cardiology rotation

Question 1

Lovenox dosing for inpatient DVT prophylaxis?

Answer 1

1mg/kg subcutanoues Q12hr or 1.5mg/kg subQ once daily

Question 2

Lovenox dosing for unstable angina/NSTEMI?

Answer 2

1mg/kg q12hr

Question 3

Lovenox dosing for a stemi?

Answer 3

30mg IV bolus followed by 1mg/kg 15 minutes later then 1mg/kg subq Q12hr

Question 4

What is the approach for preop cardiac risk evaluation?

Answer 4

Step 1- is it an emergency or not? if no move to next step
Step 2- Are they having ACS symptoms if yes treat them if no move to step 3
Step 3- Estimate MACE if low risk less than 1% no further testing
Step 4- risk is greater than 1% do a MET if it is >4 or 10 then no further testing needed. If less than 4 ask yourself will further testing impact decision if yes than do a Pharm stress test
Step 5- if pharm is abnormal do an angiogram

Question 5

Right axis deviation can mean what?

Answer 5

1. sign of pulmonary hypertension
2. Lateral myocardial infarction
3. right ventricular hypertrophy
4. COPD
5. PE

Question 6

Left axis deviation can mean what?

Answer 6

MCC is a left anteriorfasicular block

1. LVH
2. MI
3. systolic HF
4. LBBB

Question 7

Why do we worry about HF with reduced EF?

Answer 7

because it can cause VT/Vfib/sudden cardiac death

Question 8

when should ICD therapy be considered in patient post MI with ischemic cardiomyopathy causing HF?

Answer 8

Class 1A rec- it can decrease total mortality in patients at least 40 days post MI with a EF 30% or less with NYHA class 1 symptoms while on GDMT

Question 9

What are the 5 types of myocardial ischemia?

Answer 9

1. Spontaneous rupture of plaque or SVD in women
2. Demand ischemia- can be caused by decreased supply, coronary artery spasm, coronary emboli, anemia, arrhythmia’s, hypertension or hypotension
3. Sudden cardiac death- accompanied by presumably new ST elevation or new LBBB
   4a. MI associated with PCI
   4b. MI associated with stent thrombosis
4. MI associated with CABG graft failure up to one month out

Question 10

Metoprolol tartrate dose inpatient for Afib rate control?

Answer 10

2.5-5mg IV bolus over 2 mins up to 3 doses

Question 11

Verapamil dose for inpatient Afib rate control?

Answer 11

0.15mg/kg IV bolus over 2 mins. Can give an additional 10mg after 30 mins if no response then 0.005 or 0.05? mg/kg/min

Question 12

Ditiazem inpatient afib rate control dose?

Answer 12

0.25mg/kg IV bolus over 2 min then 5-15mg/hr

Question 13

Amiodarone dose for afib rate control for inpatient

Answer 13

300mg IV over an hour then 10-50mg/hr over 24 hours

Question 14

Class 1a afib catheter ablation rec?

Answer 14

sor symptomatic paroxsymal AF refractory or intolerant to at least 1 class I or Class III antiarrythmic med when rhythm control is desired

Question 15

Class 1A indications for CABG?

Answer 15

1. Left main stem disease >50%
2. Proximal LAD >70% and circumflex
3. 3 vessel disease w/or without involvement of proximal LAD
4. Patients with DM and 2 vessel disease

Question 16

Types of chest pain?

Answer 16

1. Typical chest pain- retrosternal chest discomfort with a characteristic quality and duration this either brought on with exertion or emotional stress and then relieved with rest or nitroglycerin
2. Atypical meets two out of the 3 above
3. Non-cardiac meets only one of the above

Question 17

What plot can you use to determine if a stress test is needed?

Answer 17

diamond forrester plot
Low risk- no tess
intermediate- test
High risk- go straight to angiogram

Question 18

What are the 5 types of pulmonary hypertension?

