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Coexisting 2016 > Ischemic heart disease > Flashcards

Ischemic heart disease Flashcards

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1
Q

Causes

A

Narrowing of the coronaries due to:

  1. Atherosclerosis
  2. Severe HTN or tachycardia
  3. Coronary artery vasospasm
  4. Severe hypotension
  5. Hypoxia
  6. Anemia
  7. Severe AI or AS
  8. Hypertrophied ventricle (bigger size, bigger O2 demand)
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2
Q

Clinical signs

A
  1. Angina
  2. Ischemia
  3. MI
  4. Arrhythmias
  5. Ventricular dysfunction
  6. Sudden death
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3
Q

Risk factors

A
  1. Increasing age
  2. Male gender
  3. HLD
  4. DM
  5. HTN
  6. Smoking
  7. Family history
  8. Obesity
  9. Vascular disease
  10. Menopause
  11. High-estrogen contraceptives
  12. Sedentary lifestyle
  13. Type-A personality
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4
Q

Main problem in ischemic heart disease

A

Imbalance between

myocardial O2 demand and myocardial oxygen supply

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5
Q

What is an atherosclerotic plaque composed of

A
  1. fatty acids
  2. cholesterol
  3. cellular waste products
  4. calcium deposits, other junk.
  5. Pro-inflammatory, pro-coagulant.
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6
Q

What are the chemical messengers involved in angina

A

Adenosine and bradykinin

  • these substances produce the chest pain typically associated with angina (thalamic/cortical stimulation).
  • They also slow AV conduction, decreasing contractility to hopefully improve oxygen demand/supply imbalance
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7
Q

Stable angina

A

No change in angina symptoms/precipitating factors over the past 60 or more days.

Frequency/duration of pain unchanged.

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8
Q

Unstable angina

A
  1. Crescendo
  2. Caused by less than normal activity, unpredictable
  3. New onset
  4. Lasts for prolonged periods
  5. Occurring more frequently or more severely
  6. Signals impending MI

Associated with acute plaque changes & usually partial thrombosis

Increasing medication need also indicates worsening even if symptoms are under control

Shouldn’t be operating on these folks unless its an emergency. Probably gonna ruin your day.

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9
Q

Prinzmetal angina

A

At rest, usually not provoked by a specific action

Spasm of the coronary arteries

Can occur in completely normal vessel

Often associated with migraines, Raynauds, other vasospastic diseases

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10
Q

What is stunning

A

Brief ischemic period that can cause dysfunction for several hours. Not good.

Both contraction and relaxation of the heart muscle requires ATP, which becomes depleted in ischemia/hypoxia. If coronary flow is reestablished, ventricular function will slowly return to normal. The duration of reduced performance (myocardial stunning), depends on the duration of the preceding ischemia.

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11
Q

Hibernation

A

Impaired myocardial function from prolonged ischemia, but normal function is still restored following restoration of normal flow.

With hibernation restoration of normal coronary flow (e.g., by coronary bypass) will restore normal function in the affected region.

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12
Q

Preconditioning

A

Provoked brief periods of ischemia that confer protection against future ischemia.

  • Short, repeating episodes of ischemia do not result in cumulative damage, but rather protect the heart from subsequent damage caused by a larger ischemic insult.

Shown to limit infarct size in later MI.

Pacing, exercise, opioids can evoke preconditioning

Inhaled anesthetics modulate this by blocking triggers (From what I read, this is good, but poorly understood. Interestingly COX-2 inhibitors completely abolish this protection. Who knew?)

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13
Q

Early management

A

Lifestyle modification

  1. diet
  2. execrcise
  3. smoking cessation

Treat any exacerbating factors:

  1. Fever
  2. Anemia
  3. Infection
  4. HTN
  5. HLD/Cholesterolemia

Pharmacological manipulation of O2 supply/demand

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14
Q

Drugs used in management

A
  1. BB
    • reduce contractility and HR
  2. Ca++ channel blockers
    • dilate coronaries, reduce contractility, reduce afterload
  3. ACE inhib
    • improve contractility and reduce afterload
  4. Nitrates
    • dilate coronaries and collaterals, decrease pre- and afterload (decrease in peripheral vasculat resistance and venodilation)
  5. Antiplatelets
    • reduce potential for thrombosis
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15
Q

Surgical interventions

A

PCI

  • balloons, stents, drug stents

CABG

  • off-pump, minimally invasive, robotics, all kinds of stuff

Transmyocardial revascularization- sounds impressive

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16
Q

Surgical delay post stent placement

A

Angioplasty, no stent- 4-6 weeks

Bare stent- 30-45 days

Drug stent- 1 year

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17
Q

Acute Coronary Syndrome

A

Occurs with plaque disruption leading to partial or complete occlusion of a coronary artery

