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Week 2 Flashcards

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1
Q

What issues would require an X-ray?

A
  1. on initial evaluation
  2. W/ SOB, cough, chest pain
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2
Q

How are the densities portrayed differently in x-rays?

A
  • Air is the darkest color while metal is the whitest color
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3
Q

In what order are radiography requests made? (3)

A
  1. x-ray initial evaluation
  2. CT -if abnormal X-ray
  3. CT angiography
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4
Q

What issues would require request of CT?

A

Trauma, cancer work up, interstitial lung disease

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5
Q

What are the 3 ways to preform CT?

A
  1. CT routine- no contrast
  2. CT angiography - time IV bolus of contrast to highlight vessels
  3. High resolution CT - very thin images to better visualize interstitium of lung
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6
Q
  1. What does echocardiography look for?
  2. MRI?
  3. Nuclear medicine?
  4. Catheterization?
A
  1. functional status of heart
  2. functional MRI can also check functional status of heart
  3. looks at perfusion to look and see if there are any blockages of heart
  4. Looks closely at vessels
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7
Q

What are advantages (2)and disadvantages (2) of xray?

A

Advantages

  1. Lower radiation than CT
  2. Can screen the heart and great vessels and ID non-cardiac sources of chest pain

Disadvantages

  1. Insufficient to confirm or exclude coronary artery disease
  2. Low sensitivity to diagnose cardiovascular disorders
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8
Q

What are advantages (2)and disadvantages (4) of CT?

A

Advantages

  1. accurate assessment of cardiac and non-cardiac structures
  2. Potential to examine coronary arteries and cardiac function

Disadvantages

  1. Radiation to exposure
  2. IV contrast
  3. Limited effectiveness in detecting disease in small coronary arteries
  4. Inferior to MRI for functional assessment
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9
Q

What is the systemic approach to identify and evaluate key structures in a chest radiograph?

A
  1. A-airway
  2. B-bone
  3. C-cardiac
  4. D-diaphragm
  5. E-everything

identify all of these

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10
Q

Identify Lungs, heart (if you can the different parts too), aorta, and mediastinum on chest XRay

A

image

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11
Q

Which side of the diaphragm should be higher on imaging?

A

The right side due to position of liver.

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12
Q
  1. What are the names of the standard limb leads and where are they placed?
  2. Describe their polarity
A
  1. avR (right arm), avL (left arm), avF (left leg/foot)
  2. All unipolar positive leads (negative charge moves towards positive)
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13
Q
  1. Describe the 3 augmented limb leads?
  2. Describe their polarity?
A
  1. All bipolar leads
  2. Lead 1 measures electrical potential between right arm (-) and left arm (+)
  3. Lead 2 measures electrical potential between right arm (-) and left leg (+)
  4. Lead 3 measures electrical potential between left arm (-) and left leg (+)
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14
Q

Is a positive deflection going towards or away from a positive lead?

A

towards

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15
Q
  1. Describe the position of each precordial/chest leads
  2. Describe their polarity
A
  1. V1 - 4th intercostal space, right
  2. V2 - 4th intercostal space, left
  3. V3-Between V2 and V4
  4. V4 - mid collar bone, within 5th intercostal space
  5. V5 - 5th intercostal at anterior axillary line
  6. V6 - 5th intercostal at mid-axillary line
  7. All unipolar
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16
Q

On an EKG/ECG

  1. What is the time period of one tiny box (width) vs one large box (width)
  2. What is the voltage in one tiny box (height) vs one large box (height)
A
  1. Tiny box - 0.04 sec ;;;Large box - 0.2 sec
  2. Tiny box - 0.1 mV ;;;; large box - 0.5 mV
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17
Q
  1. What is the easy shorthand to determine BPM by counting boxes?
A
  1. Look at how many boxes are between R waves
  • 1 big box = 300 bpm
  • 2 big boxes = 150 bpm
  • 3 big boxes = 100 bpm
  • 4 big boxes = 75 bpm
  • 5 big boxes = 60 bpm
  • 6 big boxes = 50 bpm
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18
Q

What is the normal length and amplitude of a P wave?

A
  1. length (time) - 0.04 -0.1 seconds
  2. Amplitude - 2-3 mm
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19
Q

What is the normal time and width in boxes of PR interval?

A
  1. 0.12-0.2 seconds (<200 ms)
  2. 3-5 little boxes
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20
Q

What is the normal time and width in boxes of QRS wave?

A
  1. 0.04-0.12 seconds
  2. 1-3 little boxes
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21
Q

How do you quickly determine if QRS axis is normal, left shifted, or right shifted? (Looking at Lead I, Lead II, and Lead aVF)

A

Look at the the deflection of QRS in each lead strip…together they tell you about axis

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22
Q

How do you determine the electrical axis using the ECG? (6 steps)

A
  • Step 1 - look at lead 1(x axis) and count how many little boxes is taken up by R wave (vertically) then look at S wave and look at how many little boxes are taken up (horizontally)
  • Step 2 -Then get the difference between the two… if 5 boxes for R (upward) wave and 1 box for S (downward) wave then 5-1 = +4
  • Step 3 - on a graph mark where +4 lands on x axis (to the right)
  • Step 4 - repeat same process as step 1 but for aVF lead (y axis)
  • Step 5 -the answer you get from step 4 should be graphed on y axis now (remember + y axis numbers go down not up on the heart axis graph)
  • Step 6 - Connect the dots which will be the end of the arrow coming off of (0,0) on graph
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23
Q

On the chart showing different electrical axis…

  1. What is the range of normal deviation
  2. What is the range of left axis deviation
  3. What is the range of right axis deviation
A
  1. -30 degrees to 90 degrees
  2. -30 degrees to -90 degrees
  3. 90 degrees to 180 degrees
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24
Q

How can the appearance of QRS indicate a bundle branch block?

