Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

!!!!! Co-Existing Disease !!!!! > Ischemic Heart Disease > Flashcards

Ischemic Heart Disease Flashcards

1
Q

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

A
  1. 24- 48hours
  2. Mostly postoperative
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

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

A
  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!)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Two pathophysiologic mechanisms that can be responsible for perioperative MI

A
  1. Acute coronary thrombosis
  2. Increased myocardial demand in the setting of comprimised myocardial oxygen supply (CAD)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Main problem in ischemic heart disease

A

Imbalance between myocardial O2 supply and demand

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is an athlerosclerotic plaque composed of?

A
  1. fatty acids
  2. cholesterol
  3. cellular waste products
  4. calcium deposits
  5. Pro-inflammatory mediators
  6. Pro-coagulant. mediators
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

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

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Define Stable angina

A
  1. No change in angina symptoms/precipitating factors within the last 60 days.
  2. Frequency and duration of pain has not changed.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Define Unstable angina

A
  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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Define Prinzmetal angina

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q
  1. What is myocardial stunning?
  2. Hibernation?
  3. Preconditioning?
A
  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.
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

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

A
  1. Troponins
  2. CPK-MB (creatine phosphokinase - myocardial bound)
  3. LDH (lactate dehydrogenase)
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Ischemic heart disease drug management and effects:

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Ischemic heart disease surgical interventions

A
  1. PCI- balloons, stents, drug stents
  2. CABG- off-pump, minimally invasive, robotics, all kinds of stuff
  3. Transmyocardial revascularization- sounds impressive
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Surgical delay post stent placement

A
  1. Baloon Angioplasty - no stent = 4-6 weeks
  2. Bare metal stent = 30-45 days
  3. Drug eluding stent = 1 year
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Acute Coronary Syndrome

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Characteristics of unstable plaques

A
  • 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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Worst kind of plaques

A

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

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Events after plaque rupture

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

What is myocardial Infarction?

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Dx of MI

A

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)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Initial Acute MI treatment

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Reperfusion therapy for ACS

A
  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
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

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

A
  1. Heparin
  2. ß-Blocker
  3. ACE inhibitor
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Unstable angina/Non-STEMI patho, Dx

A
  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 two or more contiguous leads and/or deep symmetrical T-wave inversion
  4. Troponin levels
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Tx for Non-STEMI

A
  1. Rest
  2. O2
  3. Analgesia
  4. ß-Blockers
  5. NTG
  6. ASA/Plavix
  7. Heparin
  8. Possible revascularization
26
Q

MI complications

A
  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
27
Q

Periop MI risk

A
  • Risk is less than 1% in the general population
  • Most occur in the 24-48 hours after surgery
28
Q

Prognostic determinants in ischemic heart disease

A
  1. Extent of atherosclerosis
  2. EF
  3. Plaque stability
29
Q

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

A
  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
30
Q

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

A
  1. **Tachycardia**
  2. Increased contractility (drugs)
  3. Increased preload (fluids)
  4. Increased afterload (drugs)
  5. Shivering
  6. Hyperglycemia
  7. HTN
31
Q

In a ischemic heart disease

A patient that displays tachycardias, should provoke two questions that will further assess the patient, what are they?

A
  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.
32
Q

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

A
  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.
33
Q

Why is tachycardia particularly worrisome in ischemic heart disease.

A

It effects BOTH supply and demand!!!!

  • increases demand
  • reduces supply

(doing this simultaneously and can quickly lead to CV collapse)

34
Q

Monitoring for ischemia with an EKG

  • what do we look for that indicates ischemia?
  • what can idividual leads tell us?
  • What leads are best?
A
  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)
35
Q

Ischemic heart disease Induction anesthesia considerations

A

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
36
Q

Ischemic heart disease anesthetic mainitinence GOALS

A
  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)
37
Q

Agents implicated in coronary steal

A

Isoflurane (Forane) NTP Dipyridamole

38
Q

Things to remember about VA in these pts

A

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

39
Q

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

A
  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)
40
Q

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

A
  1. PREVENTING ischeimia by optimizing myocardial supply and decreaseing demand
  2. MONITORING for ischemia
  3. TREATMENT if ischemia develops
41
Q

How does acid/base balance effects CAD

A
  1. Hypocapnea caused by hyperventilation can cause coronary artery constriction
42
Q

caractheristics of LV disfunction

A

EF

LVEDP > 18 mmHg (normal 12-14)

