBs or can –> heart block

29
Q

78 y/o woman presents w/ 45 min retrosternal chest pain associated with nausea and diaphoresis. The pain is relieved after 2 NTGs. Multiple RFs, Her EKG and cardiac enzymes are unremarkable.

The closest referral hospital is three hours away.

What is the Dx, and what should your approach be? What drug & test to give?

A

Dx = Unstable angina

Admit her to the local hospital and begin aggressive medical therapy optimizing her coronary artery disease management

Give Aspirin (COX-I anti-plt)
Perform a stress test
30
Q

Drugs for Acute angina.

A

Morphine
- If chest pain is unresponsive to nitroglycerin
- Also relieves anxiety
- Associated with increased mortality in unstable
angina/NSTEMI
Oxygen, especially if O2 saturation

31
Q

What are C-I’s for ASA?
What do NSAIDs (eg Celecoxi) do to CV risk?
What does NTG do to preload?

A

ASA would be contra-indicated in cases of a GI bleed, ulcer

*** Both non-selective & COX-2 selective (ALL NSAIDS) –> increased CV risk. ASA is unique in that it is unique, and so is cardioprotective in that at low doses it’s anti-plt effects dominate

NTG –> VD –> decreased preload –> increased venous capacitance
Morphine, to some extent, also decreases preload

32
Q

If pharmacological MGMT of angina fails (eg not able to complete stress test & reach MPHR), what test should you order next?

A

Coronary angiogram (probably going to end up in the cath lab)

33
Q

When should we time the 8-hr removal of NTG patch to avoid building tolerance?

A

Sometime throughout the day, b/c statistically, ischemic events / Mis seem to occur at 3-4 AM (early morning hrs), likely d/t surge or early morning catecholamines to help us wake up

34
Q

What kind of diuretics are most efficacious for CHF?

A

Loop diuretics (eg furosemide or ethycrynic acid)

35
Q

In a patient with CHF & CAD, what should we do next after maxing pharm therapy for CHF & BP?

A

Coronary angiography

36
Q

What to do in someone with acute Sxs, but EKG shows LBBB

A

Give furosemide for some immediate Sx relief, then A cardiac catheterization to evaluate for ischemia
(B/c of LBBB, can’t do a stress test b/c we can’t read/trust the EKG)

37
Q

42 y/o female presents w/ retrosternal CP assx w/ diaphoresis & SOB. It is brought on by jogging and in the ER relieved with two nitroglycerin. Her EKG is unremarkable. No RFs. How to stratify her risk?

A

Exercise stress test without augmentation, after medical therapy maximized