Ischemic Heart Disease- Lecture Flashcards
More than 90% of acute coronary syndrome events (angina, NSTEMI, STEMI) result from the disruption of _
More than 90% of acute coronary syndrome events (angina, NSTEMI, STEMI) result from the disruption of atherosclerotic plaque followed by platelet aggregation and thrombus formation
Atherosclerotic plaques may rupture due to _ or _
Atherosclerotic plaques may rupture due to chemical factors that destabilize the lesion or physical stress on the lesion
* Triggers include strenuous physical activity, emotional stress, SNS activation
Coronary thrombosis following atherosclerotic plaque rupture is often exacerbated by _
Coronary thrombosis following atherosclerotic plaque rupture is often exacerbated by endothelial dysfunction –> leads to vasoconstriction and diminished anti-thrombotic function
The 90% lesions have lots of _ and are not as common to rupture; the 30-40% lesions are soft with _ and are more commonly the ones to rupture
The 90% lesions have lots of calcium and are not as common to rupture; the 30-40% lesions are soft with cholesterol and are more commonly the ones to rupture
Atherosclerotic plaque rupture will stimulate thrombosis via activation of _
Atherosclerotic plaque rupture will stimulate thrombosis via activation of hemostasis
* Endothelial damage –> exposure of the thrombogenic connective tissue to the cirulating blood
* Triggers soft platelet plug (1) and then fibrin clot (2)
The ACS pathologies that are characterized by partially occlusive thrombus are _
The ACS pathologies that are characterized by partially occlusive thrombus are unstable angina and NSTEMI
The ACS pathology that is characterized by completely obstructive thrombus is _
The ACS pathology that is characterized by completely obstructive thrombus is STEMI
The difference between unstable angina and NSTEMI is _
The difference between unstable angina and NSTEMI is NSTEMIs have enough blockage that there is necrosis of the tissue
* Troponin is normal in unstable angina, abnormal in NSTEMI
A common result of acute plaque rupture and coronary artery thrombosis is _
A common result of acute plaque rupture and coronary artery thrombosis is myocardial infarction
With an MI event, blood flow can be spontaneously restored within _ hours
With an MI event, blood flow can be spontaneously restored within 12-24 hours
* Endothelium is working to dissolve the thrombus
* However, this is often too late because ischemia can result very quickly
Only _ minutes of ischemia can cause irreversible myocyte injury called infarct
Only 20-30 minutes of ischemia can cause irreversible myocyte injury called infarct
Name some of the factors that determine the severity of an infarction
- Magnitude and duration of ischemia
- Is there collateral coronary flow?
- Mass of the myocardium perfused by the blocked coronary artery
- Oxygen demand of the myocardium at risk
- Degree and timing of reperfusion (good)
- Once you do reperfuse, how big is the inflammatory response (reperfusion injury)
Within 20-30 minutes irreversible cell injury ensues; marked by _ cellular change
Within 20-30 minutes irreversible cell injury ensues; marked by loss of nuclei
* An MI occurs when the ischemia is severe enough for long enough to cause irreversible injury and necrosis
During reversible myocyte injury, there is a rapid shift from _ –> _ metabolism
During reversible myocyte injury, there is a rapid shift from aerobic –> anaerobic metabolism
* Lactic acid accumulates
* Reduction in ATP
Reversible myocyte injury is also associated with abnormal electrolyte ion shifts that can result in _ or _
Reversible myocyte injury is also associated with abnormal electrolyte ion shifts that can result in arrhythmias or edema (rising intracellular Na+)
Infarctions begin in _ layer of the heart and can progress to the entire thickness of the myocardium due to prolonged, total occlusion of _
Infarctions begin in subendocardial layer of the heart and can progress to the entire thickness of the myocardium due to prolonged, total occlusion of epicardial coronary artery
The subendocardial layer is susceptible to ischemia due to _
The subendocardial layer is susceptible to ischemia due to poor collateral flow, being adjacent to high-pressure ventricles, and being furthest from epicardial coronary arteries
Two possible ECG findings that might suggest subendocardial ischemia:
- ST depression
- T wave inversion
The most suggestive finding on the ECG for an MI is _ ; however, _ or _ can also be signs
The most suggestive finding on the ECG for an MI is ST segment elevation ; however, ST segment depression or T wave inversion can also be signs
Labile T wave inversions in the setting of chest pain are likely to suggest _
Labile T wave inversions in the setting of chest pain are likely to suggest myocardial infarction
The ST segment represents _
The ST segment represents the period between depolarization and repolarization of the left ventricle
* In a normal state, the ST segment should be isoelectric to the PR segment
ST depression in multiple leads; suggestive of ischemia/ infarction
What medications are adminstered in the setting of unstable angina/ NSTEMI?
