Cad/ Ischemic Heart Disease

Front 1

What is the # 1 cause of mortality from disease in the US?

Back 1

Ischemic Heart Disease (CAD)

Front 2

What types of patients have a high risk of Ischemic heart disease?

Back 2

> 65 years of Age
Pts with PVD (atheroscerosis is present)

Front 3

What are the modifiable risk factors for CAD/ IHD?

Back 3

Obesity
Stress
Physical inactivity
Smoking
High COOH intake
Alcohol
Diabetes Mellitus
Transunsaturated fats in diet
Low estrogen (post menopausal women)

Front 4

What are the non-modifiable risk factors in CAD/ IHD?

Back 4

Genetic abnormality in lipid metabolism
Age
Family History

Front 5

Explain the anatomy of the coronary arteries.

Back 5

Heart lies in center of chest on left side. …left side of the heart is more lateral and posterior. First chamber seen is the right ventricle. Left ventricle is more lateral.

PA comes of right ventricle and bifurcates into right and left pulmonary arteries. Aorta has three branches off of it….1) Braciocephalic artery, which branches into the right subclavian artery and the right common carotid artery 2) Left common carotid artery 3) Left subclavian artery.

2 main coronary arteries that come off the coronary cusps of the aortic valve (the aortic valve has 3 cusps). When the aortic valve is closed during end systole the blood accumulates in the cusps and then during diastole it flows to the epicardial surface of the heart. So 2 of the aortic cusps give rise to the coronary arteries: 1) Left cusp-> Left Main CA. This immediately bifurcates into the Left Anterior Descending CA and the Circumflex Artery. 2) Right cusp->Right coronary artery.

The Left Anterior descending CA pathway follows the ventricular septum. It feeds the anterior 2/3 of the septum. Diagonal branches come down (1-3) and feed the major surface of the left ventricle. Supplies most of the conduction sys of the left bundle branch.

The circumflex artery has small branches that supply blood to the left lateral surface of the left ventricle.

The right coronary artery has branches that feed the right ventricle. In the posterior part of the heart it goes down the sulcus to give rise to the posterior descending artery. (in 60% of the cases. In the other 40% of the cases the posterior descending artery comes off of the circumflex branch…won’t know til you have a cardiac cath.) It feeds the SA node, the AV node, and most of the right ventricle.

Posterior descending branch: supplies the posterior 1/3 of the intraventricular septum.

Front 6

The left anterior descending artery supplies blood to...

Back 6

The anterior 2/3 of the septum.
The major surface of the left ventricle.
Conduction system of the LEFT bundle branch.

Front 7

The circumfex artery supplies blood to

Back 7

The Left lateral surface of the left ventricle.

Front 8

The Right coronary artery supplies blood to...

Back 8

The right ventricle.
SA node
AV node
Right bundle branch

Front 9

The Posterior descending artery comes off of what main artery?

What does it feed?

Back 9

In 60% of people, if comes off the Right CA. In 40% of people, it comes off the circumflex artery.

SUPPLIES BLOOD TO:
Posteriomedial papillary muscle.
Posterior 1/3 of the intraventricular septum.

Front 10

Where do you get atheroscerosis in the left CA? the right CA? Why?

Back 10

-->Left side happens at birfurcations
-->Right side happens anywhere (less bifurcations)

both occur due to turbulent blood flow.

Front 11

Explain the patophysiology behind ischemic heart disease

Back 11

It's an imbalance b/c coronary blood flow (O2 supply), and MVO2 (O2 demand).

Front 12

_______ is the most common cause of impaired coronary blood flow and angina pectoris.

Back 12

Atheroscerosis.

Front 13

O2 supply to the myocardium depends on....

What things can affect these factors?

Back 13

* Coronary blood flow
* Intralumenal coronary diameter
* Coronary Perfusion Pressure
* Hgb O2 Content
* Duration of diastole

Stenotic CA's can decrease coronary blood flow. Increased CA resistance decreases intralumenal size.

CPP = ADP - LVEDP. So increased aortic diastolic pressure (afterload) will increase CPP. Decreased LVEDP (preload) will increase CPP. (decreased outside pressure). Aortic insufficiency will decrease CPP b/c aortic diastolic pressure is decreased.