Coag cascade is triggered–> local hypercoagulable state–> thrombus formation leading to greater occlusion

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18
Q

Characteristics of unstable plaques

A
  1. T-cell aggregation at the shoulder region with macrophage clusters
  2. Thin fibrous cap
  3. Lipid rich core
  4. Newly formed intra-wall capillaries
  5. Lymphocyte/mast cell infiltration into the adventitia
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19
Q

Worst kind of plaques

A

Plaque instability more significant than size of plaque

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20
Q

Events after plaque rupture

A

Platelet aggregation → thromboxane A released (vasoconstriction) → IIb/IIIa receptors on platelets activated → further aggregation, strengthening of thrombus → fibrin deposited → thrombus formation

  • Causes angina, infarction, sudden death
  • Microemboli can also be dislodged, clotting off smaller vessels elsewhere
  • Vasospasm also possible
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21
Q

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, collateral circulation
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22
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

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23
Q

Initial Acute MI treatment

A

Evaluate hemodynamics, what’s your BP looking like

  1. Get a 12-lead
  2. O2, don’t go crazy though
  3. Pain relief- morphine
  4. NTG
  5. ASA or plavix
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24
Q

Reperfusion therapy for ACS

A

Thrombolytic therapy - Must start within 30-60 minutes of arrival time.

