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122 Cards in this Set

  • Front
  • Back
Acute Chest pain is defined as? (3)
1. recent onset < 24 hrs, which causes the patient to seek medical tx 2. MC location is the anterior thorax 3. sensation that is regarded as distressing to the patient
p. 361
Define Unstable Angina.
No elevation in biomarkers and no elevation in pathologic ST segment elevation on EKG
p. 361
Define NSTEMI.
NSTEMI: elevation in cardiac biomarkers, but the absence of pathologic changes on EKG.
p. 361
Define STEMI.
Elevation in both serum cardiac biomarkers as well as pathologic ST segment elevation evidence on EKG.
p. 361
How do indviduals usually describe their CP when perietal and when visceral.
MC individuals describe their somatic pains as sharp. Visceral pains are MC: "discomfort, heaviness, and or aching".
p. 361
Why is a patient asked, MC with a 1-10 pain scale, to grade their pain?
To monitor response to treatment.

p. 361
What is the classic description of angina pectoris?
retrosternal left anterior chest or epigastric discomfort described as "squeezing, crushing, tightening, or pressure like".
p. 361
those who c/o of "stabbing, positional, or pleuritic pains are those who have a REDUCED (not impossible) liklihood of ACS".
What is the increase likelihood risk in a patient with chest pain and complaints of the additional sxs: dyspnea, diaphoresis, nausea, vomiting?
Two fold increase risk.

p. 361
- Additionally, an increase probability that the chest pain that begins on the left and radiates to EITHER shoulder, arm, hand, or jaw. Typically, pain lasts 2-20 minutes. If the pain lasts fgor a "split second" or for 12-24 hrs straight, consider another cause.
T/F: there is an increased likelihood of chest pain being cardiac if the pain is in the Right Arm instead of the Left arm.
TRUE
4.7 +LR for right shoulder
4.1 +LR for both arms or shoulders
2.3 + LR for left shoulder
p. 362
Atypical cardiac chest pain is most common in what people?
1. Women
2. Non-white minorities
3. DM
4. elderly
5. Psychiatric Dz patients
6. AMS patients.
p. 362
What disorders that cause CP are more common in women than men? (3)
1. Vasospastic disorders
2. Microvascular disorders
3. MVP

p. 362
What group of people will often delay examination and treatment for CP because the pain is:
1. relieved with antacids
2. pain is unrelated to exercise
3. pain is not relieved with rest or nitro
4. palpitation sensation and not "chest pain"
5. fatigue is the chief concern*
Women

p. 362
*when I was in the ER, one of the physicians said as a pearl that the MC concern expressed for cardiac concerns in women was only fatigue
What are the associated cardiac sxs that are more commonly found in women?
1. Nausea
2. Vomiting
3. jaw pain
4. neck pain
5. back pain

p. 362
(diaphoresis is more commonly found in men)
What common illegal drug is MC associated with advanced atherosclerosis and AMI- and has limted association with cardiac risk factors or a patients age?
Cocaine

p. 362
What are:
1. > 40 y/o in age
2. male gender and females who are postmenopausal
3. HTN
4. Cigarette smoking
5. Hyperlipidemia
6. DM
7. Truncal obesity
8. fhx + for risk
9. sedentary lifestyle
Major risk factors for cardiac ischemia...

p. 362
What percent of individuals will commonly report with ACS and not have pain?
1/3 (33%)
MC: Women

p. 362
What group of MI patients have an increased mortality rate, more than twice that of other MI patients?
Atypical presenters...

- these individuals are less likely to receive anti-ischemic therapies and are therefore morelikely to suffer doubled risk mortality.
p. 363
T/F: Epigastric pain, or even upper abdominal pain relieved with antacids does not require further clinical examination.
False:
Always keep suspicion for ACS/Silent ischemia...remain vigilent, esp if > 50 y/o and + hx of CAD

p. 363
What are the following?
1. dyspnea at rest or exertion
2. shoulder arm or jaw discomfort
3. nausea
4. lightheadedness
5. generalized weakness
6. acute changes in mental status
7. diaphoresis
Angina Equivalent sxs...

p. 363
What is the increased risk of SCD (sudden cardiac death) in individuals with dyspnea alone, w/o chest pain?
4 fold increase