- Beta blockers (metoprolol)
- Nitrates (nitroglycerin)
- Anti-platelet therapies (aspirin, clopidogrel)
- Anticoagulant Therapy (heparin)
- ACE inhibitor (lisinopril)
- Statin (atorvastatin)
Beta blockers are administered for ischemic heart disease for the purpose of _
Beta blockers are administered for ischemic heart disease for the purpose of decreasing oxygen demand
* Lower the heart rate –> enhances electrical stability and decreases oxygen demand
Beta blockers should be administered in the first 24 hours post MI and should be continued indefinitely because _
Beta blockers should be administered in the first 24 hours post MI and should be continued indefinitely because reduces long-term mortality
Beta blockers should almost always be used for ACS unless patient has _
Beta blockers should almost always be used for ACS unless patient has marked bradycardia, severe bronchospasm, hypotension, acute heart failure
Nitrates are used in the setting of ACS for the purpose of _
Nitrates are used in the setting of ACS for the purpose of venodilation –> decreases preload –> less wall stress –> lower oxygen demand
Additionally, coronary vasodilation improves blood flow, reduces vasospasm, and improves O2 supply
Be cautious when using nitrates for right ventricle infarctions because these patients are often _
Be cautious when using nitrates for right ventricle infarctions because these patients are often preload-dependent –> nitrates can cause hypotension
Anti-platelet therapies in the context of ACS are very important because _
Anti-platelet therapies in the context of ACS are very important because they reduce mortality
* Give them immediately and continue indefinitely
* Often combine aspirin + clopidogrel
Aspirin works as an anti-platelet therapy by _
Aspirin works as an anti-platelet therapy by inhibiting synthesis of TXA2 –> inhibits platelet activation
Clopidogrel, Ticagrelor, Prasugrel all function as _ inhibitors
Clopidogrel, Ticagrelor, Prasugrel all function as P2Y12 inhibitors (they block ADP)
Heparins are also used in the context of ACS and work by _
Heparins are also used in the context of ACS and work by enhancing antithrombin effects
* LMW heparin is technically more effective but is harder to monitor compared to unfractionated heparin
Severe occlusions require intervention via _
Severe occlusions require intervention via percutaneous coronary intervention (PCI)
All patients who receive a stent need to take a dual platelet therapy of _ + _
All patients who receive a stent need to take a dual platelet therapy of aspirin (ASA) + clopidogrel
To diagnose a STEMI on ECG, we must see ST segment elevation > _ mm in at least two anatomically contiguous leads
To diagnose a STEMI on ECG, we must see ST segment elevation > 1 mm in at least two anatomically contiguous leads
Or we can diagnose STEMI if there is > _ mm elevation in 2 contiguous precordial leads
Or we can diagnose STEMI if there is > 2 mm elevation in two contiguous precordial leads
We also proceed with STEMI treatment if we see _
We also proceed with STEMI treatment if we see new left bundle branch block
* LBBB can hide the ST elevation so we proceed with treatment
ST elevation in lead II, III, aVF
Lead II, III, aVF: inferior infarction
ST elevation in lead V2-V4
Lead V2-V4: anterior infarction
ST elevation in lead V1-V4
Lead V1-V4: anteroseptal infarction
ST elevation in I, aVL, V5, V6
Lead I, aVL, V5, V6: lateral infarction
A left bundle branch block on ECG suggests _ MI
A left bundle branch block on ECG suggests anterior MI
ST elevation in V4R
V4R: right ventricle infarction
ST depressions in V1, V2
ST depressions in V1, V2: posterior infarction
“Electrically silent” on ECG
“Electrically silent” on ECG: Left circumflex occlusion
Infarction on the anterior or anteroseptal portion of the heart is a problem at the _
Infarction on the anterior or anteroseptal portion of the heart is a problem at the left anterior descending artery (LAD)
Infarction on the lateral portion of the heart is most often a problem of the _
Infarction on the lateral portion of the heart is most often a problem of the left circumflex, can sometimes be LAD
Infarction in the inferior portion of the heart is a problem of the _
Infarction in the inferior portion of the heart is a problem of the right coronary artery
ST elevation in V4R, which suggests a right ventricle MI is usually a problem of the _
ST elevation in V4R, which suggests a right ventricle MI is usually a problem of the right coronary artery
V1 and V2 ST depressions, which suggest posterior MI, is a problem of _