Left ventricular hypertrophy will increase LVEDP and decrease CPP.

TAchycardia will decrease diastolic filling time.

Anemia will decrease Hgb O2 content. A

Front 14

A Hct of ___ is best for pts iwth CAD/ IHD for what reason?

Back 14

A Hct of 30 is best for CAD pts because it decreases the viscocity of the blood to the point to where it flows better through the vessels.

Front 15

What factors both decrease O2 supply and increase O2 demand?

Back 15

LVH - increase LVEDP (decr CPP) AND increases MVO2

Tachycardia: decrease diastolic filling time AND increases MVO2

Anemia: Decreases Hgb O2 content AND hypoxia causes increased intropy, which increases MVO2. (Increased inotropy also causes isolated systolic HTN).

Front 16

Factors that affect O2 Demand (Increase MVO2)

(what is rate-pressure-product?)

Back 16

MVO2 = HR X SBP (Anything that increases either of these will increase MVO2).

* Heart Rate
* Blood Pressure (incr afterload or preload)
* Myocardial Contractility
* LV size - wall tension/ stress
* Duration of Systole

Front 17

Things that increase afterload

Back 17

Systolic Wall stress
Aortic/ arterial stiffness
Increased BP
Aortic Stenosis
VC
Hypercarbia (d/t VC)
Aortic Cross clamping in aneurysm sx

Front 18

Things that will increase preload

Back 18

Diastolic wall stress (LVEDV)
Increase EDV
Venous wall thickness

Front 19

Why does aortic insufficiency cause angina?

Back 19

Aortic diastolic BP is decreased.

CPP = AoDP - LVEDP

So CPP will be decreased. this ischemia leads to angina.

Front 20

---% of coronary BP occurs during diastole.

Back 20

80%

Front 21

Explain atherosclerosis

Back 21

HTN, smoking, VC, etc causes turbulent blood flow.

Turbulent blood flow causes shear stress on the birfurcations of a blood vessel, damaging it. Damage causes inflammation and profliferation of the endothelial intimal layer (hardening of the arteries. Vessel damage causes plt activation and then plt aggregation forming a thrombus.

Fatty streaks develop. Then, a fibrous tissue develops. Smooth muscle cells proliferate increasing the size of the lesion and forming a fibrous plaque.

All of this causes narrowing of the vessel...making it a easy for an emboli to lodge and cause an occlusion.

Front 22

Explain Coronary Spasm

Back 22

A transient, focal increase in vascular tone. Lumen narrow and blood flow is decreased.

Variant Angina with an elevated ST segment that goes away when the angina goes away.

Spasms can trigger a thrombus formation, and MI, or an arrythmia.

Lethal arrythmias can occur....pt will die of sudden cardiac death.

At risk: Cocaine and amphetamine users, heavy smokers. (can occur with or without atherosclerotic disease).

Treat with Nifedipine: A dihydropyridine CCB.

Front 23

NY Heart Association Classification of Angina

Back 23

CLASS 1: Risk Factors present but no symptoms.

CLASS 2: Pt has modifiable risk factors adn some minor symptoms of angina that are relieved at rest.

CLASS 3: Angina is relieved at rest with nitrates.

CLASS 4: UNSTABLE/ CRESCENDO ANGINA - Acute angina at rest Or Angina that is not relieved with nitrates. Episodes last 5-10 min.

Front 24

What part of the heart is most likely to have an MI?

Back 24

Subendocardial d/t poor perfusion.

Front 25

What type of MI is more survivable? Subendocardial or transmural?

Back 25

Subendocardial.

A transmural MI can affect contractility.

Front 26

Transmural MI

Back 26

Q-Wave MI

Full thickness of ventricular wall is infarcted…necrosis of tissue.

Usually result of acute plaque changes and thrombosis. Ends up in hemorrage or rupture that causes damage to the myocardium (necrosis).

Front 27

Subendocardial MI

Back 27

Non-Q wave MI.

The result of decreased coronary perfusion d/t HOTN or increased MVO2.

Hypertrophy increases the risk d/t MVO2.