-p. 363
What are the following individuals, with regard to CP/ACS/Cardiac Disease:
- diabetes- secondary to sensory impairment
- advanced age
- psych illness
- AMS
High risk groups- for atypical presentations

p. 363
T/F: Palpitations are a common complaint of individuals, esp with benign PVC's and are therefore a common variant with little concern; unless > 3 on EKG.
False:
Palpitations can be a response to ischemia, or the cause of ischemic changes from an arrythmia. Therefore should always be concerned about c/o palpitations.
p. 363
- yet also ask about possible contributing factors: caffeine beverages, herbal medications, rx therapies, otc therapies, additional metabolic concerns and even consider electrolyte abnormalities: low potassium, low magnesium, etc. Also remember patient may have a personal or family hx...
T/F: Physiologically there are true differences in pain signal propagation and medication related to gender, age and race as well as permanent or transient metabolic influences.
True

p 363
T/F: People with acute ischemic cardiac events have a higher incidence of: abnormal heart sounds, diminshed S2, paradoxical split of the S2 and/or S3 or S4, due to changes in ventricular function or compliance.
True

p. 363
What percent of individuals with a confirmed MI have reproducible chest wall tenderness?
15%

p. 363
The sxs of a "massive PE" are MC what type in nature?
Visceral in nature and are therefore MC described as" heaviness and tightness in chest".
- Dyspnea, fever, cough and/or hemoptysis may also be present.
- can present with: CP, dyspnea, syncope, shock and/or hypoxia.
p. 363
What are some risk factors for aoritc dissection?
1. pregnancy
2. atherosclerosis
3. coarctation of the aorta
4. biscupid aoritc valves
5. aortic stenosis
6. marfan's syndrome
7. ehlers-danlos syndrome

p. 363
What MC sets in as midline substernal CP, that is often described as: "tearing, ripping, or searing and radiating to the interscapular areaof the back?
Aortic Dissection.

p. 364
- Additionally, the pain is most intense at the onset of sxs and then is felt below and above the diaphragm.
- often as the syndrome progresses, secondary sxs develop: stroke, AMI, or limb ischemia...these sxs may overshadow the initial event.
How is dx of simple spontaneous Pneumothorax (PTX) made?
Plain Chest radiograph

p. 364
Spontaneous PTX MC occurs in:
Smokers with COPD, sudden barometric pressure changes as well as idiopathic causes- bleb diseases

p. 364
Sudden, sharp lancinating, chest pain and dyspnea is most commonly associated with...
Spontaneous pneumopthorax

p. 364
Sudden sharp chest pain that will MC occur following an event of forceful vomiting.
Esophageal rupture (Boerhaaves syndrome)

- The patient will often appear toxic, be dyspneic, and diaphoretic.

p. 364
How is esophageal rupture confirmed?
Study with water soluble contrast

p. 364
What is the MOST important diagnostic finding in a patient who c/o substernal chest pain, with radiation to back, neck and shoulders. This patient c/o of the pain as worse when lying flat and with inspiration.
Friction rub with auscultation

p. 364- pericarditis.
What EKG findings are highly specific for pericarditis?
Diffuse ST segment elevation and T wave inversion. Additionally depression of the PR segment.

p. 364
What MC causes CP at rest and can also be associated with dizziness, hyperventilation, anxiety, depression, palpitations and fatigue- and is a valvular abnormality MC found in women.
MVP

p. 364
Best treated with Beta Blockers!!!
Another inflammatory process that causes sharp, pleuritic CP reproduced by light palpation over the xiphoid process?
Xiphodynia

p. 364
Short, lancinating chest discomfort that occurs in episodic bunches lasting 1-2 minutes near the cardiac apex associated with inspiration and poor posture and inactivity?
Texidor twinge or Precordial Catch Syndrome

p. 364
What is associated with reflux dz and is characterized by sudden on set of "dull, tight, or gripping substernal CP" which is MC precipitated by the consumption of hot or cold liquids or a large fluid bolus and often lasts for hours.
Esophageal Spasm

- This pain can sometimes be relieved with Nitro, but typically with a slight delay
p. 364
Postprandial, dull, boring pain in the mid-epigastric; very often even waking a patient from sleep.
Peptic Ulcer Disease

- this is different from duodenal ulcer- which is most commonly relieved by food.
p. 364
Hx of panic attacks and at least four the following:
1. palpitations
2. diaphoresis
3. choking
4. tremor
5. dyspnea
6. chest pain or discomfort
7. nausea
8. dizziness
9. derealization/depersonalization
10. fear of losing control or dying
11. paresthesias
12. chills or even hot flashes.
Panic disorder

p. 365
What is the MOST serious cause of acute chest pain?
Acute Coronary Syndrome

p. 365
What increases the diagnostic value of the EKG in the ER?
Comparing a prior EKG and examining both in light of the clinical picture- ie hx.