A

wide QRS > 120 msec

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25
Q
  1. What would a right bundle branch block (RBBB) look like on V1 and V6
  2. What about LBBB
A
  1. RBBB: On V1 you have bunny ears (R and R’) +wide QRS —V6 shows wide QRS
  2. LBBB: On V1 you see one large downward spike (wide QRS)— V6 shows opposite of V1 (inverted)
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26
Q

What is a priori hypothesis?

A

hypotheses are those based on assumed principles and deductions from the conclusions of previous research, and are generated prior to a new study taking place

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27
Q

What is a post hoc analysis?

A

A post-hoc study is conducted using data that has already been collected

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28
Q

What is subgroup analysis?

A

It’s a type of analysis done by breaking down study samples into subsets of participants based on a shared characteristic. The goal is to explore differences in how people respond to an intervention.

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29
Q

What is interim analysis?

A

an evaluation of the current data from an ongoing trial, in which the primary research question is addressed, and which has the potential for modifying the conduct of the study.

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30
Q

Describe the blood flow through the heart (from right atrium to aorta - 12)

A
  1. RA
  2. Tricuspid valve
  3. Right ventricle
  4. Pulmonary valve
  5. Pulmonary Trunk
  6. Pulmonary arteries
  7. Lungs
  8. Pulmonary veins
  9. Left atrium
  10. Mitral/bicuspid valve
  11. Left ventricle
  12. Aortic valve
  13. Aorta
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31
Q

What is considered the anterior (sternocostal surface of heart)?

A

Right atrium and both ventricles

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32
Q

Describe the inferior (diaphragmatic) surface of heart?

A

The back sides of ventricles (mostly the left)

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33
Q

Describe the posterior (base) surface of heart?

A
  1. the left atrium and four pulmonary veins
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34
Q

What is the right pulmonary surface and left pulmonary surface of heart?

A
  1. formed by right atrium
  2. formed by left ventricle and portion of left atrium
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35
Q

The right atrium is divided into what two continuous spaces?

A
  1. Atrium proper
  2. Sinus of venae cavae
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36
Q

Where is the atrium proper found in right atrium?

A
  1. the space in front of crista terminalis. It has rough ridges on walls called musculi pectinati
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37
Q

Where is the sinus of vena cavae found?

A
  1. space present posterior to crista terminalis
  2. The superior and inferior vena cavae both open into this space.
  3. Its walls are smooth and thin
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38
Q
  1. What is the atrial septum?
  2. What is it marked by?
A
  1. Separates the right atrium from the left atrium
  2. Fossa ovalis
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39
Q

What are trabeculae carneae?

A
  1. muscular bands that have one end attached to the ventricular surface, while other end attaches to tendon like fibrous cords, choradae tendineae
  2. Found in both ventricles
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40
Q
  1. What are chordae tendineae?
  2. Function?
A
  1. Attached to trabeculae carneae and to the cusps of the tricuspid valve (in right ventricle)
  2. Prevent eversion(flipping inside out) of valve cusps into atrial cavity during ventricular contraction
  3. Found in both ventricles
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41
Q
  1. What is the septomarginal trabeculae?
  2. Function?
A
  1. One of the three trabeculae carneae (papillary muscles) found in right ventricle
  2. Its function is to carry the right bundle branch to the atrioventricular bundle (bundle of His)
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42
Q

What is the infundibulum (conus arteriosus)?

A
  1. the outflow track of the right ventricle leading to pulmonary trunk
  2. It has smooth walls
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43
Q

Describe the structure of the tricuspid valve (cusps/leaflets/direction/etc)

A
  1. It has 3 cusps/leaflets
  2. Anterior, septal, and posterior cusps
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44
Q

Describe the structure of the pulmonary valve (cusps/direction/etc)

A
  1. Present at the opening of the pulmonary trunk
  2. Consists of 3 semilunar cusps - right, left, and anterior semilunar cusps
  3. cusps are concave when you look at them from above
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45
Q

Where is the left auricle found?

A

The left auricle projects from the left atrium and overlies the pulmonary trunk

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46
Q
  1. Describe the two portions of the left atrium
  2. How are the two separated?
A
  1. Posterior half (inflow portion) - receives the four pulmonary veins and has smooth walls
  2. Anterior half (continuous with left auricle) - contains musculi pectinati
  3. No distinct structure separates the two components
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47
Q

What is the valve of the foramen ovale?

A
  1. This is found behind the fossa ovalis in the right atrium - Both are structures to prevent connection between the two atrium
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48
Q

What is the aortic vestibule?

A
  1. The outflow tract from the left ventricle to the aorta
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49
Q
  1. Describe the mitral (bicuspid) valve
A
  1. Found in the left atrioventricular orifice
  2. Has two cusps each anchored to papillary muscles by tendinous cords
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50
Q

How are papillary muscles (trabeculae carneae) different in left vs right ventricles?

A
  1. In left ventricle there are only two but they are larger than those in the right ventricle
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51
Q
  1. Describe the aortic valve (cusps, direction, etc)
A
  1. Three semilunar cusps
  2. Right, left, and posterior semilunar cusps
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52
Q
  1. What is the cardiac skeleton and where is it found
A
  1. Four rings of dense, fibrous connective tissue with interconnected areas around the AV, aorta, and pulmonary trunk orifices
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53
Q

What is the function of cardiac skeleton?

