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ED fellowship-- cardiology > ACS > Flashcards

ACS Flashcards

1
Q

Define ACS

A

Constellation of disease occurring as a result of myocardial infarction.

Range from unstable angina to AMI both NSTEMI and STEMI

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2
Q

Define stable angina

A

Transient episodic chest discomfort resulting from myocardial ischaemia. Typically predictable and reproducible with frequency of attacks stable over time.

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3
Q

Define unstable angina ( history and pathophys)

A

Angina that is new onset or occurring at rest with minimal exertion.
Worsening from a previously stable patient of pain occurrence in terms of frequency or duration, resistance to previously effective medications or provocation with decreased levels of exertion or stress.

pathophys: plaque rupture accompanied by thrombus formation and vasospasm. Freqeuntly characterisedby an ECG abnormality including T-wave and ST segment changes.

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4
Q

Define prizmental angina

A

Caused by coronary artery vasospasm at rest with minimal coronary artery lesions - it may be relieved with exercise or NTG. ECG can reveal ST segment elevation that is impossible to dicern from STEMI.

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5
Q

Define AMI

A

Either of the following

1: Typicall rise and gradual fall of TNI with at least one value above the 99th percentile with at least one of the following clinical parameters
- Ischaemic symptoms
- ECG changes
- Development of pathological Q
- Imaging evidence of presumably new finding such as a loss of viable myocardium or RWMA
- identification of intracoronary thrombus by angiography or autopsy

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6
Q

Discuss types of MI

A

Type 1: Spont Mi related to ischamia resulting from a primary coronary event - plaque rupture, erosion, fissuring or dissection

Type 2: Mi secondary to myocardial ischaemia caused by increased O2 demand or decrease supply - coronary artery spasm, coronary embolism, severe anaemia or systemic hypotension

Type 3: sudden unexpected cardiac death with symptoms suggestive of MI

Type 4 Mi associated with coronary instrumentation

Type 5 MI associated with CABG

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7
Q

List causes for ST elevation

A 
MI 
Pericarditis 
LBBB 
BER 
Ventricular paced rhythm 
normal variant 
PE 
Left ventricular aneurysm 
Osborn wave of hypothermia 
Brugada's syndrome 
Acute cerebral haemorrhage 
Postelectrical cardioversion
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8
Q

Discuss the pathophysiology of ACS

A

The underlying pathophysiology of ACS is myocardial ischaemia resulting from inadequate perfusion to meet o2 demands.

Myocardial o2 demands depend on HR, after load, contractility, and wall tension.

Occlusion of more than 95% is usually required for angina at rest. With exertion or increase in o2 demand can be present at 60%

Composition of plaques can vary greatly from fibrous stable plaques to unstable fibrolipid plaques which are likley to rupture and lead to thrombosis and platelet aggregation and lead to occlusion and tissue necrosis

Angiography shows that often the initial atherosclerotic plaques is only 50% the diameter of the lumen and that the most important factors in MI are the acute events of rupture and platelet activation.

Another important factor in development of infarction is local vasospams. After a significant coronary vessel occlusion local mediators and vasoactive substances are released. Sympathetic response and release of adrenaline can lead to vasopspam and increase platelet aggregation worsening occlusion

Further damage occurs at a cellular level as inflammatory thombotic and other debris fromt he occlusive plaque lesion is released and embolisez inot the destal vessels leading to microvasculature obstruction and hypoperfusion/ischaemia. With PCI and thrombolysis CA2 o2 and cellular elements are released which can causea reperfusion injury and lead to myocardial stunning or reperfusion arrythmias

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9
Q

Describe the GRACE risk model (bonus what is killip class)

A

GRACE model uses 8 factors to predict mortality at 6 months from admission

Criteria include

  • AGE
  • SYstolic blood pressure
  • Creatinine
  • Arrest at arrival
  • HR
  • Killip class
  • abnormal cardiac enzymes
  • ECG ST elevation

Killip class system used in MI taking into account the development of heart failure to risk stratify mortality