p. 365
What can be used to detect isolated ST segment elevation in the posterior aspect in 4% of AMI patients; and would qualify patient for reperfusion secondary to STEMI.
Leads V7-V9 EKG

p. 365
What can be done to increase the sensitivity of the first EKG performed for AMI concerns?
Serial EKG's done in the first 2-3 hrs of examination.

p. 365
All tropinins are the main proteins of the thin filaments of the myofibrils. However, Which troponin subunit is inhibitory in nature?
Troponin I

p. 365
All tropinins are the main proteins of the thin filaments of the myofibrils. However, Which troponin subunit is trypomyosin binding subunit?
Troponin T

p. 365
All tropinins are the main proteins of the thin filaments of the myofibrils. However, Which troponin subunit is calcium bindings subunit?
Troponin C

p. 365
How early can triponin be detected in the serum? (Troponin I and T)
as early as 2 hours

p. 366: However they are not relioably elevated for 6-12 hours.
When do troponin levels reach their peak (in hours, and for how many days?)
Reach their peak in 12 hours.
Last for 7-10 days

p. 366
T/F: Troponin has more specificity for the heart than CK-MB.
True

p. 366
in the ABSCENCE of Coronrary Artery Disease, what do the following have in common?
1. Tachyarrythmias
2. Left Ventricular Hypertrophy (LVH)
3. Myocarditis
4. Pericarditis
5. Heart Failure
6. Pulmonary Embolism (PE)
7. Sepsis
Elevated Troponin (has been known to occur- but not a must)

p. 366
In the presence of an elevated troponin...
What is the difference for myocardial necrosis and MI- what is the difference?
MI requires the presence of troponin elevation as well as one of the following: ischemic sxs, new ST segment and T wave changes, new bundle branch block, new Q waves, or imaging evidence of a new loss of viable myocardium or new regional wall abnormality. However, myocardial necrosis occurs when the troponin is elevated and the absence of all these other things.
p. 366
When do CK levels become elevated? When do they peak? When do they return to NML?
Elevations occur in 4-8 hrs
peak in 12-24 hours
return to normal with in 3-4 days.

p. 366
remember: CK BB- brain, CK MM- skeletal, CK-MB- cardiac. However, the predominent enzyme in the heart: CK-MM, but the CK MB is found in greater preportion in the heart.
In the presence of AMI, when do myoglobin levels rise following sxs?
Myoglobin levels will often rise within 3 hours of sxs
peak in 4-9 hours
and in NML renal function resolve in 24 hours.
p. 367
B-type Natriuretic peptides: BNP and pro-BNP...
decreases blood volume- how and why?
- BNP decreases blood volume by natriuresis and decreasing peripheral resistance through vasodilation. (decreasing afterload)
- released when ventricular wall tension and pressure is too much

p. 367
What is the half life of BNP and pro-BNP?
BNP: 20 minutes
pro-BNP: 90 minutes

p. 367 (generally, tho maybe different in renal issues)
Risk stratification of Patients with unstable angina.
What is the likelihood of of short term death in the individual possessing one of the following:
- Accelerated tempo of ischemic sxs in the last 48 hrs
- pain prolonged > 20 min at rest
- Pulmonary edema; New or worse Mitral regurge murmur, S3, new or worsening rales, Hypotension, brady/tachy HR, > 75 y/o
- EKG change: Angina at rest/transient ST segment changes, BBB- new, SVT
- Elevated cardiac enzymes
High Likelihood
of short term risk death or non-fatal MI

- p. 368
Risk stratification of Patients with unstable angina.
What is the likelihood of of short term death in the individual possessing one of the following:
- Prior MI, peripheral Cerebrovascular Dz, CABG or prior ASA use
- Prolonged angina at rest > 20 minutes- now resolved, mod/high likelhood of CAD, rest angina relieved with Nitro, Nocturnal angina,
- Age > 70
- T wave changes, pathologic Q waves, resting ST depression
- slightly elevated cardiac enzymes
Intermediate Likelihood
of short term risk death or non-fatal MI

- p.368
Risk stratification of Patients with unstable angina.
What is the likelihood of of short term death in the individual possessing one of the following:
- Increased angina frequency, severity or duration; Angina provoked at a lower threshold; New onset Angina with onset 2 weeks to 2 months before presentation
- Chest discomfort, reproduced by palpation
- NML, unchanged EKG
Low Likelihood
of short term risk death or non-fatal MI

