IHD Flashcards
Risk factors for IHD
Dm, obesity, male, increasing age, hypercholesterolemia, htn, smoking, sedentary life, genetics
dysrhythmias, angina, acute MI, sudden death
Stable angina develops…..
Develops in the setting where CA is partiall or sig occluded greater than 70%. Chronic narrowing of CA.
Angina Pectoris releases what?
Release of adenosine and bradykinin
Release of adenosine and bradykinin cause…..
Cardiac nociceptors->
Afferent neurons->
send pain?
arrises at T1-T5 sympathetic ganglia
slow AV conduction
decrease cardiac contractility
dermatomes for angina/ other diagnosis
C8 – T4 dermatome,
C8 = hands
T4 = nipple line
Retrosternal chest pain, pressure, heaviness
Radiates to neck, left shoulder, left arm, or jaw
Occasionally to back or down both arms. chest pain with physical exertion cold weather or emotional tension
Chronic stable CP
Chest pain that does NOT change in frequency or severity in 2-month period
doesn’t hurt more or happening more often
Unstable CP
Chest pain increasing in frequency and/or severity without increase in cardiac biomarkers
12 lead ECG changes look for
ST segment depression
Associated T wave inversion
ST elevation
order biomarkers to correlate
previous MI changes
Exercise stress test assess….
Assessing the Relationship of cardiac stressor/ movement to chest pain
assess supply and demand balance
looking for greater degree of ST changes with stress, greater depression = increased CAD
What dx cardiac test has greater sensitivity for assessing CAD?
nuclear stress imaging
tracers accumulating = good flow
dark area = no tracer = ischemia
Nuclear stress imaging
measures…..
Size of perfusion abnormality = significance of CAD detected
Estimates LV systolic size and function
Differentiates new perfusion abnormality vs. “old” MI
Tracers for nuclear stress imaging used with/without exercise
Thallium
Atropine, dobutamine, and pacing- used to help increase hr and cause the stress.
Adenosine, dipyridamole- Help with dilating the areas after we induce stress, only dilate normal CA not going to evoke change in arteries that are atherosclerotic. Poor arteries/ inflamed from atherosclerosis, these wont dilate them anymore
Get Echo when….
patho Q wave and new BBB
Echo assesses….
Wall motion abnormalities
Valvular function
Function of Coronary angiography
Determines location of occlusive disease
Diagnose Prinzmetal (variant/spasm) angina
Assess results of angioplasty/stenting
Coronary angiography does not measure…..
Does NOT measure stability of plaque; when it will rupture
Gen treatment for IHD
Cessation of smoking
Ideal body weight
Low-fat, low-cholesterol diet; Statins;
Regular aerobic exercise
Treatment of hypertension
When are statins prescribed
increased trig
LDL > 160 mg/dl, 50% reduction is what they are looking for
ASA moa
inhibits cox 1 = inhibits thromboxane A2= decreased clotting.
Irreversible, plat life span = 7 days
Platlets given to plavix pts is effective….
24 hours after the last dose / 5 half lives
Platelet glycoprotein IIb/IIIa receptor antagonists meds and MOA
(abciximab, eptifibatide, tirofiban)
Inhibit platelet activation, adhesion, and aggregation
Plavix metabolite increases clearance by….
6-8 hrs
Thienopyridines (P2Y12inhibitors)
medications
Clopidogrel and Prasugrel
Clopidogrel MOA
Inhibits ADP receptor P2Y12 and platelet aggregation
when clopidogrel is DC’s platlets….
D/C ~ 80% of platelets recover to normal function , takes time and we are always making plat
clopidogrel hypo/hyper responsive percentage
10 - 20% of people hypo/hyper-responsive = less predictable pharmacodynamics
Clopidogrel and PPI’s
reduce the effectiveness of the drug
Pragusul compared to clopidogrel
More predictable pharmacokinetics; more potent than Plavix.
Higher risk of bleeding
Nitrates effect
Decrease frequency, duration, and severity of CP
Increase exercise to produce ST-segment depression
Dilate coronary arteries and collaterals
Decrease peripheral vascular resistance
Decreases preload
Potential anti-thrombotic effects; not well researched
Nitrates are contraindicated in……
Contraindicated with aortic stenosis and hypertrophic cardiomyopathy
AS = need more venous return for forward motion
HC = outflow obstructed
Nitrates drug interactions
Synergistic with beta-blockers/calcium channel blockers; if given in addition then the effect is more profound.
