Ischemic heart disease Flashcards
Incidence
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
Causes
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)
Clinical signs
Angina Ischemia MI Arrhythmias Ventricular dysfunction Sudden death
Risk factors
Increasing age Male gender HLD DM HTN Smoking Family history Obesity Vascular disease Menopause High-estrogen contraceptives Sedentary lifestyle Type-A personality
Main problem in ischemic heart disease
Imbalance between myocardial O2 demand and myocardial oxygen supply
What is an atherosclerotic plaque composed of
fatty acids, cholesterol, cellular waste products, calcium deposits, other junk. Pro-inflammatory, pro-coagulant.
What are the chemical messengers involved in angina
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
Stable angina
No change in angina symptoms/precipitating factors over the past 60 or more days. Frequency/duration of pain unchanged.
Unstable angina
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.
Prinzmetal angina
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
What is stunning
Brief ischemic period that can cause dysfunction for several hours.
Not good.
Hibernation
Impaired myocardial function from prolonged ischemia, but normal function is still restored following restoration of normal flow
Preconditioning
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?)
Medical management
Lifestyle mods
Treat any: Fever Anemia Infection HTN HLD/Cholesterolemia
Drugs used in management
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
Surgical interventions
PCI- balloons, stents, drug stents
CABG- off-pump, minimally invasive, robotics, all kinds of stuff
Transmyocardial revascularization- sounds impressive
Surgical delay post stent placement
Angioplasty, no stent- 4-6 weeks
Bare stent- 30-45 days
Drug stent- 1 year
ACS
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
Characteristics of unstable plaques
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
Worst kind of plaques
Plaque instability more significant than size of plaque
Events after plaque rupture
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
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, collateral circulation
Dx of MI
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
Initial Acute MI treatment
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
Reperfusion therapy for ACS
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
Adjunctive therapy
Heparin BB ACE inhibitor- anterior MI, LV failure, EF<40%, DM Glycemic control Statins
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
Tx for Non-STEMI
Rest O2 Analgesia BB NTG ASA/Plavix Heparin Possible revascularization
MI complications
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
Periop MI risk
Risk is less than 1% in the general population
Most occur in the 24-48 hours after surgery
Prognostic determinants in ischemic heart disease
Extent of atherosclerosis
EF
Plaque stability
Myocardial O2 supply
Decreased by- **Tachycardia** Hypotension Vasoconstriction O2 carrying capacity (acid/base, anemia, hypoxia) Viscosity Arterial patency Coronary spasm
Myocardial O2 demand
Increased by- **Tachycardia** Increased contractility (drugs) Increased preload (fluids) Increased afterload (drugs) Shivering Hyperglycemia HTN
In a ischemic heart disease pt that displays tachycardia, what are two questions you should immediately start thinking about?
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.
Anesthetic concerns
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.
Why is tachycardia particularly worrisome in ischemic heart disease.
It both increases demand and reduces supply simultaneously and can quickly lead to CV collapse.
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.
Induction
Minimize hemodynamic changes
Etomidate, High opioid technique (longer cases)
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
Agents implicated in coronary steal
Isoflurane (Forane)
NTP
Dipyridamole
Things to remember about VA in these pts
Decrease contractility (good)
Decrease SVR (ehhh)
Increase coronary blood flow (nice)
Sensitize heart to epi (mostly a concern with halothane)
