cardio Flashcards

1
Q

What is Dextrocardia?

A

Transposition of the heart (mirror image). May occur in isolation or other organs may be affected. Often is asymptomatic, but may be found in some genetic syndromes that leads to more significant issues

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2
Q

What is cardiomegaly?

A

In PA view, the maximum heart width should be less than ½ the total thoracic cavity width. Seen in dilated cardiomyopathy and HF. May be seen in HCM

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3
Q

What does pericardial effusion look like on CXR?

A

“Water bottle” sign. Makes the heart look enlarged and triangular in shape. Generally effusions are large if visible on CXR

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4
Q

What does CHF look like on CXR?

A

Possible CXR findings:
Pleural effusions: Bilateral costophrenic angles, fissure between lung lobes, Interlobular septa (Kerley B lines)- horizontal lines on periphery of lungs
Increased vascular markings: diffuse increase in vascular markings, cephalization of the pulmonary vessels (vessels in upper lobes more prominent) due to swelling
Fluid buildup that increases pressure in veins and capillaries and fluid will collect in spaces

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5
Q

What does CHF with pulmonary congestion/cepahlization look like on CXR?

A

Other organs that cause fluid overload state can give cephalization in the lungs like kidney failure, liver failure, etc. When there is cephalization, they show up really well in the upper lobes.

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6
Q

What does aortic dissection look like on CXR?

A

Widened mediastinum. “Calcium sign” (calcified area > 1 cm from outside curve of aortic knob). Blood is in between the layers of the wall and cause widening or separation, tend to occur where there are artherosclerotic plaques. If we didn’t have the calcium sign we couldn’t tell the difference between dissection and aneurysm

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7
Q

What do aortic dissection/Aneursysms look like on CXR?

A

Lower their blood pressure

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8
Q

What is a transthoracic echo?

A

It can be done outpatient or inpatient. Probe is placed on anterior chest in the intercostal “windows” because ribs will block out the sound waves, with standardized 4 view of the heart: the parasternal long axis (right shoulder), parasternal short axis (lef shoulder), apical 4 chamber view and subcostal (subxiphoid). Each view usually has multiple subviews obtained by “fanning” of probe by rocking the probe back and forth “technically difficult study”- usually someone with a large BMI or significant breat tissue, they tried but now they can inject contrasting solution (agitated saline and definity microspheres-aka contrast)

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9
Q

What contrast are they going to use if there is a patent opening?

A

Definity microspheres

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10
Q

What are the indications for TTE?

A

Evaluation of possible cardiac cause for sx: fatigue, dyspnea, chest pain, edema, pleural effusions, hypoxemia, syncope/near syncope, evaluation of a murmur, stroke- evaluate for clot or patent foramen ovale, congenital heart disease, cardiotoxic meds (chem)- assess for damage

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11
Q

In a new murmur, what do we need to worry about?

A

Anyone who has a new murmur, definitely getting an echo to see if they have Endocarditis

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12
Q

What are the contraindications and risks for TTE?

A

There are no contraindications and the risks are minimal

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12
Q

How do we interpret the results of an echo?

A

Report= lots of measurements, lots of words. EF= left ventricle ejection fraction (normal > 50-55%, severely bad < 25%-high risk for sudden cardiac arrest- get implantable defibrillator and leave with ife vests). Diastolic dysfunction (grades I, II, III), thickness of the walls, wall motion (akinesis- no contract, hypokinesis), enlargement of a chamber (dilatation). Valves (number of leaflets, prolapse, stenosis, regurgitation, calcifications, vegetations- bacterial balls), right ventricular systolic pressure (based off of tricuspid regurg, increased RSVP may indicate pulmonary HTN), Presence of pericardial/pleural effusions, IVC collapse (Normal for IVC to collapse-50% with inspiration, no collapse= possible volume overload)

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13
Q

What are the indications for a transesophageal echo (TEE)?

A

Nondiagnostic TTE, assessment of cardiac tumors, assessment of valves-usually before surgery, assessment of aortic dissection, assessment of native and prosthetic valves, assessment for intracardiac thrombus with repeated strokes, intraoperative monitoring. Person is put to sleep and tube is put down the esophagus

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14
Q

Where is a TEE performed and who is it done by?

A

Done in an endoscopy suite/ OR suite under anesthesia- Cardiologist

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15
Q

What are the absolute contraindications for TEE?

A

Recent esophageal/gastric surgery, esophageal stricture/obstruction, active upper GI bleed, known/suspected perforated GI organ

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16
Q

What are the relative contraindications for TEE?

A

Known coagulopathy or thrombocytopenia, malformation of nose/throat/ esophagus/cervical spine, Hx of GI surgery or bleed, Histal hernia (stomach moves up through the stomach into the thoracic avity), esophageal varices- popping one of these would cause them to bleed like crazy

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16
Q

What are the complications for TEE?

A

Esophageal rupture +/- Pneumothorax, vocal cord injury, arrhythmias, sore throat, mouth injury

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17
Q

What is stress testing?

A

Heart funciton is evaluated at rest and under stress- exercise stress or pahrmacologic stress. EKG or imagining may be done at the same time to evaluate issues with heart function, types of imaging: EKG, Echo (TTE)- “Stress Echo”, Nuclear Medicine (myocardial perfusion scan)- “Nuc Med Stress Test”, does it get taken by the heart equally and at exercise

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18
Q

What are the contraindications for a stress test?

A

Asymptomatic, low risk pts, recent MI, acute cardiac infection or inflammation, severe aortic stneosis, hemodynamically unstable, hypertensive urgency, recent stroke/ TIA

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18
Q

What are the indications for a stress test?

A

Symptomatic (chest pain, dyspnea, etc) but no EKG changes and negative workup, intermediate risk of CAD. Pre-operative evaluation of symptomatic pts undergoing noncardiac, non-emergent surgery. Can be done outpatient or inpatient. Pts w/ positive stress tests need further evaluation- heart catheterization with angiography

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18
Q

What are the complications of a stress test?

A

Arrhythmia, MI, syncope, near syncope, chest pain, dyspnea, headache (pharm)

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19
Q

What are the types of stress test?

A

Exercise stress with EKG, exercise stress with imaging (Echo or Nuc Med), Pharmacologic Stress with imaging (Echo or Nuc Med)

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20
Q

What is a stress echo?

A

Echocardiogram images are obtained before and immediately after exercise. Reduction in wall motion (hypokinesis or akinesis) after exercise is concerning for CAD, says that there is a blockage of the artery which is concerning for CAD and will need a stent or bypass. This is called a positive stress test

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21
Q

What is a nuclear Medicine stress test?

A

Cardiolite tracer is injected at rest and at exercise. Detectors pick up radioactive signal from cardiolite at rest and after exercise. Areas of the heart that have reduced cardiolite signal after exercise is concerning for CAD “reversible ischemia” there when it is stressed and returned at rest, because there is reduced blood flow.

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22
Q

When to do a stress echo vs nuc med stress test?

A

Depends on availability and comfort level of interpreting providers

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23
Q

What is an exercise stress test with EKG?

A

Best initial test if patient can exercise and low probability of CAD. EKG monitoring only**. Treadmill or stationery bike. Standardized procedure with increase in incline/resistance every 3 min.- target HR, metabolic equivalents (METs). Evidence of ischemic EKG changes (ST segment depression or elevation) and/or significant sx → further evaluation. The pt has to have a baseline EKG that is relatively normal.

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24
Q

What are the criteria for METs?

A

4 METS= 1 flight of stairs= 1.7 miles/hr with 10% incline for 3 mins
10 METS = 3.4 miles/ hr with 14% incline for 3 mins
Pts who met or exceeded 10 METS has very low risk of significant CAD

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25
Q

What does typical angina look like?

A

Substernal chest discomfort with a characteristic quality and duration, provoked by exertion or emotional stress, relieved by rest or nitroglycerin

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26
Q

Whe do we use exercise stress tests with imaging?

A

It is the best initial test if: pt can exercise and has low probability of CAD, but baseline EKG limits interpretation. Examples: LBBB, Digoxin, pacemaker, baseline, ST segment changes, accessory pathway. Pt can exercise and has intermediate/high probability of CAD. Imagining options: stress echo, nuc med myocardial perfusion scan (Nuc Med stress test)

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27
Q

What is pharmocologic stress testing?

A

Indicated in pts who can’t exercise sufficiently. Possible meds used: vasodilators like adenosine and lexiscan (adenosine derivative), dipyridamole. Sympathomimetic-dobutamine. Pt is injected with pharmacologic agent to induce stress similar to exercise. Imaging: stress echo or nuc med stress test

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28
Q

What do we order? And when do we order it?

A

Exercise is preferred over pharmacologic stress. Exercise with EKG only if low risk, normal baseline EKG, and able to exercise. Echo or NucMed imaging if: intermediate or high risk of CAD, low risk, but baseline EKG is abnormal. Echo vs Nuc Med as well as pharmacologic agent will depend on where you work. Nuc med is more common

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29
Q

How do we interpret stress test results?

A

“Positive” stress test= evidence of ischemia and pt needs further evaluation aka heart cath. Sensitivity and specificity- 80-85% no matter which type of stress test is done.

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30
Q

What does a lipid panel consist of?

A

Most common measurements of serum lipids:
Total cholesterol under 200 is normal, 200-239, over this is elevated
Triglycerides under 150 is normal, 150-199, over this is elevated
HDL > 40 , what we want, less tha 40 is worrisome
LDL under 130 is normal unless diabetic, 130-159, over this is elevated
HDL fraction is measured
LDL fraction is either measured or calculated
LDL= (total cholesterol)-(HDL)- (triglyveride/5)
Levels can vary as much as much 10-15% over the course of a year and between labs. Fasting vs non fasting: triglycerides levels are most affected by fasting and nonfasting state. Can also affect LDL level since triglycerides are used in calculation.
Extended lipid panel can measure LDL directly
HDL>60 = negative risk factor
LDL < 100 if other comorbidities present, such as CAD, PAD, CHF, DM, for DM, <70 encouraged by several diabetes groups. Calculation is valid for triglyceride concentrations up to approximately 400 mg/dl

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31
Q

A lipid panel can also include what?

A

VLDL, non-HDl, LDL/HDL ratio or chol/HDL ratio (ratio has been related to increased or decreased risk of CAD. Non-HDL may be a better indicator of CHD risk than LDL.)
LDL/HDL ratio and Chol/HDL Ratio (better since fasting not necessary)

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32
Q

What is the LDL/HDL ratio?

A

Normals Men Women
½ avg risk 1.0 1.5
Avg risk 3.6 3.2
2x avg risk 6.3 5.0
3x 8.0 6.1

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33
Q

What is the Chol/HDL ratio?

A

Normals Men Women
½ avg risk 3.4 3.3
Avg risk 5.8 4.4
2x avg risk 9.6 7.1
3x 23.4 11.0

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34
Q

Identifying and naming waves, intervals, and segments

A
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35
Q

What does pericardial effusion look like on CXR?

A

“Water bottle” sign. Makes the heart look enlarged and triangular in shape. Generally effusions are large if visible on CXR

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36
Q

What does aortic aneurysm look like on CT?

A

Entire aortic vessel is enlarged

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37
Q

What does aortic dissection look like on CT?

A

A dissection, we will be able to see it, because of the thin line of the wall of the artery and blood can be seen. This differentiates dissection and aneurysm better

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38
Q

What are the indications for TTE?

A

Evaluation of possible cardiac cause for sx: fatigue, dyspnea, chest pain, edema, pleural effusions, hypoxemia, syncope/near syncope, evaluation of a murmur, stroke- evaluate for clot or patent foramen ovale, congenital heart disease, cardiotoxic meds (chem)- assess for damage

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39
Q

What are the absolute contraindications for TEE?

A

Recent esophageal/gastric surgery, esophageal stricture/obstruction, active upper GI bleed, known/suspected perforated GI organ

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40
Q

What are the relative contraindications for TEE?

A

Known coagulopathy or thrombocytopenia, malformation of nose/throat/ esophagus/cervical spine, Hx of GI surgery or bleed, Histal hernia (stomach moves up through the stomach into the thoracic avity), esophageal varices- popping one of these would cause them to bleed like crazy

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41
Q

What are the complications for TEE?

A

Esophageal rupture +/- Pneumothorax, vocal cord injury, arrhythmias, sore throat, mouth injury

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42
Q

What is an exercise stress test with EKG?

A

Best initial test if patient can exercise and low probability of CAD. EKG monitoring only**. Treadmill or stationery bike. Standardized procedure with increase in incline/resistance every 3 min.- target HR, metabolic equivalents (METs). Evidence of ischemic EKG changes (ST segment depression or elevation) and/or significant sx → further evaluation. The pt has to have a baseline EKG that is relatively normal.

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43
Q

When do we use exercise stress tests with imaging?

A

It is the best initial test if: pt can exercise and has low probability of CAD, but baseline EKG limits interpretation. Examples: LBBB, Digoxin, pacemaker, baseline, ST segment changes, accessory pathway. Pt can exercise and has intermediate/high probability of CAD. Imagining options: stress echo, nuc med myocardial perfusion scan (Nuc Med stress test)

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44
Q

What do we order? And when do we order it?

A

Exercise is preferred over pharmacologic stress. Exercise with EKG only if low risk, normal baseline EKG, and able to exercise. Echo or NucMed imaging if: intermediate or high risk of CAD, low risk, but baseline EKG is abnormal. Echo vs Nuc Med as well as pharmacologic agent will depend on where you work. Nuc med is more common

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45
Q

What is pharmocologic stress testing?

A

Indicated in pts who can’t exercise sufficiently. Possible meds used: vasodilators like adenosine and lexiscan (adenosine derivative), dipyridamole. Sympathomimetic-dobutamine. Pt is injected with pharmacologic agent to induce stress similar to exercise. Imaging: stress echo or nuc med stress test

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46
Q

What is an exercise stress test with EKG?

A

Best initial test if patient can exercise and low probability of CAD. EKG monitoring only**. Treadmill or stationery bike. Standardized procedure with increase in incline/resistance every 3 min.- target HR, metabolic equivalents (METs). Evidence of ischemic EKG changes (ST segment depression or elevation) and/or significant sx → further evaluation. The pt has to have a baseline EKG that is relatively normal.

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47
Q

What does typical angina look like?

A

Cardiolite tracer is injected at rest and at exercise. Detectors pick up radioactive signal from cardiolite at rest and after exercise. Areas of the heart that have reduced cardiolite signal after exercise is concerning for CAD “reversible ischemia” there when it is stressed and returned at rest, because there is reduced blood flow.

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48
Q

What is a stress echo?

A

Echocardiogram images are obtained before and immediately after exercise. Reduction in wall motion (hypokinesis or akinesis) after exercise is concerning for CAD, says that there is a blockage of the artery which is concerning for CAD and will need a stent or bypass. This is called a positive stress test

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49
Q

What is the gold standard for CAD?

A

Heart cath and coronary angiography that also evaluates heart function, but it is invasive. Normally going in under fluoroscopy, if we dont see any dye where we should, we have to be concerned that there is a blockage or partially blockage. Very invasive. they will go in through the radial artery or the femoral artery and snake it up and look for any places that are narrow or stenosed.

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50
Q

Describe the cardiac conduction system and how it functions

A

A- SA node depolarizes spontaneously. At this time, there is no detectable electrical activity in the heart. Diastole neutral and AV valves are open.
B- Signal from SA node travels to the AV node, where it is slowed down to allow time for the atria to contract
C- the signal form the SA node travels from r. Atria to the l. atria, the cells depolarize which leads to contraction.
D- the AV node depolarizes and the signal travels down the AV bundle which divides into L. and R. bundle branches. Millisecond delay with AV bundle.
E- the signal is released to the ventricles via purkinje fibers. The depolarization starts in the septum then both ventricles.
F- the diagram does not show ventricular repolarization. After depolarization, the ventricles repolarize and reset for another signal.
The more you stretch, the more you constrict. Starling’s law actin and myosin overlap and contract

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51
Q

List the six limb leads and the six chest (precordial) leads

A

Ten electrodes are placed on the body, one on each limb and six on the chest wall. Limb electrodes were originally placed on the limbs- wrists ad ankles- bony places with less muscles but are now placed on the shoulders and hips with overall les interference/artifact in the signal. R. leg lead serves as a ground-detects background signal that is subtracted out from other leads. We don’t want to place leads on muscle, because we will get a lot of background noise.
Limb leads: I, II, III, aVR, aVL, aVF
Chest Leads: V1,V2, V3,V4, V5, V6

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52
Q

one small box in the horizontal axis

A

1 small box (1mm)= 40 ms (0.04 sec)

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53
Q

QRS wave

A

60-100 ms - Normal 100-120 ms- gray zone >120 ms is abnormal or wide
QRS complex is < 3 small boxes

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54
Q

PR interval

A

120-200 ms
= 1 big box

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55
Q

QT interval

A

360-440 ms. QT interval varies by HR. QT corrected (QTc) accounts for this. QTc is more important to follow clinically. < 440 ms (11 small boxes or just over 2 big boxes) in men and < 460 ms in women.

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56
Q

Draw the following
QRS wave
QS wave
RS wave
RSR’ wave
QR wave

A
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57
Q

List several ways to calculate rate on an EKG and when you would use them

A

Several options for calculating rate from an EKG
300-150-100
6 second count
10 second count rule on 12 lead EKGs

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58
Q

What is the 300-150-100 method for calculating rate on EKG?

A

Memorize this sequence of numbers: 300-150-100-75-60-50
Look at the lead used as the rhythm strip (usually lead II)
Find an R wave that falls directly on the start of a “big” box.
CCount along each big box and use the numbers you just memorized until you fall on another R wave. This will be an estimate of your rate.

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59
Q

Use the 350-150-100 to calculate rhythm on this strip

A

Normal HR is 3-5 big boxes between R waves. If between numbers, can estimate the rate based on the difference. If the second R wave falls between 2 big boxes, estimate the rate based on the difference between the 2 closet numbers and normal heart rate= 60-100 bpm=3-5 big boxes between R waves

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60
Q

What if the rate is below 50?

A

For bradycardic rates, or very irregular rates, use the 6 second method or 10 second rule. Some sources say count QRS complexes, some say count R-R intervals. Either way, this is an estimation. If you want to accurately know your pts HR, count their pulse at 60 secs of telemetry.

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61
Q

So which method does not work well if the rhythm is irregular?

A

350-150-100. Measure R-R intervals with calipers to determine if rhythm is regular or irregular

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62
Q

What is the 6 second count for calculating rate on EKG?

A

Find the hash marks at the top/bottom that mark out 3 sec intervals. Count the number of R waves in a 6 second interval and multiple by 10.

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63
Q

What is the 10 second count for calculating rate on EKG?

A

On a 10 second 12 lead EKG: Count all QRS complexes and multiply by 6 . Count all QRS complexes on 12 lead EKG and multiple by 6

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64
Q

There are several different methods to determine rate in beats per minute, what are they?

A

Use the 30-150-100-75-60-50 method (IF RHYTHM IS REGULAR)
Count the number of complexes over a 6 sec period and then multiply by 10.
If it is a 10 second standard EKG (standard 12-lead), count total QRS waves and multiply by 6
Or count your pts pulse

65
Q

List the rhythmas that are sinus rhythms

A

Normal
Normal Sinus Rhythm
Sinus arrhythmia (normal variant)
True sinus arrhythmias
Sinus tachycardia
Sinus bradycardia
Sinus pause
Sick sinus syndrome

66
Q

List the rhythmas that originate in the atria

A

Atrial arrhythmias
Atrial escape rhythm (Ectopic atrial)
Ectopic atrial tachycardia
Wandering atrial pacer (multi-focal)
Multifocal atrial tachycardia
Supraventricular tachycardia
Atrial Fibrillations
Ventricular response (slow, normal, rapid_
Atrial Flutter

67
Q

List the rhythmas that originate in the ventricles

A

Ventricular arrhythmias
Idioventricular (Ventricular escape)
Accelerated ventricular escape
Ventricular tachycardia (monofocal)
Multifocal ventricular tachycardia/ Torsades des Pointes
Ventricular flutter
Ventricular fibrillation

68
Q

List the rhythms with a wide QRS

A

IDIOVENTRICULAR (VENTRICULAR ESCAPE)
ACCELERATED IDIOVENTRICULAR
VENTRICULAR TACHYCARDIA (V TAC)
VENTRICULAR FLUTTER
POLYMORPHIC VENTRICULAR TACHYCARDIA (TORSADES DE POINTES)
Ventricular foci
Atrial foci with a bundle branch conduction issue
Ventricular escape

69
Q

Explain when you should be concerned with a pause on an EKG.

A

When to be concerned:
Pause is 3 secs or more (1 second is 5 big boxes, so 3 secs is 15 big boxes)
Multiple frequent pauses
Pt is symptomatic

69
Q

List the rhythmas that are irregular

A

Junctional Arrhythmias
Junctional escape
Accelerated junctional
Heart blocks
AV node block
1st degree
2nd degree
3rd degree
Bundle branch block
Left
Right
SVT with aberrancy
Accessory pathways
WPW
LGL

70
Q

List the leads you use to evaluate axis

A

These leads view the heart from six different angles along the frontal plane:
Lead I: 0 degrees
Lead II: 60 degrees
aVF: 90 degrees
Lead III: 120 degrees
aVR: -150 degrees
aVL: -30 degrees

71
Q

What is atrial enlargement?

A

1st part of P wav represents right atrium, 2nd part represents left atrium
Assess P wave in V1 and Lead II for signs of atrial enlargement
Have to have P waves
Normal P wave characteristics
Max height 2.5 mm in Lead II
Positive in II and aVF
P wave duration is <120 ms
Evidence of atrial enlargement
Biphasic P wave (Both possitive and negative) OR…
Dipahsic/bifid (notched) P wave or…
Very tall or very wide P waves

72
Q

What are the criteria for right atrial enlargement?

A

P wave is >2.5 mm tall in any of the inferior leads. Really tall

73
Q

What are the criteria for left atrial enlargement?

A

Diphasic P wave in Lead II or III with terminal portion of P wave > 40 ms
AND
Biphasic P wave in Lead V1 with terminal negative portion > 40 ms duration and >1mm deep

74
Q

Define Right ventricular hypertrophy (RVH)?

A

In RVH, there will be much larger vectors towards the right side of the heart
EKG findings- NEED TO MEET ALL CRITERIA
Right axis deviation of +100 degrees or more (Lead I QRS is more negative)
Dominant R wave in V1 (R>S)
Dominant S wave in V6 (S>R)
QRS <120 ms

75
Q

What is left Ventricular Hypertrophy (LVH)?

A

In LVH, there will be much larger vectors towards the LEFT side of the heart
Several different criteria to assess for LVH
Most common is Sokolow-Lyon Index:
Measure S wave in V1 or V2 (whichever is greater/deeper)
Measure R wave in V5 or V6 (whichever is greater/taller)
Add together → greater than or equal to 35 mm (7 big boxes) is diagnostic for LVH
May show inverted T waves

76
Q

What are some other ventricular hypertrophy changes?

A

Severe LV hypertrophy
I, aVL, V5, V6
Changes:
T wave inversion
Asymmetric T waves
Downsloping ST segment

77
Q

What is a summary of hypertrophy?

A

Atrial enlargement
Look at the P waves in Lead II and V1
Biphasic, diphasic, wide or tall, concern for atrial enlargement
Examine for criteria for RAE and LAE
Look for good R wave progression
If R wave is present in V1 and is larger than R wave in V2, examine for criteria for RVH
Look at size of S wave in V1, R wave in V5 or V6 (largest)
If sum of those two is more than 35mm then basic criteria for LVH is met

78
Q

Describe how to evaluate an EKG for ischemic changes.

A

T wave inversions are indicative of ischemia without tissue damage. This may be seen in stable angina, unstable angina, or initially in NSTEMI.
Subtotal occlusion or total occlusion of a coronary artery are seen in different ways.
Subtle occlusion=subendocardial=ST segment depression
Typically seen in NSTEMI but can also be seen in unstable angina. Total occlusion=transmural=ST segment elevation. STEMI
Necrosis=permanent tissue death= completed MI. Pathological Q waves on EKG. Area around scar tissue becomes foci for irritability which can cause PVCs or arrhythmias

79
Q

An EKG can give information regarding:

A

Location of ischemia/infarction, artery that has occlusion (STEMI), whether the infarction is affecting the conduction system

80
Q

What are the situations where the EKG may be less helpful?

A

Chronic LBBB, ventricular pacing. Dont look at PVCs to evaluate for ST and T changes. But may be present during an event and is indicative of underlying ischemia/irritable myocardium. If a pt is not pacemaker dependent, consider turning off a pacemaker (via magnet) to evaluate underlying conduction system.

81
Q

What are the Contiguous Leads?

A

EKG changes due to ischemia need to be seen in two or more contiguous leads

82
Q

What do T wave inversion indicate?

A

Decreased blood flow to an area that leads to localized hypoxia. Characteristic EKG findings is new inverted T waves where they are symmetrical. May be transient (ie stable or unstable) and only appear during episodes of pain. Ischemic T wave inversions are defined as T waves at least >0.1 mV (on small box) in two contiguous leads that go the opposite direction from the baseline from normal. You cannot always localize ischemic TWI to an artery

83
Q

What do pathologic Q waves look like?

A

Dead myocardium will show up as pathologic Q waves. They will usually remain permanently after tissue death

84
Q

What are the criteria for pathologic Q waves?

A

> 40 ms wide (>1 small box) AND >2mm deep (>2 small boxes and below the baseline) AND >25% of QRS complex (from bottom of Q wave to top of R wave) OR any Q in V1-V3 (look closely for any Rs- if it goes a little bit up then down it is an R wave, not an S wave). Have to be present in at least 2 contiguous leads NOT aVR

85
Q

What do pathologic Q waves look like on EKG?

86
Q

What is Wellens Syndrome?

A

EKG manifestation of sveere stenosis of the left anterior descending artery (inverted T waves without chest pain). This is an impending heart attack though. Characterized by deep, symmetric T wave inversions in V2, V3 (can also be seen in biphasic T waves with terminal negative portion in V2 and V3). At high risk for impending MI and scary because they will be asymptomatic. These are the two different types. This pt will need to be evaluated to see if they need an open heart catherization

87
Q

What is acute pericarditis?

A

Inflammation of the pericardium (may involve the myocardium) (acute perimyocarditis)
Leads to diffuse EKG changes
classic= diffuse ST elevation across most leads
Lack of reciprocal ST changes (not a STEMI)
PR segment depression in several leads
PR segment elevation in aVR
Late stages will show T wave inversion across most leads

88
Q

What does acute pericarditis look like on EKG?

A

Diffuse ST elevation across most leads. Lack of reciprocal ST changes. This pt has the kind of chest pain that is better when you lean forward

89
Q

What are the electrical alternans?

A

Alternating heights of QRS waves
Causes: cardiac tamponade, pulmonary embolism (large)

90
Q

How can we assess pulmonary pathologies like PE on EKG?

A

Acute PE causes acute pulmonary hypertension.
Possible findings:
Sinus tachycardia (most common finding-40%) right ventricular strain-T wave inversion in inferior and right precordial leads (II, III, aVF, and V1-4) Non-specific ST segment and T wave changes, RAE, RAD, RBBB, Pathognomonic finding is S1Q3T3 pattern (only seen in 20%). S wave in lead I, Q wave in lead III, inverted T wave in lead III. Atrial arrhythmias.

91
Q

What does a PE with a classic S1Q3T3 pattern look like on EKG?

92
Q

What kind of electrolyte abnormalities can occur?

A

potassium and calcium

93
Q

how can potassium cause an electrolyte abnormality?

A

Hyperkalemia: peaked T waves, QRS eventually widens into a non perfusing rhythm (when K is very high, EKG appears as a sine wave, this is really bad)
Hypokalemia: flattened T waves, may see a “U” wave after T wave

94
Q

How can calcium cause an electrolyte abnormality?

A

Hypercalcemia: shorter QT interval
Hypocalcemia: prolonger QT interval (watch for TORSADES)

95
Q

What does hyperkalemia look like on EKG?

A

Tall T waves

96
Q

What does severe hyperkalemia look like on EKG?

A

Sine wave. P waves are present, so this is not idioventricular

97
Q

What does hypokalemia look like on EKG?

A

Flat T waves and U waves

98
Q

What does hypercalemia look like on EKG?

A

Short QT interval

99
Q

What does Hypocalcemia look like on EKG?

A

Long QT interval. Typically if the end of the T wave sits more than halfway between two R wave the QT is likely long. QT interval varies by HR thus the QTc is more important to follow clinically <440 ms in men and <460 ms in women

100
Q

What are pacemakers?

A

They pace the heart and deliver socks as needed. We insert pacemakers to correct SA node dysfunction to pace the atria and let the normal conduction system conduct. The AV nodal block to pace the ventricle while sensing the SA node. Sinus node dysfunction and AV-nodal block to pace the atria and the ventricle. BBB and heart failure to pace the right ventricle and the left ventricle together to improve EF. Some pace all the time, some only when rate drops below a set point. WILL SEE PACEMAKER “SPIKES”-vertical lines when pacer fires.

101
Q

Define what a pacemaker vs a defibrillator is

A

pacemaker= PPM (permanent pacemaker)
defibrillator= AICD (automatic impantable cardioverter-defibrilator)
ICDs are implanted for primary (or secondary) prevention of sudden cardiac death is different populations. Most common being patients with systolic heart failure and an EF < 35% after 3 or so months of optimal medical therapy.

102
Q

ow can we assess pulmonary pathologies like COPD on EKG?

A

Hyperexpansion of the chest causes heart to increase in vertical orientation and to rotate to the left. Chronic elevation in pulmonary arterial pressure due to loss of lung tissue and chronic hypoxemia increase RV workload.
Possible findings: mutli-focal atrial tachycardia, atrial fibrillation, small QRS amplitude in left-sided leads- I, aVL, V4-6 due to increased AP diameter, right axis deviation, right atrial enlargement, right ventricular hypertrophy

103
Q

What does COPD-MAT look like on EKG?

104
Q

What does COPD with low QRS in lateral leads, RAE look like on EKG?

105
Q

What is brugada syndrome?

A

Genetic syndrome
Most common mutation is related to sodium channels but there are subgroups for calcium and potassium channels
Predisposed to sudden v-fib arrest: most common in asian descent, cause of unexplained sudden death.
Characteristic EKG findings: Right BBB with ST elevation (V1, V2, V3) (sometimes called a shark fin, the second R wave has this funny curve to it)

106
Q

What can hypothermia causes?

A

Bradycardia, QT prolongation, Characteristic osborne waves (AKA “J” waves), low temp

107
Q

Describe electromechanical dissociation

A

Another way to remember causes (these being the more common)
Severe hypovolemia (trauma)
Pump failure (massive MI =/- wall rupture, severe heart failure)
Obstruction to circulation
Tension Pneumothroax
Cardiac Tamponade
Massive PE

108
Q

What are the electrical alternans?

A

Alternating heights of QRS waves
Causes: cardiac tamponade, pulmonary embolism (large)

109
Q

What does intracranial hemorrhage look like on EKG?

A

Bradycardia and deep inverted T waves
Sx: HA and AMS

110
Q

Describe the 5 possible pathophysiologies underlying arrhythmias.

A

Arrhythmias of the SA node:
SA node is the pacemaker, but it isn’t working correctly
Ectopic arrhythmias (rhythm is somewhere else in the the heart, not SA node)
SA node is not working and the rhythm originates somewhere else
ATRIAL arrhythmias
JUNCTIONAL arrhythmias
VENTRICULAR arrhythmias
Re-entrant arrhythmias
An electrical circuit develops where the signal is racing (doesn’t stop) around and around the circuit and sending out waves of depolarization-reentrant pathway
Blocks
The SA node IS the pacemaker, but another part of the conduction system ISN’T working.
Preexcitation syndromes:
There is an accessory conduction system that carries the signal to the ventricles too early

111
Q

What is troponin?

A

Protein complex that regulates contraction of striated muscle.
Three forms of cardiac troponin (cTn)
cTnC- identical to that found in skeletal muscle
cTnT- specific to heart muscle
cTnI- specific to heart muscle
Pts sometimes present > 24 hours after onset of sx, troponin remains elevated. In Mi, troponin has a sustained release from intracellular contractile apparatus to which it is normally tightly bound. Low levels of troponin are found in the reference population. Increases in troponin do indicated some type of cardiac distress, but not cause or mechanism

112
Q

What are troponin assays?

A

cTnT or cTnl- 4th gen assays (0.25 was a heart attack)
Can’t compare between assays between hospitals with different brands
manufacturer -defined cutoffs/upper reference limits
Levels can be increased due to other causes than myocardial injury
Change in level is monitored over time- time intervals depend on specific protocol used

112
Q

What time frame do we need to do a troponin in?

A

Detectable within 3-12 hours post MI. because the troponin is leaking but it may take a while for the troponin to get to a blood vessel for blood flow. Peaks in 12 hrs to 2 days (cTnT) o 24 hours (cTnI). Remains elevated up to 2 weeks. cTnT: 5-14 days. cTnI: 5-10 days. Increased levels with chronic kidney disease, PE, myocarditis, trauma

113
Q

What are the newer troponin tests?

A

High sensitivity troponin assays (hs-Tn)
5th gen assay
Available in US as of late 2017
Most people will have baseline low levels
Have to look at “delta” troponin, or change in troponin level over time, gender specific cutoffs
Each assay will have specifics for cutoffs that rule in or out MI, as well as how much change is needed to rule in MI

114
Q

What is a BNP?

A

Brain natriuretic peptide (BNP). aka opposite of aldosterone. Natriuretic peptides:
Released by the heart/vasculature in response to volume overload
Promote sodium excretion and water in the urine, vasodilation

115
Q

What are the types of natriuretic peptide?

A

Types:
Atrial natriuretic peptide (ANP)
Brain natriuretic peptide (BNP)
C-type natriuretic peptide (CNP)

116
Q

What are the advantages of BNP?

A

Hormone released from ventricular myocytes in response to high ventricular filling pressures
Remains in circulation longer than ANP or CNP- better for lab measurement
Elevated BNP not specific for heart disease, rather indicative of hemodynamic stress and fluid overload states
Increased in pts with asymptomatic and symptomatic left ventricular dysfunction

117
Q

What are the characteristics of a BNP?

A

Has a high negative predictive value where the BNP < 100 pg/mL and helps rule out CHF
BNP > 400 pg/mL is consistent with a diagnosis of CHF, but does not rule it in. BNP also elevated in pts w/ MI, renal failure, a fib, pulmonary hypertension. Decreased in obesity

118
Q

Should a BNP be used alone?

A

Should not be used as a stand-alone marker for CHF or as a marker for treatment efficacy. Increased level of BNP does correlate with increased hospital mortality. Afib associated with higher BNP levels in pts who did not have a final diagnosis of CHF.

119
Q

What is a NT-proBNP?

A

proBNP cleaved into BNP and NT-proBNP. In pts with LV dysfunction, NT-proBNP rises ore than BNP. NT-proBNP level < 300 pg/mL roughly equivalent to BNP of <100 mg/mL

120
Q

What are the reference ranges for NT-proBNP?

A

Reference ranges must account for age, gender, and BMI.
Age: < 50 yrs > 450
50-75 > 900
>75 >1800
Plasma concentrations of NT-proBNP are higher in older individuals and in women than men, but lower in obese individuals. Also NT-proBNP increases with renal failure-optimal cut-off not clearly established.

121
Q

What is ankle brachial index (ABI)?

A

Resting systolic pressure measured in brachial artery and either dorsalis pedis or posterior tibial artery of same side.
Ratio is calculated-ABI
Can also use ABI to assess adequacy of blood flow to feet to evaluate how well foot ulcers, amputations, etc will heal. Screening tool to see who might need more invasive testing of vasculature (such as angiography)

122
Q

What are the normal rates for ABI?

A

ABI 0.9-1.3= normal
ABI < 0.9 = likely occlusive peripheral artery disease with > 50% stenosis
Lower values indicate worse disease
Correlated with increased risk of CVD
ABI > 1.3 = likely calcifications of the artery walls
Also correlated with increased risk of CVD

123
Q

What is arterial plethysmography?

A

Inflatable cuffs placed on extremities (arms, legs, or both) and pulse wave is recorded. Normal= tall, sharp peak with notch in downslope
abnormal = decreased peak, no notch
“Arterial studies”

124
Q

What are the indications for arterial plethysmography?

A

Lower extremity ulcers/ wounds, surgical pre-planning, thoracic outlet syndrome (where the subclavian gets clamped off) evaluation, diabetic foot wounds. Talking where to amputate for good blood flow

125
Q

What is an ankle brachial index (ABI)?

A

Resting systolic pressure measured in brachial artery and either dorsalis pedis or posterior tibial artery of same side. Ratio is calculated- ABI. ABI 0.9-1.3= normal. ABI < 0.9 = likely occlusive peripheral artery disease with > 50% stenosis. Lower values indicate worse disease. Correlated with increased risk of CVD. ABI > 1.3= likely calcifications of the artery walls. Also correlated with increased risk of CVD. Can also use ABI to assess adequacy of blood flow to feet to evaluate how well foot ulcers, amputations, etc will heal. Screening tool to see who might need more invasive testing of vasculature (Such as angiography)

126
Q

What is angiography?

A

GOLD STANDARD. But very invasive. Dye injected via catheter, fluoroscopy used to visualize vessels.

127
Q

What are the benefits and complications of angiography?

A

Benefits: excellent visualization of vessels. Can also use therapeutic interventions at the same time
Complications: perforation/bleeding, thrombus formation, vessel dissection, allergic rxn to dye

128
Q

What are specialized types of angiography?