Only drug to prolong life in CAD pts
Beta blockers
Decreases risk of death and reinfarction in MI pts
Beta blockers effects
Anti-ischemic, anti-hypertensive, anti-dysrhythmic
medication that Increased risk of bronchospasm in reactive airway disease
Beta 2 adrenergic blockers
(propranolol, nadolol)
Beta 1 blockers
Blockade of β1- receptors (atenolol, metoprolol, acebutolol, or bisoprolol)
Beta blockers effect
Decrease Heart rate
Inrease Diastolic time
Reduce Myocardial contractility
Decrease Myocardial oxygen demand
Helping heart to relax and refill, when increasing diastolic time = increases coronary perfusion time.
medication that is Uniquely effective for decreasing frequency/severity of spasm in coronary arteries (prinzmental)
CCB
Dilate coronary arteries,
CCB decrease ……
Vascular smooth muscle tone
Contractility
Oxygen consumption
Systemic BP
Beta blockers compared to CCBs
Not as effective as beta blockers in decreasing incidence of myocardial reinfarction
Angiotensin II increases….
Myocardial hypertrophy
Interstitial myocardial fibrosis
Coronary vasoconstriction
Inflammatory responses
ace i
ACE i treat
Hypertension
Heart failure
Cardioprotective ; reduce the workload to decrease demand and prevent vent remodeling and stabilize the repercussed heart and prevent the reoccurrence of reperfusion arrhythmias.
Medication that helps with coronary plaque stabilization
statins by Decreases, Lipid oxidation, Inflammation, Matrix metalloproteinase, Cell death
Statins reduce the mortality noncardiac surgery and vascular surgery by….
Reduces mortality noncardiac surgery (44%) and vascular surgery (59%)
Revasularization for what pts….
Failure of medical therapy
> 50% L main coronary artery
> 70% epicardial coronary artery
Impaired EF <40%
CABG > PCI when……
L main disease; 2 or 3 vessel CAD, DM and have 2 or 3 Vessels
what is Acute Coronary Syndrome
Acute or worsening imbalance of myocardial oxygen supply to demand
Events leading to ACS
Atheromatous plaque
Coagulation cascade
Thrombin generation
Arterial occlusion (partial or complete)
No st seg elevation and negative biomarkers
unstable angina
No st seg elevation with positive biomarkers
NSTEMI
St elevation with positive biomarkers
STEMI
What forms at the site of the ruptured plaque
plat monolayer and Vulnerable plaques; likely to ruputure.
Chemicals that stim plat aggregation
Collagen, ADP, epinephrine, serotonin-> stim plat aggregations
TXA2 = vasoconstriction
Glycoprotein 2b/3a function
Glycoprotein IIb/IIIa receptors; activated on plat and that enhances the ability to interact with adhesive proteins/ make stickier and make clot bigger -> growth-> stabilize thrombus
Troponin increases within….
3 hours after myocardial injury , stay elevated for 7 to 10 days
More specific than CK-MB
STEMI Dx
evidence of myocardial necrosis with myocardial ischemia; troponin, st changes, patho q wave,
reperfusion medical therapy
Tissue plasminogen activator (tPA), streptokinase, reteplase, or tenecteplase- started within 30 min of hospital arrival/ 12 hr or symptom onset.
catalyze plasminogen-> plasmin to break down the clot
Restores normal antegrade blood flow
When are imaging studies ordered
new LBB or abnormal ECG
Regional wall motion abnormalities
Ad look at valves, if pt has evidence of EKG with an MI. echo is not warranted. Only indictive if the pt needs an echo. Not everyone with an MI will have an echo.
Indications for PCI
-Contraindications to thrombolytic therapy
-Severe HF and/or pulmonary edema
-Symptoms present for 2 - 3 hours
-Mature clot
Indications for CABG
CABG recommended based on Coronary anatomy
failed angioplasty
Evidence of infarction-related ventricular septal rupture or mitral regurgitation
Drug therapy for ACS
MONA; morphine, oxygen, nitrates, asa
P2Y12inhibitors (clopidogrel, prasugrel, or ticagrelor)
Platelet glycoprotein IIb/IIIa inhibitors
Unfractionated heparin (esp for PCI/ thrombolytic therapy is planned)
βblockers
RAAS; ACEi, ARB, prevent vent remodeling.
Causes of unstable angina
Rupture or erosion of a coronary plaque
Dynamic obstruction due tovasoconstriction(prinzmental/ cold temp)
Worsening coronary luminal narrowing (atherosclerosis/ stent restenosis)
Inflammation (vasculitis)
Myocardial ischemia due to increased oxygen demand
Unstable Angina/ NSTEMI
Angina at rest, lasting >10 minutes
Chronic angina pectoris
Cp thats more frequent and more easily provoked
Crescendo pattern; gaining momentum
New-onset angina
severe,prolonged, or disabling cp
Treatment for unstable angina/ NSTEMI
Bed rest, oxygen, analgesia, andβ-blocker therapy
Sublingual or IV nitroglycerin
Calcium channel blockers
Aspirin, clopidogrel, prasugrel, or ticagrelor and heparin therapy (unfractionated heparin or LMWH)
Thrombolytic therapy not indicated in what pts
unstable angina/ NSTEMI because the fibin is not there and pts still have flow
Types of PCI
Balloon angioplasty, bare-metal stent, drug eluding stent……Destruction of endothelium of the vessel
Reendovasualrization post balloon angioplasty can take…..