Answer 18

1. PAH- arteris in the lungs become narrowed or thickened
   a. IPAH- no clear cause
   b. Heritable linked genes, can be linked to congential heart disease, HIV, connective tissue like scleroderma and lupus
   c. Can be due to drug use i.e methamphetamines or diet pills
2. from left sided heart disease can be either diastolic or systolic
3. due to lung disease, most common. Examples are COPD, emphysema. Lung airways narrow making it harder to exhale
   b. can also be from restrictive lung disease- interstitial lung disease, sleep apnea, high altitude. This causes arteries in lungs to tighten up so blood can go to areas receiving most O2. The tightening causes increased pressure.
4. Chronic thromboembolic pulmonary hypertension- occurs when the body can not dissolve blood clots in the lungs leading to scar tissue in blood vessels blocking normal blood flow making the RV work harder
5. Due to unknown cause

Question 19

What does MONA stand for?

Answer 19

1. Morphine
2. Oxygen
3. Nitro
4. Aspirin

Question 20

Stemi guidelines?

Answer 20

1. give 325mg of aspirin, 600mg of plavix or 180 of brillenta, and heparin 60units/kg bolus up to 4000units/hr

Question 21

If someone has to wait for the cath lab and they have received the aspirin, plavix, and bolus of heparin what should you do?

Answer 21

Start them on a heparin drip of 12units/kg up to 1000units/hr

Question 22

What should you do if someone is having a STEMI and onset was within a 12 hour period but they cant get into the cath lab for the next 2 hours?

Answer 22

Can use fibrolytic therapy, and give 325mg of aspirin and 300mg of plavix if less than 75 years old. If greater than 75 years old they get 75mg of plavix

Question 23

If someone has a CrCl <30 and requires lovenox therapy what should their dose and frequency be?

Answer 23

still 1mg/kg subq but ever 24 hours instead of Q12h

Question 24

Post MI medicaions?

Answer 24

Aspirin 
Beta blocker 
Plavix 
ACEi
statin high dose

Question 25

What is the MOA of nitrites? how do they increase blood flow/vasodilate?

Answer 25

1. Nitrates get converted to NO near the plasma membrane of vascular smooth muscle. 2. NO then stimulates conversion of GTP to cGMP, having more cGMP causes vascular smooth muscle to relax resulting in vasodilation

Question 26

MOA of ranolazine? It is a strange one, due to something that occurs with ischemia?

Answer 26

When cardiac muscle is ischemic it leads to a lat Na+ current, this can lead to Na+ intracellular overload which then leads to reversal of the Na/Ca exchanger so it end up pumping in way more Ca++ which causes increased contraction So ranolazine stops this late Na+ current.

Question 27

Do nitrates decrease pre-load or afterload?

Answer 27

Preload

Question 28

Do CCBs decrease Preload or afterload

Answer 28

Afterload by reducing vasoconstriction in both coronary and noncoronary vessels, which increases coronary blood flow.

Question 29

What two medications can reverse atrial spasm?

Answer 29

Nitrates and CCB's

Question 30

Describe the different class 1 anti arrhythmic?

Answer 30

Class 1A- Procainamide, Moderate Na+ channel blockade with K+ channel blockade, delaying repolarization Class 1B- Lidocaine, Mild Na+ channel blockade without K+ channel blockade. Repolarization is accelerated Class 1C- Flecainide, Propafenone, Marked Na+ channel blockade without K+ channel blockade, slows down depolarization and can widen QRS

Question 31

Describe class 2 anti-arrythmics?

Answer 31

These act on nodal cell conduction. They block B1 adrenergic receptors which slows down phase 4 and phase 0 of the AV node. Phase 4 is the start of depolarization when slow Ca+ channels open and phase 0 is the rapid depolarization when faster Ca+ channels open.

Question 32

Describe class III anti arrhythmics

Answer 32

These are amiodarone, sotalol, tikosyn These work on cardiac muscle cells and cause a delay of phase 2-3 by blocking potassium channels which results in an increased actional potential and refractory period, delaying the ability for the cell to depolarize again. This reduces the heart ability to respond to rapid tachycardias Amiodarone also has class 1A properties by moderately blocking Na+ channels in phase 0

Question 33

Describe class IV anti arrhythmics?

Answer 33

These are diltiazem, verapamil They block L-type Ca+ channels, this effect on the SA and AV node delay depolarization slowing down the conduction rate and repolarization.

Question 34

Magnesium can be used for which arrhythmias?

Answer 34

torsade de pointes and digoxin-induced arrhythmia