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pharmacotherapy 1 > acute coronary syndrome > Flashcards

acute coronary syndrome Flashcards

1
Q

pathophysiology of ACS

A

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

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2
Q

what is ACS

A

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.

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3
Q

Different types of ACS

A
  1. ST-segment elevation myocardial infarction (STEMI).
  2. Non-ST-segment elevation acute coronary syndrome (NSTE-ACS).
    3.Unstable angina.
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4
Q

STEMI

A

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.

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5
Q

NSTE-ACS

A

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.

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6
Q

what are the subjective symptoms of STEMI

A
  • worsening of chest pain and pressure
  • catagorize as viselike
  • suffocating, squeezing, aching and gripping
  • radiate to the arms, neck, or jaw
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7
Q

objective finding of STEMI

A
  • ECG typically shows ST-segment elevation >1mm in two or more contiguous leads.
  • Positive biomarkers ( troponin )
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8
Q

STEMI extent of injury

A

cardiac necrosis: complete blockage of a coronary artery

most severe type of ACS

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9
Q

symtoms of NSTE-ACS including both unstable angina and NSTEMI

A
  1. chest pain occur at rest or minimal exertion
  2. start in retrosternal can radiate down to arm neck or jaw
  3. diaphorisis, dyspnea, nausea, abdominal pain or synope
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10
Q

difference between findings and extent of injury of unstable angina and NSTEMI

A
  • 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
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11
Q

Clinical Assessment and Initial Evaluation of ACS

A
  1. 12-lead ECG within 10 minutes of presentation
  2. Serial ECGs, If the initial ECG is nondiagnostic
  3. Serial cardiac troponins: at presentation and again 3-6 hours after symptom onset
  4. TIMI risk score predicting 30-day and 1-year mortality in patients with NSTE-ACS.
  5. SCr and CrCl
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12
Q

seven indicators that are used to calculate the TIMI score?

A
  1. age 65 or older.
  2. Three or more risk factors for CAD.
  3. Prior coronary stenosis 50% or greater.
  4. ST deviation on ECG.
  5. Two or more** anginal events** in the previous 24 hours.
  6. Aspirin use in previous 7 days.
  7. Elevated cardiac biomarkers.
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13
Q

TIMI Risk Stratification “STEMI” 3 points for?

A
  1. Age ≥ 75 years
  2. SBP < 100 mm Hg

age 75 or more
SBP less than 100mm hg

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14
Q

TIMI Risk Stratification “STEMI” 2 points for?

A
  1. Age 65–75 years
  2. Heart rate > 100 BPM
  3. Killip class II–IV

Higher Killip classes (II-IV) indicate worse heart function and carry higher risk.

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15
Q

TIMI Risk Stratification “STEMI” 1 points for?

A
  1. 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
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16
Q

(TIMI)
High-Risk , medium and low risk?

A
  • high: TIMI Risk Score > 4 points
  • medium: TIMI Risk Score 3 points
  • low: TIMI Risk Score 0–2 points
17
Q

ElectroCardioGram “ECG”

A
  • 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

18
Q

immediate therapeutic objectives in both STEMI and NSTEMI?

A
  1. Re-perfusion: Restore blood flow to the infarct-related artery
  2. Prevent infarct expansion (if MI) or prevent MI (if UA)
  3. Alleviate symptoms
  4. 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.

19
Q

primary and secondary goals in STEMI managment

A

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).

20
Q

NSTE-ACS goal and treament

A

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.

21
Q

Primary Percutaneous coronary intervention (PCI) vs fibrinolytic therapy

A

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.

22
Q

when Fibrinolytic Therapy is given?

A
  1. Indicated for patients with a STEMI in whom PCI cannot be done within 120 mins, Not recommended in patients with NSTE-ACS
  2. time frame: benefit only when given between 12 and 24 hours.
  3. door-to-needle time of less than 30 minute hospital arrival for optimal effectiveness.
23
Q

Fibrinolytic Therapy drugs?

A
  1. Fibrin-specific agent (Alteplase, Reteplase & Tenecteplase)
  2. non-fibrin-specific agent (. Streptokinase)

**fibrin speciifc agent preffered over non fibrin open greater percentage of artery
**

24
Q

Ischemia-guided Therapy

A

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.

25
Q

initial anti-ischemic and analgesic medications

A

**MONA-B.
1. **morphine
1. oxygen
1. nitroglycerine
1. asprin
1. betablocker

26
Q

aspirin recommendation in ACS initial and mentaince doe?

A
  1. first-line therapy in ACS regardless of the type (STEMI or NSTEMI).

initial dose: (Avoid enteric-coated aspirin)
1. 162-325mg is recommended for patients who haven’t been taking aspirin regularly (naive)
2. for PCI (81-325mg) depending on their pre-existing aspirin regimen.

