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Coexisting+Basics > Ischemic heart disease > Flashcards

Ischemic heart disease Flashcards

1
Q

Incidence

A

Leading cause of death in US men and women

Major cause of periop M+M

about 30% of surgical pts, approximately 500,000-900,000 periop MIs worldwide every year

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2
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)
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3
Q

Clinical signs

A 
Angina
Ischemia
MI
Arrhythmias
Ventricular dysfunction
Sudden death
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4
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
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5
Q

Main problem in ischemic heart disease

A

Imbalance between myocardial O2 demand and myocardial oxygen supply

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6
Q

What is an atherosclerotic plaque composed of

A

fatty acids, cholesterol, cellular waste products, calcium deposits, other junk. Pro-inflammatory, pro-coagulant.

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7
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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8
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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9
Q

Unstable angina

A

Caused by less than normal activity, unpredictable
New onset
Lasts for prolonged periods

Occurring more frequently or more severely signals impending MI, 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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10
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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11
Q

What is stunning

A

Brief ischemic period that can cause dysfunction for several hours.

Not good.

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12
Q

Hibernation

A

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

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13
Q

Preconditioning

A

Provoked brief periods of ischemia that confer protection against future ischemia. Shown to limit infarct size in later MI.

Pacing, exercise, opioids can evoke preconditioning (I’ll take the drugs, please)

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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14
Q

Medical management

A

Lifestyle mods

Treat any:
Fever
Anemia
Infection
HTN
HLD/Cholesterolemia
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15
Q

Drugs used in management

A

BB- reduce contractility and HR
Ca channel blockers- dilate coronaries, reduce contractility, reduce afterload
ACE inhib- improve contractility and reduce afterload
Nitrates- dilate coronaries and collaterals, decrease pre- and afterload
Antiplatelets- reduce potential for thrombosis

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16
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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17
Q

Surgical delay post stent placement

A

Angioplasty, no stent- 4-6 weeks

Bare stent- 30-45 days

Drug stent- 1 year

18
Q

ACS

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

19
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

20
Q

Worst kind of plaques

A

Plaque instability more significant than size of plaque

21
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

22
Q

Infarction

A

Necrosis caused by ischemia

In the heart, begins to occur within 20-30 minutes of ischemia onset

Typically starts in the subendocardium

Full infarct size usually occurs in 3-6 hours

Size depends on proximity of lesion, collateral circulation

23
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

24
Q

Initial Acute MI treatment

A 
Evaluate hemodynamics, what's your BP looking like
Get a 12-lead
O2, don't go crazy though
Pain relief- morphine, NTG
ASA or plavix
25
Q

Reperfusion therapy for ACS

A

Thrombolytic therapy- streptokinase, TPA, reteplase, tenecteplase. Must start within 30-60 minutes of arrival time.

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

26
Q

Adjunctive therapy

A 
Heparin
BB
ACE inhibitor- anterior MI, LV failure, EF<40%, DM
Glycemic control
Statins
27
Q

Unstable angina/Non-STEMI patho, Dx

A

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

28
Q

Tx for Non-STEMI

A 
Rest
O2
Analgesia
BB
NTG
ASA/Plavix
Heparin
Possible revascularization
29
Q

MI complications

A

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

30
Q

Periop MI risk

A

Risk is less than 1% in the general population

Most occur in the 24-48 hours after surgery

31
Q

Prognostic determinants in ischemic heart disease

A

Extent of atherosclerosis

EF

Plaque stability

32
Q

Myocardial O2 supply

A 
Decreased by-
**Tachycardia**
Hypotension
Vasoconstriction
O2 carrying capacity (acid/base, anemia, hypoxia)
Viscosity
Arterial patency
Coronary spasm
33
Q

Myocardial O2 demand

A 
Increased by-
**Tachycardia**
Increased contractility (drugs)
Increased preload (fluids)
Increased afterload (drugs)
Shivering
Hyperglycemia
HTN
34
Q

In a ischemic heart disease pt that displays tachycardia, what are two questions you should immediately start thinking about?

A

What’s the BP?
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.

35
Q

Anesthetic concerns

A

Regional- sympathectomy will likely lead to hypotension, treat with phenylephrine. Use ephedrine if bradycardia also present.

General- Maintain O2 supply/demand balance. Do not allow for sustained periods of hypo/hypertension or tachycardia.

36
Q

Why is tachycardia particularly worrisome in ischemic heart disease.

A

It both increases demand and reduces supply simultaneously and can quickly lead to CV collapse.

37
Q

Monitoring for ischemia

A

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.

38
Q

Induction

A

Minimize hemodynamic changes

Etomidate, High opioid technique (longer cases)

39
Q

Maintenance

A 
**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
40
Q

Agents implicated in coronary steal

A

Isoflurane (Forane)
NTP
Dipyridamole

41
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)

Coexisting+Basics (10 decks)

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