Ischemic Heart Disease

Question 1

What is the leading cause of death in men and women in the US?

Answer 1

CAD

Question 2

About ___% of our patients will have CAD

Answer 2

30%

Question 3

Causes of CAD

Answer 3

Narrowing of the arteries due to:
Atherosclerosis
Severe HTN or tachycardia
Coronary vasospasm
Severe hypotension
Hypoxia
Anemia
Severe AI or AS (these patients will have hypertrophied ventricles and higher O2 demands)

Question 4

Clinical Manifestations of CAD

Answer 4

Ischemia
Angina
MI
Arrhythmia
Ventricular dysfunction (CHF)
Sudden Death

Question 5

___% of MIs are silent

Answer 5

70%

Remember that if you suspect your patient has CAD, but no angina, they probably have it. It’s just silent.

Question 6

Risk factors for CAD

Answer 6

Age
Men
HTN
DM
Hyperlipidemia
Smoking
Family history
Obesity and sedentary lifestyle
PVD
Menopause
Use of high estrogen contraceptives
Psychosocial characteristics (Type A personalities)

Question 7

What is the source of pain from cardiac ischemia?

Answer 7

Adenosine and bradykinin released during ischemia.

• These chemicals stimulate neurons in the heart that produce thalamic and cortical stimulation, resulting in the typical chest pain associated with angina
• These substances also slow AV nodal conduction and decrease contractility, improving the O2 supply and demand balance

Question 8

What is unstable angina?

Answer 8

Angina that has changed its characteristics within the past few weeks of surgery.

• Occurring more frequently or more severely
• Lasts for long periods
• Caused by less than normal activity
• Signals impending MI***

Question 9

Do we take patients to the OR with unstable angina?

Answer 9

FUCK NO

Only exceptions are emergencies

Question 10

What is stable angina?

Answer 10

No change in pattern for at least 60 days.

Question 11

What is stunning?

Answer 11

Dat ass.

BRIEF periods of ischemia that lead to myocardial dysfunction that can last several hours

Question 12

What is hibernation?

Answer 12

Impaired myocardial function from ongoing impaired coronary BF, but is relieved following return of normal BF

Question 13

What is preconditioning?

Answer 13

Brief intermittent periods of ischemia allow for some protection against a subsequent larger ischemic insult, and therefore limits infarct size (I guess because the heart is kind of used to having ischemia on and off)

Question 14

These things can evoke preconditioning

Answer 14

Exercise, pacing, and opioids.

IAs also modulate preconditioning by blocking triggers.

Question 15

Pharm management of CAD

Answer 15

BBs- reduce HR and contractility

CCBs- dilate coronaries, reduce contractility and afterload. Not used for long-term therapy anymore.

Nitrates- dilate coronaries and collaterals, decreases preload and afterload (decreases cardiac stretch and force it has to push against)

Anti-plts- reduce potential for thrombosis

Question 16

Procedures we may have to manage for CAD

Answer 16

1) PCI
- Balloon angio
- Bare metal stenting
- Drug eluting stenting

2) CABG
- OPCAB (off-pump CABG)
- MIDCAB (minimally invasive direct CABG)

3) TMR (transmyocardial revascularization)

Question 17

Stenting and surgical delays

Answer 17

Will have to delay d/t length of antiplt therapy needed

Coronary angioplasty (4-6 weeks)
Bare metal stents (30-45 days)
Drug eluting stents (1 year)

Question 18

What is acute coronary syndrome?

Answer 18

An acute decrease in coronary blood flow due to:

Plaque rupture triggers coagulation cascade and leads to a hypercoagulable state, platelet accummulation, formation of a thrombus, and acute partial or total occlusion of the coronary artery.

Question 19

Which is more of a threat to a vessel, a plaque that is large? Or a plaque that is unstable?

Answer 19

A plaque that is unstable.

Question 20

Characteristics of disrupted plaques

Answer 20

Eccentric (not uniform)
Large, necrotic, soft, lipid-rich core (Mmmmm)
Covered by a THIN fibrous cap
Righ in macrophages and T cells

Question 21

What happens when a plaque ruptures?

Answer 21

Platelet aggregation at site
Release of Thromboane A2 by activated platelets (potent vasoconstrictor)
Activation of IIb/IIIa receptors on platelets, which allows plts to stick together and strengthen the thrombus
Fibrin is deposited
Thrombus is thusly formed.

This process can cause angina, infarction, or sudden death.
Can dislodge and send microemboli to smaller vessels.
Vasospasm can occur.