V1 and V2 ST depressions, which suggest posterior MI, is a problem of right coronary artery (usually) can sometimes be the left circumflex
Pathologic Q waves are indicative of _
Pathologic Q waves are indicative of prior transmural MI
3 criteria for Q waves to be “pathologic”
Criteria for Q waves to be pathologic:
1. Q waves > 1 mm wide
2. Q waves > 25% of QRS amplitude
3. Pathologic Q waves should be present in at least 2 contiguous leads
Name 3 major complications post MI
- Decreased contractility (inc risk of thrombus)
- Electrical instability (arrhythmias)
- Tissue necrosis (papillary muscle tear, VSD, ventricular rupture)
Ventricular fibrillation
Ventricular tachycardia
Ventricular septal rupture is a post MI complication that can occur _ days post MI and causes _
Ventricular septal rupture is a post MI complication that can occur 3-7 days post MI and causes VSD
* A hole forms in the interventricular septum: causes shunting from LV –> RV
* This causes a holosystolic murmur
* Diagnosis with echo
* This can lead to heart failure due to an overload of pulmonary circulation
Ventricular free wall rupture is a post MI complication that can occur within _ days of an MI
Ventricular free wall rupture is a post MI complication that can occur within 14 days of an MI
* Blood fills the pericardial splace –> cardiogenic shock/ tamponade
* This can form a pseudoaneurysm if the thrombus forms to plug the rupture
Describe the most common acute findings/ complication after an MI
Pericarditis involves inflammation extending from the injured myocardium to the pericardium
* Patients experience sharp, pleuritic pain, fever, pericardial friction rub on auscultation
* We treat with aspirin and avoid anticoagulants
- QRS duration is prolonged beyond normal (.10 seconds)
- The normal Q wave in lead V5 or V6 that represents septal depolarization is absent
- There is no secondary R’ wave in VI as occurs in RBBE
Several other ECG changes that may occur in LBBB are seen in this ECG although they are not essential to make the diagnosis. The QRS complexes in leads facing the left ventricle (I, aVL and V6) show an M shaped pattern and there are secondary changes in the ST segments which are depressed and accompanied by T wave inversion. The initial R waves that are normally seen in the right sided precordial leads are absent in this record and the complexes in these leads are changes in these leads – the ST segments are elevated and the T waves are tall. As explained elsewhere these changes should not be interpreted to indicate ischaemia in the presence of LBBB
Describe what to look for in a left bundle branch block on ECG
- Prolonged QRS (more than 3 small boxes)
- rS or QS wave in V1
- Broad and notched/slurred R wave in lead I and V6
_ is a sudden increase in the tempo or severity of anginal episodes that occur at less exertion or at rest
Unstable angina is a sudden increase in the tempo or severity of anginal episodes that occur at less exertion or at rest
* Result of rupture of unstable atherosclerotic plaque with subsequent platlet aggregation and thrombosis
* Can progress to NSTEMI
Metabolic factors that contribute to vascular tone:
Metabolic factors that contribute to vascular tone:
* Acidosis –> vasodilation
* Hypoxia –> vasodilation
* Citrate –> vasodilation
* Adenosine –> vasodilation
Endothelial factors that contribute to vascular tone:
Endothelial factors that contribute to vascular tone:
* Nitric oxide –> vasodilation
* Endothelin-1 –> vasoconstriction
The humoral factors that contribute to vascular tone:
The humoral factors that contribute to vascular tone:
* Angiotensin II –> vasoconstriction
* Prostaglandins –> vasodilation
The neural factors that contribute to vascular tone:
The neural factors that contribute to vascular tone:
* alpha1, alpha2 –> vasoconstriction
* beta2 –> vasodilation
* serotonin –> vasodilation
* acetylcholine –> vasodilation
The most important factors for determining vascular tone and vascular resistance are _ and _
The most important factors for determining vascular tone and vascular resistance are metabolic molecules and nitric oxide (from the endothelial cells)
The three major determinants of myocardial oxygen demand are _ , _ , and _
The three major determinants of myocardial oxygen demand are heart rate , wall tension , and contractility
* These are all proportional to oxygen demand
Define wall stress
Wall stress = pressure * radius / 2 * wall thickness
Chronic stable angina is mostly a (supply/ demand) problem
Chronic stable angina is mostly a demand problem
* Treatment is mostly directed at reducing demand
Atherosclerosis causes a (supply/ demand) problem
Atherosclerosis causes a supply problem
