Cardiac Part II- Arrhythmias and Ischemia Flashcards

1
Q

What HR is the AV node beating at?

A

40-60 bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

What HR are the Purkinje fibers beating at?

A

20-40 bpm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What length of time is a little box in an EKG?

A

0.04 secs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What length of time is a big box in an EKG?

A

0.2 secs

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What does a p-wave represent?

A

Atrial depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What does a QRS segment represent?

A

Ventricular depolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

What does a T-wave represent?

A

Ventricular repolarization

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Sinus tachycardia

A

Upright P wave in lead II preceding every QRS with a ventricular rate >100/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Causes of sinus tach

A
Exercise
Anemia
Dehydration or shock
Fever
Sepsis
Infection
Hypoxia
Chronic pulmonary disease
Hyperthyroidism
Pheochromocytoma
Medications/stimulants
Heart failure
Pulmonary embolus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

What is the rate when you count the boxes for the next QRS segment?

A
1st box: 300
2nd box: 150
3rd box: 100
4th box: 75
5th box: 60
6th box: 50
7th box: 43
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

Sinus bradycardia

A

Upright P wave in lead II preceding every QRS with a ventricular rate <60/min

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

Causes of sinus bradycardia

A
AV blocking meds
Heightened vagal tone
Sick sinus syndrome
Hypothyroidism
Hypothermia
Obstructive sleep apnea
Hypoglycemia
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Sinus arrhythmia

A

Changing sinus node rate with resp cycle
Common in young healthy individuals
HR increases with inspiration and decreases with expiration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Premature atrial contractions (PAC)

A

Occurs when a focus in the atrium (not the SA node), generates an action potential before the next scheduled SA node action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Characteristics of premature atrial contractions (PAC)

A
Premature
Ectopic
P-wave looks morphologically different
Narrow QRS
Compensatory pause
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Atrial fibrillation

A

Occurs when action potentials fire very rapidly within the pulmonary veins or atrium in a chaotic manner resulting in a VERY fast atrial rate (300-600 bpm)
Ventricular rate is usually 100-200 due to the AV node that becomes intermittently refractory
No P-waves

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Risk factors for A fib

A
HTN
Valvular heart disease
CAD
Cardiomyopathy
COPD
Obesity
Sleep apnea
Excessive EtOH
DM
Thyrotoxicosis
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

S/Sx of A fib

A
Asymptomatic
Palpitations
Fainting
SOB
CP
CVA
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

Classifications of A fib

A
First detected
-Only one diagnosed episode
Paroxysmal
-Recurrent episodes that stop on their own in <7 days
Persistent
-Recurrent episodes that last >7 days
Permanent
-An ongoing long-term episode
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

Management of A fib

A

Rate control- beta blockers, calcium channel blockers, digoxin
Rhythm control
Anticoagulation
-Warfarin, heparin, dabigatran, rivaroxaban, apixaban
-ASA
Cardioversion
-Electrical or chemical (amiodarone, etc.)
Ablation/MAZE procedure

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

Atrial flutter

A

Occurs when a “reentrant circuit” is present causing a repeated loop of electrical activity to depolarize the atria at a fast rate of ~250-350 bpm
Produces a “sawtooth” pattern of the P waves with lack of P waves
A narrow complex tachycardia at a ventricular rate of exactly 150 bpm is very commonly atrial flutter

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Supraventricular tachycardia (SVT)

A

Any tachycardia that begins above the ventricles (at or above the AV node)
-Paroxysmal (comes and goes) supraventricular tachycardia (PSVT)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Mechanisms of supraventricular tachycardia (SVT)

A

Re-entry: often quick acceleration to 200 bpm

Automaticity: atrial tachycardia, junctional ectopic tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

Antidromic

A

Going in a clockwise direction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

Orthodromic

A

Going in a counterclockwise direction

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

S/sx of supraventricular tachycardia (SVT)

A
Palpitations
SOB
CP
Tachypnea
Dizziness
Loss of consciousness
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

EKG findings in supraventricular tachycardia (SVT)

A

Narrow QRS complex

Tachycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

Tx for supraventricular tachycardia (SVT)

A
Physical maneuvers
-Valsava, coughing, carotid massage, drinking ice water, plunging the face into cold water
Medications
-Adenosine
Cardioversion
-Synchronized
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

Junctional rhythm

A

Occurs when the electrical activation of the heart originates near or within the AV node instead of from the SA node

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

Characteristics of junctional rhythm

A

Narrow QRS complex
P wave frequently is not seen (may be buried)
P waves sometimes seen after QRS
May be slow or fast

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

What does accelerated indicate if it precedes the words junctional bradycardia?