This area is poorly perfused so lack of blood flow is damaging.

Can also be caused by plaque disruption leading to an occlusion BEFORE necrosis develops. (once necrosis develops its a tranmural MI).

Front 28

What can cause sudden cardiac death?

Back 28

Lethal arrythmias
Coronary vasospasms
Sudden ischemia to the CONDUCTION SYSTEM (blockage of the right CA).

Pts die with no complaints of chest pain.

Front 29

The severity of an MI depends on...

Back 29

* Location, severity and rate of development of lesions
* Size of vascular bed perfused by vessel. (The higher up on the CA that the obstruction occurs, the more severe the infarct.)
*Duration of occlusion (PCA in 90 min)
* Metabolic needs of the myocardium at risk (hypertrophy or tachycardia more)
* Extent of collateral blood vessels (seen with chronic ischemia)
* Presence, site and severity of spasm
* Alterations in BP, HR, and rhythm

Front 30

Complications that can occur after an MI.

Back 30

* Contractile dysfunction
* Arrhythmias
* Myocardial rupture
* RV infarction d/t back up of blood (can cause death!!!)
* Infarct extension (if not tx well)
* Pericarditis(fluid accum in pericardial sac..rubs on heart muscle..rubs it raw!!)
* Mural thrombus (decr contractility and can break off and emboli).
* Ventricular aneurysm: acute or during healing (4-6 mths post MI)
* Papillary muscle dysfunction / rupture (d/t remodeling of the heart)
* Progressive heart failure

Front 31

Ventricular ectopy or Vtac/ Vfib is the result of ischemia to what part of the heart?

Back 31

Ischemia to the subendocardia. conduction system.

Front 32

What complication of an MI can mimic an MI extension?

Back 32

Pericarditis.

S/S: Chest pain on deep inspiration. ST segment is elevated.

Occurs 2-3 days after an MI (fluid must accumulate in pericardial sac). Can occur mths after an MI (Dressler's Syndrome).

Treat with ASA and Indomethicin (Goal is to decrease the inflammation.). Steroids if refractory.

Front 33

Explain the pathology of papillary muscle dysfunction.

What happens with a papillary muscle rupture?

Back 33

A lesion the left anterior descending artery causes ischemia to LV pap muscles. They can't contract. This causes mitral regurgitation.

They can also rupture. This will cause acute mitral regurg, high PAP, Cardiogenic shock, CHF.

Front 34

List the types of reperfusion therapy for tx of IHD.

Back 34

Thrombolysis (TPA)
PCI with angioplasty ( in 90 min)
CABG (rare)

Front 35

List medical therapy for IHD

Back 35

* Beta Blockers (decr HR and MVO2)
* Statins (anti-inflammatory and remodel arteries, incr HDL)
* Antiplt meds (ASA)
* Nitrates
* ACEI's/ ARBs
* CCB's (VD and decr HR)

Boy Scouts of America and the Night Acute Care Nurses

Front 36

STEMI pts have ___ to ___ min to be reperfused.

Back 36

60-120 min.

Stent placement can also occur.

Front 37

What increase the risk of a periop MI?

Back 37

* Pt status uncontrolled/ unstable preop.
* Specific surgical procedures: CV, thoracic, etc
* Low surgeon expertise...takes longer.
* Lack of diagnostic criteria to define sichemia or MI.
* Tachycardia, HTN intraop and decreased CPP
* Pts with severe CAD

Front 38

How are periop MI's diagnosed?

Back 38

ECG Changes
Draw blood and check cardiac enzyme levels.

Front 39

When can you see a subendocardial, non-Q wave MI??

What are the S/S?

Back 39

At the end of a case during emergence.

24-48 hours post-op.

S/S: Tachycardia and ST depression.

Front 40

8 step algorithm for determining the need for preoperative cardiac evaluation

Back 40

Step I – assesses the urgency of the surgery (can it be delayed?)

Step II – assesses whether the patient has undergone revascularization (CABG, stent, PCA, TPA)

Step III – if and when the patient underwent invasive or noninvasive coronary evaluation

Next steps – integrate risk stratification according to clinical risk factors, functional capacity and surgery-specific factors

Front 41

List procedures with high risk, medium risk, and low risk of periop CAD.

