Ischemic Heart Disease Flashcards
What are the two most important risk factors for the development of atherosclerosis involving the coronary arteries?
Male gender
Increasing age
____% of our surgical pts are at increased risk for IHD
30
What are the common manifestations for IHD?
Angina pectoris
Acute MI
Sudden Death
What is the full list of risk factors for IHD?
Male gender
Increasing age
Hypercholesterolemia
Hypertension
Smoking
Diabetes
Obesity
Sedentary lifestyle
Genetic factors/family history
Things that cause sudden cardiac death
CAD
Overdose
Cardiomyopathy
What is angina pectoris?
Imbalance between coronary blood flow (supply) and myocardial oxygen consumption (demand)
Can precipitate ischemia, which frequently manifests as chest pain
Release of what 2 cardiac nociceptors occurs in angina?
Adenosine
Bradykinin
Stable angina typical develops in the setting of _______ or significant (what percent?) ________ of a segment of coronary artery
Partial occlusion
Chronic narrowing (>70%)
With adenosine and bradykinin, the afferent neurons converge with the upper __________ and _________ in the spinal cord
5 thoracic sympathetic ganglia
Somatic nerve fibers
After the afferent neurons converge, they produce what type of stimulation? What does this result in?
Thalamic and cortical stimulation
Chest pain of angina pectoris
What does bradykinin and adenosine slow?
What do they decrease?
AV conduction
Cardiac contractility
What is the most common cause of impaired coronary blood flow resulting in angina pectoris?
Atherosclerosis
Angina pectoris may also occur in the absence of coronary obstruction, as a result of what 3 things?
myocardial hypertrophy
severe aortic stenosis
aortic regurgitation
What are causes of decreased coronary blood flow?
Reduction in lumen size
clot/plaque in vessel
decrease in BP (anesthesia can cause this)
With angina pectoris, we don’t really worry about the chest pain, but we worry about:
The decrease in cardiac contractility and decreased AV conduction
What are the symptoms of angina?
Retrosternal chest pain, pressure, heaviness (from C8 to T4)
Radiates to neck, left shoulder, left arm, or jaw
- Occasionally to back or down both arms
Shortness of breath, dyspnea
Lasts several minutes
What other factors can induce angina?
Physical exertion
Emotional tension
Cold weather
What two pt populations have a weird presentation of chest pain?
Women
Diabetics
Other causes of chest pain?
How do differentiate?
- GERD: give GI cocktail
- Musculoskeletal: if you touch it and it hurts, it’s MS
- Pericarditis: WBC elevated, ST elevation in all leads
-PE: gold standard is CT angio, ABGs - AAA dissection: tearing pain in back and chest (if aortic root is involved, more chest than back pain)
How does a saddle PE present?
o2 levels low
syncope
confused
air hungry
may be combative
demarcation line on chest b/c one side of body is oxygenated and the other is not
Chronic stable vs unstable angina?
Chronic:
- Chest pain that does NOT change in frequency or severity in 2-month period
Unstable:
- Chest pain increasing in frequency and/or severity without increase in cardiac biomarkers (troponin, cp-k)
- If elevated cardiac biomarkers but no EKG changes, then probably NSTEMI
- typically lasts >10 minutes
Chest pain differential chart:
What are the most dangerous ones we would treat first?
Aortic dissection, PE, MI
Pneumothorax causes:
Trauma
Spontaneous
Diagnostic tools for chest pain:
Which one is the gold standard?
12 lead EKG
Exercise stress test
Nuclear stress imaging
Echo
Coronary angiography (gold standard)
When is an echo useful?
Pts with a LBBB or an abnormal EKG in whom the diagnosis of AMI is uncertain
You will see what type of abnormality on an echo in pts with an AMI?
Regional wall motion
How fast does a troponin jump in an MI? How long is it elevated for?
3-4 hours
up to 2 weeks
What type of EKG change is a characteristic of subendocardial ischemia?
What else may accompany this?
ST segment depression
transient T wave inversion
Pts with chronically inverted _____ waves resulting from previous MI may show a return of the _____ waves to normal upright position during MI.
What is this called
T waves (for both blanks)
Pseudonormalization of the T wave
What is an exercise stress test useful for?
Detecting signs of myocardial ischemia and establishing their relationship to chest pain and determining the relationship to exercise capacity
Exercise testing if often combined with what imaging studies?
Nuclear
Echo
MRI
Why is exercise testing not always feasible?
Inability of the pt to exercise, d/t peripheral vascular or MS disease, deconditioning, dyspnea on exertion, prior stroke, or the presence of chest pain at rest or with minimal activity
The _____ the degree of ST segment depression, the _____ the likelihood of significant CAD
Greater (for both)
At least ___ mm of horizontal or downscoping ST segment depression during or within ___ minutes after exercise indicates CAD
1 mm
4 min
What is the overall sensitivity of the exercise test?
around 75%
What test has a greater sensitivity than exercise testing for detection of IHD?
Nuclear stress imaging
During a nuclear stress test, what will cause tracer activity to be LESS present?
A significant coronary obstructive lesion causing a reduction in blood flow
What are the tracers in a nuclear stress test made of?
