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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:
Atherosclerosis
Severe HTN or tachycardia
Coronary vasospasm
Severe hypotension
Hypoxia
Anemia
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 
Ischemia
Angina
MI
Arrhythmia
Ventricular dysfunction (CHF)
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 
Age
Men
HTN
DM
Hyperlipidemia
Smoking
Family history
Obesity and sedentary lifestyle
PVD
Menopause
Use of high estrogen contraceptives
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

Dat ass.

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)

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.

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.

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

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.

22
Q

Infarction begins within __-__ minutes of ischemia

A

20-30min

23
Q

Infarction usually reaches its full size in __-__ hours

A

3-6

24
Q

Size of an infarction depends on

A

Location of the lesion

Amount of collateral circulation

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

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
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

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 < 40%, or DM)
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

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.

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)

32
Q

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

A

less than 1%

33
Q

When do most peri-op MIs occur?

A

24-48 hours AFTER surgery!!

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
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)

Co-Existing Disease (10 decks)

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