Back 41

HIGH RISK:
(>5% risk of morbidity or mortality)
--->Vascular surgery
--->Long procedures with fluid shifts
--->Emergency surgery (esp incr with age)
--->Aortic and other major vascular sx (endovascular repairs are associated with low risk).
--->Peripheral vascular sx

INTERMEDIATE RISK
(< 5% risk of morbidity/mortality)
---> Carotid endarterectomy
---> Head and neck sx
---> Intraperitoneal or intrathoracic sx
---> Orthopedic sx
---> Prostate sx

LOW RISK
(< 1% risk of morbidity and mortality)
---> Endoscopic Surgery
---> Superficial surgery
---> Cataract Surgery
---> Breast Surgery

Front 42

As you move up on the aorta, the risk of ischemia with the sx ______.

Back 42

Increase.

Front 43

List some Major, Intermediate, and Minor predictors of perioperative cardiac events (PCE).

Back 43

MAJOR
---> Unstable angina
---> MI within 7 – 30 days
---> Decompensated heart failure (no wiggle room..cannot handle stress changes)
---> LVH with a low EF.
---> Ventricular Dysrhythmias
---> Supraventricular Dysrythmias with uncontrolled rates (loss of atrial kick and no diastolic filling.)
---> High degree AV block
---> Severe valvular disease

INTERMEDIATE:
---> Chronic stable angina
---> Prior MI by history
---> Q – waves on ECG
---> Compensated or prior heart failure
----> DM
---> Renal Insufficiency (creat > 2 mg/dL)

MINOR:
Abnormal ECG
LVH
LBBB
ST-T wave
Dyrhythmias – atrial fiblrillation
Advanced age
History of stroke
Uncontrolled HTN
Low functional capacity

Front 44

How many metabolic equivalents to eat, dress, etc?

How many to walk up one flight of stairs?

How many to run, swim, etc?

Back 44

1 MET = Eat, dress
4 METs = walking up one flight of stairs
10 METs = Swimming, running, etc.

Front 45

How many metabolic equivalents are required for surgery?

Back 45

4 - pt must be able to walk up one flight of stairs.

This can be found measured via a stress test or just by questioning about funcitonal status.

Front 46

T/F

Prophylactic revascularization of asymptomatic pts is the most effective method for preventing ischemic intraop cardiac events.

Back 46

FALSE

Prophylactic revascularization in asymptomatic patients – no benefit over medical therapy

Front 47

T/F

A previous revascularization (PCI or CABG) w/n 5 yrs w/o recurrent signs or symptoms of ischemia is sufficient and no further testing is required before a surgery.

Back 47

TRUE

Front 48

What are the Hemodynamic Goals for a patient with IHD having NONcardiac surgery?

Back 48

HR: Slow - BB (avoid stimulants)

PRELOAD: Normal to Slightly decreased - venodilators like NTG or diuretics (Avoid vol overload)...keeps LVEDV down so you can maintian CPP.

AFTERLOAD: Normal to Slightly Increased - Use Neosynephrine. (Avoid arterial vasodilators). Keeps ADBP up so you can maintain CPP.

CONTRACTILITY: Normal to Decreased - BBs/Vol Anesthetics (Avoid Stimulants)

Front 49

T/F

If your patient has stable angina that has been chronic for years and has had revascularization w/n 2 yrs and is scheduled for surgery...you don't need to do another cardiac cath as long as no change in symptoms.

Back 49

TRUE.

Front 50

What is a Drug Eluting Stent?

How long should sx be delayed after placement and why?

Back 50

A drug-eluting stent (DES) is a peripheral or coronary stent placed into narrowed, diseased peripheral or coronary arteries that slowly releases a drug to inhibit clot formation.

Elective sx should be delayed for 1 year and continue dual antiplatelet therapy (ASA and fibrinolytic).

Front 51

What is bare metal stent?

How long do you hold elective sx after placement?

Back 51

A vascular stent without a coating (as used in drug-eluting stents). It is a mesh-like tube of thin wire.