Maintenance therapy:
1. given indefinitely at a preferred dose of 81mg after ACS with or without PCI.
2. lower doses are generally preferred for long-term use. below 160mg due to higher risk of bleeding

27
Q

dual antiplatet recommendation

A

aspirin+p2y12 inhibtor

ischemia-guided strategy: aspirin+Clopidogrel and ticagrelor
NST-ACS: asprin + Clopidogrel, prasugurl and ticagrelor
STEMI PCI: asprin + Clopidogrel, prasugurl and ticagrelor
STEMI Fibrinolytics: Clopidogrel

The efficacy of ticagrelor is decreased in patients treated with higher doses of aspirin (greater than 300 mg daily) compared with lower doses (less than 100 mg daily).

28
Q

Anticoagulant Recommendations for fibronolytic therapy

A
  • Patients undergoing reperfusion with fibrinolytic should receive anticoagulant therapy after fibrinolysis:
  • At least 48 hours with intravenous UFH
  • intravenous/subcutaneous enoxaparin or fondaparinux during hospitalization, up to 8 days.

Anticoagulant Recommendations for pci: 1. ufh and bivalirudin

29
Q

long term managment drugs

A

DAPT
betablocker
ace
statin

ABAS= ASPRIN+ BETABLOCKER+ ACE+STATIN

30
Q

Long term managment DAPT:

A
  • duration:Given at least 12 months after ACS.
  • Shorter-duration DAPT: for patients with stable ischemic heart disease who have undergone PCI with elective stent placement
    benefit: reduces mortality after ACS, regardless of whether the patient received stenting.

short duration: high bleeding risk and lower ischemic risk
long duration:higher ischemic risk and a lower bleeding risk

31
Q

Long term managment B-BLOCKER

A
  • Indicated for all patients unless contraindicated.
  • initiated within the first day,
  • Continue for at least 3 years (when EF is greater than 40%).
  • Continue indefinitely in patients with an EF less than 40%.
  • If moderate or severe LV failure, initiate carvedilol, bisoprolol, or metoprolol succinate with gradual titration.
32
Q

Long term managment ace inhibtor

A

ACE inhibitors should be initiated and continued indefinitely for all patients with an LVEF of 40% or less and in those with hypertension, diabetes mellitus, or stable chronic kidney disease unless contraindicated.
ACE inhibitors may be acceptable in all other patients with cardiac or other vascular disease.
Angiotensin receptor blockers (ARBs) are indicated if the patient has contraindications to or is intolerant of ACE inhibitors.
Contraindications include hypotension, pregnancy, and bilateral renal artery stenosis.

33
Q

Long term managment Lipid-Lowering Therapies

A

High-intensity statins are indicated in all patients after ACS without contraindication and within the first 24 hours.

In high-risk patients achieving a less-than-expected response to statins or in those who are completely statin intolerant, non-statin therapy may be considered for CV benefit.

either ezetimibe or a PCSK9 inhibitor “Alirocumab and Evolocumab” can be considered in combination with statin therapy in very high-risk patients.

34
Q

drugs to use for pain control

A

Pain should be treated with acetaminophen, nonacetylated salicylates, tramadol, or narcotics at the lowest dose to control symptoms.
It is reasonable to use nonselective NSAIDs, such as Naproxen, if initial therapy is insufficient.

Monitor regularly for sustained hypertension, edema, worsening renal function, or GI bleeding.
If these occur, consider dose reduction or discontinuation.

35
Q

other factors and drugs to consider in pain control stratgies

A

NSAIDs and select cyclooxygenase-2 inhibitors should be discontinued at the time of presentation because they have been associated with an increased risk of major adverse cardiac events.

Antiemetic + Stool Softener should be administered to minimize the undesirable effects of morphine and also because straining has negative impact on the CVS.

Before discharge, the patient’s musculoskeletal discomfort should be addressed, and a stepped-care approach should be used to select therapy.

36
Q

Evaluation Of Therapeutic Outcomes

A

Relief of ischemic discomfort
Return of ECG changes to normal / baseline
Absence or resolution of HF signs and symptoms.

In general, the most common adverse reactions from ACS therapies include hypotension and bleeding.

37
Q

Fibrinolytic Therapy why not recommended in nste-acs

A

Not recommended in patients with NSTE-ACS as thrombi in these patients are not typically fibrin rich, so they are less responsive to therapy.

38
Q

Best timing is 2-6 hours after the clot forms. Maximum time is 12 hrs–Why

A

This is because older clots (>12hrs old) are resistant to lysis & also because cardiac tissue necrosis is already established
In MI, intracoronary delivery within 2-6 hours & IV administration after 6 hours (rapid, inexpensive and lower risk)

pharmacotherapy 1 (7 decks)

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