acute coronary syndrome Flashcards
pathophysiology of ACS
Atherogenic plaque rupture is the underlying pathophysiology for ACS, causing several prothrombotic substances to be released, which results in platelet activation and aggregation and eventual thrombus formation leading to partial or total occlusion of the coronary artery.
1- atherogenic plaque rupture
2- prothromic substance release
3- platelte activation and aggregation
4- thrombus formation and occulsion
what is ACS
Acute coronary syndrome (ACS): is a spectrum of conditions compatible with acute myocardial ischemia or infarction caused by an abrupt reduction in coronary blood flow.
Different types of ACS
- ST-segment elevation myocardial infarction (STEMI).
- Non-ST-segment elevation acute coronary syndrome (NSTE-ACS).
3.Unstable angina.
STEMI
Defined by characteristic symptoms of myocardial ischemia in association with persistent ST-segment elevation on ECG with positive troponins
* STEMI is an indication for immediate coronary angiography to determine whether reperfusion can be done.
NSTE-ACS
Suggested by the absence of persistent ST-segment elevation on ECG
NSTE-ACS can be divided into unstable angina (UA) and NSTEMI according to whether cardiac biomarkers of necrosis are present.
UA and NSTEMI are closely related conditions whose pathogenesis and clinical presentation are similar but vary in risk and severity.
what are the subjective symptoms of STEMI
- worsening of chest pain and pressure
- catagorize as viselike
- suffocating, squeezing, aching and gripping
- radiate to the arms, neck, or jaw
objective finding of STEMI
- ECG typically shows ST-segment elevation >1mm in two or more contiguous leads.
- Positive biomarkers ( troponin )
STEMI extent of injury
cardiac necrosis: complete blockage of a coronary artery
most severe type of ACS
symtoms of NSTE-ACS including both unstable angina and NSTEMI
- chest pain occur at rest or minimal exertion
- start in retrosternal can radiate down to arm neck or jaw
- diaphorisis, dyspnea, nausea, abdominal pain or synope
difference between findings and extent of injury of unstable angina and NSTEMI
- both have st-segment depression T wave inversion or non specific ecg change and both are partial occulsion of coronary artery
- UA: no positive biomarker for cardiac necrosis and no myocardiac injury
- NStEMI: have positive biomarker and myocardiac injury
Clinical Assessment and Initial Evaluation of ACS
- 12-lead ECG within 10 minutes of presentation
- Serial ECGs, If the initial ECG is nondiagnostic
- Serial cardiac troponins: at presentation and again 3-6 hours after symptom onset
- TIMI risk score predicting 30-day and 1-year mortality in patients with NSTE-ACS.
- SCr and CrCl
seven indicators that are used to calculate the TIMI score?
- age 65 or older.
- Three or more risk factors for CAD.
- Prior coronary stenosis 50% or greater.
- ST deviation on ECG.
- Two or more** anginal events** in the previous 24 hours.
- Aspirin use in previous 7 days.
- Elevated cardiac biomarkers.
TIMI Risk Stratification “STEMI” 3 points for?
- Age ≥ 75 years
- SBP < 100 mm Hg
age 75 or more
SBP less than 100mm hg
TIMI Risk Stratification “STEMI” 2 points for?
- Age 65–75 years
- Heart rate > 100 BPM
- Killip class II–IV
Higher Killip classes (II-IV) indicate worse heart function and carry higher risk.
TIMI Risk Stratification “STEMI” 1 points for?
- Weight < 67 kg
2.History of HTN, DM, or angina
3.Time to reperfusion > 4 hs
4.Anterior ST segment elevation
or left bundle branch block
(TIMI)
High-Risk , medium and low risk?
- high: TIMI Risk Score > 4 points
- medium: TIMI Risk Score 3 points
- low: TIMI Risk Score 0–2 points
ElectroCardioGram “ECG”
- ECG / EKG is the recording of the electrical current generated by the heart.
- **electrodes: **detect electrical impulse during depolarization and repolarization.
The graphic drawing of this electrical activity is called an electrocardiogram (ECG or EKG).
12-lead.ECG is standard type
U wave (seen in patients with hypokalemia).
Each of the waveforms represents different aspects of cardiac depolarization and repolarization.
The ECG is composed of several waveforms, including the P wave, QRS complex, T wave, ST segment, the PR interval
immediate therapeutic objectives in both STEMI and NSTEMI?
- Re-perfusion: Restore blood flow to the infarct-related artery
- Prevent infarct expansion (if MI) or prevent MI (if UA)
- Alleviate symptoms
- Prevent death.
achieved primarily by restoring coronary blood flow and lowering myocardial oxygen demand.
Time is crucial!!! The faster the occluded artery is opened, the more muscle is saved.
primary and secondary goals in STEMI managment
primary goals
1. restore the patency of the infarct-related artery
2. Minimize infarct size
secondary goals:
* preventing complications :Arrhythmias, Death.
* Controlling chest pain and associated symptoms.
Requires urgent revascularization either interventionally or with drug therapy (i.e., fibrinolysis).
NSTE-ACS goal and treament
1.prevent total occlusion of the related artery
2.control chest pain and associated symptoms.
treatment: (treated on the basis of risk (TIMI, GRACE)
1. early invasive strategy: diagnostic angiography-> do revascularization
2. ischemia-guided strategy.
Routine invasive therapy superior to an ischemia-guided strategy (results in lower rates of recurrent UA, recurrent hospitalization, MI, and death) in high-risk patients.
Primary Percutaneous coronary intervention (PCI) vs fibrinolytic therapy
pci ( within 90 mins) is preffered over fibrinolyitc
1. Higher success rate in opening arteries (>90% vs. <60% with fibrinolytics).
2. Lower risk of intracranial hemorrhage and major bleeding compared to fibrinolytics.
3. If PCI cannot be done within 120 minutes, lytic administration includes a door-to-needle time of 30 minutes.
when Fibrinolytic Therapy is given?
- Indicated for patients with a STEMI in whom PCI cannot be done within 120 mins, Not recommended in patients with NSTE-ACS
- time frame: benefit only when given between 12 and 24 hours.
- door-to-needle time of less than 30 minute hospital arrival for optimal effectiveness.
Fibrinolytic Therapy drugs?
- Fibrin-specific agent (Alteplase, Reteplase & Tenecteplase)
- non-fibrin-specific agent (. Streptokinase)
**fibrin speciifc agent preffered over non fibrin open greater percentage of artery
**
Ischemia-guided Therapy
to avoid the routine early use of invasive procedures unless patients have refractory or recurrent ischemic symptoms or develop hemodynamic instability.
1 low-risk score (TIMI 0 or 1, GRACE less than 109)
1 low likelihood of ACS who are troponin negative(preferred for low-risk women)
1. Can be chosen according to clinician and patient preference.