A
  1. maintains integrity of orifices
  2. Attachment site for muscles and cusps
  3. Electrically isolates atria from ventricles
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54
Q

Where is the best place to auscultate for the mitral valve?

A
  1. Left fifth intercostal space, midclavicular line, cardiac apex
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55
Q

Where is the best place to auscultate for the tricuspid valve?

A
  1. Left lower sternal border, fifth intercostal space
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56
Q

Where is the best place to auscultate for the pulmonary valve?

A
  1. second intercostal space, left sternal border
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57
Q

Where is the best place to auscultate for the aortic valve?

A
  1. second intercostal space, right sternal border
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58
Q

What path does the right coronary artery (RCA) follow?

A
  1. Arises from right aortic sinus
  2. Descends downward in the coronary sulcus between the right atrium and right ventricle
  3. continues in the sulcus onto the diaphragmatic surface of the heart
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59
Q
  1. What path does the left coronary artery (LCA) follow?
  2. What does it bifurcate into
A
  1. arises from the left aortic sinus
  2. Passes between the pulmonary trunk and left auricle before entering coronary sulcus
  3. Within the coronary sulcus in bifurcates into anterior interventricular and circumflex branch
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60
Q

What are the branches of RCA? (4)

A
  1. Sinoatrial nodal branch
  2. Right marginal branch
  3. Atrioventricular nodal branch
  4. Posterior descending artery (PDA) (commonly branches off of RCA but in some people it is LCA)
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61
Q

What does the right coronary artery supply?

A

right coronary artery supplies blood to the

right ventricle,

the right atrium

SA (sinoatrial) and AV (atrioventricular) nodes

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62
Q

What does the left coronary artery supply?

A

Left atrium and left ventricle

  • plus interventricular septum
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63
Q

What artery supplies the SA and AV node?

A

Right coronary artery

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64
Q

What is the dominant coronary artery?

A

The artery that gives way to the posterior interventricular branch

  • in most people it is the right coronary artery
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65
Q

What is the main vein draining venous blood from heart muscle?

A

The coronary sinus

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66
Q

What is the path of the coronary sinus? (origination, path, end)

A
  1. A continuation of the great cardiac vein
  2. Runs from left to right on the hearts posterior surface - within coronary sulcus
  3. It opens into the right atrium between inferior vena cava and atrioventricular orifice
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67
Q

What veins contribute to the coronary sinus?

A
  1. Great cardiac vein (seen in anterior side of heart)
  2. Small cardiac vein (on other side of sinus and wraps around to front)
  3. Middle cardiac vein
  4. Posterior cardiac vein
  5. Left marginal vein
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68
Q

What are smallest cardiac veins (venae cordis minimae)?

A

Small veins that open directly into the chambers of the heart

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69
Q
  1. the great cardiac vein drains areas of the heart supplied by ???
  2. Middle and small cardiac vein drain areas supplied by ???
A
  1. LCA
  2. RCA
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70
Q
  1. What forms the cardiac plexus?
  2. What does the cardiac plexus innervate?
A
  1. sympathetic fibers, parasympathetic fibers (vagus), visceral afferents
  2. innervate the heart
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71
Q

The cardiac plexus is formed by the superficial and deep part. Where is each part found?

A
  1. Superficial part - between aortic arch and pulmonary trunk
  2. Deep part: between aortic arch and tracheal bifurcation
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72
Q

At what level of the spine does the pulmonary trunk end up dividing into right and left pulmonary arteries?

A
  1. T5 and T6 (just below sternal angle)
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73
Q

Where is the superior mediastinum found?

A
  1. Posterior to the manubrium of the sternum and anterior to T1-T4 vertebrae
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74
Q
  1. What forms the brachiocephalic veins?
  2. What does left and right brachiocephalic veins form?
A
  1. Union of internal jugular and subclavian veins
  2. left and right unite to make superior vena cava
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75
Q

Where does the brachiocephalic vein receive blood from?

A
  1. head, neck, and upper limbs

*thus superior vena cava returns blood from all places above diaphragm except lungs and heart

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76
Q
  1. At what point in the skeletal system is the brachiocephalic vein formed?
  2. What about the superior vena cava?
A
  1. sternoclavicular joint
  2. first costal cartilage
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77
Q

What is the only part of the aorta that is in the superior mediastinum?

A

The arch of the aorta

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78
Q

Where is the arch of the aorta in relation to skeletal system?

A
  1. behind the second right costal cartilage at level of sternal angle (T4/T5)
  2. it goes upward, backward, and to the left and arches over left lung root to continue into thoracic descending aorta
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79
Q

What is the ligamentum arteriosum?

A

Connects the pulmonary trunk to the arch of aorta. It allows blood to bypass lungs during development

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80
Q

What does the phrenic nerve innervate?

  1. Send Motor information to??
  2. Receive Sensory information from??
A
  1. Motor: The diaphragm
  2. Sensory: Diaphragm, mediastinal pleura, and pericardium
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81
Q

What is the path of the phrenic nerve?

A
  1. Originates in cervical plexus
  2. enter superior mediastinum between subclavian artery and brachiocephalic vein origin
  3. Descend anterior to the root of the lungs and rung along pericardium to reach diaphragm
82
Q

What plexus does the vagus nerve contribute to?

A

The esophagus, cardiac, and pulmonary plexus

83
Q

Atrial Fibrillation

  1. Describe the rate of pulse
  2. How is it diagnosed?
A
  1. irregularly irregular pulse
  2. EKG
84
Q
  1. What does an EKG of atrial fibrillation look like?
A
  1. Do not show regular P waves, instead show fibrillatory waves
  2. QRS complexes are occurring at an irregularly irregular rate (no pattern)
85
Q

What is happening in the heart that causes atria fibrillation?