Put pt on a combo of ASA and fibrinolytics. Wait 4 weeks for surgery.

Front 52

If a pt has to have emergency surgery and has recently had a stent placed is on dual combination antiplatelet therapy...what should you continue and what should you discontinue?

Back 52

Continue the ASA

Discontinue the fibrinolytics.

Front 53

What is the baseline of functional status that tells you a pt needs a beta blocker intraop?

Back 53

Patients with ischemia on stress test or Class I indications.

Front 54

Explain Statins and statin therapy intraop.

Back 54

STATIN EFFECTS:
* Anti-inflammatory action to stabilize plaque
* Statin therapy should be used perioperatively in all patients with CAD or CAD mx risk factors.
* Enhance the production of NO-->causing vasodilation.
* Decreased proliferation of smooth muscle in response to injury (statins scavenge O2 free radicals so they don't cause damage. )

USE: Give them the morning of sx and restart them as soon as sx is over.

Front 55

T/F

For pts with CAD/ IHD you always continue antiplatelet therapy (ASA) intraop.

Back 55

TRUE.

Front 56

Describe the preop management of Ischemic Heart Disease

Back 56

Determine extent of Ischemic heart disease and prior interventions (CABG or PCI?)
Determine stability of the disease…having symptoms now? How severe?
Review medications that can increase risk of surgery or contra-indicate a particular anesthetic technique

Front 57

What is the most sensitive test for ischemic heart disease?

What are other testing methods and their sensitivity rates?

Back 57

Coronary Angiography (gold standard).

Standard Electrocardiography (nonspecific test)
Low sensitivity rates – 54%
Exercise Electrocardiography (nonspecific test)
Low sensitivity rate – 74%
Echocardiography (better)
Radionuclide Imaging (better)
CT scan (low predictability)

Front 58

What is a good way to estimate systolic wall stress?

Back 58

MVO2 ~= Systolic wall stress = HR X SBP

"rate pressure product"

Front 59

ST segment depression represents ______ ischemia.

When this is seen with chest pain and returns to normal once the chest pain is over it is called.....

Back 59

ST segment depression represents subendocardial ischemia.

When this is seen with chest pain and returns to normal once the chest pain is over it is called angina pectoris.

Front 60

Diastolic wall stress = ?

What heart chamber is the most resilient to wall stress?

Back 60

Preload.

An increase in preload increases your diastolic wall stress.

The left ventricle is the most resilient chamber to wall stress. It is the thickest.

Front 61

What is pseudonormalization in an ECG?

Back 61

Inverted T waves from previous MI may manifest a return of the T waves to the normal upright position (“pseudonormalization”) during myocardial ischemia

Front 62

ST segment elevation during an anginal episode that returns to normal once ischemia is relieved is called...

Back 62

ST segment elevation during an anginal episide that returns to normal once ischemia is relieved is called variant angina. This is a symptom of a coronary vasospasm....differentiate from stable angina because of the ST segment elevation instead of depression.

Front 63

T/F

Most patients with Angina Pectoris have an abnormal ECG.

Back 63

TRUE

ECG (and usually LV function) at rest is normal in ONLY about 30% of patients with a typical history of angina pectoris.

Front 64

What changes during an exercise electrocardiography indicate that you have ischemic heart disease? What needs to happen before surgery?

Back 64

>= 1mm horizontal or down-sloping ST segment depression during or w/n 4 minutes after exercise.

A systolic murmur of mitral regurgitation or a decrease in BP (decr contractility w/ ischemia) during exercise adds to the diagnostic value of this test.

HOTN and ventricular arrythmias indicate a left main CA stenosis. (STOP THE TEST ASAP!!)

If any of these happen, you need to get a cardiac consult before surgery.

Front 65

What drug is contraindicated in severe CHF?

Back 65

CCB's

Front 66

HOTN during a stress test or ventricular arrhythmias means what? What do you do?

Back 66

Left main CA stenosis.

STOP THE TEST ASAP!!

Front 67

Contraindications to exercise electrocardiography...

Back 67

Inability to exercise
Severe aortic stenosis
Severe hypertension
Acute myocarditis or endocarditis
Uncontrolled heart failure

Front 68

T/F

A negative stress test means you do not have CAD.

