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

Ischemic Heart Disease Flashcards

1
Q

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

A

CAD

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2
Q

About ___% of our patients will have CAD

A

30%

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3
Q

Causes of CAD

A

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)
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4
Q

Clinical Manifestations of CAD

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

___% of MIs are silent

A

70%

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

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6
Q

Risk factors for CAD

A
  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)
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7
Q

What is the source of pain from cardiac ischemia?

A

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

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8
Q

What is unstable angina?

A

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***

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9
Q

Do we take patients to the OR with unstable angina?

A

FUCK NO

Only exceptions are emergencies

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10
Q

What is stable angina?

A

No change in pattern for at least 60 days.

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11
Q

What is stunning?

A

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

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12
Q

What is hibernation?

A

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

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13
Q

What is preconditioning?

A

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)

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14
Q

These things can evoke preconditioning

A

Exercise, pacing, and opioids. IAs also modulate preconditioning by blocking triggers.

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15
Q

Pharm management of CAD

A

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

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16
Q

Procedures we may have to manage for CAD

A

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)

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17
Q

Stenting and surgical delays

A

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)

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18
Q

What is acute coronary syndrome?

A

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.

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19
Q

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

A

A plaque that is unstable.

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20
Q

Characteristics of disrupted plaques

A

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

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21
Q

What happens when a plaque ruptures?

A

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.

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22
Q

Infarction begins within __-__ minutes of ischemia

A

20-30min

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23
Q

Infarction usually reaches its full size in __-__ hours

A

3-6

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24
Q

Size of an infarction depends on

A

Location of the lesion Amount of collateral circulation

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25
Q

How is an MI diagnosed?

A

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

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26
Q

INITIAL treatment of an MI

A

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

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27
Q

Reperfusion therapies for MI

A

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

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28
Q

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

A

Heparin BBs Glycemic Control Statins ACE Inhibitors (if anterior wall MI, LV failure, EF

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29
Q

Diagnosis of unstable angina / non-STEMI

A

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

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30
Q

Treatment for unstable angina

A

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.

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31
Q

Complications of infarction

A

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)

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32
Q

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

A

less than 1%

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33
Q

When do most peri-op MIs occur?

A

24-48 hours AFTER surgery!!

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34
Q

Factors that will decrease O2 supply to the heart

A

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

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35
Q

Factors that will increase O2 demand on the heart

A

Tachycardia Increased contractility Increased preload and afterload Shivering Hyperglycemia HTN

36
Q

Monitors for ischemia

A

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)

37
Q

Induction for those with CAD

A

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.

38
Q

Main intra-op goals for CAD

A

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

39
Q

What is coronary steal?

A

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.

40
Q

Coronary steal may occur with these medications

A

Isoflurane (Forane) Nitroprusside (SNP) Dipyridamole

41
Q

Are IAs generally good or bad for CAD?

A

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)

42
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
43
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!)

44
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)
45
Q

Causes

A

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)

46
Q

Clinical signs

A

Angina Ischemia MI Arrhythmias Ventricular dysfunction Sudden death

47
Q

Risk factors

A

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

48
Q

Main problem in ischemic heart disease

A

Imbalance between myocardial O2 supply and demand

49
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
50
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
51
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.
52
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.
53
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
54
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.
55
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)
56
Q

Medical management

A

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

57
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
58
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
59
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
60
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
61
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
62
Q

Worst kind of plaques

A

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

63
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
64
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
65
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)

66
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
67
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
68
Q

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

A
  1. Heparin
  2. ß-Blocker
  3. ACE inhibitor
69
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
70
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
71
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
72
Q

Periop MI risk

A
  • Risk is less than 1% in the general population
  • Most occur in the 24-48 hours after surgery
73
Q

Prognostic determinants in ischemic heart disease

A
  1. Extent of atherosclerosis
  2. EF
  3. Plaque stability
74
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
75
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
76
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.
77
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.
78
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)

79
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)
80
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
81
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)
82
Q

Agents implicated in coronary steal

A

Isoflurane (Forane) NTP Dipyridamole

83
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)

84
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)
85
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
86
Q

How does acid/base balance effects CAD

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

*** Co-Existing Disease *** (10 decks)

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