A
  1. Normally the depolarization/signal for heart beat starts at SA node
  2. In atrial fibrillation - there is depolarization in MANY places within both atrium
  3. Some depolarizations will reach AV node and lead to QRS wave/heart contraction.
  4. This is why the rate is irregularly irregular. Sort of happens by chance which depolarizations reach AV node
86
Q

Define

  1. Paroxysmal fibrillation
  2. Persistant fibrillation
  3. Permanent fibrillation
A
  1. Comes and goes; spontaneous conversion to sinus rhythm
  2. Lasts days/weeks; often requires cardioversion procedure
  3. Permanent lasting
87
Q

What symptoms are seen in patients with symptomatic atrial fibrillation?

A
  1. Palpitations
  2. Dyspnea
  3. Fatigue
  4. Heart rate >100 bpm
88
Q

Untreated rapid atrial fibrillation can cause…what disease?

A
  • Cardiopmyopathy (tachycardia-induced cardiomyopaty)
  • ejection fraction will decline (decreased LVEF)
  • Systolic heart failure
  • For patients who are asymptomatic, heart failure can be the first sign that they have atrial fib
89
Q

What function in the heart determines heart rate?

A
  1. AV node refractory period
  2. If AV node is in refractory period then it cannot take on another depolarization.
  3. If it has recooperated and not in refractory period then it can send signal to ventricles.
  4. This determines heart rate
90
Q

What is the difference in AV node with age?

A
  1. Younger, healthy patients have healthier AV node - so have higher heart rate
  2. Older patients - don’t have AV node that is not capable of fast conduction and have lower heart rate
91
Q
  1. Atrial rate in fibrillation vs ventricular rate?
  2. why the difference?
A
  1. Atrial rate in fibrillation is around 300-500 bpm
  2. ventricular rate is 70-180
  3. AV node refractory period doesn’t allow the full 300-500 bpm to occur
92
Q

How does atrial fibrillation affect preload?

A
  1. Eliminates ventricular pre-filling
  2. Loss of atrial kick which decreases pre load
93
Q

What are some dangerous outcomes of atrial fibrillation when it comes to clots?

A
  1. cardiac embolism
  2. brain (stroke)
  3. Gut (mesenteric ischemia)
  4. Spleen
  • Do to thrombi that form in the atrium which can break off and go somewhere else in body
94
Q

What are some triggers of atrial fibrillation?

A
  1. Often no trigger needed
  2. Binge drinking
  3. Increased catecholamines
95
Q

Atrial flutter

  1. What is the difference between this and atrial fibrillation? (in EKG)
A
  1. Atrial flutter shows shark tooth type waves (flutter waves) before QRS complex
  2. Found in every lead of EKG
96
Q

What is happening in the heart with atrial flutter?

A
  1. The many points of depolarization in the atria are more organized than in atrial fibrillation
  2. These points of depolarization go around in a circle in the atria, each circle representing a saw tooth wave
  3. Some of these depolarizations go to AV node and conduct signals to rest of body
97
Q

Symptoms of arial flutter?

A
  1. some are asymptomatic
  2. Some are symptomatic with palpitations, dyspnea, and fatigue
98
Q
  1. What is paroxysmal supraventricular tachychardia?
  2. What is the origin of activity?
  3. What occurs to QRS complex
A
  1. Intermittent tachycardias (HR >100 bpm) - sudden onset/offset
  2. Origin of electrical activity is above ventricle (meaning electrical signal still goes through AV node, bundle of His, purkinje fibers - so still makes normal or narrow looking QRS complex)
99
Q

How can you tell on a EKG if there is PSVT?

A
  1. around 150 bpm - sudden onset
  2. Normal or NARROW QRS complex (<120 msec)
100
Q

One of the causes of PSVT is AVNRT (atrioventricular nodal reentrant tachycardia)

  1. What is AVNRT?
A
  1. AVNRT requires an individual to have a dual pathway AV node (a slow and fast pathway)
  2. Slow pathway is able to be re-excited pretty fast while fast pathway takes longer.
  3. Subsequent atrial signal go down preferentially through slow path bc fast pathway is not ready and leads to ventricular excitation and retroverse signalling back up fast pathway (once its ready to be excited)
  4. This leads to dual atrial and ventricular contraction
101
Q

What is the dual AV node pathway?

A
  1. When the AV node has some cells with slow conduction with short refractory period
  2. And other cells with fast conduction and long refractory period
  3. In normal heart rate conducted by SA node this dual pathway doesn’t induce any issues because fast conduction cells cancel out slow conduction
  4. With premature atrial contraction - you can have slow conduction cells propel signal even when fast cells cannot and by the time they reach end of AV node they can excite fast conduction cells
  5. This creates a circuit where signal goes up the fast conduction cells to depolarize atria BUT ALSO go down to depolarize bundle of His - tachycardia situation begins
102
Q

How can you identify AVNRT in ECG?

A
  1. Sudden onset tachycardia
  2. Presence of retro grade P waves that comes AFTER QRS complex - seen on every beat
103
Q

what is Wolff-Parkinson White?

A

cardiac electrical disorder

  • Patient has an accessory atrioventricular pathway (bundle of kent) that conducts impulses from atria to ventricles bypassing the AV node
  • Causes pre-excitation where ventricular depolarization occurs before AV nodal impulse
104
Q

How can diagnosis of WPW be made via EKG?

A
  1. Presence of delta wave (at the R spike it is not going straight up but goes up at an incline)
  2. Presence of short PR interval
105
Q

What does delta wave mean in WPW syndrome?