  • Killip class I includes individuals with no clinical signs of heart failure.
  • Killip class II includes individuals with rales or crackles in the lungs, an S3, and elevated jugular venous pressure.
  • Killip class III describes individuals with frank acute pulmonary edema.
  • Killip class IV describes individuals in cardiogenic shock or hypotension (measured as systolic blood pressure lower than 90 mmHg), and evidence of peripheral vasoconstriction (oliguria, cyanosis or sweating).
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10
Q

Discuss TIMI risk socre for STEMI

A

The TIMI score was developed from the inTIME2 trial of 15000 STEMI patient and looked at 30 day mortality all cause. Thrombolytic trial and did not look at PCI-
Also used new LBBB as a STEMI equivilant which it is no longer considered especially with scarbossi criteria

Uses 8 crieteria

1) Age >65, 65-75, >75
2) systolic BP <100
3) HR> 100
4) diabetes, HTN or angina
5) anterior ST elevation
6) Killip class 2-4
7) weight less than 67kg
8) time to treatment > 4

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11
Q

Discuss TIMI risk score for UA/NSTEMI

A

Uses 7 criteria to predict composite all-cause mortality, myocardial infarction, or urgent revascularization up to 14 days

Criteria include

1) age >65
2) 3 or greater CAD risk factors
3) known CAD >50%
4) ASA use in the past 7 days
5) severe angina (2 episodes in the past 24 hours)
6) ECG changes
7) Postive TNI

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12
Q

Describe the classic history of ACS

A

Classic angina pectoris is described a discomfort with squeezing pressure tightness fulness heaviness or burning sensation.
Classically substernal or precordial in location and radiates to the neck, jaw, shoulders or arms

Symptoms assoiated include dyspnoea, nausea and vomting, diaphoresis weakness, dizziness, excessive fatique and anxiety

ACS can masquarde as GIT abnormalities

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13
Q

Describe population that commonly present with atypical symptoms of ACS

A

Women, the elderly, diabetics, dementia patients

Patient with nil prior history of MI or risk factors

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14
Q

List DDX for chest pain (more than 20)

A

Cardiac
-MI, Unstable angina, stable angina, pericarditi, myocardial or pulmonary contusion, prizmetal’s angina

Resp:
-Pneumonia, PE, pneumothorax, pulmonary htn, pleurisy

GIT:
-GORD, mallory weiss syndrome, Boerhaavés syndrom, PUD, oesophageal spasm, gastritis , cholecysitis, panceatitis

Vascular
- disection,

Infectious
- VZV

MSK

Trauma

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15
Q

Discuss complications of MI

A

1) Arrythmias
- Bradydysrhythmia and AV block occur in 25-30% of patient with AMI - sinus brady is usualy seen
- Symptomatic bradycardias in the first few hours after MI tend to be atropine responisve
- Conduction block associated with anterior stemi has poor prognosis and respnds poorly to treatment
- Tachyarrhythmias are common and can be atrial or ventricular in origin

2) Cardiogenic shock
- seen with patient with alrge infarcts, prior MI, older age and DM

3) LV free wall rupture is uncommon - 1/3 of cases occur in the first 24 hours and the remainder 3-5 days later
- Clinically associated with sudden death

4) Interventricular septal rupture
- massive deterioation and a new harsh murmur heard best at the left sternal edge should prompt this diagnosis
-ECHO can show
-Vasopressor, inotropic support and intraortic balloon
pulsation are important measure to temporise until cardiac surgery

5) pericarditis ( MI related and post (Dressler’s syndrome)
Dresslers syndrome unlike infarct related pericarditi does not requir transmural involvement
-uncommon late complication occuring 1 week to several months post MI

6) Stroke both thrombotic and haemorrhagic
7) valvular complications

8) procedural complictation
- arterial injury with haemorrhage related to percutaneous interventions - pseudoaneyrsms

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16
Q

Discuss LVH as a mimic of ACS

A

LVH features prominent left sided forces manifesting as large rS or QS complexes in the right precoridal leads. THese changes rarely extend beyond V1-2
COnsistent with the rule of appropriate discordance (ST segment should be oppoisite the majority of the QRS) the leads with this paitten may feature ST elevation