A

> 60 bpm HR

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Premature ventricular contraction (PVC)

A

Occurs when a focus in the ventricle generates an action potential before the next schedule SA nodal action potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Characteristics of premature ventricular contractions (PVC)

A

Premature
Ectopic
Wide complexes
Compensatory pause

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

V tach

A

Wide QRS complex (>120 ms) originating in the ventricles at a rate >100 bpm
Considered to be hemodynamically unstable life-threatening
-May or may not have a pulse

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Tx for v tach

A

ACLS (defibrillation, epi, antiarrhythmics)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Classifications of v tach

A

Sustained- lasts more than 30 secs or symptomatic
Non-sustained VT: lasts less than 30 secs and is asymptomatic
Monomorphic- same pattern
Polymorphic- changing pattern

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

What electrolyte finding occurs with Torsades de Pointes?

A

Hypomagnesemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Steps of pulseless V-tach

A
  1. No pulse
  2. IV, O2, monitor
  3. Start CPR (2 min), hook up AED
  4. Evaluate rhythm and pulse
  5. Defibrillation
  6. Continue CPR (2 mins)
  7. Evaluate rhythm and pulse
  8. Defibrillation
  9. Continue CPR (2 mins) and epinephrine q3-5 mins
  10. Evaluate rhythm and pulse
  11. Continue CPR (2 mins) and Amiodarine 300 mg bolus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

V-tach tx

A

Treat with IV Mg

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

Clinical pearl about V-tach

A

Pts with a prolonged QT interval have a higher risk of developing polymorphic VT

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Idioventricular rhythm

A

It is very similar to ventricular tachycardia (VT) except the ventricular rate is <60
Often called “slow VT”
When ventricular rate is between 60-100, it is referred to as an accelerated idioventricular rhythm or AIVR (common with MI)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

V fib

A

Quivering of the ventricles with virtually NO forward CO

Main cause of sudden death in pts with MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

Tx of V fib

A
  1. No pulse
  2. IV, O2, monitor
  3. Start CPR (2 min), hook up AED
  4. Evaluate rhythm and pulse
  5. Defibrillation
  6. Continue CPR (2 min)
  7. Evaluate rhythm and pulse
  8. Defibrillation
  9. Continue CPR (2 min) and epi q3-5 min
  10. Evaluate rhythm and pulse
  11. Continue CPR (2 min) and amiodarone 300 mg bolus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

Tx of asystole

A

High-quality CPR, epi

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

First-degree AV block

A

Fixed prolonged PR interval (>0.20 sec)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

Causes of 1st degree AV block

A

Medications
Ischemia
Lyme disease

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

2nd degree AV block

Mobitz Type I (Wenckebach)

A

Progressive PR interval prolongation with each beat until a QRS wave is not conducted
Longer, longer, longer…drop QRS

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

Mobitz type II

A

Extra P waves with dropped QRS
Usually associated with bradycardia
PR interval may be nl or prolonged

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
49
Q

Tx for Mobitz type II

A

Pacemaker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
50
Q

3rd degree heart block

A

No communication between atria and ventricle
P waves: equal distance between all
QRS: WIDE, slow, and equal distance between all
Usually symptomatic

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
51
Q

Tx for third degree heart block

A

Pacemaker

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
52
Q

What is an EKG finding in hypokalemia?

A

U wave

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
53
Q

What are EKG findings in hyperkalemia?

A

Peaked T waves
Widening of the QRS
Increase in PR interval
Bradycardia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
54
Q

What is an EKG finding in hypocalcemia?

A

Prolonged QT interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
55
Q

What is an EKG finding in hypercalcemia?

A

Shortened QT interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
56
Q

Long QT syndrome

A

May lead to potentially fatal arrhythmia polymorphic ventricular tachycardia (torsades de pointes)

57
Q

S/sx of long QT syndrome

A

Palpitations
Fainting
Sudden death

58
Q

Nl range of QT

A

<0.440

59
Q

Prolonged QT interval causes

A
Congenital
Acquired
-Medications
-Disease states
-Electrolyte abnormalities
60
Q

Medication causes of prolonged QT interval

A
Macrolides
FQs
TCA
Antipsychotics
Ondanstron
61
Q

Diseases that cause prolonged QT interval

A

Intracranial hemorrhage

62
Q

Electrolyte abnormalities that cause long QT syndrome

A

Hypocalcemia
Hypomagnesemia
Hypokalemia

63
Q

Brugada syndrome

A

Genetic disorder that results in sudden cardiac death from polymorphic ventricular tachycardia or ventricular fibrillation in the setting of a structurally nl heart
-Most commonly from a mutation in the Na channel gene SCN5A
QT interval is nl

64
Q

Type I EKG findings in Brugada syndrome

A

Lead V1 has a “covered” ST segment elevation of at least 2 mm followed by a neg T wave

65
Q

Type II EKG findings in Brugada syndrome

A

There is a “saddleback” appearance of the ST segment in lead V1 with ST elevation of at least 2 mm. This can be present in nl individuals as well

66
Q

Type III EKG findings in Brugada syndrome

A

Features of type I or type II with a <2 mm of ST segment elevation

67
Q

Wolff-Parkinson-White (WPW)

A

Accessory pathway that connects the electrical system of the atria directly to the ventricles allowing conduction to avoid passing through the AV node
Shortened PR interval
Delta wave

68
Q

Tx for Wolff-Parkinson-White

A

Procainamide +/- electrical cardioversion

69
Q

Class I Vaughan-Williams classification- antiarrhythmic meds

A

Block membrane sodium channels

70
Q

Class II Vaughan-Williams classification- antiarrhythmic meds

A

Beta-blockers that decrease automaticity, prolong AV conduction, and prolong refractoriness

71
Q

Class III Vaughan-Williams classification- antiarrhythmic meds

A

Block potassium channels and prolong repolarization, widening the QRS and prolonging the QT interval

72
Q

Class IV Vaughan-Williams classification- antiarrhythmic meds

A

Calcium channel blockers that decrease automaticity and AV conduction

73
Q

Class I

Ia

A

Quinidine, Procainamide, Disopyramide

-SVT, VT, prevention of VF, symptomatic ventricular premature beats

74
Q

Class I

Ib

A

Lidocaine, Mexiletine

-VT, prevention of VF, symptomatic ventricular beats

75
Q

Class I

Ic

A

Flecinide, Propafenone

-Life-threatening VT or VF, refractory SVT

76
Q

Class II MOA

A

Slows AV conduction

77
Q

Class II indications

A

SVT, may prevent VF

  • Esmolol
  • Propranolol
  • Metoprolol
78
Q

Side effects of Class II

A

Fatigue
Bradycardia
AV block
Decreases LV function

79
Q

Class III- Amiodarone

A

Refractory VT, SVT, prevention of VT, A fib, VF

80
Q

Side effects of Amiodarone

A
Hypotension
Corneal micro-deposits
Thyroid dysfunction
-Hypothyroidism > Hyperthyroidism
Pulmonary fibrosis
Blue-gray skin discoloration
81
Q

Class III- Dronedaron

A

Side effects:

  • QT prolongation
  • Contraindicated in severe heart failure
82
Q

Class III- sotalol

A

VT, A fib

Side effects: Torsades de pointes, bradycardia

83
Q

Class III- Dofetilide

A

A fib and flutter

Side effects: Torsades de pointes in 3% of pts

84
Q

Class III- Ibutilide

A

Conversion of A fib and flutter

Side effects: Torsades de pointes in 5% of pts

85
Q

Class IV indications

A

SVT

86
Q

Class IV- Verapamil

A

Side effects:

  • Constipation
  • Decreases LV function
87
Q

Class IV- Diltiazem

A

Side effects:

  • Hypotension
  • Decreases LV function
88
Q

Class V indications

A

SVT

89
Q

Class V adenosine MOA

A

Blocks AV nodal conduction and shortens atrial refractoriness

90
Q

Class V- adenosine SEs

A

Transient flushing
Dyspnea
AV block
Sinus bradycardia

91
Q

Class V- digoxin MOA

A

Inhibits the Na, K, ATPase pump and prolongs AV nodal conduction and AV nodal refractory period

92
Q

Class V- digoxin SEs

A

AV block
Arrhythmias
GI
Visual changes

93
Q

Tx for Brugada syndrome

A

Implantable cardioverter-defibrillator (ICD)

94
Q

Tx for long QT syndrome

A

Beta blockers

Implantable cardioverter-defibrillator (ICD)

95
Q

Coronary artery disease

A

MOST pts have identifiable and modifiable risk factors

96
Q

Risk factors of CAD

A
Aging
Male gender/post-menopausal women
FHx of premature CAD
DM
HTN
Hyperlipidemia
Smoking- #1 preventable cause
Obesity and inactivity
97
Q

What is responsible for almost all cases of coronary heart disease?

A

Atherosclerosis
-Insidious process: Begins with fatty streaks that are first seen in adolescence- progress into plaques into early adulthood- culminate in thrombotic occlusions and coronary events in middle age and later life

98
Q

Ischemic heart disease

A

Often associated with other ischemic disease:

  • PAD
  • Coronary artery stenosis
  • Cerebrovascular disease/stroke/TIA
  • Renal artery stenosis
  • Mesenteric ischemia
99
Q

Angina pectoris

A

Precordial CP precipitated by stress or exertion and relieved by rest or nitrates
Angina is the term used when CP is thought to be attributable to myocardial ischemia
Occurs whenever myocardial oxygen demand exceeds oxygen supply

100
Q

Most common cause of angina pectoris

A

Atherosclerotic obstruction of one or more coronary arteries

-Other causes: coronary artery vasospasm, congenital anomalies, emboli, arteritis, LVH, dissection

101
Q

Sx of angina pectoris

A
Pressure, pain, squeezing, tightness, heaviness
Exertion and relieved with rest
Atypical sx:
-Dyspnea
-Indigestion
-Arm or jaw pain
-Exertional SOB
-Nausea
-Diaphoresis
-Fatigue
102
Q

Activities that promote angina pectoris

A
Physical activity
Cold
Emotional stress
Sexual intercourse
Meals
Lying down
More commonly in the morning
Generally lasts for 2-5 minutes
103
Q

Stable angina pectoris

A

Pattern to the pain, predictable
Chest discomfort can be reproduced at a certain level of exertion and is relieved with rest or nitro
Lasts 5-15 minutes

104
Q

Workup for stable angina pectoris

A

EKG
Stress test
+/- coronary angiography

105
Q

Labs for angina pectoris

A

Negative troponins

106
Q

EKG for angina pectoris

A

Usually nl at rest
Ischemic changes: T wave flattening or inversion, ST depression
Exercise EKG is the most commonly used noninvasive procedure for evaluating for inducible ischemia

107
Q

Precautions and risk for exercise EKG for angina pectoris

A

1 infarction or death per 1,000 tests

Symptomatic aortic stenosis is a relative contraindication

108
Q

Indications for exercise EKG for angina pectoris

A

Comfirm dx of angina, determine severity of limitations of activity due to angina, assess prognosis in pts with known CAD, evaluate responses to therapy

109
Q

Exercise EKG positive test for angina pectoris

A

1 mm horizontal or downsloping ST-segment depression measured 80 msec after the J point
60-80% of pts with anatomically significant coronary dz will have a pos test

110
Q

Tx for angina pectoris

A

SL nitro

111
Q

Prevention of further attacks for angina pectoris

A

Beta blockers- prolongs life
ASA or alternative clopidogrel
Ranolazine- may prolong QT
Calcium channel blockers- generally used as last line agent

112
Q

Printzmetal’s or variant angina

A
Angina pain at rest (often b/w midnight-early morning)
Most common in early women
Each episode generally lasts 5-15 mins
Coronary artery vasospasm
ST segment elevation
Treated with CCBs
Avoidance of nicotine, caffeine, ergots
113
Q

Unstable angina and non-ST elevation MI

A

“Preinfarction” acute coronary syndrome
New or worsening sx of myocardial ischemia
-Angina may come on at rest or with minimal exertion and may last >30 min
Changing pattern:
-Frequency, duration, intensity
-Requires longer rest periods/more nitro

114
Q

Labs for unstable angina and NSTEMI myocardial infarction

A

Troponin neg with unstable angina
Troponin pos with NSTEMI
Check BMP for K and Crt

115
Q

EKG for unstable angina and NSTEMI myocardial infarction

A

Unstable angina- usually ST depression

NSTEMI- non ST elevation MI (+ troponins)

