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:

1. Atherosclerosis
2. Severe HTN or tachycardia
3. Coronary vasospasm
4. Severe hypotension
5. Hypoxia
6. Anemia
7. Severe AI or AS (these patients will have hypertrophied ventricles and higher O2 demands)

Question 4

Clinical Manifestations of CAD

Answer 4

1. Ischemia
2. Angina
3. MI
4. Arrhythmia
5. Ventricular dysfunction (CHF)
6. 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

1. Age
2. Men
3. HTN
4. DM
5. Hyperlipidemia
6. Smoking
7. Family history
8. Obesity and sedentary lifestyle
9. PVD
10. Menopause
11. Use of high estrogen contraceptives
12. 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

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

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)

Question 42

Most perioperative MIs occur within \_\_\_\_\_\_\_\_\_\_\_\_. what are the typical diagnosis patterns

Answer 42

1. 24- 48hours 2. Mostly **post**operative 3. Mostly **N-STEMI** and diagnosed with EKG and cardiac biomarkers 4. they are usually **preceeded** by tachycardia and ST depression * tachycardia increases O2 consumption→ with CAD the coronaries inability to dialate leads to the MI

Question 43

What physiologic changes post-op that lead to a **pro-thrombotic** state and plaque rupture

Answer 43

1. increased blood **viscosity** 2. ∆s in **catecholamine** levels 3. ∆s in **cortisol** levels 4. ∆s in endogenous tissue plasminogen **activator** levels 5. ∆s in plasminogen activator **inhibitor** levels. (post op autopsies have shown significant numbers of deths via trhombus in a coronary artery that is **NOT** critically stenosed→even MORE reason to make sure to blunt the stress response!)

Question 44

Two pathophysiologic mechanisms that can be responsible for perioperative MI

Answer 44

1. Acute coronary thrombosis 2. Increased myocardial demand in the setting of comprimised myocardial oxygen supply (CAD)

Question 45

Causes

Answer 45

Narrowing of the coronaries due to: Atherosclerosis Severe HTN or tachycardia Coronary artery vasospasm Severe hypotension Hypoxia Anemia Severe AI or AS Hypertrophied ventricle (bigger size, bigger O2 demand)

Question 46

Clinical signs

Answer 46

Angina Ischemia MI Arrhythmias Ventricular dysfunction Sudden death

Question 47

Risk factors

Answer 47

Increasing age Male gender HLD DM HTN Smoking Family history Obesity Vascular disease Menopause High-estrogen contraceptives Sedentary lifestyle Type-A personality

Question 48

Main problem in ischemic heart disease

Answer 48

Imbalance between **myocardial** O2 supply and **demand**

Question 49

What is an athlerosclerotic plaque composed of?

Answer 49

1. fatty acids 2. cholesterol 3. cellular waste products 4. calcium deposits 5. Pro-inflammatory mediators 6. Pro-coagulant. mediators

Question 50

What chemical messengers involved in angina? What is their roll?

Answer 50

1. **Adenosine** and **Bradykinin** * these substances produce the chest pain typically associated with angina (thalamic/cortical stimulation). * They **slow AV conduction →** decreasing contractility **→** which will improve oxygen demand/supply imbalance

Question 51

Define Stable angina

Answer 51

1. **No change** in angina symptoms/precipitating factors within the **last 60 days**. 2. **Frequency** and **duration** of pain has not changed.

Question 52

Define Unstable angina

Answer 52

1. Is caused by less than normal activity, unpredictable 2. New onset 3. Lasts for prolonged periods 4. Occurring more frequently or more severel **Unstable angina signals an impending MI,** * Note: Increasing medication need also indicates worsening even if symptoms are under control 1. Shouldn't be operating on these folks unless its an emergency. 2. Probably gonna ruin your day.