The ST elevation is generally concave in LVH

The left precordial eads may show evidence of repolarization abnormality (strain pattern) with ST segment depression and asymmetrically inverted t-waves

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17
Q

Discuss Takotsubo cardiomyopathy

A

Left apical ballooning
Typically occurs in the setting of severe emotional distress
Patient have normal coronary arteries

Mimic STEMI and can have +ve TNI
Diagnosis
-New ecg changes (STE or TWI) or moderate TNI rise
-Transient akinesis/ dyskinesis of left ventricle with RWMA

Typicall it occurs in post menopausal women expierincing sudden emotional stress associated with a cathecolamine surge

Typically recovery wall motion within a month

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18
Q

Discuss the limitations of ECG in ACS

A

Single ECG is 60% sensitivity and 90% specific for AMI. Serial ECGs in the setting of continued or recurrent pain increases diagnostic value

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19
Q

Discuss the utility of a CXR in ACS

A

Exclude or confirm other DDX
Able to gather information conerning apllication of other therapies – ie. widened mediastinum and the use pf thrombolytics
SIgns of congestion can suggest Killip class of heart failure which can be used as a prognosticator on GRACE and TIMI

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20
Q

Discuss non ACS cardiac conditions in which there is a rise in TNI level

A

Can be seen in patient with myocarditis, pericarditis, CHF, LVH and non presnetrating cardiac trauma

Although the presence of TNI in these condition may be considered a false positive for ACS the source of these levels is likley underlying myocyte damage and have a significant prognostic effect

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21
Q

Discuss non cardiac condition that can lead to a rise in TNI

A

Massive and sub massive PE – right heart strain leads to right ventricular dysfunction and TNI rise – is a poor prognostic sign

Can also be seen in sepsis, extreme physical exertion, renal failure and essential hypertension

again a rise in troponin in any of these condition is associted with poorer outcome

Aortic dissection
Acute CNS pathology
Burns <30%
HCOM

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22
Q

Discuss elevated TNI in renal failure

A

These patient are at high risk for ACS

should not be ascribed to renal failure and poor clearance unless trend to show the same

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23
Q

Discuss CK-MB as an alternative to TNI

A

Myocardial cells are the most abundant source of CK-MB so elevated levels are suggetive of MI

It is however found in other cells especially pelvic muscle cells

To improve sensitive and specificity for MI a CK ratio is perfomred in which at least 5% of total CK must be CK-MB for it to be positive finding

24
Q

Discuss the use of exercise stress testing in low-moderate risk patient

A

Exercise stress testing in low risk patient had a -ve predictive vaule of 98.7%

Absoulate contraindication to stressing including recent AMI, high risk UA, unctrolled cardiac dysrhythmias, symptomaitc severe aortic stenosis, uncontrolled symptoamtic heart failure, P or pulmonary infarct, acute myo or pericarditis and acute aortic dissection

Specificty of the test is decereased in the presence of underlying ECG abnormalities, LVH or artifact

False postiive results can occur from aortic stenosis or insufficiency, HCOM, HTN, AV fistula, aneamia, haemoglobinopathies, low cardiac outpaute states, COPD, digitalis toxic stattes, LVH, hyperventilation, MV prolpase and BBB

25
Q

Discuss the use of ECHO in the diagnosis of AMI

A

Echo allows bed side assessment of RWMA due to the close correlation between wall motion and blood flow.

Imparied myocardial contractility ranges from hypokinesis to akinesis

After AMI parodixcal wall motion and decreased EF can be observed due to loss of muiscle tone.