Thallium
Technetium
What is the most important indicator of the significance of the coronary artery disease detected?
The size of the perfusion abnormality
What can you administer to produce rapid heart rate to create cardiac stress during nuclear testing?
Atropine
Dobutamine
Institution of artificial cardiac pacing
Cardiac stress can be produced by administration of what?
Coronary vasodilator such as adenosine or dipyridamole
What is an echo used for?
Wall motion abnormalities
Valvular function
_____ provides the best information about the condition of the coronary arteries
Stress echocardiography
Who is a stress echocardiography indicated in?
- patients with known or possible angina pectoris who have survived sudden cardiac death
- those who continue to have angina pectoris despite maximal medical therapy
- those who are being considered for coronary revascularization
- those who develop a recurrence of symptoms after coronary revascularization
- those with chest pain of uncertain cause
- those with a cardiomyopathy of unknown cause
What is a coronary spasm?
What does this result in?
a sudden, temporary narrowing or tightening of a small part of an artery
a temporary situation where the heart does not get enough blood
What is variant angina?
How is this diagnosed?
angina that results from coronary vasospasm rather than occlusive coronary artery disease
diagnosed by ST-segment elevation during an episode of angina pectoris.
What is a vulnerable plaque?
What are the characteristics of this?
those most likely to rupture and form an occlusive thrombus
a thin fibrous cap and a large lipid core containing a large number of macrophages
T/F
The presence of vulnerable plaque predicts a greater risk of MI regardless of the degree of coronary artery stenosis.
True
AMI most often results from rupture of a plaque that had produced less than ___% stenosis of a coronary artery
50
Prevention of IHD
- Smoking cessation
- Ideal body weight
- Low fat, low cholesterol diet (statins if not)
- Regular aerobic exercise
- HTN treatment
- GLP-1 agonists
Losing ____ % of body weight decreased CAD risk by _____ %
10
50
When is drug treatment recommended baed on LDL?
What is the goal?
LDL exceeds 160 mg/dl
Goal is >50% reduction or <70 mg/dl
HTN increases risk of coronary events, such as what?
direct vascular injury
left ventricular hypertrophy
increased myocardial oxygen demand
Drug therapy for IHD includes:
- ASA
- Platelet glycoprotein IIb/IIIa receptor antagonists
- Thienopyridines (P2Y12 inhibitors)
- Nitrates
- Beta blockers
- Calcium channel blockers
- ACE inhibitors
- statins
MOA of ASA?
What is the dose?
Inhibits COX-1… thromboxane A2
- Irreversible, platelet life span
75-235 mg/day
What is the alternative for AMI pts who are allergic to aspirin?
P2Y12 inhibitors
What is TXA2?
Thromboxane A2 (TXA2) is a type of thromboxane that is produced by activated platelets during hemostasis and has prothrombotic properties: it stimulates activation of new platelets as well as increases platelet aggregation.
What is the platelet lifespan?
7-14 days
What are examples of Platelet glycoprotein IIb/IIIa receptor antagonists?
MOA?
abciximab, eptifibatide, tirofiban
Inhibit platelet activation, adhesion, and aggregation
What are examples of P2Y12 inhibitors?
MOA?
Clopidogrel, prasugrel
Inhibits ADP receptor P2Y12 and platelet aggregation
P2Y12 inhibitors can be a prodrug. What is the % of people that are hypo/hyper responsive?
10-20
Between clopidogrel and prasugrel, which has a higher risk of bleeding?
Prasugrel
What type of drug can affect the enzyme that metabolizes clopidogrel to its active compound and thereby can reduce the effectiveness of it?
PPIs
What are two common blood tests to check platelet function?
P2Y12 panels
TEG
Nitrates decrease what 3 things about angina
frequency, duration, and severity
Antianginal effects of nitrates are greater when these drugs are used in combination with what other two drug classes?
Beta blockers
Calcium channel blockers
What do nitrates do?
- Dilate coronary arteries and collaterals
- Decrease peripheral vascular resistance
- Decreases preload
- Potential anti-thrombotic effects
T/F
People taking chronic nitrates respond to sublingual nitrates just as well
False!
Will have to have IV nitrates before they respond appropriately
What are nitrates contraindicated in?
aortic stenosis and hypertrophic cardiomyopathy
What is the only drug to prolong life in CAD pts?
Beta blockers
What are the 3 main purposes of beta blockers??
Anti-ischemic, anti-hypertensive, anti-dysrhythmic
If someone is on beta blockers, do we continue them or d/c them for surgery?
Continue them or at least give a dose
What is a consideration of beta blockers with anesthesia induction?
They have an exaggerated hypotensive response
What is the difference in blockade of B1 vs B2?
What are the different drugs?
Beta 1: atenolol, metoprolol, acebutolol, or bisoprolol
- Heart rate
- Diastolic time
- Myocardial contractility
- Myocardial oxygen demand
Beta 2: propranolol, nadolol
- Increased risk of bronchospasm in reactive airway disease
What are two other things that propranolol is used for?
anxiety
tremors
Which beta blocker do we give in the OR most often?