Question 53

Define Prinzmetal angina

Answer 53

1. Occurs at **rest** 2. It is usually **not** **provoked** by a specific action 3. **Spasm** of the coronary arteries that can **occur in completely normal vessel** 4. Is often associated with **migraines**, **Raynauds**, other **vasospastic** diseases

Question 54

1. What is myocardial **stunning**? 2. **Hibernation**? 3. **Preconditioning**?

Answer 54

1. **Stunning** = breif ischemic period cause temporary loss of **contractile** funtion that cn last for several hours to days. Not good. 2. **Hibernation** = Tissue that is persistantly ischemic undergoes **metabolic** **adaption** to prolong myocyte **survival** until perfuson is restored 3. **Peconditioning** = Provoked brief periods of ischemia that confer **protection against future** ischemia. * Shown to limit infarct size in later MI. * Pacing, exercise, opioids evoke preconditioning * Inhaled anesthetics modulate this by blocking triggers * Interestingly COX-2 inhibitors completely abolish this protection.

Question 55

What labs are the cardiac biomarkers and what do they indicate?

Answer 55

1. **Troponins** 2. **CPK-MB** (creatine phosphokinase - myocardial bound) 3. **LDH** (lactate dehydrogenase)

Question 56

Medical management

Answer 56

Lifestyle mods Treat any: Fever Anemia Infection HTN HLD/Cholesterolemia

Question 57

Ischemic heart disease drug management and effects:

Answer 57

1. **ß-Blockers**- * decreases HR and contractility 2. **Ca⁺⁺ Channel Blockers** * **​**dilates coronaries, decreases contractility, decreases afterload 3. **ACE inhibitors** * **​**improve contractility via decreased afterload 4. **Nitrates** * **​**dilates coronaries and collaterals, decreases preload (vasodilation) and afterload (decreases periperal vascular resistance) 5. **Antiplatelets**- * reduce potential for thrombosis

Question 58

Ischemic heart disease surgical interventions

Answer 58

1. **PCI-** balloons, stents, drug stents 2. **CABG**- off-pump, minimally invasive, robotics, all kinds of stuff 3. **Transmyocardial revascularization**- sounds impressive

Question 59

Surgical delay post stent placement

Answer 59

1. Baloon Angioplasty - no stent = **4-6 weeks** 2. Bare metal stent = **30-45 days** 3. Drug eluding stent = **1 year**

Question 60

Acute Coronary Syndrome

Answer 60

* Occurs with **plaque disruption** leading to partial or complete occlusion of a coronary artery * Coagulation cascade is triggered → local hypercoagulable state → thrombus formation leads to complete occlusion

Question 61

Characteristics of unstable plaques

Answer 61

* **T-cell** aggregation at the shoulder region with macrophage clusters * **Thin** fibrous cap * **Lipid** rich core * Newly formed intra-wall **capillaries** * Lymphocyte/mast cell **infiltration** into the adventitia

Question 62

Worst kind of plaques

Answer 62

Plaque instability more likely than those that have a llarger size.

Question 63

Events after plaque rupture

Answer 63

1. Platelet aggregation 2. **thromboxane** A released (vasoconstriction) 3. **IIb/IIIa** receptors on platelets activated→further aggregation 4. strengthening of thrombus→**fibrin** deposited 5. **Thrombus** formation causes: 1. angina, infarction, sudden death 6. **Microemboli** can also be dislodged, clotting off smaller vessels elsewhere 7. **Vasospasm** also possible

Question 64

What is myocardial Infarction?

