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IPAP > EMED Block 3 > Flashcards

EMED Block 3 Flashcards

1
Q

What is the leading cause of death among US adults?

What disease process causes this?

A

Ischemic heart dz

Atherosclerotic dz of epicardial coronary arteries (CADz)

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2
Q

What is the predominant Sx of CAD

PTs w/ NSTEMIs usually present w/ ?

A

Chest pain

Angina at rest

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3
Q

What are the 3 different presentations of unstable angina?

A

Rest- angina lasts >20min

New- limited activity

Increased- previous dx, more frequent/longer

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4
Q

High likelihoods for short term risk of death or non-fatal MI risk stratification

A

Inc Sx tempo past 48hrs
Lasting >20min

Pulmonary edema
New/worsening MR
S3/new/worsening rales
HOTN, Brady/Tachy
>75y/o

Angina at rest w/ ST >0.5mm
BBB
Sustained V-tach

Inc TnT

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5
Q

Intermediate likelihood of death from MI

A

Hx of MI/CVDz/CA bypass
ASA use

Angina >20min of rest self resolved/resolved w/ Nitro
Nocturnal angina
New onset angina <2wks

> 70y/o

Twave cahnges
Pathologic Q waves
Resting ST depressions <2mm

Slightly elevated TnT

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6
Q

Low likelihood of death from MI

A

Inc angina frequency/severity/duration
Angina provoked at lower thresholds
New onset in past 2wks-2mon

Chest discomfort reproduced by palpitations

Normal EKG/markers

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7
Q

Left coronary artery divides into ? and ? to supply ?

What does the RCA supply?

A

Circumflex- ant/lat wall
LAD- anterior/septal regions

RV, inferior LV vis right posterior descending artery

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8
Q

AV conduction system receives blood from ?

What supplies the RBB and posterior division of LBB?

What supplies the posteromedial papillary muscles?

A 
Antrioventriuclar (RCA)
Septal perforating (LAD)

LAD and RCA

RCA

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9
Q

What influences O2 supply to the heart?

What influences O2 carrying capacity?

A

O2 carrying capacity /CAD flow

Hbg, O2 saturation

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10
Q

What determines coronary blood flow?

Exercise induced MI occurs as result of ?

A

Duration of diastolic relaxation in heart
Peripheral resistance

Fixed atherosclerotic lesions

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11
Q

Atherosclerotic plaque from due to ?

ACS can be caused by reduced flow due to secondary causes including ?

A

Repetitive injury to vessel wall

Coronary spasm
Microvascular dysfunction
Disrupted/erosion of plaques
Platelet aggregation or thrombus formation at lesion

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12
Q

What are the three factors that can cause a plaque to rupture?

After this rupture happens, what response occurs?

A

Composition/shape
Local factors
Artery movement

Platelet activation

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13
Q

How is ischemia produced during stable angina?

A

Activity induces O2 demands higher than supply

Ischemia occurs at fixed point, slowly over time

Atherosclerotic plaque has not ruptures, no thrombus

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14
Q

What causes ischemia to occur during ACS?

What is the main Sx of ischemic heart Dz

A

Plaque rupture/platelet rich thrombus develop
Coronary flow reduced

Chest pain

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15
Q

What 5 characteristics of ischemic heart dz Sxs may be helpful?

Sxs of acute MI can be described as ?

Less common descriptions include?

A

Severity Location Radiation
Duration Quality

Pressure Heavy Tight Fullness Squeeze

Knife Sharp Stab

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16
Q

What is the classic location of acute MI pain?

What are the three classic triggers that precipitate angina and how long does it last?

A

Sub-sternal/Left chest w/ radiation to arm, neck or jaw

Stress Exercise Cold
<10min

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17
Q

Acute myocardial ischemia pain usually lasts longer than angina and has ? 3 more prominent Sxs?

What is the difference in angina and AMI response to initial therapy?

A

Diaphoresis Nausea SOB

Angina: improves <5min w/ rest/nitro
AMI: little response to nitro

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18
Q

What are the 3 non-classic ACS presentations?

What gender is more likely to present w/ a silent MI w/out pain?

A

Advanced age
Female
DM

Female

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19
Q

PTs have poor prognosis if they present w/ ? non-classic MI Sxs

What are the traditional cardiac risk factorsfor CAD that are not helpful to predict ACS in PTs >40y/o?

