8/10- Acute Coronary Syndromes at the Bedside Flashcards
(36 cards)
- 62 yo man reports 6 mo of chest discomfort on fast walking
- Sx occur every time he walks 500 feet and beyond, are associated with SOB and are relieved after few min of rest.
What is your most likely clinical diagnosis?
A. Unstable angina
B. Acute coronary syndrome
C. Chronic stable angina
D. Prinztmetal’s angina
E. Pericarditis
F. Aortic dissection
G. Pulmonary embolism
What is your most likely clinical diagnosis?
A. Unstable angina
B. Acute coronary syndrome
C. Chronic stable angina
D. Prinztmetal’s angina
E. Pericarditis
F. Aortic dissection
G. Pulmonary embolism
- 30 yo woman reports sudden onset of sharp chest pain, increasing with deep inspiration and lying in the supine position, and relieved by sitting up
What is your most likely clinical diagnosis?
A. Unstable angina
B. Acute coronary syndrome
C. Chronic stable angina
D. Prinztmetal’s angina
E. Pericarditis
F. Aortic dissection
G. Pulmonary embolism
What is your most likely clinical diagnosis?
A. Unstable angina
B. Acute coronary syndrome
C. Chronic stable angina
D. Prinztmetal’s angina
E. Pericarditis
F. Aortic dissection
G. Pulmonary embolism
- This lady is also hypoxemic and tachycardic (not told)
- Pain is sharp (like pulmonary embolism pain) but pain is positional (quite diagnostic for pericarditis)
What are included under “acute coronary syndromes??
Acute Coronary Syndromes:
- Unstable angina
- Myocardial infarction
A pt with stable angina is also described as having what?
Stable CAD (coronary artery disease)
Atherosclerosis causes what main disease?
Coronary heart disease (CHD)
Coronary heart disease may manifest in what 2 main ways?
Categories within these?
Acute coronary syndromes
- Non ST elevation acute coronary syndromes (unstable angina or non-ST elevation MI)
- ST elevation MI
- Sudden cardiac death
Chronic stable angina
What is the pathophysiology of chronic stable angina?
- Stable plaque causing fixed obstruction and exertional symptoms of MI
- Usually when the plaque reaches 70% diameter stenosis in the epicardial coronary artery (typically seen in 4th-6th decades of life)
What is the clinical presentation of chronic stable angina?
Exertional chest discomfort (angina) reproducible at a constant level of effort and of unchanged pattern and severity
What is the overall process of atherosclerosis (leading to chronic stable angina)?
Endothelial injury
- 0% diameter stenosis
- Infancy/childhood-1st decade
Fatty-Streak formation
- 10% diameter stenosis
- 1st-2nd decade
Well developed atherosclerotic plaque
- 70% diameter stenosis
- 4th-5th-6th decade
Why does chronic stable angina correlate with __% diameter stenosis?
When coronary narrowing reaches 70% diameter stenosis, there is no more coronary flow reserve
- The arterioles (in microvasculature) are maximally dilated to increase coronary blood flow maximally at rest (400%) and cannot afford further vasodilation to increase myocardial oxygen supply when needed during exertion (i.e. already working maximal capacity at rest)
- Because of the inability to further increase CBF (b/c coronary flow reserve is abolished) at 70% stenosis, this causes ISCHEMIA (and its clinical manifestations: angina) secondary to IMBALANCE in myocardial O2 demand-supply DURING exertion
With chronic stable angina, what are the symptoms/their pathophysiology that result upon exertion?
(Lack of coronary flow reserve at 70% diameter stenosis causes):
- IMBALANCE in myocardial O2 Demand-Supply during exertion
- ISCHEMIA (secondary to above imbalance) with clinical manifestation of angina
In what ways (list) can chronic stable angina be treated?
- Anti-platelet medication (e.g. aspirin, a thromboxane A inhibitor)
- Anti-ischemic/anti-anginal medications
- Coronary angiography (cardiac catheterization)
- Revascularization
What anti-ischemic/anti-anginal meds can be used to treat chronic stable angina? Effect?