The abscence of RWMA or diffuse abnormalities on ECHO has a negative predictive value as high as 98%

Stress echo with dobutamine stressing may eb more accurate in CAD for females compared to stress treadmill

26
Q

Discuss pro and cons of bedside ECHO in ACS

A

Pros

  • readily accessibloe and portable
  • inexpensive
  • Detection of RWMA useful for early diagnosis and if diagnositc uncertainty
  • Identification of nonishcaemic causes of symtpms including ( vavluar heart disease, aortic dissection, pericardtitis, mtral valve prolpase and PE)
  • Idenitifaction of complications of MI (acute MR, free wall rupture, ventrical wall rupture, intracardiac thrombus formation)

Cons

  • Skill level of operator
  • Limited sensitivity particularly in small area of myocardial injury
  • limited visual windows
  • inability to distinguish acute from chronic RWMA
27
Q

Discuss myocardial perfusion scan (Myocardial scintigraphy)

A

Radionuclide tracer injection and scintigraphy allows real time assessment of mycoardial perfusion,

In pateint with a normal intial study the likleyhood of ACS is extremly low
IN those with abnormal dristribution (ie reduced uptake) soe form of sichaemic heart disease is likley

Two pattern of follow-up scan result after an abnormal iniatial scan

1) normal redistribution (consistent with active coronary ishcaemia)
2) persistant reduction in distribution (MI remote or recent)

The incidence of cardiac event is 1% in 30 days for patient with a normal scan. High sensitivity and good specificity for CAD

28
Q

Discuss CTCA

A

In low to intermediate pretest probability of CA CTCA has a very high negative predictive value. Will also identify other DDX of chest pain

29
Q

Discuss PCI and Fibronolytic management of ACS

A

Early patency resulting in myocardial salvage is the key beneift of emergent repufusion therapy

Timely treatment within the first hour of symptoms leads to if not complete substantial myocardial salvage. Treatment between 2-12 hours have more modest results but still significant benefit.

The opening of occluded vessels causes less adverse ventricular modelling, reduced ventricular aneurysms and improve electrophysiological stability.

With each 30 minute delay to PCI the 12 month mortality risk increases by 7.5%

Thrombolytics should be administered 30 minutes from admission to hospital and PCI within 90minutes

30
Q

Discuss resons for delay in administration of PCI or thrombolytics

A

Delays can occur at 4 main times which can be remebered as the 4 ds

1) Door events prior to arrival to the ED – patient calling primary care, trying to drive themselves, waiting for EMS
2) Data ( time to obtain data ie ECG)
3) Decision ( time to come to decision for treatment – can be delayed by uneccesary consultation)
4) Drug ( administoring the drug or taking patient to cath)

Often EMS will call ahead and can circumvent the ED completly if Cath is available

31
Q

Discuss the use of oxygen in the management of ACS

A

Oxygen is a drug with potential for significant benefit and harm

Patient with ACS often will have respiratory compromise secondary to APOor chronic pulmonary disease. patient with ACS and respiratory distress and poor oxygenation should receive supplemental oxygen as standard to maximise oxygen saturation for perfusion of the myocardium

IN patient without respiratory compromise and desaturation o2 can be harmful. The AVOID trial demonstrated that o2 therapy in patient without respiratory compromise led to earlier MI and larger area of infraction, Furthermore re-infarction and dysrhythmia were increased in the o2 arm

32
Q

Discuss the use of GTN in the management of ACS

A

Nitrates decrease mycoadial preload and to a lesser extent afterload causing a reduction in myocardial o2 demand.

Nil contempary evidence to suggest improved outcome with use of nitrates,

Useful for symptomatic releif –
Avoid in patient with hypotension or signs of right heart infarct ( inferior MI, ST elevation in V1 >AVR, st depression in V2, right sided lead infarct)

Can use infusion 10mic/min titrated to effect and BP, alternatively spray and sublingual are effective pain relief

33
Q

Discuss the use of opiod analgesia in ACS

A

Useful as a pain relief and anxiolytic
Also shows some vasodilatory effect which can reduce preload

All of the above reduce myocardial o2 demand
Care for narcosis

34
Q

Discuss B-Blocker

A

Prior to contempary re-vascularisation techniques IV blockade was used as a standard therapy to control catecholamine induced tachycardia, including VF, increasing contractility and reducing myocardial o2 demand

Several large studies have however shown increase rate of heart faiulure, higher rate of death, recurrent ischaemia and pace maker need – not part of acute management

35
Q

Discuss use of ACE and Statins

A

Benifical post MI – reduce mortality, heartfailure, re-infarct

36
Q

Discuss antiplatlet therapy in AMI in general

A

In patient with non AMI ACS dramatic reduction to acute infarct is noted with appropriate antiplatelet therapy. ASpirin is indicated for all patient suscpected of ACS wihtout contrindication

The administartion of aspirin and other antiplatlets is associatged with reduction in mortality ranging from 25-50%

37
Q

Discuss the use of Aspirin in AMI

A

Aspirin irreversibly acetylates platelet cyclooxygenease therby removing all acitivity for the lifespan of the platelet 8-10 days

Also reduces antiaggregatory prostacyicn

Benefit alone of 23% reduced mortality and synergistic with firbinolytics 42% reduction

38
Q

Discuss use of PSY12 receptor inhibtor agents

A

The thienopyridines ticlopidine, clopidogreal and prasugreal are more potent platelet inhibitors than aspirin. They inhbit the transformation of the PSY 1 receptor into its high-affinity ligand binding stat irreversible inhibiting platelet aggregation for the life of the platelet

Clopi has been the preferred agent. ACCOAST trial showed nil improved outcome for patient treated with prasugrel

Ticagrelor acts differently then above is rapidly absorbed and does not require hepatic activation. Ticagrelor causes less death from cardiovascular causes but has a higher rate of nonprovedure related bleeding. The PLATO trial assessed increased cost of ticagrelor vs clopi and found ticagrelor to be superior

The AHA have suggested in the form of a calss 1 reccomendation that clopi or ticagrelor should be withheld for at least 24 hours befeor urgent on pump CABG if possible. If CABG is performed within 5 days of clopi patient ahve increase incidence of operative and postoperative haemorrhage , need for trasnfusion need for reoperation for haemostasis and post op mortality.

39
Q

Discuss the use of UFH in ACS

A

UFH binds to anti-thrombin 3 forming a complex that is able to inactive thrombin and activate factor 10. This prevent conversion of fibrinogen to fibrin

Has a profound synergistic effect with aspirin in the prevtion of death in AMI

Iniital bolus of 60units/kg followed by infusion of 12 units per kg

Recommended in those going for immedicate PCI over LMWH

40
Q

Discuss the use of LMWH in ACS

A

One third of the heparin molecules binds to antithrombin and thrombin. The remaining molecule bind only to factor 10 a.

Potentional advantages include easier administration, greater bioavailbaility more consistent therapeutic responce and longer serum half life

Reccomended over UFH in the use for paitent with AMI who are being treated conservatively – PCI >24hours from onset of pain

41
Q

Discuss the use of firbinolytic therapy in ACS

A

Options include stretptokinase – obselete, Tissue plasminogen activator – recombinant tissue tupe plasminogen activators (reteplase and tenecteplase)

Tenecteplase has severeal benefit in STEMI when compared to the other agents

1) longer half life allows it to be given as a bolus
2) it is 14 times more fribrin specifc than TPA and even more so than r-PA
3) 80 times more resistent to plasminogen activator inhibitor type 1

There is little difference in mortality between tenecteplase and TPA prior to 4 hours. Late presentation after 4 hours show 30 day motrality beneifit with tenecteplase
Also slightly less adverse reaction with tenectoplase
Given single dose markedly easier to use in the prehospital setting

42
Q

Discuss elgibility criteria for fibrinolytic agent therapy

A

In the absence of contraindications fibrinolytic therapy should be offered to any who present with 12 hours of symptom onset with STEMI who is unlikley to get primary PCI within 120minutes of first medical contact

43
Q

Discuss BP in thrombyltics

A

Patient with a history of chronic high blood pressure should not be excluded from fibrinolytic therapy if BP is adequately controlled
It has been show that the risk of cerebral haemorrhage is increased with systolic BP higher than 150 and even high when pressures exceed 175 . THe literalure appears to show a risk-benefit ratio for patient with substantial increase in BP. Despite this persisant pressure of greater than 200/120 is considered an absolute contraindication

The beneift in patient with hypotension is less clear. Multiple trials have shown no apparanet mortality beneift with fibrinolytics in killip class 3-4. Howevere review of data on STEMI have shown patient with a systolic under 100 intiially beneiftted most from thrombolytics

44
Q

Discuss retinopathy and thrombolytics

A

Active diabetic haeorrhagic retinopathy is a strong relative contraindication due to the risk of blindness from bleeding.