CI 2

marked or multiple wall motion abnormalities

43
Q

major

clinical predictors of increased periop cardiovascular risk

A

may require delay of elective surgery to get cardiology evaluation

  1. unstable coronary syndrome
  2. acute/recent MI
  3. unstable/severe angina
  4. decompensated heart failure
  5. significan dysrhythmia
  6. high grade AV block
  7. sympromatic ventricular dysrhythmia with underlyining heart disease
  8. SVT with uncontrolled rate
  9. severe valvular disease
44
Q

intermediate

clinical predictors of increased periop cardiovascular risk

A

well validated markers of increased cardiac risk

  1. mild angina
  2. previous MI
  3. compensated heart failure
  4. diabetes (esp insulin dependent)
  5. renal insuficiency
45
Q

minor

clinical predictors of increased periop cardiovascular risk

A

markers of coronary disease not demonstrated to increase peri-op risk

  1. advanced age (>70yo)
  2. abnormal EKG (left ventr hyperthrophy, LBBB, etc)
  3. rhythm other than sinus
  4. low fxn capacity
  5. hx of stroke
  6. uncontrolled HTN
46
Q

who gets further testing before going into OR

A
  1. pts with two of these factors:
    1. high risk surgery
    2. low exercse tolerance
    3. moderate clinical factors
  2. pts with low funtional capacity
  3. pts whose functional capacity cannot be assessed
47
Q

high risk surgeries

A
  • abdominal aortic aneurysm (AAA)
  • aortic or major vascular surgery
  • peripheral vascular surgery
  • thoracotomy
  • major abdominal surgery
  • prolonged surgery with large fluid shift
48
Q

intermediate risk surgery

A

carotid edarterectomy

head & neck surgery

intraperitoneal and thoracic surgery

ortho

prostate

49
Q

low risk surgery

A

endoscopic surgery

superficial surgery

cataract surgery

breast surgery

50
Q

who can go to surgery without need of stress testing

A
  • no prior revascularization but stable CAD & good exercise tolerance
  • unstable CAD/low exercise tolerance BUT EKG and non invasive testing came negative
  • unstable CAD/low exercise tolerance BUT the cardiac cath showed no left main disease
  • had CABG (
  • PCI with bare-metal stent in > 6 weeks, minila anti-platelet & no change in medical condition
51
Q

who needs cardiac consult before surgery

A
  • PCI in the last 12 months with DES and dual antiplatelet therapy
  • unstable CAD or decreased exercise tolerance w/ positive EKG and left main artery disease on cardiac cath
52
Q

best muscle relaxants in CAD

A

those with minimal or no effects on the heart rateand Systemic vascular pressure

  1. vecuronium
  2. rocuronium
  3. cisatricurium
53
Q

CAD

glycopyrolate or atropine

A

glycopyrolate

d/t anticholinergic effects & less increase in HR

54
Q

normal stroke volume

A

60-90 ml

55
Q

normal stroke index

A

40-60 ml/m2

56
Q

normal SVR

A

80 x (MAP-CVP)/CO

900-1500 dynes.sec.cm-5

57
Q

normal PVR

A

80 (PAP-PCWP)/CO

50-150 dynes.sec.cm-5

58
Q

treat:

increased BP and increased PCWP

(akaincreased SVR, afterload and work on the heart & oxygen consumtion)

A

increase anesthetic depth - dilates vasculature

and/or

give nitroglycerin or sodium nitroprusside - to dilate veins and decrease venous return

normal PCWP = 2-10 mmHg

59
Q

treat

increased HR

A

beta antagonist

  • esmolol, metoprolol, labetalol, propanolol

calcium channel blocker

  • nifedipine, verapamil, dlitiazem
60
Q

treat:

decreased in arterial BP w/ normal or decreased PCWP

(aka decreased SVR and coronary perfusion/flow)

A

decrease anesthetic depth

  • contricts vasculature

phenylephrine

  • increases BP and improves coronary perfusion
61
Q

treat:

decreased arterial blood pressure and increased PCWP

(aka left vetricular failure)

A

phenylephrine

  • increases BP
  • impproves coronary perfusion

nitroglycerin w/ positive inotrope

  • dilate veins & increase contractility

normal PCWP = 2-10 mmHg

62
Q

hormal hemodynamics

ex: PCWP 10, BP 140/85, HR 75

A

nitroglycerin

or

calcium channel blocker

(nifedipine - potent coronary dilator)

!!!!! Co-Existing Disease !!!!! (15 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions