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Clin Specialties - EMed > Lecture 3 - Cardiac > Flashcards

Lecture 3 - Cardiac Flashcards

1
Q

What is the treatment for myocarditis?

A

steroids

and heart transplant

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2
Q

Where do most aortic aneurysms occur?

A

abdomen

typically do not cause pain

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3
Q

What causes pain during a pneumothorax?

A

damage to the pleura

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4
Q

When does PNA cause chest pain?

A

once the infection advances to the lining of the lung

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5
Q

Where on the bone is there sensory innervation?

A

only at the periosteum

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6
Q

Who are we more worried about in regards to bone fracture, a 16 year old or a 50 year old?

A

The 50 year old

more likely to be pathologic

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7
Q

Which chest pain can you NOT miss?

A 
PNA 
MI 
PE
ACS
Dissection
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8
Q

What are the official vs not official cardiac risk factors?

A 
Cardiac RF: 
HTN 
Cholesterol 
DM
Family Hx (really only if they have familial hypercholesterolemia) 
Tobacco 
Non-official: 
sedentary lifestyle 
obesity 
prior MI 
age
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9
Q

Right sided heart failure can manifest how?

A

peripheral edema

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10
Q

What is one of the most common reasons for decreased breath sounds?

A

broken ribs

the pt is avoiding breathing in all the way

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11
Q

What tests will you order for chest pain?

A

EKG (first and best)
Troponin
Chest Xray

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12
Q

D - Dimer

A

tests when a clot is being broken down by the body

it is a good test for aortic dissection because the blood trapped in the false lumen is clotting

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13
Q

BNP

A

test that can help differentiate between CHF and COPD

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14
Q

What is the gold standard for dx dissection?

A

CT scan with contrast

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15
Q

Who should get a D-dimer?

A

pts in low risk with a 15% pre-test probability AND sxs less than 72 hours (mature clots come back negative)

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16
Q

Who are we worried about with aortic dissection?

A

Marfan’s Syndrome: tall, lanky arms and legs, bluish tinge to sclera, high arched palate

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17
Q

If esophageal spasm manifests similarly to chest pain and is even released by nitro, how can you differentiate this from MI?

A

troponin

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18
Q

What causes esophageal rupture?

A

vomiting (not coughing) really hard

you may even see pink dots on cheeks from where they’ve ruptured blood vessels on their face

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19
Q

What is the initial presentation of ischemic heart disease?

A

Stable angina

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20
Q

What is the underlying pathology behind stable angina?

A

Atherosclerosis — end result of an inflammatory process instigated by endothelial disruption

Stable angina is limited flow from progressive athersoclerotic narrowing of epicardial vessels

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21
Q

What are the s/s of stable angina?

A

Persistent, exertional chest discomfort

Relief with rest or nitro

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22
Q

Unstable angina?

A

Sxs are accelerating (increasing in frequency, duration, intensity) or occur at rest

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23
Q

What is the treatment for stable ischemic heart disease?

A

Nitro

Beta blocker (or BBC if contraindications for BB)

Daily ASA (or clopidogrel if ASA CI)

Lifestyle modifications

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24
Q

NSTEMI

A

Intermittent occlusion/pre-profusion

Unlike STEMI which complete occlusion of coronary blood flow

+ cardiac enzymes in both STEMI and NSTEMI (not found in unstable angina)

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25
Q

How is STEMI dx?

A

Clinical intuition + EKG

Move quickly to treatment —> time is muscle

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26
Q

What is the treatment for an NSTEMI?

A

PCI within 72 hours of symptom onset (more urgent than emergent)

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27
Q

What is the treatment for angina?

A

Oxygen and IV saline

If they are stable you can observe them, contact their PCP (most often stable angina pts do not present to the ED), and send them home

Unstable: (getting admitted)
Oxygen NC 
Aspirin (Chew)
Heparin 
Nitro
BB (esmolol)

CCB only have a place in Prizmetal angina

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28
Q

How can you tell which leads belong to which area of the heart?

A

Big I, lil I, Ass up, All down

L S. L
I L. S. L
I. I. A. A

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29
Q

What is the gold standard for dx MI?

A

Troponin

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30
Q

What is the goal of “door to balloon time”?

A

90 minutes to PTCA (percutaneous transluminal coronary angioplasty)

If that is unavailable then 30minutes to fibrinolysis

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31
Q

What are thrombolysis agents that are used for MI treatment when cath lab is not available?

A

Tissue plasminogen activator
Streptokinase
Tenecteplase

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32
Q

What supportive therapy is given to pts with MI in the ED?

A

MONA

Morphine (helps with pain and lowers BP, decreasing afterload)
Oxygen (NC only if <90% or respiratory distress)
Nitro (decrease afterload and preload
ASA (aspirin)
+/- statin therapy (helps decrease inflammation)

+/- ACEI

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33
Q

What does the morphine part of MONA do?

A

Reduce afterload

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34
Q

For MI pt, when do you not want to do MONA?

A

Don’t give nitro (we dont want to decrease pre-load) for pts with a right (RCA) occlusion

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35
Q

When do we not give nitro?