Nil reason to withold if only evidence of simple diabetic retinopathy

45
Q

Discuss cardiac arrest requiring CPR and thrombolytics

A

CPR is not a contraindication unless is prolonger greater than 10 minutes or obvious signs of trauma from the CPR.

Mortaliity is higher in patient with arrest and CPR with thrombolytics but rates of bleeding complications are not found to be higher. Specifically the rates of haemothorax and cardiac tamponade were not diagnosed in arrest patients

46
Q

Discuss previous stroke or TIA and Previous MI with thrombolytics

A

Previous stroke is a strong relative contraindication as rates of bleeding are much high

Patient with previous MI +- PCI +- CABG are not contraindicated from thrombolysis. These patient however fair better with PCI or CABG as 75% of cases are due to occlusion of the grafted vessel. Due to the large mass of thrombus and absent flowin the graft fibronolytics may not be effective

47
Q

Discuss previous surgery and thromboltytics

A

Relative contraindication
Facial trauma within the past 3 months and intracranial or intraspinal surgery wihtin the past 2 months are considered to be absolute contraindications
Major surgery within the past 3 weeks and recent internal bleeding 2-4 weeks are also relative contraindications

48
Q

Discuss Menstruation and thrombolytics

A

Eostrogen is a partially cardioprotective there is very little clinical experience with fibrinolyiss in premenopausal women. Gynecologists have indeicated that fibrinolytic therapy should be readily controlled by vaginal packing and therefore considered as a compressible site of bleeding

49
Q

Discuss thrombolytic therapy vs PCI

A

PCI is the preferred choice for reperfusion if available
It is less effected by time in the first couple of hours compared to thromboyltics
Thrombolytic effectivness rapidly declines with passage of time
Further high risk STEMI should have PCI if available and include
-late presenters (3 hours of symptoms )
-patient in cardiogenic shock
-individuals with contraindication to lysis

In general the following can be applied
-Primary PCI is preferred reperfusion therapy in patient with STEMI if it can be performed within 90 minutes of first medical contact - otherwise lysis is preferred

Situations in which fibrinolytic therapy should be considered the default approach (assuming door to needle time <30minutes)

  • Patients presenting to the ED within 60 minutes of onset of symptoms
  • patients in presenting 60-120 minutes after symptoms in who PCI is expected to be delayed 90 minutes
  • Unacceptable delays in cath lab activation
  • significant factors likely to impede successful performance of PCI - severe contrast allergy or poor vascular access

Situations in which primary PCI may be the preferred repurfision strategy due to reduced efficacy or icnreased blleding risk

  • Longer patient delay from symptoms onset (2-4hours) primary PIC preferred if delay is expected to be less than 120 minutes
  • Late presentation after 4 hours of onset - low efficacy of fibrinolytics
  • patients with HD compromise or cardiogenic shock with the option of urgent CABG
50
Q

Discuss lysis in patient with cardiogenic shock

A

Occurs in 10% of cases of STEMI and has a mortality rate of 80%. Fibrinolysis is not effect likley owing to a significantly lower coronary artery perfusion pressure. IN circulatory failure states the lytic agent is not exposed to the thrombus

PCI shows 6 months mortality improvement compared to medical therapy

51
Q

Discuss post cardiac arrest care

A

Consist of four main facets

1) Prevent further cardiac arrest
- optimise fio2 -94-98% (hyperoxemia increase cardiac damage) - decrease fio2 as soon as possible aiming for the above target
- Protective lung strategy - ETT
- commence sedation
- ventilate for normocarbia
- correct elevtrolyte
- maintain euglycaemia
- administer appropriate antiarrythmics - amioderone

2) define the underlying pathology
- diagnosis and treat cause (PCI or thrombolysis)
- Treat complications ( heart fialure hypotension, rib fracture pneumo)
- Cath lab on ECMO if available

3) limit organ damage
- If uconcious despite ROSC TTM aiming at 36C as per Nielsen et el
- Invasive monitoring
- Maintain Map over 70 – inotropes as needed

4) predict non survivors

52
Q

Describe the Heart score

A

Used in patients >21 years of age presenting with symptoms suggesitve of ACS to predict 6 week risk of ACE.

