Ischemia & CAD Flashcards
Most perioperative MIs occur within ____________. what are the typical diagnosis patterns
24- 48hours
Typical diagnosis patterns not on slides!
- Mostly postoperative
- Mostly N-STEMI and diagnosed with EKG and cardiac biomarkers
- they are usually preceeded by tachycardia and ST depression
- tachycardia increases O2 consumption→ with CAD the coronaries inability to dialate leads to the MI
What physiologic changes post-op that lead to a pro-thrombotic state and plaque rupture
(NOT IN LECTURE)
- increased blood viscosity
- ∆s in catecholamine levels
- ∆s in cortisol levels
- ∆s in endogenous tissue plasminogen activator levels
- ∆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!)
Main problem in ischemic heart disease
Imbalance between myocardial O2 supply and demand
Compare Stable, Unstable and Prinmental Angina
Stable:
- no ∆ in frequency or duration in the last 60 days
- associated with a fixed narrowing (usually 75%+)
- relieved by rest or NTG
Unstable:
- becoming more frequent, longer, or more severe
- occuring at rest or with less exertion;
- associated with an unstable plaque/thrombosis;
- signals impending MI
Prinzmetal: coronary vasospastic disease
What are the casues of ischemic heart disease?
Caused by increased oxygen demand or decreased oxygen supply
- Athlerosclerosis is the mose common casue
- Severe Hypertension or tachycardia
- Coronary Vasospasm
- Severe Hypotension
- Hypoxemia
- Anemia
- Severe aortic insuficiency or Aortic Stenosis
What are the Clinical manifestations of ischemic heart disease?
- Angina
- Ischemia
- Myocardial Infarction
- Arrythmias
- Ventricualr dysfunction
- Congestive heart failure
- Sudden death
Ischemic heart disease drug management and effects:
-
ß-Blockers-
- decreases HR and contractility
-
Ca++ Channel Blockers
- dilates coronaries, decreases contractility, decreases afterload
-
ACE inhibitors
- improve contractility via decreased afterload
-
Nitrates
- dilates coronaries and collaterals, decreases preload (vasodilation) and afterload (decreases periperal vascular resistance)
-
Antiplatelets-
- reduce potential for thrombosis
Ischemic heart disease surgical interventions
- PCI- balloons, stents, drug stents
- CABG- off-pump, minimally invasive, robotics, all kinds of stuff
- Transmyocardial revascularization- sounds impressive
What is myocardial Infarction?
- 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 and collateral circulation
Periop MI risk
- Risk is less than 1% in the general population
- Most occur in the 24-48 hours after surgery
What decreases Myocardial O2 SUPPLY and should be avoided/prevented/promtly treated in patients with CAD?
- **Tachycardia** (sympathetic stimulation)
- Hypotension (decreases coronary blood fow)
- Vasoconstriction
- disruptions in O2 carrying capacity
- acid/base (hypocapnea from hyperventilation will also cause coronary vasoconstiction)
- anemia
- hypoxia
- Blood Viscosity
- Arterial patency
- Coronary spasm
What increases myocardial O2 DEMAND and should be avoided/prevented/promtly treated in patients with CAD?
- **Tachycardia**
- Increased contractility (drugs)
- Increased preload (fluids)
- Increased afterload (drugs)
- Shivering
- Hyperglycemia
- HTN
regoional vs general anesthesia in patients with Ischemic heart disease/CAD
-
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.
Monitoring for ischemia with an EKG
- EKG indicators of ischemia?
- what can individual leads tell us?
- What leads are best?
-
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
- Leads II, III and aVF reflect: Right coronary artery
-
supplies:
- Right atrium and right ventricle
- Inferior aspect of left ventricle
- SA node and AV node
-
supplies:
- Leads V3-V5 reflect: Left anterior descening
- supplies: Anterolateral aspect of left ventricle
- Leads I and aVL reflect: Left circumflex artery
- supplies: Lateral aspect of left ventricle
- Best lead combos (II and aV5) or (II, V4, V5) or (V3, V4, V5)
(Slide says we can also use TEE and PA catheters)
Ischemic heart disease Induction anesthesia considerations
The goal is to minimixe hemodynamic changes
- Decrease the duration of laryngoscopy
- Minimize SNS response
- USE: gas, lidocaine, Propofol, opioids esmolol
- Ketamine is definately a NO!!
-
For severe LV dysfunction
- May not tolerate anesthesia induced myocardial depression
- USE: high opioid technique and Etomidate!