A

If SBP is <90
Inferior infarct pattern
Use of viagara/sildenafil in last 24 hours

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36
Q

What is the dose of ASA that should first be chewed by the pt having an MI?

A

325mg followed by a daily dose of 81mg

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37
Q

What is the goal of anticoagulation therapy?

A

Limitation of thrombin

Achieved by attacking various portions of the coagulation cascase

38
Q

What role do statins play in ACS?

A

Should be given to every pt with ACS regardless of their lipid levels
Should be started on day of presentation and continued indefinitely

It:

  • stableizes plaques
  • reverses endothelial dysfunction
  • decreases thrombogenicity
  • anti-inflammatory
39
Q

Beta blockers use in the setting of ACS?

A

Negative inotropic properties

Positive effects on remodeling

Reduction of myocardial oxygen demand in the acute setting

40
Q

What is the difference between NSTEMI and STEMI in regards to treatment?

A

STEMI has to go to the cath lab right away

NSTEMI will EVENTUALLY go to the cath lab (24-48 hours)

41
Q

How does PCI (cath lab) work?

A

Access via radial or femoral artery

Catheter advanced to aorta and coronaries via fluoroscopy

42
Q

If a pt with ACS begins to show signs of heart failure and have a heart murmur, what type of valve problem is this?

A

Acute mitral regurgitation

43
Q

Loud, harsh mid-systolic murmur primarily localized to the RUSB and projecting to the carotids

A

Aortic stenosis

44
Q

How do pts with aortic stenosis present?

A

Dyspnea
Syncope
Angina with exertion

Harsh systolic murmur

Left ventricular hypertrophy

45
Q

What is the treatment for aortic stenosis?

A

Eventually valve replacement

Admit with syncope, cardiac chest pain, CHF, arrythmias

Treatment in the ED is really focused on what NOT to do since these pts have a fixed cardiac output
NOT:
Nitrates/diuretics: exacerbate sxs by reducing pre-load
BB: reduce inotropes —> exacerbate sxs (basically decrease contractility)
CCBs: reduce in afterload —> lead to deminished outflow

46
Q

Which murmur might you see with endocarditis?

A

Aortic regurgitation (diastolic murmur)

47
Q

Aortic regurgitation

A

Incompetence of aortic valve leading to reduction in cardiac output —> heart failure

Acute:
Endocarditis
Retrograde dissection

Chronic:
Bicuspid valve (MC in US)
Rheumatic heart disease (MC in world)
Infective endocarditis

48
Q

Soft, high pitched, early diastolic decrescendo murmur localized to 3rd intercostal space on the left (Erbs point)

A

Aortic regurg

Accentuated at end expiration with pt sitting up and leaning forward

49
Q

What is the mainstay of treatment for aortic regurg in the ER?

A

Check for underlying infection (endocarditis can be a major cause)

Control HTN to alleviate pressure

NOT:
BB - may prolong diastole and lead to increased regurg

50
Q

What causes acute aortic regurg?

A 
Infective endocarditis
Aortic dissection (retrograde)

Traumatic deceleration injury

51
Q

What is the pathophysiology behind chronic aortic regurg?

A

Left ventricle dilates to accommodate the regurgitant volume while maintaining cardiac output. Increasing end-diastolic volume (pre-load) is the primary hemodynamic compensation for aortic regurg —> eventually this fails leading to CHF

52
Q

How do pts with aortic regurg present?

A

Pts present late in disease

May complain of uncomfortable awareness of their heart beat or palpitations, especially in bed, for years before exertional sxs develop

As ventricle fails, sxs of left sided and then right sided heart failure develop

53
Q

With which valvular disease do you see widened pulse pressure?

A

Aortic regurg

54
Q

Mitral stenosis

A

W > M

Rheumatic fever (autoimmune attack on the heart in response to strep infection)

Decreased left ventricle filling
Marked atrial enlargment and elevated atrial pressures

Leads to pulmonary hypertension and right sided heart failure

Sxs: exertional dyspnea and cough progressing to sxs of CHF and then right sided heart failure
Hemoptysis

55
Q

What are the sxs of someone with mitral stenosis?

A

Dyspnea on exertion (d/t pulmonary HTN)
Right heart failure

Elevated jugular venous pressure
Narrow pulse pressure

Diastolic opening snap
Low pitch rumble

56
Q

What is the treatment for mitral stenosis?

A

BB/CCB: increase diastolic filling time to augment cardiac output

Warfarin for A. Fib

Balloon vulvuoplasty

57
Q

What is the most common valvular disease in US?

A

Mitral regurgitation

58
Q

What are the sxs of mitral regurg?

A

Acute
-often associated with ischemia
-occur with chordal rupture
Sxs are abrupt onset and associated with FLASH PULMONARY EDEMA

Chronic:
Progressive dyspnea
A. Fib
Worsening heart failure

59
Q

What is the treatment for someone with mitral regurg?