- p. 368
What is Coronary artery blood flow determined by?
Duration of diastolic relaxation as well as peripheral vascular resistance.

p. 369
What is ACS caused by?
Secondary reduction of blood flow from:
1. vasospasm (coronary arterial spasm)
2. disruption or erosion of atherosclerotic plaques
3. platelet aggregation or thrombus formation or thrombus formation at the site of atherosclerotic lesion

p. 369
What are secondary causes of coronary artery ischemia from?
Factors extrinsic to the coronary arteries:
1. Increased myocardial demand: fever, tachycardia, thyrotoxicosis
2. reduced bloodflow (hypotension)
3. reduced O2 delivery: anemia, hypoxemia

p. 369
The mainstay of ischemic heart disease is Chest Pain, the history should include what about the nature of the chest pain?
It should be characterized into:
- severity
- location
- duration
- quality
In addition, the presence of additional sxs:
- nausea
- vomiting
- diaphoresis
- dyspnea
- lightheadedness
- syncope
- palpitations

-p 369
also: onset/duration of sxs; as well as activities that precipitated the event, and prior evaluations for similar sxs (risk stratification)
Chest wall pain can be reproducible in some cases of cardiac related discomfort, why?
It is believed to be from the inflammed pericardium sitting just posterior to the chest wall...

- p. 369
How might sxs of acute myocardial ischemia be discribed?
MC as a "discomfort"

p. 369
Angina pectoris, what MC provokes sxs (possibilities are endless, but what was provided in the book)
Exercise
Stress
Cold environments

MC sxs last < 10 minutes (but up to 20)
MC relieved w/in 2-5 minutes of rest or Nitro administration

p. 369
In the ED what are poor predictors of risk for MI or other ACS?
Cardiac Risk factors

p. 369
What has more predictive value for an acute coronary event: Risk factors for CAD or the presence of sxs consistent with CAD?
The presence of sxs has more predictive value of acute event

p. 369
Bradycardic rhythms are MC associated with an MI where in the heart?
Inferior wall

p. 369
T/F: Extremes in Blood pressure (high and low) are associated with a worse prognosis
True

p. 369
What is an ominous sign for a patient with cardiac disease, because it may signify papillary muscle dysfunction...
New Systolic Murmur...

- a flail leaflet of the mitral valve with resultant mitral regurge, or ventricular septal defect...

p. 370
An S4 is common in what two patient types? (2 diagnoses)
1. Long Standing HTN
2. Myocardial Dysfunction

p. 370
What is the single best test to indentify patients with AMI on presentation to the ED?
EKG

p. 370- this should be done and interpreted with in 10 minutes of arrival to the ED
Reciprocal ST segment changes predict what 5 things?
1. larger infarct distribution
2. increased severity of underlying CAD
3. more severe pump failure
4. higher likelihood of cardiovascular complications
5. increased mortality

p. 370
In the appropriate clinical setting, patients with even NML or non-specific EKG's have what % incidence of AMI and % incidence of unstable angina?
1-5% (AMI)
4-23% (Angina)

p. 371
Demonstration of new Ischemia in EKG increases risk of AMI to what % and unstable angina to what %?
25-73% (AMI)
14-43% (Angina)

p. 371
What is the % risk of patients with non-diagnostic EKGs or ischemia that is age indeterminant for AMI and angina?
4-7% (AMI)
21-48% (Angina)
In the setting of left bundle branch block, what three ST segment patterns are indicative of AMI?
1. ST segment elevation 1 mm or more and concordant (the same direction as the main deflection) with QRS complex
2. ST segment depression 1 mm or more in leads V1, V2, V3
3. ST segment elevation 5 mm or more and discordant (opposite direction) with QRS complex

p. 371
What is ST segment elevation concordant with QRS complex in a predominantly positive QRS complex HIGHLY specific for?
AMI (Acute myocardial infarction)

p. 372
ST segment depression in leads V1-V3 has an 80% specificity for what?
AMI (Acute myocardial infarction)

p. 372
T/F: Patients with ST segment elevation on their intial EKG do not need serum cardiac biomarkers...
True and False:
True: it is not necessary to obtain these biomarker to begin tx and dispo plans
However,
False: they should be obtained anyway. These serum markers will be used for risk stratification.
[risk stratification of NSTEMI/STEMI, unstable angina; additionally to help non-diagnostic EKG's for dx of NSTEMI]

p. 372
T/F: Elevations in troponin have been seen in those with renal failure, owing to what some believe are false positives.
True