Answer 64

1. Necrosis caused by ischemia 2. In the heart, begins to occur within 20-30 minutes of ischemia onset 3. Typically starts in the **subendocardium** 4. Full infarct size usually occurs in 3-6 hours 5. Size depends on proximity of lesion and collateral circulation

Question 65

Dx of MI

Answer 65

Need 2 out of 3: * Chest pain * Serial EKG changes indicative of MI→ST changes * Increase and decrease in serum cardiac enzymes (Cardiac MRI helpful to determine extent of infarct)

Question 66

Initial Acute MI treatment

Answer 66

1. **Evaluate hemodynamics**, what's your BP looking like? 2. **Get a 12-lead** 3. **O2** (don't go crazy though hypocpnea caused by respiratory acidosis can cause coronary artery constriction- Stoelting) 4. **Pain relief**- morphine, NTG ASA or plavix

Question 67

Reperfusion therapy for ACS

Answer 67

1. **Thrombolytic therapy** * streptokinase, TPA, reteplase, tenecteplase. * Must start w/ in **30-60 minutes** of arrival 2. **Direct angioplasty** * Perform within **90 minutes** of arrival, 12 hours of symptom onset. 5% fail and require surg. CABG- high mortality if in the first 3-7 days post MI

Question 68

Adjunctive therapy for Myocardial infarction (anterior MI, LV failure, EF)

Answer 68

1. Heparin 2. ß-Blocker 3. ACE inhibitor

Question 69

Unstable angina/Non-STEMI patho, Dx

Answer 69

1. Reduction in **myocardial O2 supply** 2. **Change** in angina symptoms- angina at rest, chronic angina that is becoming more frequent/severe, 3. new onset **EKG changes** **ST depression in** t**wo or more contiguous** leads and/or deep symmetrical T-wave inversion 4. Troponin levels

Question 70

Tx for Non-STEMI

Answer 70

1. Rest 2. O2 3. Analgesia 4. **ß-**Blockers 5. NTG 6. ASA/Plavix 7. Heparin 8. Possible revascularization

Question 71

MI complications

Answer 71

1. Arrhythmias 2. LVF/CHF/pulmonary 3. HTN 4. Cardiogenic shock 5. Thromboembolism/Stroke 6. Papillary muscle dysfunction, valvular disease 7. External infarct rupture: most common day 4-7, leads to acute tamponade, followed by death 8. Ventricular aneurysm

Question 72

Periop MI risk

Answer 72

* Risk is less than **1%** in the general population * Most occur in the **24-48 hours** after surgery

Question 73

Prognostic determinants in ischemic heart disease

Answer 73

1. Extent of atherosclerosis 2. EF 3. Plaque stability

Question 74

What decreases Myocardial O2 **SUPPLY** and should be avoided/prevented/promtly treated in patiens with CAD?

Answer 74

1. \*\*Tachycardia\*\* (sympathetic stimulation) 2. Hypotension (decreases coronary blood fow) 3. Vasoconstriction 4. disruptions in O2 carrying capacity 1. acid/base (**hypocapnea** from hyperventilation will also cause coronary vasoconstiction) 2. anemia 3. hypoxia 5. Blood Viscosity 6. Arterial patency 7. Coronary spasm

Question 75

What **increases** myocardial O2 **DEMAND** and should be avoided/prevented/promtly treated in patiens with CAD?

Answer 75

1. \*\*Tachycardia\*\* 2. Increased contractility (drugs) 3. Increased preload (fluids) 4. Increased afterload (drugs) 5. Shivering 6. Hyperglycemia 7. HTN

Question 76

In a ischemic heart disease A patient that displays tachycardias, should provoke two questions that will further assess the patient, what are they?

Answer 76

1. What's the BP? 2. What's the cause? * Beta blockers and NTG (if BP is ok) are great **short term,** but the **underlying cause** must be found and corrected.

Question 77

Ischemic heart disease/CAD Anesthetic management considerations with **regoional vs general** anesthesia

Answer 77

1. **Regional** * **sympathectomy** will likely lead to hypotension * treat with **phenylephrine**. * Use **ephedrine** if bradycardia also present. 2. **General** * **Maintain O2 supply/demand** balance * DO NOT allow for **sustained periods** of hypo/hypertension or tachycardia.

Question 78

Why is **tachycardia** particularly worrisome in ischemic heart disease.