A

Fluorescein angiography
Microangiography- this is the skin. skin grafts to make sure there is good blood supply

129
Q

Identify what you would expect to see on a TTE for the following a patient with a systolic crescendo-decrescendo murmur best heard on the right upper sternal border

A

aortic stenosis

130
Q

Identify what you would expect to see on a TTE for the following a patient with a diastolic murmur best heard at the apex

A

mitral stenosis

131
Q

Identify what you would expect to see on a TTE for a patient with a recent STEMI in the left anterior descending artery

A

hypokinesis or akinesis in the left ventricle from MI

131
Q

Identify what you would expect to see on a TTE for a patient with dilated cardiomyopathy

A

Systolic failure with thin heart wall and reduced EF

131
Q

Identify what you would expect to see on a TTE for a patient who uses IV drugs with a new pansystolic murmur at the left lower sternal border

A

tricuspid regurgitation

132
Q

Identify what you would expect to see on a TTE for a patient with heart failure with reduced ejection fraction (HFrEF) vs a patient with heart failure with preserved ejection fraction (HFpEF)

A

systolic dysfunction w/ reduced ejection fraction. diastolic dysfunction w/ preserved ejection fraction

133
Q

What is ankle brachial index (ABI)?

A

Resting systolic pressure measured in brachial artery and either dorsalis pedis or posterior tibial artery of same side.
Ratio is calculated-ABI
Can also use ABI to assess adequacy of blood flow to feet to evaluate how well foot ulcers, amputations, etc will heal. Screening tool to see who might need more invasive testing of vasculature (such as angiography)

134
Q

What are the normal rates for ABI?

A

ABI 0.9-1.3= normal
ABI < 0.9 = likely occlusive peripheral artery disease with > 50% stenosis
Lower values indicate worse disease
Correlated with increased risk of CVD
ABI > 1.3 = likely calcifications of the artery walls
Also correlated with increased risk of CVD

135
Q

What are the other tests for HF?

A

Galectin-3: involved in cell growth and apoptosis. Associated with cancer, stroke, severe heart failure, multiple types of fibrosis. Heart failure- Galectin-3 increased in patients with worsening heart disease. Elevated levels correlate with increased risk of death (prognostic marker)

136
Q

What are the indications for cardiac monitoring?

A

s/sx of arrhythmias, not captured on EKG. s/sx

137
Q

What are the types of cardiac monitoring?

A

Inpatient→ telemetry. Outpatient: Holter monitor. Event monitor. Patch monitor. Mobile cardiac telemetry, implantable recorder (Ling)-multiple years

137
Q

What is a holter monitor?

A

Near daily symptoms. for 24-48 hours continuous recording

138
Q

What is an event monitor?

A

requires pt to push a button when symptoms occur, up to 30 days.

139
Q

What are patch (zio) monitors?

A

14 days continuous recording (1 lead). No button to press but just has continuous monitoring and get it placed and taken off by the cardiologist

140
Q

What is mobile cardiac telemetry?

A

30 days, continuous monitoring

141
Q

Which cardiac monitor do I choose?

A

Decide if the pt is symptomatic and for how long.
Daily sx→ Holter monitor
sx but less often→ event monitor
Sx very infrequent but severe → implantable, like strokes from a fib
No sx →holter, patch, mobile cardiac telemetry, implantable

142
Q

Describe the following tests that can be used to further assess a patient’s risk of ASCVD coronary artery calcium score

A

Reported score 0-400.
0= no evidence of calcification
1-10= minimal
11-100= mild
101-400=moderate
401+ = severe
CT chest w/o contrast shows calcification in plaques in the left anterior descending artery. CAC- CT scan of heart measures calcification of the coronary arteries. The extent of CAD is graded according to a calcium score: statins stabilize plaques. Genetics plays a large role

143
Q

Describe the following tests that can be used to further assess a patient’s risk of ASCVD hsCRP

A

High sensitivity CRP. Detects same protein (CRP), but more sensitive to lower levels. < 1 mg/L = lower risk, >3mg/ L = high risk of CVD. Can’t be used for risk assessment in people with chronic inflammatory conditions. CRP higher in females, higher in African American. Also elevated by hormone replacement therapy and birth control pills.

144
Q

Describe the following tests that can be used to further assess a patient’s risk of ASCVD carotid doppler?

A

Internal carotid artery. Carotids easy to analyze with US, and provide non-invasive estimate for how much atherosclerosis is happening elsewhere in the body. Carotid bifurcation is more prone to atherosclerosis than other areas.

145
Q

A patient has an acute CHF exacerbation. Which of the following would NOT be seen on CXR?

A

widened mediastinum

146
Q

Which of the following descriptions would be consistent with a pericardial effusion?

A

water bottle heart

147
Q

a widened mediastinum would be associated with?

A

aortic dissection

148
Q

A patient has a diastolic murmur best heard at the apex. Which of the following would be expected on auscultation?

A

mitral stenosis

149
Q

Which of the floowing woul be an indication for TEE?

A

suspected endocarditis with a negative TTE

150
Q

Which os the following correctly describes HFrEF?

A

An EF < 55% on echo

151
Q

Which of the preferred test in healthy patients with pain, no ischemic EKG changes, and negative serial troponin

A

Exercise stress test with EKG

152
Q

Which of the following findings would indicate a positive stress test?

A

area of hypokinesis on stress echo after exercise

153
Q

A patient has a positive stress test. What would be the next best step?

A

consult cardio for a left heart cath

154
Q

What is the normal range for an ABI?

155
Q

Which of the following is included in the criteria for diagnosing acute coronary syndrome?

A

an increase or decrease in troponin

156
Q

A patient needs an amputation of his lower leg. Which of the following would NOT be helpful in surgical planning?

A

Venous doppler US

157
Q

What pathology is shown on the CT?

A

aortic dissection

158
Q

This EKG shows electrical alternates-alternating heights of QRS complexes. What condition is associated with this?

A

cardiac tamponade

159
Q

Based on the EKG, what would be expected on a CXR

A

pericardial effusion