Acute Coronary Syndromes Flashcards
90% result from plaque rupture which leads to thrombus formation
Acute Coronary Syndromes
Plaque rupture leads to exposure of
Thrombogenic CT
Begins within seconds and we see platelet plug formation as platelets adhere to subendothelial collagen
Primary Hemostasis
Exposure to tissue factor citrates the clotting cascade, ultimately activating thrombin which forms a fibrin clot
Secondary hemostasis
Platelet plug formation
Primary hemostasis
Clotting cascade
Secondary Hemostasis
Irreversibly binds thrombin and other factors and it activity is modulated by heparin sulfate
Antithrombin
Inactivate factors Va and VIIIa which are important in accelerating the coagulation cascade
Protein C and S and thrombomodulin
Negative feedback inhibitor for the extrinsic coagulation pathway
Tissue Factor Pathway Inhibitor (TFPI)
Released by endothelial cells in response to thrombus formation and it converts plasminogen to plasmin
Tissue Plasminogen Activator (tPA)
Degrades fibrin clots
Plasmin
Inhibits cyclic AMP formation, thereby decreasing platelet activation and aggregation
Prostacyclin
Nitric Oxide inhibits
Platelet activation
Decreases the vasodilatory and antithrombic properties
Coronary thrombosis
Small plaque ruptures with low thrombus burden may get incorporated into the vessel wall and increase
Stenosis
Involves the full thickness of the myocardium as a result of prolonged, completely occluded vessels (STEMI)
-Endocardium to epicardium
Transmural Infarction
Only a partial thickness infarction and typically the subendocardium is the most susceptible
Subendocardial infarction
In a myocardial infarction, a more proximal occlusion results in a
Greater territory of infarction
A rapid shift from aerobic or anaerobic metabolism, leading to the accumulation of lactic acid and thus lower pH
Myocardial Infarction
During an infarct, we see decreased myocardial function in as early as
2 Minutes
In an infarction, we see irreversible cell injury after
20 Minutes
We can see myocardial edema due to increased vascular permeability and an interstitial oncotic pressure rise from leaked proteins in
4-12 hours
Interstitial edema separating myocardial cells give the histologic characteristic of an MI which is
Wavy Myofibers
In an MI, sarcomeres are contracted and consolidated, seen at infarct borders. This histologic characteristic is called
Contraction bands
-Seen at infarct borders
In24-48 hours post infarction, histologically we can see
Inflammatory cells and coagulation necrosis
Start at about 4 hours after infarct
Inflammatory Cells
Charcterized by pyknotic or shrinking nuclei and bland eosinophilia cytoplasm
-Seen 18-24 hours
Coagulation Necrosis
5 days following an MI, neutrophils are replaced by macrophages that remove necrotic connective tissue and dead cells. This is known as
Yellow Softening
This causes thinning and dilation of the infarcted zone, which can result in
Myocardial wall rupture
We see granulation tissue with neovascularization and mild chronic inflammation at
10 days post MI
At 10 days post MI, we see
Lymphocytes and Fibroblasts
1-2 months following an MI, we see dense
Dense fibrosis
Abnormal wall motion of the affected area
Systolic Dysfunction
We see a rise in LVEDP due to both systolic and diastolic dysfunction in an
MI
Chronically ischemic tissue due to severe stenosis that then becomes an MI
Ischemic preconditioning
Patients with recent angina that precedes an MI have less
Morbidity and mortality
The infarcted tissue becomes thin and dilated, so infarct expansion without further myocyte death can
Occur
Non-infarcted tissue can dilate to compensate for cardiac output. This can also lead to continued
LV enlargement and HF
ACE inhibitors and ARBs may help to decrease
Ventricular remodeling
Left-sided substernal pain that radiates to jaw or arm. May be more intense than angina pain or last longer
Acute MI
The physical exam for a patient with ACS is mainly just symptoms of
Congestive Heart Failure
Shows T-wave inversion or ST depression
Unstable angina
Shows T-wave inversion or ST depression
NSTEMI
Shows ST segment elevation
STEMI
A proximal RCA occlusion will show up in EKG leads involving the
RV branches
We can perform a right sides EKG to check for
RV infarct
An isolated posterior infarct typically involves the distal
-Supplies the posterior part of the LV located just beneath the AV sulcus
Left Circumflex Artery
Shows tall R waves in V1-V3, with ST depressions and upright T waves
Posterior infarct
To catch a posterior infarct, we can place
Posterior leads
Most often, a posterior infarct will be combined with an
Inferior (RCA) or lateral (proximal LCx) infarct
Shows ST elevation in inferior leads with tall R waves and ST depression seen in anterior leads
Inferno-posterior Infarct
An inferno-posterior infarct is confirmed with
Posterior leads
Protein that controls interaction between actin and myosin
Troponin
Very specific to cardiac tissue
Troponin I and Troponin T
Is not specific to cardiac tissue
Troponin C
Begins to rise 3-4 hours after symptoms and peak at 18-36 hours
Cardiac Troponin
How long after an MI are cardiac troponins detectable for?
10 days
Begins to rise 3-8 hours after symptoms and returns to normal 48-72 hours
CK-MB
Used for anti-ischemic therapy because they reduce myocardial oxygen demand
Beta-blockers
What are three things used for anti-ischemic therapy?
Beta-blockers, Nitrates, and Ca2+ channel blockers
Re-occlusion of the artery. More common in patients treated with tPA than PCI but can also happen with PCI
Recurrent Ischemia
Severely decreased cardiac output which is a vicious cycle as hypotension leads to worsening of coronary perfusion
Cardiogenic Shock
Leads to profound hypotension and right sided heart failure
Right Ventricular Infarct
Acute inflammation post MI can cause acute
-Pain, fevers, and a friction rub
Pericarditis
Delayed pericarditis after an MI due to an immune process against damaged myocardial tissue
Dresser syndrome
We may see pericardial effusion and elevated inflammatory markers with
Dressler Syndrome
Can form in the area of blood stasis due to the MI
Thromboembolism