Back 68

FALSE

only 75% sensitivity.

Front 69

What is Radionucleotide Imaging

Back 69

Assesses coronary perfusion – SPECT scan

* Identifies areas of limited coronary blood flow and can estimate left ventricular systolic size and function.

* Tracers (e.g., thallium, technetium) are injected into the patient to. detect areas of myocardial ischemia
.
*The pt then exercises. As exercise increases the area of poor uptake is more obvious.

Imaging immediately after cessation of exercise detects regional ischemia ( you can see it...it's not dyed.)

* Image again 4 hours later to detect reversible ischemia....these areas can be reperfused (are not dead). Correlate these areas to the CA involved.

* Areas of persistently absent uptake signify old MI (dead tissue).

Front 70

What is a stress Echocardiography?

Back 70

Performed on pts that cannot do a stress test because of contraindications.

*IV contrast dye is used to detect ventricular wall motion abnormalities (WMA) at the site of ischemia.

* Allows localization of the coronary lesion

* Use of Dobutamine to ↑ HR and contractility or(+/- atropine) if you don’t want pt to exercise.

Front 71

What meds are used in a Stress Echocardiography?

Back 71

Dobutamine and Atropine

Front 72

What is the use of CT scans in diagnosing ischemic heart disease?

Back 72

* Coronary artery calcification can be detected by electron beam computed tomography.

Other than that...nothing. Not a specific test...false positives. Not recommended.

Front 73

What is the gold standard in diagnosing CAD? Describe it.

Back 73

Coronary Angiography

Cath lab procedure. Put catheter up the aorta to the left coronary osteum and then inject a radioopaque dye to visualize the CA's and the area of blockage.

* Allows for localization of stenotic lesions in specific CA's.

* Diagnose CA vasospasm!!

* Diagnose wall motion abnormalities (WMA)

* Diagnose structural abnormalities

Front 74

How do you diagnose a CA vasospasm?

Back 74

ST segment elevated with angina that goes away with anginal episode.

Coronary Angiography: Inject medication to precipitate a spasm, then you give meds to dilate the CA and release the spasm.

That way you know exactly where it's at.

Front 75

Differentiate between Chronic Coronary Syndrome and Acute Coronary Syndrome

Back 75

Chronic Coronary Syndrome is just angina with no myocardial damage.

Acute Coronary Syndrome is angina with myocardial damage.

Front 76

Tx For Chronic Coronary Syndrome

Back 76

* Lifestyle modification
* Smoking cessation
* Weight loss
* Hypertension control
* Lowering low density lipoprotein cholesterol
* Medical Therapy (nitrates)
* Surgical Therapy (stents)

Front 77

Medical Therapy for CAD

Back 77

* Statin Therapy: Reduce low-density lipoprotein (LDL) cholesterol and C-reactive protein (CRP)

* Hypertension Control
---> ACE Inhibitors / ARBs
---> Alpha agonists

* Beta blockade Therapy

* Calcium channel blockers

*Antiplatelet drugs
---> Low-dose ASA (75-325 mg/day)
---> Clopidogrel (Plavix) and ticlopidine (Ticlid) effectively inhibit plt aggregation by blocking adenosine diphosphate receptors.
---> Platelet GP IIb/ IIIa receptor antagonists (abciximab, eptifibatide, tirofiban) inhibit platelet adhesion, activation, and aggregation.

*Nitrates

Front 78

Clopidogrel (Plavix)

Back 78

Effectively inhibit platelet aggregation by blocking adenosine diphosphate receptors.

Front 79

How does plavix inhibit platelet aggregation?

Back 79

By blocking ADP receptors (adenosine diphosphate receptors).

Front 80

How do abciximab, eptifibatide, tirofiban inhibit platelet aggregation?

Back 80

They are antagonists to platelet receptors.

Abciximab is given in the cath lab to break up a thrombus.

glycoprotein IIb/IIIa receptor antagonist

Front 81

What are the principal drug of choice to treat Ischemic Heart Disease?

Why?

Back 81

Beta Blockers.