A

Ultimately surgery

Can help with decrease remodeling with BB and afterload reduction

60
Q

Previously healthy person presents to the ED with pulmonary edema

A

Be thinking acute mitral regurg

61
Q

Holosystolic murmur

A

Mitral regurg

62
Q

Aortic dissection

A

Precipitated by tear of vascular intima

HTN biggest RF

Excrutiating/ “tearing” pain with abrupt onset and marked distress
Decresendo

Pain located to chest or back/abdomin depending on location

HTN
Pulse variance or BP differential (difference in BP between right and left arm)
Mediastinal widening on xray

Tx: strict BP control with BB, fluid support, surgery

63
Q

Mediastinal widening on chest x-ray

A

Aortic dissection

Also you will see:
Abrupt onset of tearing pain in chest or abdomen
Variance in BP or pulse between arms

64
Q

What is the treatment for aortic dissection?

A

BB —> control that BP
Fluids

Surgery

65
Q

What size aneurysm is dx for aortic aneurysm?

A

> 4cm

66
Q

At what cm do pts with aortic aneurysms get surgery?

A

5.5cm or greater

67
Q

Ascending vs descending aortic aneurysm

A

Ascending = before ligamentum arteriosum

Descending = distal to ligamentum arterisoum

68
Q

Pericarditis

A

Non=specific inflammation of the pericardial sac surrounding the heart

Typically viral etiology (HIV, TB, neoplasia, autoimmune)

Acute vs recurrent vs effusive

Often see systemic signs of inflammation/infection
URI prodrome common

95% present with acute, sharp/pleuritic pain
Worse when laying flat, relieved when leaning forward

Pericardial friction rub
Muffled heart sounds
Pulsus paradoxus

Diffuse ST elevations

Echo - assess for effusion

Tx: NSAIDs
Colchicine
Glucocorticoids (Prednisone) —> only for refractory cases

69
Q

Presentation of pericarditis?

A

Often see systemic signs of inflammation/infection
URI prodrome common

95% present with acute, sharp/pleuritic pain
Worse when laying flat, relieved when leaning forward

Pericardial friction rub
Muffled heart sounds
Pulsus paradoxus

Diffuse ST elevations

Echo - assess for effusion

70
Q

What is the treatment for pericarditis?

A

NSAIDs

Colchicine

71
Q

Pericardial tamponade

A

Ventricular compromise d/t effusion around the heart
Rate of fluid accumulation rather than volume is predictor of severity

Commonly caused by trauma

Becks triad:
Neck vein distention
Hypotension
Muffled heart sounds

Kussmauls sign (increased JVD with inspiration)

EKG: electrical alternans

Tx: pericadiocenteiss
Dobutamine
Admit to ICU

72
Q

Becks Traid

A

Seen with pericardial tamponade

Muffled heart sounds
Hypotension
JVD

73
Q

Kussmaul sign

A

Increase JVD with inspriation

Seen with tamponade

74
Q

Electrical alternans

A

Seen on EKG for cardiac tamponade

75
Q

How do you treat HTN in pregnancy?

A

Labetolol (first line)
Nifedipine
Methyldopa

76
Q

How do you treat HTN in DM?

A

ACEI/ARB, CCB, diuretic

77
Q

Sxs of HTN emergency

A 
Dydpnea
Chest pain 
HA 
Dizziness 
Neurological deficit

Flash edema is common initial presentation

78
Q

HTN emergency

A

In general, MAP reduction of 25% in the first 2 hours

Then target 160/100 gradually over 6 hours

Labatelol (BB first line therapy)
Nicardpine

79
Q

What is the treatment for acute pulmonary edema?

A

Nitroprusside with loop diuretic

80
Q

What is the treatment acute aortic dissection?

A

Nitroprusside + metoprolol

81
Q

When do we admit syncope pts?

A

CHF hx
Ventricular arrythmias
Valvular disease
Abnormal ECG

82
Q

Treatment for CHF in the ED focuses on?

A

Symptom stabilization and referral to ultimate care

Based on presentation 
Wet and cold 
Wet and warm 
Dry and cold
Dry and warm
83
Q

Treatment for wet and cold CHF?

A

Dobutamine (inotropic support to help with decongestion)

Or dapamine or milrinone

84
Q

What is the most dangerous zone to be in for CHF pts?

A

Dry and cold
(Poor perfusion even at optimal hemodynamics

Pts need mechanical support or transplant

85
Q

What is the treatment for bradycardic rhythms?

A

Atropine to improve rate

If unstable: transcutaneous pacing

Always look for reversible causes

Ultimate management is with pacemaker

86
Q

Treatment for tachy arrhythmias?

A

Unstable: shock

Stable: consider adenosine or vagal

87
Q

Afib vs aflutter on EKG?

A

Afib is irregularly irregular

Aflutter is usually regular (organized atrial activity increases suspicion of flutter)

88
Q

What is the treatment for afib and aflutter in a stable pt?

A

Rate control vis CCB or BB

Unstable: cardioversion (ONLY IF SXS ARE LESS THAN hours)
Anticoagulation is based on risk calculation with CHADSVASC score

89
Q

V Tach

A

MEDICAL EMERGENCY

Cardioversion
Rhythm control —> amiodarone

90
Q

What imaging provides the highest yield when assessing someone for aortic dissection?

A

CT

Clin Specialties - EMed (11 decks)

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