Question 22

Infarction begins within __-__ minutes of ischemia

Answer 22

20-30min

Question 23

Infarction usually reaches its full size in __-__ hours

Answer 23

3-6

Question 24

Size of an infarction depends on

Answer 24

Location of the lesion

Amount of collateral circulation

Question 25

How is an MI diagnosed?

Answer 25

Requires 2 of these 3 criteria: - Chest pain - EKG changes indicative of MI - Elevated cardiac enzymes Can also get a cardiac MRI to evaluate the extent of the infarction

Question 26

INITIAL treatment of an MI

Answer 26

``` Get a BP (how is their pressure holding up with these cardiac changes?) 12 lead-EKG MONA - Morphine - O2 - NTG - ASA or clopidogrel ```

Question 27

Reperfusion therapies for MI

Answer 27

1) Thrombolytics - tPa, streptokinase, reteplase, tenecteplase - Begin within 30-60 min of arrival 2) Direct coronary angioplasty - Must be performed within 90 minutes of arrival and 12 hours of onset - About 5% will fail and require surgery 3) CABG - High risk of mortality if performed within 3-7 days after an MI

Question 28

Adjunct medical treatment for MI after all the initial shit has been done

Answer 28

``` Heparin BBs Glycemic Control Statins ACE Inhibitors (if anterior wall MI, LV failure, EF < 40%, or DM) ```

Question 29

Diagnosis of unstable angina / non-STEMI

Answer 29

Change in angina symptoms EKG changes ST depression in 2 or more contiguous leads and/or symmetrical T wave inversions Troponin Levels

Question 30

Treatment for unstable angina

Answer 30

Maximize perfusion and minimize O2 consumption! Basically, same as treatment for CAD, but also bed rest, O2, pain control, and possible coronary intervention. Remember that unstable = impending MI! ``` Bed rest Give O2 Give analgesia (decrease SNS response) BBs NTG ASA or plavix or hepatin May require revascularization surgery ``` If this happens in the OR, all we can really do is decrease O2 demand and give O2. So we can give BBs, NTG, and O2.

Question 31

Complications of infarction

Answer 31

Arrhythmias Thromboembolism (can cause stroke) Cardiogenic Shock LV failure and pulm edema Papillary muscle dysfunction (causes valvular disease) Ventricular aneurysm (fibrous outpouching of the ventricle (most commonly in the anteroapical region) External rupture of infarct (may happen 4-7 days post-MI and cause effusion/tamponade) Acute pericarditis (2-4 days post-MI)

Question 32

For the general population, risk of peri-op death from cardiac causes is _____

Answer 32

less than 1%

Question 33

When do most peri-op MIs occur?

Answer 33

24-48 hours AFTER surgery!!

Question 34

Factors that will decrease O2 supply to the heart

Answer 34

``` Tachycardia (less time in diastole) Hypotension Vasoconstriction Low O2 carrying capacity (anemia, hypoxia, acid/base balance) High viscosity Arterial patency Coronary spasm ```

Question 35

Factors that will increase O2 demand on the heart

Answer 35

``` Tachycardia Increased contractility Increased preload and afterload Shivering Hyperglycemia HTN ```

Question 36

Monitors for ischemia

Answer 36

EKG - V5 reflects LV function and is supplied by the LAD - Lead II reflects ischemia in the RCA PA Cath (overall heart function) TEE (looks for clots in LA and valvular/heart wall function)

Question 37

Induction for those with CAD

Answer 37

Etomidate - Remember etomidate won’t blunt response to DVL→ maybe follow-up with esmolol High opioid technique (for longer cases) Use what the pt already takes (BBs vs. CCBs) to blunt DVL We want a smooth induction and quick intubation in these pts.

Question 38

Main intra-op goals for CAD

Answer 38

Remember that overall, we want to decrease demand!! ``` AVOID TACHYCARDIA Preload and afterload- normal Contractility- low-normal HR- avoid tachy!! Rhythm- NSR is best obviously MVO2- decrease O2 demand and attenuate the SNS response to stuff ```

Question 39

What is coronary steal?

Answer 39

Basically, shitty coronaries are already maximally dilated in their shitty attempt to deliver O2. So, dilating the coronaries will steal blood/O2 away from these areas. HOWEVER, THIS IS ONLY THEORETICAL. It has never been demonstrated in the lab and WHY THE HELL ARE WE LEARNING THIS STUPID SHIT.

Question 40

Coronary steal may occur with these medications

Answer 40

Isoflurane (Forane) Nitroprusside (SNP) Dipyridamole

Question 41

Are IAs generally good or bad for CAD?

Answer 41

BAD They decrease contractility Decrease SVR (will decrease BP and perfusion pressure) Increase coronary blood flow Sensitizes the heart to the effects of epi (especially halothane and enflurane)