A
  1. It means that the ventricles are getting excited prematurely before the normal QRS complex is set to occur via normal signaling
  2. Delta wave causes a short PR interval
106
Q

What are the two types of tachycardia seen with wolff-parkinson-white syndrome?

A
  1. Orthodromic AV re-entrant tachycardia
  2. Antidromic AV re-entrant tachycardia
107
Q

What is Orthodromic AV re-entrant tachycardia

A
  1. Remember that an accessory atrioventricular pathway can direct electrical signal both ways creating circuits with ventricle, atria, and AV node
  2. Orthodromic is when AV node sends a signal down to ventricles and signal uses accessory atrioventricular pathway to go back into the atria and excite AV node again
108
Q

What is Orthodromic AV re-entrant tachycardia

A
  1. Remember that an accessory atrioventricular pathway can direct electrical signal both ways creating circuits with ventricle, atria, and AV node
  2. Antidromic is when electrical signal goes down accessory atrioventricular pathway and up the AV node to create a circuit this way
109
Q

What does the EKG look like for Orthodromic AVRT?

A
  1. Narrow QRS complex tachycardia
110
Q

What does the EKG look like for Antidromic AVRT?

A
  1. creates a WIDE QRS complex tachycardia
111
Q

What is WPW patten vs WPW syndrome?

A
  1. pattern means patient is asymptomatic but does show delta wave on EKG
  2. syndrome is when patient presents with tachycardias, palpitations
112
Q

Why is atrial fibrillation in WPW life threatening?

A
  1. Usually in A-fib the rate of depolarization is 300-500 bpm but it is slowed down to <200 bpm bc AV node can’t conduct that fast
  2. The accessory atrioventricular pathway can conduct rapidly though so you get these very high bpm (300-500) and this leads to minimal atrial filling and low cardiac output which can be life threatening
113
Q
  1. What is an AV block?
    1. What does this cause on EKG?
    2. What about severe block on EKG?
A
  1. Slowed or blocked conduction from atria to ventricles
  2. Prolongs PR interval
  3. This can show as a non conducted P wave meaning no generation of QRS
114
Q

What is type I AV Block

A
  1. Prolongation of PR interval only
  2. All P waves + QRS are conducted
115
Q

What is general Type II AV block?

(What are the subdivisions called?)

A
  1. Some p waves are conducted and some p waves are not conducted through to create QRS complexes
  2. Mobitz I and Mobitz II
116
Q

What is general Type III AV block?

A
  1. No impulse conduction form atria to ventricles
117
Q

In 1st degree/Type I AV block

  1. Where is the block usually found?
  2. What are the symptoms
A
  1. usually in AV node
  2. Usually no symptoms because all QRS complexes are made its just the PR is prolonged -found incidentally
118
Q

In 2nd degree/Type II AV block

  1. What is mobitz type I
  2. Where is block usually found
A
  1. Progressive PR prolongation followed by dropped beat
  2. Grouped beating (you see two QRS together followed by a space -dropped beat)
  3. Block is usually in AV node
119
Q

In 2nd degree/Type II AV block

  1. What is mobitz type II
  2. Where is block usually found
A
  1. No progressive prolongation, you may even see normal PR intervals
  2. It is irregularly irregular bc can have normal/prolonged PR interval (but same PR interval each time) + QRS followed by non-conducted P wave and so on in random order
  3. Block is usually in HIS-Purkinje system
  4. Often seen with bundle branch block
120
Q

In 3rd degree/Type 3 AV block

  1. Where is block usually found?
  2. What does EKG look like?
A
  1. Block is usually in HIS-purkinje system
  2. P waves that don’t lead to QRS because signal from atria doesnt go into ventricle
  3. Some QRS signals may appear but they are conducted from a different lower pace maker tissue
121
Q

How to differentiate between 3rd degree AV block and 2nd degree AV block-mobitz type I in EKG?

A
  1. The R-R interval (R between QRS complexes) in 3rd degree AV block are REGULAR (w/irregular PR intervals)
  2. In Mobitz type I R-R intervals are NOT regular (w/irregular PR intervals)
122
Q

What is ventricular tachycardia?

A
  1. Rapid depolarization of ventricles via an electrical foci within the ventricle (outside normal conduction)
123
Q

How is ventricular tachycardia seen on EKG?

A
  1. Wide QRS complexes
  2. Between wide QRS complexes you may be able to see tiny bumps which are P waves coming in from atria
  • Ventricular tachycardia occurs has AV dissociation in absence of heart block
124
Q

What is AV dissociation?

A
  1. Atria and ventricular depolarization have become uncoupled (dissociated)
125
Q
  1. What is ventricular fibrillation?
  2. What does EKG look like
A
  1. disorganized heart signals cause the lower heart chambers (ventricles) to twitch (quiver) uselessly. As a result, the heart doesn’t pump blood to the rest of the body. -this is fatal!
  2. image
126
Q
  1. What is seen in EKG with either right or left bundle branch blocks?
  2. Explain why it is like this
A
  1. PR interval is normal and QRS is wide
  2. SA node depolarizes normally (causing P wave) → then electrical signal moves to AV node and His bundle → reaches bundle branches, one will be blocked. → since one branch is NOT BLOCKED then QRS complex does begin on time (normal PR interval) but it is wider because it takes longer to depolarized both ventricles via one bundle branch
127
Q

What is the difference in right and left bundle branch block in EKG? explain the differences

A
  1. Right bundle branch block shows wide QRS and QRS complex is pointing upward + bunny ears
  2. Left bundle branch block shows wide QRS and QRS complex is pointing downward
  3. Remember deflection is based on where the electrical impulse is moving towards or away from Positive lead…this changes on whether electrical impulse has to move leftward/rightward to depolarize ventricle being blocked from excitation
128
Q

Do bundle branch blocks cause symptoms?

