ACS Flashcards
Absolute contraindications for nitrate use
Hypotension
Use of sildenafil or PDE5 inhibitors within the previous 24-48 hours
Oral BB target heart rate
50-60 bpm
Antiplatelet in TIMI trial
Prasugrel
increased major bleeding compared to clopidogrel
Antiplatelet in PLATO trial
Ticagrelor
May be used in NSTE and UA patients whose symptoms are not relieved adequately by nitrates or BBs, or unable to tolerate these agents
CCBs
May be given for symptoms not relieved after 3 serial SL NTG tablets
Morphine
Coronary plaques prone to disruption
Rich lipid core and thin fibrous cap
Activated in the coagulation cascade converting prothrombin to thrombin which converts fibrinogen to fibrin
Factor VII
Factor X
MC presenting complaint of patients with STEMI
Pain (deep and visceral)
Painless STEMI is greater
Patients with DM, increases with age
PE manifestations of anterior MI
Usually sympathetic
PE manifestations of inferior MI
Usually Parasympathetic
Temporal stages of STEMI
Acute: first few hours-7days
Healing: 7-28 days
Healed: >29 days
Cardiac troponins remain elevated after STEMI
7-10 days after STEMI
Two serious complications of STEMI
VSD
Mitral Regurgitation
(by Doppler echo)
Prognosis relates to 2 general classes of complications of STEMI
Electrical complications
Mechanical compilations
Cause of most out-of-hospital deaths from STEMI
VFib
Classification of Myocardial Infarction Type I
Spontaneous MI
Classification of Myocardial Infarction Type II
MI 2 to an Ischemic Imbalance
Classification of Myocardial Infarction Type III
MI resulting in death when biomarker values are unavailable
Classification of Myocardial Infarction Type IVa
MI related to PCI
Classification of Myocardial Infarction Type IVb
MI related to stent thrombosis
Classification of Myocardial Infarction Type V
MI related to CABG
Time to initiate fibrinolytic therapy
Door-to-Needle (D-N) time
= 30 mins
Time to move the patient to cath lab for PCI
Door-to-Balloon (D-B)
= 60 mins
Goal of initiating PCI
Within 120 minutes of first medical contact
Role of buccal absorption of aspirin in STEMI
Rapid inhibition of cyclooxygenase1 in platelets followed by a reduction in thromboxane A2 levels
Role of SL NTG
Capable of decreasing o2 demand (lowering preload) and increasing o2 supply (dilating infarcted or collateral vessels)
AE of morphine
May reduce cardiac output and arterial pressure
Vagotonic effect
STEMI candidate for reperfusion therapy
ST elevation of at least
2mm: two contiguous precordial leads
1mm: two adjacent limb leads
Meds avoided in STEMI
Glucocorticoids and NSAID(except asprin)
may result in a larger infarct scar
Principal goal of fibrinolysis
prompt restoration of full coronary arterial patency
Role of fibrinolytics
Promoting conversion of plasminogen to PLASMIN, which subsequently lyses fibrin thrombi
Absolute contraindications to use of fibrinolytic agents
Hx of CV hemorrhage at ANY TIME
Non hemorrhagic stroke or other cerebrovascular event within 1 YEAR
Marked hypertension (>180 and/or >110mmHg) anytime of the attack
Suspicion of aortic dissection
Active internal bleeding (EXCLUDING menses)
Relative contraindications to fibrinolytic therapy
Concurrent use of anticoagulants (INR >2)
Recent (<2weeks) invasive or surgical procedure or prolonged (>10min) CP resuscitation
Bleeding diathesis
Pregnancy
Hemorrhagic ophthalmic condition
Active PUD
Hx of severe HPN currently controlled
Allergic reaction to streptokinase
Avoided if had received the preceding 5 days to 2 years
Most frequent and potentially the most serious complication of fibrinolysis
Hemorrhage
Cardiac carh and coronary angio should be carried out after fibrinloysis
Failed reperfusion (persistent chest pain and ST elevation >90mins)
Coronary artery reocclusion
Rationale for dangling the feet over the side of bed or sitting in a chair within the first 24hours
Reduction of pulmonary capillary wedge pressure
Primary goal of treatment with antiplatelet and anticoagulants in conjunction with reperfusion strategies
Maintain patency of infarct-related artery
Benefits of ACEI in STEMI
Reduction in ventricular remodeling after infarction with a subsequent reduction in the risk of CHF
LV undergoes series of changes in shape, size and thickness in both infarcted and non infarcted segments
Ventricular remodeling
Primary cause of in-hospital death from STEMI
Pump failure
MC clinical SSx of pump failure
Pulmonary rales
S3 and S4 gallop
Prescribed for EF<40% +|- heart failure
ACEI or ARBS
Agent effective in abolishing ventricular ectopic activity in patients with STEMI and in the prevention of VFib
Beta Blockers
Electrolyte imbalances which are risk factors for Vfib
Hypokalemia (goal: 4.5)
Hypomagnesemia (goal: 2)
Sustained Vtach and hemodynamically stable
IV amiodarone or procainamide
Ventricular rhythm with a rate of 60-100bpm often occuring transiently during fibrinolytic therapy at the time of reperfusion
Accelerated Idioventricular Rhythm
benign; do not require therapy
MC supraventrecticular arrhythmia
Sinus tachycardia
ICD after STEMI indications
At least 40 days after STEMI
No spontaneous VT or VF post-STEMI
FC I: LVEF <30-35%
FC II-III: LVEF <30-40%
NO ICD FOR LVEF >40%
Treatment of choice for supraventricular arrhythmias if heart failure is present
Digoxin
Treatment for persistent bradycardia despite atropine
Electrical pacing
Other indications:
Mobitz II second-degree AV block
Third degree heart block
Bilateral bundle branch block
Can cause tamponade in the presence of acute pericarditis
Anticoagulants
After recovery from STEMI, recommended for stable patients to prevent reinfarction
Submaximal exercise stress test to detect residual ischemia and ventricular ectopy
Maximal (symptom-limited) exercise stress test 4-6 weeks after