Labetolol
- We give this one because it affects both heart rate and blood pressure
Esmolol affects ____, but not _____
Heart rate
Contractility
Metoprolol affects ______, but not ____
Contractility
Heart rate
Calcium channel blockers are uniquely effective for what?
Decreasing frequency/severity of spasm
What are CCB used for?
Dilate coronary arteries
Decrease
- Vascular smooth muscle tone
- Contractility
- Oxygen consumption
- Systemic BP
Which works better in decreasing incidence of MI, CCB or BB?
BB
CCB do a good job of controlling symptoms but not at reducing mortality
Angiotensin pathway picture
Angiotensin II increases what 4 things?
- Myocardial hypertrophy
- Interstitial myocardial fibrosis
- Coronary vasoconstriction
- Inflammatory responses
ACE inhibitors are used to treat what 3 things?
Hypertension
Heart failure
Cardioprotective
Statins decrease what 4 things?
Lipid oxidation
Inflammation
Matrix metalloproteinase
Cell death
When is revascularization indicated?
Failure of medical therapy
> 50% L main coronary artery
> 70% epicardial coronary artery
Impaired EF <40%
When is CABG preferred over PCI?
- patients with significant left main coronary artery disease,
- those with three-vessel coronary artery disease
- patients with diabetes mellitus who have two- or three-vessel coronary artery disease.
What is angioplasty?
Putting balloon in plaque to push it back against the walls
What is transluminal intervention?
devices uses net and grinder to grind plaque off vessel and it catches pieces of plaque off vessel – potentially could replace CABG
– also seen in cerebral interventions
What 4 things happen in acute coronary syndrome?
- Focal disruption of atheromatous plaque
- Triggers coagulation cascade
- Thrombin generation
- Arterial occlusion by a thrombus
Define acute coronary syndrome
Acute or worsening imbalance of myocardial oxygen supply to demand
What are the 3 categories of ACS?
What are these based on?
STEMI
NSTEMI
Unstable angina
12 lead EKG or cardiac specific biomarkers (troponin)
Decision tree picture for ACS
T/F
Some cardiac ischemia may not show up with cardiac biomarkers or EKG changes
True
What happens in a STEMI?
Coronary blood flow decreases abruptly
Acute thrombus formation
- Vulnerable plaques
Thrombogenesis
- Collagen, ADP, epinephrine, serotonin
- Thromboxane A2
- Glycoprotein IIb/IIIa receptors
- Fibrin deposit
What are the majority of STEMIS caused by?
In rare cases, what else can they be caused by?
Thrombotic occlusion of a coronary artery
coronary emboli, congenital abnormalities, coronary spasm, or inflammatory diseases
STEMI plaque pathway
(This card is stupid long, I’m sorry lol)
- A platelet monolayer forms at the site of ruptured plaque, and various chemical mediators such as collagen, ADP, epinephrine, and serotonin stimulate platelet aggregation.
- The potent vasoconstrictor thromboxane A2 is released, which further compromises coronary blood flow.
- Glycoprotein IIb/IIIa receptors on the platelets are activated, which enhances the ability of platelets to interact with adhesive proteins and other platelets and causes growth and stabilization of the thrombus.
- Further activation of coagulation leads to strengthening of the clot by fibrin deposition. This makes the clot more resistant to thrombolysis
- Plaques that rupture and lead to acute coronary occlusion are rarely of a size that causes significant coronary obstruction. - - By contrast, flow-restrictive plaques that produce chronic stable angina and stimulate development of collateral circulation are less likely to rupture.
STEMI diagnosis picture
What fraction of pts describe new-onset angina pectoris or a change in their anginal pattern during the 30 days preceding an AMI?
2/3
About a quarter of patients, especially the elderly and those with diabetes, have what type of pain at the time of AMI?
None or mild
How does a STEMI pt usually present on physical exam?
anxious, pale, and diaphoretic
- Sinus tachycardia is usually present.
- Hypotension caused by left or right ventricular dysfunction
- cardiac dysrhythmias may be present
What is the development of a Q wave on EKG more dependent on?
volume of the infarcted tissue
What two diagnostic test are powerful predictors of adverse cardiac events in patients with anginal pain?
Elevated troponins
EKG
The _____ the level of troponin, the _____ the MI is
Greater
Larger
Drug therapy for STEMIS include:
MONA
P2Y12 inhibitors (clopidogrel, prasugrel, or ticagrelor)
Platelet glycoprotein IIb/IIIa inhibitors
Unfractionated heparin
β blockers
RAAS
What is the primary goal in management of a STEMI?
reestablish blood flow in the obstructed coronary artery as soon as possible
Why is MONA necessary in STEMI treatment?
to reduce catecholamine release and the resultant increase in myocardial oxygen requirements.
What type of drugs should be avoided in a STEMI?
Glucocorticoids
NSAIDS
The time from ______ to ______ strongly influences the outcome of an acute STEMI.
Onset of symptoms
Reperfusion
Reperfusion therapy includes:
Tissue plasminogen activator (tPA), streptokinase, reteplase, or tenecteplase
When should thrombolytic therapy for STEMI be initiated?
Within 30-60 minutes of hospital arrival and within 12 hours of symptom onset