A

No they are incidentally found

129
Q
  1. What is torsades de pointes?
  2. What does it look like on EKG?
A
  1. A type of very fast heart rhythm (tachycardia) that starts in your heart’s lower chambers (ventricles)
  2. On EKG looks like party streamer
130
Q
  1. What is Brugada syndrome?
  2. What does it look like on EKG?
A
  1. Genetic dysfunction in voltage gated sodium channels which can lead to sudden cardiac death during sleep -> have an increased risk of having irregular heart rhythms beginning in the lower chambers of the heart (ventricles)
  2. Coving ST segments. Type I has this more than in Type 2 or 3.
131
Q

What does ventricular hypertrophy change in electrical conduction and EKG?

A
  1. thickened heart muscle increases voltages seen in EKG during QRS complexes
132
Q
  1. What does hyperkalemia do to electrical conduction in heart?
  2. What does it look like in EKG?
A
  1. Extracellular Hyperkalemia is too much K+ (potassium) outside of cells. This makes cells be partially depolarized and easier to generate AP
  2. Mild elevation in K+ leads to peaked T waves and prolonged PR segment
  3. Moderate K+ elevation - loss of P wave with prolonged QRS complex with ST segment elevation
  4. Severe elevation - widening of QRS
133
Q
  1. What does prolonged QT interval mean?
  2. What can this lead to?
A
  1. It means abnormal cardiac re-polarization
  2. Can throw a person into ventricular tachycardia or torsade de pointes
134
Q

Prolonged QT interval

What is

  1. LQT1
  2. LQT2
  3. LQT3
A
  1. Most common - problem is with the IKs current in the heart. Swimming (activities like this) can trigger.
  2. Problem is the IKr current - auditory triggers
  3. Least common - occurs during sleep
135
Q

What drugs are included in anticoagulant category? (4)

A
  1. heparins
  2. direct thrombin inhibitors
  3. direct factor Xa inhbiitors
  4. Warfarin
136
Q

What drugs are included in thrombolytics category? (2)

A
  1. t-PA derivatives
  2. Streptokinase
137
Q

What drugs are included in Antiplatelet category? (4)

A
  1. Aspirin
  2. Glycoprotein IIb/IIIa inhibitors
  3. ADP inhibitors (clopidogrel)
  4. PDE/adenosine uptake inhibitors
138
Q

Aspirin

  1. What class of drug is this (antiplatelets, anticoagulants, thrombolytics)
  2. What is its MOA
A
  1. antiplatelets
  2. COX1 and COX2 inhibitor to prevent formation of thromboxane A2 and prostaglandins
  3. Thromboxane is a precursor to platelets!
139
Q

Abciximab, eptifibatide, tirofiban

  1. What class of drug is this (antiplatelets, anticoagulants, thrombolytics)
  2. What is its MOA
A
  1. antiplatelets
  2. GPIIb/IIIa inhibitors- binds to GP IIb/IIIa receptors on platelet and inhibits the common pathway that allows for platelets to aggregate
140
Q

Clopidogrel, prasugrel, tricagrelor, cangrelor

  1. What class of drug is this (antiplatelets, anticoagulants, thrombolytics)
  2. What is its MOA
A
  1. antiplatelets
  2. ADP receptor (P2Y12) antagonists - this inhibits the ADP mediated platelet activation at P2Y12 receptor
141
Q

Dipyridamole, cilastazol

  1. What class of drug is this (antiplatelets, anticoagulants, thrombolytics)
  2. What is its MOA
A
  1. antiplatelets
  2. cAMP PDE inhibitors - by inhibiting this enzyme you prevent degradation of cAMP and cGMP → results in prolonging the platelet-inhibiting action and vasodilation effect
142
Q

Lepirudin, argatroban, dabigatran

  1. What class of drug is this (antiplatelets, anticoagulants, thrombolytics)
  2. What is its MOA
  3. Used in what clinical situation?
A
  1. anticoagulants
  2. Direct thrombin inhibitors (inhibit activity of thrombin)
  3. Used in patients with HIT (heparin induced thrombocytopenia)
143
Q

Heparin

  1. What class of drug is this (antiplatelets, anticoagulants, thrombolytics)
  2. What is its MOA
  3. What are the two forms of heparin
A
  1. anticoagulants
  2. indirect thrombin inhibitors- Activates antithrombin III which is a protein that inhibits coagulation (via lysing of thrombin and factor Xa (Xa cleaves prothrombin to thrombin which then acts on fibrinogen to make fibrin…clots))
  3. unfractionated and low molecular weight
144
Q

warfarin

  1. What class of drug is this (antiplatelets, anticoagulants, thrombolytics)
  2. What is its MOA
A
  1. anticoagulant
  2. Vitamin K reductase inhibitors - interferes with synthesis of vitamin K dependent clotting factors (2,7,9,10) and anticoagulant protein c and s
145
Q

Rivaroxaban, apixaban, edoxaban

  1. What class of drug is this (antiplatelets, anticoagulants, thrombolytics)
  2. What is its MOA
  3. In what clinical situation is it used?
A
  1. anticoagulants
  2. Direct Xa inhibitors
  3. Atrial fibrillation (as alternative to warfarin)
146
Q

Alteplase, reteplase, streptokinase

  1. What class of drug is this (antiplatelets, anticoagulants, thrombolytics)
  2. What is its MOA
  3. What is major side effect?
A
  1. thrombolytics AKA fibrinolytics
  2. Plasminogen activators - plasminogen degrades fibrin clots
  3. bleeding
147
Q

What heart conditions is aspirin used for?