- however, these are regarded as accurate measures/assessments and are believed to suggest a worse prognosis.

p. 373
What is the difference in sensitivity and specificity of single versus serial sampling of cardiac biomarkers?
Single Markers:
- Sensitivity 39%
- Specificity 93%

Serial Markers:
- Sensitivity 90-100%
- Specificity 83-96%

p. 372-373
What has independent predictive value for the prediction of adverse events and diagnosis of ACS?
Cardiac Troponins and MB fraction of CK myocardial bands

p. 373
ie, when just one is elevated the outcome is likely to be worse.
However, elevations in multiple markers have higher likelhood of ACS and adverse events.

p. 373
BNP is elevated in heart failure patients, but also has been found to be elevated in what other patients?
ACS patients

p. 373
- in fact some submit that this can identify ACS patients who are at risk for adverse cardiovascular events, heart failure and death.

p. 373
Tx for ACS is individualized. However, in general, patients with persistent sxs and STEMI should receive what?
Reperfusion with either PCI or fibrinolytic therapy.

p. 374
- PCI should be done w/in 9o minutes. If not gonna be done in 90 min. Fibrinolysis should be done w/in 30 min. of ED arrival.
Tx with antiplatelet agents, antithrombins, Beta blockers, and nitrates are recommended for what patients?
STEMI

- p. 374
ACEI should also be considered based on: sxs, VS, and the presence of HF (particularly important if diastolic HF hx, defined as EF < 40%)
NSTEMI and UNstable angina patients are treated with what therapies (3)?
1. Antiplatelet and antithrombins
2. Betablockers
3. Nitrates (maybe)

- p. 374

Pts refractory to these therapies or w/positive cardiac markers and those scheduled to undergo PCI also benefit from GP IIb/IIIa blockers
T/F: If a patient has NML o2 sat, do not provide supplemental O2.
True and False:
2LO2 via NC is appropriate, however, little benefit to those w/o hypoxia (<90%). Yet, while this is reasonable and often practiced. Some studies report detrimental effects when given high flow. Do not exceed 2L.
-p. 374
If this treatment can be provided in under 90 minutes (1.5 hrs), it is the preferred reperfusion tx...
PCI

-. 374

AHA, ACC and ESC recommend PCI as long as door to balloon time is less than 90 minutes.
What is the MC PCI?
- Angioplasty w or w/o Stent placement.

p. 374
- the greater the intraluminal size of the stent, the less likely the risk of restenosis following stent placement. However, there is a risk with larger size of: dissection, platelet deposition, thrombus formation, and plaque hemorrhage.
What is more effective at establishing flow in the vessel, reducing reocclusion in the infarct related artery that fibrinolytic therapy- and is associated with a decreased incidence of short and long term death, non-fatal reinfarction, and intracranial hemorrhage?
PCI

p. 375
ASA and Clopidogrel are what kind of agents?
Antiplatelet

p. 375
UNfractionated Heparin, Enoxaparin (LMWH) and Fondaparinux, are what kind of agents?
Antithrombin

p. 375
Streptokinase, Anistreplase, Alteplase, Reteplase, Tenectaplase are what kind of agents?
Fibrinolytics

p. 375
Abciximab, Eptifibatide (Integrillin), Tirofiban are what agents?
Glycoprotein IIb/IIIa inhibitors

p. 375
Nitroglycerin, Morphine, Metoprolol, Atenolol are what kind of agents?
Other anti-ischemic agents

p. 375
What kind of agent is Bivalirudin (angiomax)?
Direct Thrombin Inhibitor

p. 376
What pharmacotherapy class improves left ventricular function as well as short and long term mortality?
Fibrinolytics

p. 376
What therapy may be indicated for STEMI patient, EKG with at least 1 mm ST segment elevation in two of more leads, and time to treat is < 6 - 12 hours from sx onset?
Fibrinolytics

p. 376
What is the most catastrophic complication of fibrinolytic therapies?
Intracranial hemorrhage

p. 376
What are the two limitations (bad things) for fibrinolytic therapies (though regarded as standard of care)?
1. 40-50% will not achieve complete restoration of coronary blood flow
2. 0.5-1.0% of individuals will suffer intracranial hemorrhage, leading to disabling CVA or death.