Answer 78

**It effects BOTH supply and demand!!!!** * increases demand * reduces supply (doing this simultaneously and can quickly lead to CV collapse)

Question 79

Monitoring for ischemia with an EKG * what do we look for that indicates ischemia? * what can idividual leads tell us? * What leads are best?

Answer 79

1. **EKG - Ischemia is manifested by** * **ST elevation or depression** **(****+/- 1 mm MUST be detected****)** * **T-wave changes** (may have inverted T waves from an old MI and ischemia a is manifested as T waves that are right-side-up) * **R-wave changes** 2. Leads **II, III** and **aVF** reflect: **Right coronary artery** * **​​supplies:** * Right atrium​ * right ventricle * Inferior aspect of left ventricle * SA node and AV node 3. Leads **V3-V5** reflect: **Left anterior descening** * **supplies**: * Anterolateral aspect of left ventricle 4. Leads **I** and **aVL** reflect: **Left circumflex artery** * **supplies**: * Lateral aspect of left ventricle 5. ​​​​​​Best lead combos (**II and aV₅**) or (**II, V₄, V₅**) or (**V₃, V₄, V₅**)

Question 80

Ischemic heart disease **Induction** anesthesia considerations

Answer 80

**The goal is to minimixe hemodynamic changes** 1. Use induction agents like **Etomidate** or **Propofol** * Ketamine is definately a NO!! 2. **For severe LV dysfunction** * May not tolerate anesthesia induced myocardial depression consider a **high opioid technique** (but anticipate prolonged intubation) Also USE Etomidate! 3. Other ways to minimize hymodynamic changes * **​High MAC** * **Lidocaine** * **Esmolol**

Question 81

Ischemic heart disease anesthetic mainitinence **GOALS**

Answer 81

1. **\*\*Avoid tachycardia\*\*** * pretreat for anything that will elicit a sympathetic resopnse (DVL, incision) * ß-blocker - **esmolol** * **Opioids** 2. **Normal Preload** * do not want to rapidly increase preload, it will increases myocardial demand - steeady smooth fluid balance (consider **phenylephrine** or **dobutamine**) 3. **Normal Afterload** * **​​**too low = decreased coronary profusion pressure (decreases supply) * too high = myocardial contractility must increase to overcome (increases demand) (vasodilate **IAs** or **NTG**) 4. **Decrease Contractility** (if LVF normal) * this will decrease the myocardial O₂ demand * **ß**-**blockers** * Gas 5. **Maintain NSR if possible** 6. MVO2 - **much easier to control demand**, attenuate SNS outflow as needed (**avoid** **sympathomimetics**)

Question 82

Agents implicated in coronary steal

Answer 82

Isoflurane (Forane) NTP Dipyridamole

Question 83

Things to remember about VA in these pts

Answer 83

Decrease contractility (good) Decrease SVR (ehhh) Increase coronary blood flow (nice) Sensitize heart to epi (mostly a concern with halothane)

Question 84

Oxygen ratio and Clinical triad of right ventricular infarction. Why is it imprtant to recognize?

Answer 84

1. 1/3 of inferior wall MIs are RV and isolated RV infarctions are very unusual 2. RV has a more **favorable** O₂ supply/demand ratio because: * it has less muscle mass than the LV * it gets coronary blood flow in systole and diastole 3. **Clinical triad** * hypotesion * increased juggular venous distension * clear lung fields 4. Important to recognize because tx for LV failure (vasodilators and diuretics) actually **worsen** RV failure * Initial tx intraop for RV failure is **FLUID**!!! Then **vasoressors** for hypotension, ithen **counterpulsation** (balloon pump)

Question 85

Three intraoperative challenges in management of patients with CAD according to stoelting.

Answer 85

1. **PREVENTING** ischeimia by optimizing myocardial supply and decreaseing demand 2. **MONITORING** for ischemia 3. **TREATMENT** if ischemia develops

Question 86

How does acid/base balance effects CAD

Answer 86

1. Hypocapnea caused by hyperventilation can cause coronary artery constriction