116
Q

Tx for unstable angina and non-ST elevation MI

A
MONA-B
-CCB if BB contraindicated
Antiplatelet and anticoagulation therapy
Hospital admission
Risk-stratification tools
Early invasive coronary catheterization
Statins
117
Q

MONA-B components- Nitro

A

1st line therapy
SL tablet, spray or paste
Contraindicated if PDE-5 inhibitors used in past 24 hrs

118
Q

MONA-B components- ASA

A

162-325 mg loading dose

Then 81-325 mg daily for at least one month

119
Q

MONA-B components: Beta blockers, morphine, and oxygen

A

Oral or IV
Morphine-chest discomfort
Oxygen- supplemental

120
Q

P2Y12 inhibitors

A

Antiplatelet therapy for unstable angina and NSTEMI
Clopidogrel
Prasugrel
Ticagrelor

121
Q

Glycoproetin IIB/IIIA inhibitors

A

Antiplatelet therapy from unstable angina and
Tirofiban, Eptifibatide, Abciximab
Usually started in cath lab

122
Q

Heparin

A

Anticoagulant therapy for unstable angina and STEMI

Enoxaparin (LMWH) or unfractionated heparin

123
Q

Fondaparinux

A

Anticoagulant therapy for unstable angina and NSTEMI

Slightly better for high risk bleeders

124
Q

Direct thrombin inhibitors

A

Anticoagulant therapy for unstable angina and NSTEMI

Bivalirudin + glycoprotein IIb/IIIa inhibitor

125
Q

Risk stratification tools for unstable angina and NSTEMI- GRACE risk score

A

BP
ST-segment deviation Cardiac arrest at presentation
Serum Crt Elevated troponin or CK-MB
HR

126
Q

Risk-stratification tools for unstable angina and NSTEMI: TIMI risk score

A
Age 65 or older
3 or more risk factors
Prior coronary stenosis 50% or more
ST-segment deviation
Two anginal events in prior 24 hrs
ASA in prior 7 days
Elevated cardiac markers
127
Q

Indications for cardiac catheterization and PCI in unstable angina and NSTEMI

A
Recurrent angina/ischemia at rest or with low-level activity
Elevated troponin
ST-segment depression
Recurrent ischemia with evidence of HF
EF <40%
Hemodynamic instability
Sustained VT
PCI within 6 mos
Prior CABG
128
Q

PCI

A
AKA: coronary angioplasty
Balloon angioplasty
Implantation of stents
-Bare metal or drug eluding
Rotational or laser atherectomy
Brachytherapy
-Radioactive source to inhibit restenosis
129
Q

STEMI

A

EMERGENCY
Acute episode of chest discomfort that results in most cases, from an occlusive coronary thrombus at the site of a preexisting atherosclerotic plaque
Other causes: prolonged vasospasm, inadequate myocardial blood flow, emboli, coronary dissection, cocaine

130
Q

STEMI risk

A

Risk of cardiac biomarkers with at least one value above the 99th percentile of the upper reference limit together with evidence of myocardial ischemia with at least two of the following:

  • Sx of ischemia
  • EKG changes of new ischemia
  • New Q waves
  • Imaging evidence of new loss of viable myocardium or new wall motion abnormality
131
Q

Sx of STEMI

A

Worsening in the pattern of angina or at rest
-May occur with minimal exertion
Pain may be more severe
-Nitro also has little effect
Associated sx
-Cold sweat feel weak and apprehensive, and move about trying to see a position of comfort
-Light-headedness, syncope, dyspnea, orthopnea, cough, wheezing, nausea, vomiting, abdominal bloating

132
Q

Painless infarction in STEMI

A

Older pts
Women
Pts with diabetes

133
Q

Sudden death and early arrhythmias in STEMI

A

50% of deaths occur before the pts arrive at the hospital

Death is presumably caused by v fib

134
Q

General signs of STEMI

A

Anxious, resp distress, sweating
Bradycardia, tachycardia, arrhythmias
Hypertension, hypotension

135
Q

Heart signs of STEMI

A

Murmurs, S3, pericardial friction rubs

136
Q

Extremity signs of STEMI

A

Usually nl

Cyanosis, peripheral pulses, edema

137
Q

Labs for STEMI

A

Pos troponin or CK-MB

138
Q

EKG of STEMI

A
Peaked hyperacute T waves
ST-segment elevation
Q wave development
T wave inversion
NEW LBBB