A
  1. Low dose aspirin for primary prevention of cardiovascular disease and colorectal cancer
148
Q

what is main adverse effect of aspirin?

A

bleeding, gastric ulcers, and tinnitus

149
Q

What are considered pro-drugs and active drugs in the ADP receptor antagonists drugs of antiplatelet medications?

A
  1. Pro drug - clopidogrel and prasugrel
    1. these need to be broken down by enzyme to function
  2. Active drug - ticagrelor and cangrelor (these don’t need enzyme to work on them)
150
Q
  1. In what situations would you use ADP receptor antagonists (antiplatelets)? (2)
  2. Major side effect?
A
  1. Patients with acute coronary syndrome (a term used to describe a range of conditions associated with sudden, reduced blood flow to the heart)
  2. Patients with recent arterial stent placement + aspirin
  3. Side effect: Bleeding
151
Q
  1. In what situation would you use GP IIb/IIIa inhibitors (class of antiplatelets)?
  2. What is the major side effect
A
  1. Acute coronary syndromes (a term used to describe a range of conditions associated with sudden, reduced blood flow to the heart)
  2. bleeding
152
Q

Differentiate unfractionated vs low molecular weight heparin?

A
  1. Unfractionated - activates antithrombin III which breaks down many coagulation factors → increases PTT → main side effect is bleeding
  2. Low molecular weight- affect is limited to factor Xa. → lower incidence of heparin induced thrombocytopenia and less need for patient monitoring
153
Q

What is the reversal agent of heparin?

A
  1. protamine (binds to heparin to neutralize it)
154
Q

Common clinical uses of heparin

A
  1. DVT
  2. PE
  3. Acute MI
155
Q

Benefits of Low molecular weight heparin over unfractionated heparin?

A
  1. longer half life
  2. predictable effect
  3. decreased risk of heparin induced thrombocytopenia
156
Q

What factors are synthesized by vitamin K

A
  1. Vitamin II, VII, IX, and X
  2. Protein C and S
157
Q

What is the major side effect of warfarin?

A
  1. Bleeding
  2. potential drug-drug/food interactions
158
Q
  1. What should be monitored in people taking warfarin?
  2. What is antidote of warfarin
  3. Who shouldn’t take warfarin
  4. What type of patient should be taking warfarin
A
  1. Prothrombin time or INR (goal of INR of 2-3)
  2. Vitamin K
  3. pregnant women
  4. Individuals with end stage renal disease- warfarin is anticoagulant of choice
159
Q

Heparin vs warfarin

  1. What coagulation pathway does it effect
  2. Teratogenic
  3. Onset
  4. Duration
  5. Elimination
  6. Monitoring test
A

Heparin

  1. Intrinsic pathway
  2. No
  3. rapid
  4. brief- some hours
  5. eliminated renally
  6. aPTT

Warfarin

  1. affects extrinsic pathway
  2. Yes!
  3. Slow -takes hours
  4. Prolonged (days)
  5. eliminated hepatically
  6. PT
160
Q
  1. What medications are in Class IA of anti-arrhythmic drugs?
  2. What channels do they affect?
A
  1. Quinidine, Procainamide, Disopyramide
  2. Intermediate Na+ Channel blockers
161
Q
  1. What medications are in Class IB of anti-arrhythmic drugs?
  2. What channels do they affect?
A
  1. Lidocaine, Mexiletine
  2. FAST Na+ channel blocker
162
Q
  1. What medications are in Class IC of anti-arrhythmic drugs?
  2. What channels do they affect?
A
  1. Flecainide, propafenone
  2. Slow Na+ Channel Blockers
163
Q
  1. What medications are in Class II of anti-arrhythmic drugs?
  2. Mechanism of action?
A
  1. Beta Blockers
  2. work by blocking the effects of the hormone epinephrine, also known as adrenaline
164
Q
  1. What medications are in Class III of anti-arrhythmic drugs?
  2. What channels do they affect?
A
  1. Amiodarone, sofalol
  2. K+ Channel Blockers
165
Q
  1. What medications are in Class IV of anti-arrhythmic drugs?
  2. What channels do they affect?
A
  1. Verapamil, diltiazem
  2. Calcium channel blockers
166
Q

Class IA

  1. Mechanism of Action
  2. What does this do to AP
A
  1. Blocks OPEN sodium channels
  2. Changes slope in phase 0 → which prolongs repolarization in phase 3 ;;;there is slight increase in threshold voltage (harder to excite)
167
Q

Quinidine (Class IA)

  1. When is this drug used? (clinical indications?)
A
  1. This is not usually first line drug! - can be used for both atrial and ventricular arrhythmias
168
Q

Class IB drugs

  1. Mechanism of action
  2. Side effects
  3. How does this affect AP?
A
  1. Blocks sodium channels mainly in inactive state, but also open state - with fast unbinding
  2. CNS stimulation/depression, cardiovascular depression
  3. AP in ventricles - Mildly affects slope at phase 0 and mildly affects repolarization in phase 3
169
Q

Class IB drugs

  1. How does this affect EKG?
A
  1. minimal to no effects on QRS, QT, or PR intervals
170
Q

Class IC drugs

  1. Mechanism of action
  2. How does this affect AP?
A
  1. Blocks open Na channels with very slow unbinding
  2. Decreases slope
171
Q

Major use of beta blockers (Class II)?