* Decrease the risk of death and of myocardial reinfarction in pts who have had an MI. Decr cat damage to the heart....apoptysis of myocardial cells and heart remodeling.

* Decrease myocardial O2 demand by decreasing heart rate and decreasing MVO2

* Slowing heart rate also increases diastole and increases coronary perfusion time.

Front 82

What are the most common SE of beta blockers?

Adverse Effects?

Contraindications?

Back 82

The most common side effects are fatigue and insomnia.

ADVERSE EFFECTS:
---> Mask the signs of hypoglycemia in DM.

CONTRAINDICATIONS:
---> Severe bradycardia
---> Sick sinus syndrome
---> Severe reactive airway disease
---> Atrioventricular heart block
---> Uncontrolled CHF (d/t decr contractility).

Front 83

What is the drug of choice for tx of coronary vasospasm and how does it work?

Back 83

Nifedipine

Dihydropyridine CCB

Decreases the frequency and severity of angina pectoris due to vasospasm by dilating the spasming CA.

Front 84

How do CCB's work?

List them

Contrainidications?

Back 84

USE: HTN and angina

MOA: Block Ca uptake by cells
* Decrease vascular smooth muscle tone (decr BP)
* Dilate CA's
* Decrease myocardial contractility and MVO2

Amlodipine
Nicardipine
Isradipine
Felodipine
Long-acting nefedipine

CONTRAINDICATIONS:
--> Severe congestive heart failure
---> Use with Beta Blockers (both cause myocardial depression).

SIDE EFFECTS:
---> HOTN, Peripheral Edema, Headache

Front 85

How do nitrates work to tx CAD?

Contraindications?

Back 85

MOA: Nitrates work by increasing NO. NO diffuses into smooth muscle cells and increases cGMP. cGMP causes smooth muscle relaxation. Mainly this is venodilation, but arterial vasodilation can occur in high doses. Except with sodium nitroprusside.

DESIRED EFFECTS:
---> Decreased frequency, duration, and severity of angina pectoris
---> Dilate CA's AND collateral blood vessels. Dilate stenotic AND unstenotic vessels (so no coronary steal!)
---> Decrease SVR, which decreases left ventricular afterload and MVO2.
---> Decreased preload via venodilation. This decreases the load on the heart muscle. This decreases MVO2.

SIDE EFFECTS
---> Headache via increased ICP.
---> HOTN in a hypovolemic pt.
---> Tolerance w/ longterm use.
---> Reflex Tachycardia
---> Methemoglobinemia
---> Pulmonary shunting (no HPV)

CONTRAINDICATIONS:
---> Severe aortic stenosis (DBP is already low, this will make it even lower...this will drop CPP.
---> Hypertrophic Obstructive Cardiomyopathy (Will cause a decreased afterload. LVEDV is elevated. This will decrease CPP!!!!)
---> Do no use w/n 24 hrs sildenafil (viagra), tadalafil (Cialis), Vardenafil (Levitra). These are all phosphodiesterase inhibitors (end in "-afil". The combination can cause severe HOTN.!!

Front 86

What are all of bad derrogatory cardiac effects of Ang II?

What blocks these????

Back 86

Myocardial Hypertrophy
Interstitial Myocardial fibrosis
Increased coronary vasoconstriction
Endothelial Dysfunction
Promotes inflammatory responses
Atheroma formation.

These bad effects can be blocked with ACEIs.

Front 87

When should a pt with CAD/ IHD be prescribed an ACEI?

Back 87

ACEIs shoule be prescribed for ALL pts with IHD.

They block all the cardio-negative effects of AngII and cause a remodeling and restructuring of the ventricle.

Especially if they have HTN, Left ventricular dyfunction, or DM.

Front 88

Contrainidications for ACE Inhibitors

Back 88

Documented intolerance or allergy (angioedema)

Hyperkalemia (aldosterone inhibition will increase hyperkalemia)

Bilateral renal artery stenosis (renovascular disease).

Renal Failure.

Front 89

Your hemodynamic goals for HR, preload, afterload, and contractility during anesthesia on a pt with CAD include a normal to decreased value for all of hte above variable EXCEPT..._____. Why?