Nitrates + beta blockers (or Ca blockers) to decrease myocadial O2 demand
How/why is coronary angiography (cardiac catheterization) used to treat chronic stable angina?
- To confirm the diagnosis of Chronic Stable Angina (by visualizing the fixed severe but stable coronary narrowing)
- To dictate Revascularization strategy
How is revascularization used to treat chronic stable angina?
Either:
- PCI (percutaneous coronary intervention) with balloon angioplasty and/or stenting (usually for 1 or 2 vessel CHD technically amenable to PCI)
OR
- CABG (coronary artery bypass graft surgery) (usually of 3 vessel CHD, 2-vessel CHD with decreased EF, 2 vessel CHD with proximal LAD, left main CHD)
Acute Coronary Syndromes can be broken down how?
Non-ST Elevation Acute Coronary Syndromes (NE-ACS)
- Unstable Angina
- Non ST-Elevation MI (NSTEMI)
ST Elevation MI (STEMI)
Sudden cardiac death
What is the pathophysiology behind acute coronary syndromes?
Vulnerable plaque (or unstable) that ruptures or erodes -> acute thrombus (clot) formation
- ACS develops when vulnerable or high-risk plaque undergoes disruption of the fibrous cap
- Disruption of the plaque is the stimulus for thrombogenesis
- Sometimes, thrombus resorption may be followed by collagen accumulation and smooth muscle cell growth
- Following disruption of a vulnerable or high-risk plaque, pts experience ischemic discomfort resulting from a reduction of flow through the affected epicardial coronary artery
The burden of Acute Coronary Syndromes:
- __ killer in western world
- __ million arrest suddenly
- __ million suffer heart attacks
- __ million are hospitalized with acute chest pain
- __ million suffer angina
The burden of Acute Coronary Syndromes:
- No. 1 killer in western world
- 1/2 million arrest suddenly
- 1 million suffer heart attacks
- 5 million are hospitalized with acute chest pain
- 7 million suffer angina
How can unstable angina be subdivided?
- Rest angina
- New onset angina
- Increasing angina
What may happen if unstable angina is not treated?
Unstable angina can evolve into acute MI if not treated promptly and if ischemia (2ndary to acute coronary narrowing from plaque rupture/erosion and superimposed thrombus) persists > 15-20 minutes (time needed for myocardial necrosis to start occurring)
Unlike unstable angina, how is acute MI characterized?
Elevated cardiac biomarkers of myonecrosis (such as troponin and CK-MB)
Why is it important to differentiated between both acute coronary syndromes?
1. Slightly different pathophysiology (non-occlusive vs. occlusive thrombus)
2. Different initial ECG presentation (sub-endocardial ischemia: ST depression, T wave inversion vs. acute MI pattern: ST elevation pattern)
3. Need different initial treatments (early invasive strategy vs. acute reperfusion for STEMI; both on top of medical treatment)
Pathophysiology and characteristics of NSE-ACS? Treatment?
- Usually has acute sub-occlusive thrombotic occlusion of the coronary artery (70-99% occlusion)
- Typically manifests as sub-endocardial ischemia [ST depression, T wave inversion], and usually resulting in no Q wave formation [therefore, called non-Q wave MI])
- INITIAL TREATMENT: early invasive strategy (early cath, and revascularization) on top of medical treatment.
Pathophysiology and characteristics of STEMI? Treatment?
- Usually has acute complete thrombotic occlusion of the coronary artery (usually acute 100% obstruction)
- Typically manifests as initial ST-elevation on ECG [acute myocardial injury pattern], and usually resulting in Q waves formation [eventually after few hours of persistent occlusion; thus, called also Q-wave MI]
- INITIAL TREATMENT: acute reperfusion therapy (immediate cath and mechanical recanalization with PCI , or Fibrinolytic therapy [clot buster]) on top of medical treatment.