2-3 weeks- 2-3 weeks of therapy
Reendovasualrization post baremetal stend angioplasty can take…..
12 weeks- 6 weeks of therapy
Reendovasualrization post DES angioplasty can take…..
1 year
DC clopidogrel or ticagrelor….
5 days to reduce bleeding risk
continue asa if possible
DC prasugrel ……
7 days
Angioplasty without stenting time to wait for elective sx
2-4 weeks
Bare metal stent placement time to wait for elective surgery
at least 30 days ; 12 weeks preferable
CABG time to wait for elective surgery
at least 6 weeks; 12 weeks preferable
DES time to wait for elective surgery
at least 6 months; at least 12 months after acute coronary syndrome
what anesthetic to avoid with post-cardiac intervention pts
Anesthetic technique; avoid spinal/ epidural
Pre op beta blockers
continue throughtout peri- op
treatment for bradycardia with beta blockers
Glycopyrrolate > atropine
____ has less potential to cause arrhythmias
glycopyrrolate
α2-Agonists MOA
Decrease sympathetic outflow, blood pressure, and heart rate
Continue because of rebound effects.
Rebound effects; tachycardia/ htn
DC ACEi…..
D/C 24 hours before surgery
Sympathomimetics to treat hypotension
Control hyperglycemia to…
< 180mg/dL
Components of RCRI
High risk sx; intraperiotoneal, intrathoracic, subringuinal vasular procedure
ischemic heart dz
hx of CHF
hx of CVA
Dm w/ insulin
Creat > 2.0
RCRI score
0=0.4%
1= 1%
2 = 2.4$
>3 = 5.4%
Low risk - <1%= ≤1 RCRI risk factor
Elevated risk - >1%= >2 RCRI risk factors
Functional capacity assesses….
cardiopulmonary fitness
Poor functional capacity = increased peri-operative risk
Mets
metabolic equivalent of task
Rate of energy consumption at rest
1 MET = 3.5 mL/kg/min
want > 4 METs
Emergency surgery
life or limb would be threatened if surgery did not proceed within 6 hours or less
-Proceed directly to emergency surgery w/o pre-op cardiac assessment
-Focus on surveillance and early treatment
Urgent surgery
life or limb would be threatened if surgery did not proceed within 6 to 24 hours
Time-sensitive surgery
delays exceeding 1 to 6 weeks would adversely affect patient outcomes
2, 3, avF artery
RCA
areas; RA, RV, SA node, interior LV, AV node
1, AVL artery
circumflex
area; lateral aspect of the LV
V3-V5 artery
LAD
area; anterolateral aspect of LV
Goals of IHD with anesthesia
Prevent myocardial ischemia
Monitor for ischemia
Treat ischemia
Prevent
Persistent tachycardia
Systolic HTN
SNS stimulation
Arterial hypoxemia
Hypotension
Maintain BP and HR w/in normal awake baseline 20%
Causes of decrease oxygen delivery
decrease coronary blood flow
tachycardia
hypotension
hypocapnia
Coronary artery spasm
decreased oxygen content
anemia
arterial hypoxemia
shift of the oxyghbg dissociation cure to the L
Increased oxygen requirements
symathetic nervous sytem stimulation
tachycardia
htn
increase Mypocardial contraciltiy
increased afterload
increased preload
Anesthetic considerations for induction
Succinylcholine, vecuronium, rocuronium, & cisatracurium—avoid histamine release
DL ≤15 seconds
Laryngotracheal lidocaine, IV lidocaine, esmolol, fentanyl, remifentanil, and dexmedetomidine
Volatile anesthetics
Nitrous oxide
Opioids; Severe LV function
Neuraxial anesthesia- avoid if ont DAPT therapy
med to give for tachycardia
esmolol
Tx for hypotension
Fluid bolus
Sympathomimetic drugs (ephedrine, phenylephrine)
Pragusul compared to clopidogrel
More predictable pharmacokinetics; more potent than Plavix.
Higher risk of bleeding
What forms at the site of the ruptured plaque
plat monolayer and Vulnerable plaques; likely to ruputure.
New-onset angina
severe,prolonged, or disabling cp