A
  1. supraventricular arrhythmias
  2. Ventricular arrhythmias
  • described as safest and most widely used anti-arrhythmic available
172
Q

Major use of Class IB- lidocaine?

A
  1. Ventricular Tachyarrhythmias
  2. Frequent PVCs (Premature ventricular contractions)
173
Q

Major side effects of Class IB-lidocaine?

A
  1. CNS effects
174
Q

Contraindications for Class IB - lidocaine and mexilatine?

A

NOT FOR SUPRAVENTRICULAR ARRHYTHMIAS

175
Q

Major use of Class IB- Mexiletine?

A
  1. Ventricular arrythmias
  2. often used with other drugs
176
Q

Major side effects of Class IB-Mexiletine?

A
  1. Tremor
  2. Nausea
177
Q
  1. Major use of Class IC - Flecainide?
  2. Side effects?
A
  1. Atrial Arrhythmias (A-fib)
  2. SA node dysfunction, decreased conduction velocity, and conduction block
178
Q

Contraindications of Class IC - Flecainide?

A
  1. Ventricular arrhythmias due to ischemia (makes arrhythmia worse)
179
Q

How doe beta blockers affect..

  1. SA node
  2. AV node
  3. Phase 4 in AP
  4. Refractory period
A
  1. decreases If current in SA node
  2. Increases Ca and K currents in AV node
  3. Decreases phase 4 velocity (funny current)
  4. Prolongs refractory period
180
Q

Side effects of beta blockers (class II)

A
  1. heart block
  2. negative inotropy
  3. bradychardia
181
Q

What are contraindications for Class II- beta blockers?

A
  1. Severe heart failure where decreased inotropy would be a problem
  2. conduction blocks
  3. Sinus bradycardia
  4. Asthma
182
Q
  1. Mechanism of action of Class III drugs (ibutilide and dofetilide)
  2. Mainly used in what clinical conditions?
  3. Contraindications?
A
  1. Blocks K channels which prolongs repolarization in phase 3. - overall prolongs AP
  2. Atrial fibrillation and atrial flutter
  3. Pre-existing prolonged QT interval
183
Q

What is sotalol (Class III) mainly used for?

A
  1. Severe ventricular arrhythmias (esp. those who can’t tolerate amiodarone)
  2. To prevent atrial fib and flutter
184
Q

What is Amiodarone (Class III) mainly used for?

A
  1. Ventricular tachycardial
  2. Ventricular fibrillation
  3. Atrial fibrillation
  4. Atrial flutter
185
Q

What is contraindication for sotalol (Class III)?

A
  1. Pre-existing prolonged QT interval
186
Q

What is contraindication for amiodarone (Class III)?

A
  1. Cardiogenic shock
  2. 2nd or 2rd degree heart block
  3. Severe SA node dysfunction
  4. Sinus bradycardia
187
Q

Which class III drugs can be used in children?

A
  1. sotalol
188
Q

Mechanism of action of Class IV medications (verapamil an diltiazem)?

A
  1. Blocks alpha subunit of L type calcium channels to slow heart rate. Calcium L type channels are in charge of activity in phase 0
189
Q

When are class IV drugs mainly used for?

A
  1. Supraventricular tachyarrhythmias
  2. Prinzmetal angina
  3. Hypertension
190
Q

Contraindications for Class IV drugs?

A
  1. heart block
  2. heart failure
191
Q

What is the mechanism of action of adenosine (as an antiarrhythmic drug)?

A
  1. Opens G coupled K channels, inhibits conduction of SA and AV nodes
  2. Suppresses Ca dependent action potentials
192
Q

When is adenosine (as an antiarrhythmic drug) mainly used for?

A
  1. Narrow complex paroxysmal supraventricular tachycardia (SVT)
193
Q
  1. What is the mechanism of action of ranolazine (as an antiarrhythmic drug)?
  2. What is it mainly used for?
A
  1. Inhibits beta oxidation of fats favoring glucose → prolongs AP duration and QT interval
  2. stable angina
194
Q
  1. What is the mechanism of action of ivabradine (as an antiarrhythmic drug)?
  2. What is it mainly used for?
  3. Contraindications?
A
  1. Inhibits IF current in SA node to slow firing rate and decrease heart rate
  2. Stable angina, occasionally sinus tachy
  3. bradycardia
195
Q
  1. What is mechanism of action of atropine (antiarrhythmatic drug)?
  2. For what clinical situation is it used for?
A
  1. competitive antagonists for muscarinic acetylcholine receptors (acetylcholine typically decreases heart rate)
  2. symptomatic bradycardia
196
Q
  1. What is mechanism of action of epinephrine (antiarrhythmatic drug)?
  2. For what clinical situation is it used for?
A
  1. acts as an alpha 1 adrenergic agonist (sympathetic activation)
  2. symptomatic bradycardia
197
Q
  1. What is mechanism of action of dopamine (antiarrhythmatic drug)?
  2. For what clinical situation is it used for?
A
  1. Acts as beta 1 adrenergic agonist at mid range doses
  2. symptomatic bradycardia
198
Q

How do you manage sinus tachycardia first?

A
  1. treat underlying cause
  2. fluids- but don’t overload
199
Q
  1. What is Digoxin (anti-arrhythmic drug) used for?
A
  1. Rate control in supraventricular tachycardia and atrial fibrillation
200
Q

Describe what ions are moving and where are they moving in Phase 4, Phase 0, Phase 3 of AP in SA node

A
  1. Image
201
Q

Describe what ions are moving and where are they moving in Phase 4, Phase 0, Phase 1, Phase 2, and Phase 3 of AP in ventricular tissue

A
  1. image

Block 4 (8 decks)

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