A

Fatigue Weakness Not well
Vague discomfort

HTN DM Tobacco FamHx Hypercholesterolemia

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20
Q

What type of HR is usually noted w/ inferior wall MIs

What are two poor prognosis factors for anterior wall MIs?

A

Brady

Brady/new heart block

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21
Q

What PE finding usually indicates a failing myocardium due to MI?

Presence of a new systolic murmur is ominous sign and may signify ? three issues?

A

S3 (can be normal: young pregnant athlete)

Papillary muscle dysfucntion
Flail leaflet of MV w/ MR
VSD

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22
Q

The presence of ? w/ or w/out S3 indicates S3 LV dysfunction and L-sided HF

Presence of what 3 findings suggest R-sided HF?

A

Rales

JVD
Hepato-jugular reflex
Peripheral edema

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23
Q

Dx of STEMI requires ?

Dx of NSTEMI requires ?

How is unstable angina Dx

A

EKG

Abnormaly elevated cardiac biomarkers

Hx

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24
Q

What is the TIMI score for unstable angina

What is the max score?

A 
\+65y/o
3 or more RFs for CADz
Hx coronary stenosis >50%
ST deviation on EKG
2 + anginal events <24hrs
ASA w/in 7d prior
Elevated cardiac markers

7pts, one each

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25
Q

How fast do EKGs need to be obtained and interpreted for MIs?

What is the “general” definition of a STEMI?

A

10min of presentation

ST elevations of 1mm or more in 2 contiguous leads w/ reciprocal changes

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26
Q

ST elevations on EKG suggest ?

ST depressions suggest ?

A

Transmural injury/infarction

Ischemia

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27
Q

Inferior wall MIs need to have ? obtained

Why does this step need to be taken?

A

R sided V4

ST elevation in V4R= highly suggestive of RV infarction

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28
Q

PTs w/ RV infarctions are ? dependent

What two meds need to be used w/ caution in these PTs?

A

Preload

Nitro and BBs

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29
Q

PT w/ non-diagnostic EKG and persistent MI like Sxs needs to have ? done next

PT w/ new LBBB is equivalent to ? Dx

A

Repeat EKG

STEMI

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30
Q

What causes the reciprocal changes on EKGs?

How does the size of EKG changes correlate to the severity?

A

Subendocardial ischemia

Larger= more extensive injury

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31
Q

What leads are involved in each of the locations of MIs

A 
Anteroseptal: V1-3
Anterior: V1-4
Anterolateral: V1-5, 1, aVL
Lat: 1, aVL
Inferior: 2, 3, aVF
Inferolateral: 2, 3, aVF, V5-6
True posterior: R waves in V1-2 >0.04s, R/S ratio +1
RV: 2, 3, aVF and ST elevation on R sided V4
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32
Q

? test is the risk stratifier for PTs w/ ACS

When are leads V7-9 used?

A

12 lead EKG

Posterior MI from circumflex lesion

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33
Q

Criteria for pre-existing LBBB

What is the MC pacemaker lead location and what EKG issue does this cause?

A

Elevation >1mm and concordant
Depression >1mm V1-3
Elevation +5mm and discordant

RV pacing- secondary repol of opposing polarity

34
Q

Where is Wellens seen on an EKG?

What is this finding associated with?

What abnormality occurs during this condition?

A

V2-3

Critical stenosis of LAD, pending future anterior MI

T-waves when pain free
Normal EKS w/ pain

35
Q

PTs w/ diagnostic ST elevations on initial EKG don’t need ?

When is this missing step preferably done?

A

Serum labs drawn

Non-Dx EKG of NSTEMI
Risk stratification for NSTEMI, unstable angina

36
Q

What type of serum marker is used for Dx of ACS

What types of results indicate a very low risk for ACS

A

D-troponin over 1-3hrs

Undetectable high sensitivity troponin + no EKG evidence

37
Q

Results showing elevated and __ are a worse prognosis

How long does it take troponin to rise, peak and return to normal?

A

BNP

Rise: 3-12hrs
Peak: 12-24hrs
Norm: 5-14d

38
Q

How are STEMIs Tx

What is the time frame this Tx must be done within?

What alternative Tx is done if the primary STEMI Tx is unavailable?

A

PCI

<90min w/ PCI capability
<120min w/out PCI capability

Fibrinolysis <30min

39
Q

PTs w/ ACS get ? 3 drugs in the ED

What is added if they’re refractory to these therapies or about to undergo PCI?

A

Antiplatelets
Antithrombins
Nitrates

Glycoprotein 2b/3a antagonist

40
Q

When is the aggressive STEMI Tx method applied to the NSTEMI PT

Guide lines recommend if unstable angina/NSTEMI Pts are hemodynamically unstable, then invasive Tx strategies are implemented within ?

A

One or more of:
Refractory angina
Hemo/electric instability
PTs at increased risk

2hrs

41
Q

___ is the preferred reperfusion Tx method if contact to Tx time is between ?

A

PCI

90-120min

42
Q

What is the MC PCI?

What medications are added if stents are used?

A

Coronary angioplasty w/ or w/out stent placement

Antiplatelet therayp- Thienopyridines, Glycoprotein 2b3a inhibitors

43
Q

What is the MOA of fibrinolytics

What part of the heart does this Tx improve?

A

Plasminogen activators acting on thrombosis

LV function

44
Q

When can fibrinolytics be used for STEMI PTs

Fibrinolytic therapy is more beneficial for ? types of MIs

A

Time to Tx is 6-12hrs from Sx onset and,
EKG has 1mm ST elevation in two leads

Larger, anterior

45
Q

If fibrinolytics fail, rescue PCI is recommended for ? PTs?

A

<75y/o in cardiogenic shock

Severe HF/Pulm Edema

Hemodynamic compromising ventricular arrhythmia

Large are of myocardium at risk

46
Q

What is the most catastrophic complication of fibrinolytic Tx

Differen benefits of using ASA or Glycoprotien 2b/3a inhibitors

A

Intracranial bleeding

ASA: inhibits platelet aggregation stimulated by thromboxane A2 mediated by arachidonic acid pathway

G2b/3a: stronger, interrupt platelet activation regardless of agonist present

47
Q

Absolute c/is for Fibrinolytics

Relative c/is for Fibrinolytics

A

Slide 85

48
Q

PTs receiving fibrinolytics should get ? for how long?

When is Clopidogrel used instead of ASA?

A

Full dose anticoagulant (UFH, Enox, Fonda) x 48hrs

True ASA allergy
Active PUD

49
Q

What ADP antagonists are used and when is it c/i?

A

Prasurgel- irreversible platelet receptor antagonist
Prior CVA/TIA or bleeding

Ticagrelor- reversible P2y12 antagonist, gone w/in 3d of d/c

Clopidogrel- addition to ASA and antithrombin therapy improves STEMI PTs receiving fibrinolysis

50
Q

? reduces risk of AMI and death during the acute phase of unstable angina

Combining this w/ __ dec risk by over 50%

A

UFH

ASA

51
Q

D/c use of UFH w/in ?hrs of therapy to prevent development of ?

Why would LMWH heparin be preferred?

A

<48hrs
HIT

Greater BioAvail
Lower protein binding
Longer t1/2

52
Q

LMWH (Enoxaparin) is not considered a first line antithrombin for ? PTs unless they’re already on it?

What class of drugs are used to reduce the infarct size?

A

Primary PCI for STEMI

Nitrates- relax smooth muscles , inhibit platelet aggregation

53
Q

What are the 3 benefits of using Nitro in AMI PTs not Tx w/ thrombolytics?

When using nitrates in AMI, titrate flow to ?

A

Dec infarct size
Improves regional function
Dec rate of CV complications

BP reduction, not pain

54
Q

Avoid Nitrates in PTs who took phosphodiesterase inhibitors in the past ?hrs

BBs hold what 3 beneficial properties

A

24hrs- Sildenafil
48hrs- Tadalafil

Anti dysrhythmic, ischemic and HTN properties

55
Q

Usually ? meds are given post-MI w/in 24hrs

BBs can only be given if PT has none of ?

A

PO Metoprolol
ACEIs

Signs of HF
Low output
Cardiogenic shock risks

56
Q

Use of BBs are still c/i in ? PTs

What class of drug may be used for limiting infarct size but doesn’t improve mortality

A

2/3rd degree blocks
PR interval >0.24sec
Asthma
Reactive airway dz

CCBs

57
Q

What PTs may find benefit from CCBs?

A 
Ischemia
A-fib w/out CHF
LV dysfunction
AV blocks
C/i BB use
58
Q

Anterior AMIs tend to cause TPs to develop ? sequelae dysrhthmia that indicates poor prognosis?

PTs w/ SVT, Afib/flutter w/ hemodynamic compromise are best Tx w/ ?

A

Sinus tach

Cardioversion

59
Q

? is used for Tx sinus bradycardia causing HOTN, ischemia or ventricular escape rhythms?

Anterior and inferior wall MIs can cause PTs to develop ?

A

Atropine

Complete heart blocks from occlusion of RCA/LAD

60
Q

What type of rhythms occur from anterior/inferior MIs

How does a mechanical complication present?

A

Transient junctional <48hrs of infarct

Previously stable PT suddenly decompensates- usually due to tearing/rupture of infarcted tissue

61
Q

When do ventricular free wall ruptures tend to occur?

What doe these usually lead to?

If this occurs, what is the dx test of choice?

A

1-5 days after infarct

Pericardial tamponade
Death

Echo

62
Q

How does a rupture of the interventricular septal wall present?

What is the Dx procedure of choice?

A

Chest pain
Dyspnea
Sudden/new holosystolic murmur

Doppler echo

63
Q

What PTs are more likely to have a septal rupture?

Papillary muscle rupture is more common after ? MI and presents w/ ?

A

Anterior wall MI
Three vessel CADz

Inferior MI
Dyspnea Inc HF/Dyspnea
Pulm edema
New holosystolic murmur w/ MR

64
Q

When are AMI PTs more likely to develop pericarditis

How are these PTs Tx

A

Transmural AMI and delayed presentation

ASA
Colchicine
Do not use Ibuprofen

65
Q

How does Dressler’s Syndrome present?

How is it Tx

A

Chest pain
Fever
Pleuropericarditis

ASA
Colchicine

66
Q

What Tx/PE finding suggests PT may be having RV infarction

Although not always available, what images can be Dx?

A

JVD/HOTN in response to Nitro

Echo/nuclear imaging

67
Q

What is the most serious complication that can occur from RV infarcts?

How are these types of infarcts Tx

A

Shock

Maintain pre-load (NS)
Reduce RV afterload
Inotropic support of RV
Early reperfusion

68
Q

Post-PCI PT presenting w/ chest pain has ? until proven other wise?

What biomarker is the most sensitive for detecting cocaine associated biomarker?

A

Abrupt vessel closure

Cardiac troponin

69
Q

How is cocaine induced ACS Tx

What meds are c/i in the first 24hrs

A

Benzos ASA Nitrates

BBs

70
Q

Define HF

What are the cardinal manifestations?

A

Structural/functional impairment of ventricular filling/ejection

Fatigue
Fluid retention
Edema
Dyspnea

71
Q

What is the most endogenous counter regulatory response to HF?

What are the three types of this response?

A

Natriuretic peptides

A: atria
B: ventricles
C: endotelium

72
Q

What two effects are stimulated by natriuretic peptide release?

A

Dilation

RAAS inhibition

73
Q

What are the 6 classifications of acute HF?

A

HTN: SBP >140

High Output: tachy, warm extremities, pulmonary congestion

Cardiogenic shock: Hypoperfusion w/ SBP <90

RHF: low output w/ JCD, hepatomegaly

Acute on Chronic: peripheral edema but doesn’t fit other categories

PEdema: rales, dec O2 sat

74
Q

How do PTs w/ acute on chronic HF present

How is higt output HF distinguished?

A

Gradual Sxs
Weight gain over days/wks

Normal ejection fraction
Caused by anemia/thyrotoxicosis

75
Q

Normal ejection fraction is ?

Reduced ejection fraction is ?

A

60%

<50%

76
Q

Define Systolic Dysfunction

Define Diastolic Dysfunction

A

HF w/ reduced EF <50%

HF w/ preserved ejection fraction, impaired ventricular relaxation

77
Q

How is HF Dx

What are the RFs for HF

A

Clinical Dx w/ Hx and PE

HTN 
DM 
Valvular dz
Age
Male 
Obese
78
Q

What Sx has the highest sensitivity for Dx of HF

What 3 Dxs have the highest specificity?

A

Dyspnea on exertion

Paroxysmal nocturnal dyspnea, Orthopnea and Edema

79
Q

What result has equivocal accuracy as clinical gestalt for Dx HF?

? test/image results are most specific for a final Dx of acute HF?

A

BNP value

CXR w/ congestion, cardiomegaly and edema

80
Q

What EKG finding has the highest likelihood ratio for HF?

A

Afib

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