Back 89

HR, Preload, and Contractility you all want to be normal or decreased. This decreases MVO2, which can prevent perioperative ischemic events.

Afterload you want to be normal or INCREASED. Why? Afterload - aortic diastolic BP. CPP = AoDP - LVEDP. If afterload gets too low, you will have decreased coronary perfusion pressure during diastole.

Therefore you would use neo (phenylephrine) to keep BP from getting too low and you would avoid vasodilators.

Beta blockers will be used to keep the HR and contractiltiy low and diuretics/ venodilators can be used to keep the preload down.

Front 90

Describe the perfect induction and intubation of a patient with CAD.

Back 90

Avoid tachycardia and HOTN to pvt myocardial ischemia!!!

1) Preoxgenate well!

2) Give Fentanyl, IV LIdocaine, and/or Esmolol to blunt the SNS response to DL.

3) Use etomidate instead of propofol (NEVER use ketamine).

4) Push induction meds SLOW...a little at a time, to avoid HOTN.

5) DL less than 15 secs to avoid stimulation.

6) Use an LTA kit to the cords before intubating.

Front 91

What are the good and bad effects of volatile agents in anesthesia on a pt with Ischemic Heart Disease?

Back 91

BENEFITS:
---> Provide controlled myocardial depression, which minimizes SNS activity.
---> Precondition the heart to better tolerate ischemic events
---> Nitrous Oxide use can allow you to use less volatile agent and avoid HOTN.

BAD EFFECTS:
---> Can cause decreases in BP and associated decreases in CPP. (HOTN must be avoided).
---> Nitrous Oxide increases PVR, which can increase MVO2. (Use concentrations of 50% or less).

Front 92

Describe the risks of regional anesthesia in a pt with CAD. IHD.

Back 92

Spinals can cause sudden HOTN, which can decrease CPP. Epidurals are preferred.

Keep BP at 20% of baseline.

Front 93

Describe the perfect maintenance anesthesia for a patient with CAD/ IHD.

Back 93

Low dose volatile agents with < 50% nitrous oxide.
Use Opiods, benzo's, and esmolol to keep HR at 70 bpm.
NMBs with no histamine release ( no atracurium).
Reverse with GLYCOPYROLLATE and not atropine to pvt tachcardia.

Front 94

How should you tailor your NMB's and reversal agents to IHD?

Back 94

Use ones with no histamine release (avoid atracurium).

Use glycopyrrolate and no atropine with anticholinesterase to pvt tachycardia.

Pancuronium is used alot.

Front 95

What Perioperative ECG changes inidcate myocardial ischemia??

What leads should you be able to monitor for these changes?

Back 95

* ST Segment depression or elevation of at least 1mm

* T-wave inversion (or a normally inverted T wave that un-inverts)

* R-wave changes

LEADS:
* Lead II - shows you arrythmias
* Lead V5 - shows you ischemia (ST seg elevation).
* Leads V3 -V5: Show you the left ventricle.

Front 96

What change seen via a PA cath can inidicate myocardial ischemia?

Back 96

Elevation in PAP (HPV) combined with a wedge waveform that has large "v" waves.

Large wedge v waves - mitral regurgitation d/t ischemia of the papillary muscles of the mitral valve. (The v wave is when the left atrium is passively filling).

Front 97

T/F

A PA cath is an accurate predictor of myocardia ischemia

Back 97

FALSE

Most changes in PAP and wedge pressure are NOT d/t ischemia, so it's very non-specific.

Front 98

How can an transesophageal echocardiogram help you determine myocardia ischemia?

Is this a realistic method to use intraop?

Back 98

THIS IS THE MOST SENSITIVE AND SPECIFIC MONITOR FOR HEART ISCHEMIA.

It show you the wall motion of the heart. Wall motion abnormalities are VERY SENSITIVE to ischemia. They happen almost immediately, 3-5 min before any EKG changes.

So this is a great monitor of myocardial ischemia!!! (the best)

Problem: Its not practical...you need a trained sonographer to use it in the room and you don't always have that.

Front 99

What is the most sensitive and specific monitor for myocardial sichemia?

Back 99

A transesophageal echocardiogram.

But a coronary angiography is the gold standard.