  • streptokinase
  • TPA
  • reteplase
  • tenecteplase

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
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25
Adjunctive therapy
* Heparin * BB * ACE inhibitor - anterior MI, LV failure, EF
26
Unstable angina/Non-STEMI patho, Dx
Reduction in myocardial O2 supply Change in angina symptoms * angina at rest * chronic angina that is becoming more frequent/severe, or * new onset EKG changes ST depression in two or more contiguous leads and/or * deep symmetrical T-wave inversion Troponin levels
27
Tx for Non-STEMI
1. Rest 2. O2 3. Analgesia 4. BB 5. NTG 6. ASA/Plavix 7. Heparin 8. Possible revascularization
28
MI complications
1. Arrhythmias 2. LVF/CHF/pulmonary HTN 3. Cardiogenic shock 4. Thromboembolism/Stroke 5. Papillary muscle dysfunction, valvular disease 6. External infarct rupture * most common day 4-7 * leads to acute tamponade, followed by death 7. Ventricular aneurysm
29
Periop MI risk
Risk is less than 1% in the general population Most occur in the 24-48 hours after surgery
30
Prognostic determinants in ischemic heart disease
1. Extent of atherosclerosis 2. EF 3. Plaque stability
31
Myocardial O2 supply
Decreased by * \*\*Tachycardia\*\* * Hypotension * Vasoconstriction * O2 carrying capacity (acid/base, anemia, hypoxia) * Viscosity * Arterial patency * Coronary spasm
32
Myocardial O2 demand
Increased by * \*\*Tachycardia\*\* * Increased contractility (drugs) * Increased preload (fluids) * Increased afterload (drugs) * Shivering * Hyperglycemia * HTN
33
In a ischemic heart disease pt that displays tachycardia, what are two questions you should immediately start thinking about?
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.
34
Anesthetic concerns regional, general
Regional * sympathectomy will likely lead to hypotension * treat with phenylephrine * or ephedrine if bradycardia also present General * Maintain O2 supply/demand balance. * Do not allow for sustained periods of hypo/hypertension or tachycardia.
35
Why is tachycardia particularly worrisome in ischemic heart disease.
It both increases demand and reduces supply simultaneously and can quickly lead to CV collapse.
36
Monitoring for ischemia
EKG - simplest method Look for ST, T-wave, and R-wave changes. V5 reflects LV supplied by anterior descending. Lead II reflects ischemia from RCA, rhythm disturbances.
37
Induction
Minimize hemodynamic changes * Lidocaine – 1 mg/kg IV 90 sec before beginning DVL * Esmolol – 5-10mg IV before DVL * Fentanyl – 1-3 mcg/kg to blunt circulatory response For pts with severe cardiac dysf(x) or longer cases: * Etomidate or high opioid technique (opioids ↓ HR via direct vagal stimulation) keep DVL to 15sec or less! AVOID Ketamine and Pancuronium (sympathomimetics) and histamine-releasing drugs (mivacurium, atracurium) Choose NMR with minimal to no effects on HR and SBP (vecuronium, rocuronium, cisatracurium)
38
Maintenance
* \*\***Avoid tachycardia**\*\* * Preload- normal * Afterload- normal * Contractility- decrease if LVF normal * Maintain NSR if possible * MVO2- much easier to control demand, attenuate SNS outflow as needed * avoid prolonged periods of hypotension
39
Agents implicated in coronary steal
1. Isoflurane (Forane) 2. NTP 3. Dipyridamole
40
Things to remember about IA in these pts
Inhaled anesthetics will: 1. Decrease contractility (good) * enflurane \> halothane \> iso/des/sevo 2. Decrease SVR (ehhh) * iso/des/sevo \> enflurane \> Halothane 3. Increase coronary blood flow (nice) * halothane \> enflurane \> iso/des/sevo 4. Sensitize heart to epi (mostly a concern with halothane) * halothane \> enflurane \> iso/des/sevo
41
Emergence
* Minimize shivering which causes ↑ myocardial O2 demand * supplemental O2 * aggressively tx of post-op pain * SMOOTH emergence with minimal hemodynamic effects * Consider using low-end dosing of anticholinergic w/reversal agent to avoid excessive ↑ HR
42
Most perioperative MIs occur within \_\_\_\_\_\_\_\_\_\_\_\_. what are the typical diagnosis patterns
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
43
What physiologic changes post-op that lead to a **pro-thrombotic** state and plaque rupture
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!)
44
Adjunctive therapy for Myocardial infarction (anterior MI, LV failure, EF)
1. Heparin 2. ß-Blocker 3. ACE inhibitor
45
Oxygen ratio and Clinical triad of right ventricular infarction. Why is it imprtant to recognize?
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)
46
Three intraoperative challenges in management of patients with CAD according to stoelting.
1. **PREVENTING** ischeimia by optimizing myocardial supply and decreaseing demand 2. **MONITORING** for ischemia 3. **TREATMENT** if ischemia develops
47
How does acid/base balance effects CAD
1. Hypocapnea caused by hyperventilation can cause coronary artery constriction
48
caractheristics of LV disfunction
EF \< 50% LVEDP \> 18 mmHg (normal 12-14) CI \< 2.2 L/min/m2 marked or multiple wall motion abnormalities
49
**major** clinical predictors of increased periop cardiovascular risk
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
50
**intermediate** clinical predictors of increased periop cardiovascular risk
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
51
**minor** clinical predictors of increased periop cardiovascular risk
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
52
who gets further testing before going into OR
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
53
high risk surgeries
* abdominal aortic aneurysm (AAA) * aortic or major vascular surgery * peripheral vascular surgery * thoracotomy * major abdominal surgery * prolonged surgery with large fluid shift
54
intermediate risk surgery
carotid edarterectomy head & neck surgery intraperitoneal and thoracic surgery ortho prostate
55
low risk surgery
endoscopic surgery superficial surgery cataract surgery breast surgery
56
who can go to surgery without need of stress testing
* 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 (\<5years) & no change in medical condition * PCI with bare-metal stent in \> 6 weeks, minila anti-platelet & no change in medical condition
57
who needs cardiac consult before surgery
* 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
58
best muscle relaxants in CAD
those with minimal or no effects on the heart rateand Systemic vascular pressure 1. vecuronium 2. rocuronium 3. cisatricurium
59
CAD glycopyrolate or atropine
glycopyrolate d/t anticholinergic effects & less increase in HR
60
normal stroke volume
60-90 ml
61
normal stroke index
40-60 ml/m2
62
normal SVR
80 x (MAP-CVP)/CO 900-1500 dynes.sec.cm-5
63
normal PVR
80 (PAP-PCWP)/CO 50-150 dynes.sec.cm-5
64
treat: increased BP and increased PCWP (akaincreased SVR, afterload and work on the heart & oxygen consumtion)
increase anesthetic depth - dilates vasculature and/or give nitroglycerin or sodium nitroprusside - to dilate veins and decrease venous return normal PCWP = 2-10 mmHg
65
treat increased HR
beta antagonist * esmolol, metoprolol, labetalol, propanolol calcium channel blocker * nifedipine, verapamil, dlitiazem
66
treat: decreased in arterial BP w/ normal or decreased PCWP (aka decreased SVR and coronary perfusion/flow)
decrease anesthetic depth * contricts vasculature phenylephrine * increases BP and improves coronary perfusion
67
treat: decreased arterial blood pressure and increased PCWP (aka left vetricular failure)
phenylephrine * increases BP * impproves coronary perfusion nitroglycerin w/ positive inotrope * dilate veins & increase contractility normal PCWP = 2-10 mmHg
68
hormal hemodynamics ex: PCWP 10, BP 140/85, HR 75
nitroglycerin or calcium channel blocker (nifedipine - potent coronary dilator)

Coexisting 2016 (12 decks)

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