p. 376
T/F: STEMI patients who receive fibrinolytics should receive full dose anticoagulants for 48 hrs.
True

p. 376
What decides the fibrinolytic therapy used on a patient in the ED?
The institution decides the fibrinolytic therapies that will be used.

p. 377
The ACC/AHA recommends what intervention for the following as mgt for unstable angina/NSTEMI:
1. patients with recurrent angina/ischemia w or w/o sxs of CHF
2. elevated cardiac troponin
3. new (presumed new) ST segment depression
4. high risk findings on non-invasive stress test
5. depressed left vent fxn
6. hemodynamic instability
7. left vent tachycardia
8 PCI in last 6 months
9. Prior hx CABG
Early invasive therapy (PCI)

p. 377
- early is defined as w/in first 48 hrs
What are regarded as the "core" of coronary artery thrombosis?
Platelets

p. 378
final common pathway of platelet activation is IIb/IIIa receptors on the platelet surface.
T/F: ASA should be given at a dose >165mg and is preferred 325 mg, as soon as possible. And will reversibly bind to the platelets for the life of the platelets: 8-12 days.
True

p. 378
T/F" ASA has its risks associated with it, so even in those in ACS event, ASA should be witheld even if vague hx of allergy, peptic ulcer or GI bleed.
False...can still ASA. However, if real allergy to ASA...provide plavix instead.

p. 378
How many days prior to CABG should plavix be held, secondary to bleeding risk?
5 days

- however, ACS- plavix is provided in the ED. Additionally, secondary to Current-OASIS trial, 600 mg Plavix is provided in the ED...to overwhelm the platelets. (dual antiplatelet therapy)
T/F: it is more effective, and superior, to administer GP IIb/IIIa inhibitor with fibrinolytic therapies.
False: there currently exists no role in current tx for the use of this combination of therapies.

p. 379
When compared to ASA alone, wh\at medication when added can decrease risk of death or AMI up to 56% in cases of unstable angina. It is currently recommended in patients with ACS.
The combination of heparin (UFH- unfractionated heparin) and ASA are indicated in in patients with ACS.

p. 379

- UFH is unpredictable as anticoagulant, because its bioavailability is unpredictable.
Why should unfractionated heparin be d/c'd with in the first 48 hrs?
to reduce the risk of heparin induced thrombocytopenia.

P. 379
If patient is on LMWH an d has a pending CABG, what should be done (med mgt/how ling prior)
Unfranctionated Heparin- this should be done 12-24 hrs prior to the CABG

p. 380
What is synthretic, acts as heparin as an antithrombin III to form antithrombic complexes, but is very specific for Factor 10a?
Fondaparinux

p. 380
- lower rate of bleeding with Fondaparinux that with Enoxaparin.
It is recommended, NOT as a monotherapy, but inmstead with Heparin or Angiomax just prior to PCI
T/F: Nitroglycerin has antiplatelet effects
True
-used primarily as peripheral and coronary vasodilator, it also has the effect of inhibition of plately aggregation

p. 380
How should Nitro be titrated in AMI?
To mean arterial pressure, not to patient sx improvement.

p. 380
- reduction 10% in normotensive patient
- reduction 30% in hypertensive patient
AHA/ACC recomends what agent in the first 24-48 hrs for patients with: STEMI, recurrent ischemia, CHF, or HTN...
Nitrates

- p. 380

Be very cautious in patients with known inferior wall ischemia; one third of patients may have RV involvement.
What are the current guidelines for Beta blocker therapy and STEMI or NSTEMI?
1. needs to be PO not IV
2. When started, should be w/in 24 hrs.
...providing none of the following is reported:
- signs of HF
- low cardiac output
- risk of cardiogenic shock (cumulitively, age >70; SBP <120, sinus Tach >110, or brady < 60, longer sxs before dx and tx) as well as standard relative contraindications: prolonged PR interval, 2-3rd degree AV block, active asthma or reactive airway dz.
p. 380
ACC and AHA recommend the tx of ACEI within what time frame for STEMI and HF?
w/in 24 hrs.

p/ 381

- in unstable angina as well as NSTEMI...provided when HTN persists s/p tx with nitroglycerin and B-blocker in patients with depressed LV EF.
What agent:
- produces systemic and coronary vasodilation effects
- possess anti-platelet effects
- suppresses automaticity
- protects myocytes from calcium influx during reperfusion
Magnesiun

p. 381
T/F: there is mortality benefit in the use of CCB in those with AMI.
False: there is zero mortality benfit to CCB's in those with acute MI. In fact, there has been some evidence to support more risk of harm.

p. 381