Exclusion

  • New STE 1mm or other new ECG changes
  • hypotension
  • life expectancy less than 1 year

History

  • slightly suspicious -0
  • Moderately -1
  • Highly -2

ECG

  • Normal - 0
  • Non specific repolarization disturbance (LBBB, LVH)1+
  • Significant ST deviation

AGE

  • <45 -0
  • 45-64 +1
  • > 65

Risk factors

  • nil 0-
  • 1-2 +1
  • 3 or more +2

Initial TNI
< normal limit -0
1-3x normal limit +1
>3x normal limit

Low risk 0-3
-0.9-1.7%

Moderate risk 4-6
-12-16.6%

High risk 7-10
-50-65%

53
Q

List high risk criteria for possible cardiac causes of chest pain and low risk criteria

A

High risk

  • ongoing or recurrent chest discomfort despite initial treatment
  • eleavated TNI
  • New ischaemic ECG changes or new t-wave inversion in more than 2 leads
  • diaphoresis
  • HD compromise
  • Sustained VT
  • syncope
  • known left ventricular systolic dysufnction
  • prior AMI PCI or CABG (6months)

Low risk all of the follow-up

  • age <40 years
  • symtpoms atypical for angina
  • remian symptoms free
  • absence of known CAD
  • normal TNI
  • normal ECG

intermediate neither high or low

54
Q

Discuss STEMI criteria

A

1) >2.5mm STE in leads V2-3 for men under 40 or >2mm in men over 40
2) >1.5mm STE in V2-3 in women
3) >1mm in other leads

55
Q

Discuss lysis pathway

A

Give aspirin and clopidogreal 300mg j
+either clexane 30mg bolus if under 75 followed by 1mg/kg (max 100) BD 15 minutes after bolus or if over 75 nil bolus and 0.75mg/kg (max 75) BD
If signifiacnt renal impairment consider heparin 60mg/kg bolus (4000 units max) followed by 12 units/kg/hr (1000 units)

Tenectaplase is 0.5mg/kg or 10 units per kg upper weight range to a max of 10000 
<60 -30mg (6000 IU) 
60-70- 35mg (7000 IU)
70-80 - 40mg (8000 IU) 
80-90 -45mg (9000 IU) 
>90 -50mg (10000IU)

Alteplase accelerated infusion
>67 kg - 15 mg boluse followed by 50mg over 30 minutes and then 35 mg of 60 minutes
<67 kg - 15 mg bolus followed by 0.75mg/kg over 30 minutes followed by 0.5mg/kg over 60 minutes

56
Q

Discuss relative(11) and absolute (7) contraindications to lysis in STEMI

A

Absolute

  • active bleeding or bleeding diathesis
  • suspected dissection
  • signifaicnt closed head or facial trauma within the past 3 months
  • any prior intracranial haemorrahge
  • Ischaemic stroke within the last 3 months
  • Known cerebral vascular lesions
  • Known malignant intracranial neoplasm

Relative

  • current anticoagulation
  • non compressible vascular puncture
  • recent major surgery <3weeks
  • traumatic or prolonged CPR >10 minutes
  • recent internal bleeding wihtin 4 weeks/ Active peptic ulcer
  • Suspected pericarditis
  • Advanced liver disease/ mets
  • History of chronic severe poorly controlled HTN
  • Severe uncontrolled HTN on this presentation
  • Ischaemic stroke >3months ago
  • Pregnancy or within 1 week post partum

ED fellowship-- cardiology (10 decks)

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