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Cardiovascular System - 3rd year > Review Q's Week 2 > Flashcards

Review Q's Week 2 Flashcards

1. anatomy: Histology of blood vessels (1-40) 2. cardiac muscle action potentials physiology (41-70) 3. heart anatomy development part 1 (71-94) 4. heart anatomy part 2 (95-110) 5. antiarrhuthmic drugs (111-140) 6. ECG part 1 (141-161) 7. ECG part 2 (162-177) 8. pathophysiology of arrhythmias (178-197) 9. cardiac arrhythmias (198-end)

1
Q

Which of the following is thickest in veins?

a. tunica intima
b. tunica media
c. tunica externa

A

c. tunica externa

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2
Q

Which of the following is thickest in large arteries?

a. tunica intima
b. tunica media
c. tunica externa

A

b. tunica media

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3
Q

T/F: the tunica media of the aorta is mostly made up of elastic fibers

A

true

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4
Q

What kind of cells make up the tunica intima?

A

simple squamous

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5
Q

T/F: the tunica intermedia of capillaries is very thin

A

false, capillaries have only an endothelium, with no subendothelial layer or other tunics.

(Because capillaries are only one cell layer thick, they only have a tunica intima.)

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6
Q

Which of the following has a tunica media that has more smooth muscles?

a. aorta
b. vena cava

A

b. vena cava

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7
Q

What two layers make up the tunica intima?

A

subendothelial layer

+

endothelium

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8
Q

What two layers make up the inner and outer limit of the tunica media (surround it)?

A

internal elastic lamina

+

external elastic lamina

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9
Q

Which layer of veins makes folds to form valves?

A

tunica intima

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10
Q

Where are vasa vasorum found?

A

in arteries and larger veins

(found specifically in the adventitia of the aorta.)

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11
Q

How is the tunica intima separated from the tunica media?

A

by the internal elastic lamina (IEL), a prominent sheet of elastin.

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12
Q

T/F: elastic fibers are only found in the tunica media

A

false, elastic fibers are also present in the tunica adventitia (which is bigger in veins)

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13
Q

Why do the large arteries need a blood supply (vasa vasorum)?

A

Their walls are so thick that the blood they carry cannot diffuse through- they need another source of blood to supply their outer side

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14
Q

What kind of nerves are found in the adventitia, along vasa vasorum? What do they do?

A

small sympathetic nerves for vasoconstriction.

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15
Q

T/F: Large-sized and middle-sized arteries both have vasa vasorum

A

false, most middle-sized arteries don’t have a vasa vasorum (the largest of the middle-sized have it)

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16
Q

What separates the tunica media from tunica externa/adventitia?

A

external elastic laminae

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17
Q

The tunica media of which of the following has more elongated nuclei?

a. Large-sized artery
b. Medium-sized artery

A

b. Medium-sized artery

(more smooth muscle)

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18
Q

Which of the following allow blood to enter in a pulsatile fashion?

a. thoroughfare channel
b. precapillary sphincters
c. metarterioles
d. postcapillary venules

A

b. precapillary sphincters

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19
Q

Which of the following lacks any smooth muscle cells.?

a. thoroughfare channel
b. precapillary sphincters
c. metarterioles
d. postcapillary venules

A

a. thoroughfare channel

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20
Q

Which of the following has the highest diameter?

a. arterioles
b. venules
c. small capillaries

A

b. venules

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21
Q

T/F: tight junctions between the endothelial cells of the arterioles allow fluid to pass between them to allow diffusion

A

false, the tight junctions stop the leakage of fluids

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22
Q

Which doesn’t have a tunica intima?

a. arterioles
b. capillaries
c. both
d. neither

A

d. neither

(Because capillaries are only one cell layer thick, they only have a tunica intima.)

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23
Q

What are pericytes? What do they do?

A

they’re extra cells in the periphery of blood vessels that proliferate when there’s endothelial damage. They can proliferate to become endothelial cells or smooth muscles of the capillaries.

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24
Q

What are transcytotic vesicles used for?

A

to transport things through the epithelial cells of the capillaries to the surrounding tissue

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25
Q

Which is most likely found in BM?

a. Fenestrated capillaries
b. Sinusoids
c. Continuous capillaries

A

b. Sinusoids

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26
Q

Which forces molecules to cross via diffusion/transcytosis?

a. Fenestrated capillaries
b. Sinusoids
c. Continuous capillaries

A

c. Continuous capillaries

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27
Q

Which is found in the choroid plexus?

a. Fenestrated capillaries
b. Sinusoids
c. Continuous capillaries

A

a. Fenestrated capillaries

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28
Q

Which of the following are closed by diaphragms?

a. Fenestrated capillaries
b. Sinusoids
c. Continuous capillaries

A

a. Fenestrated capillaries

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29
Q

Which of the following doesn’t have s continuous external lamina?

a. Fenestrated capillaries
b. Sinusoids
c. Continuous capillaries

A

b. Sinusoids

(the rest have continuous basement membrane)

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30
Q

Which of the following has the largest diameter?

a. Fenestrated capillaries
b. Sinusoids
c. Continuous capillaries

A

b. Sinusoids

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31
Q

Which acts as a valve in veins?

a. tunica intima
b. tunica media
c. tunica externa

A

a. tunica intima

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32
Q

Which has more pericytes?

a. Postcapillary venules
b. Large collecting venules

A

b. Large collecting venules

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33
Q

Which is thin in small and medium-sized veins?

a. tunica intima
b. tunica media
c. tunica externa

A

a. tunica intima

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34
Q

Which is thin in large-sized veins?

a. tunica intima
b. tunica media
c. tunica externa

A

b. tunica media

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35
Q

How do you differentiate between normal versus lymphatic capillaries

A

lymphatic capillaries don’t have blood cells (usually)

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36
Q

Which are bigger, endothelial cells of blood vessels OR endothelial cells of lymphatic vessels?

A

endothelial cells of lymphatic vessels

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37
Q

How are the spaces between the endothelial cells formed?

A

they’re anchored by anchoring filaments (made up of elastin and endothelium)

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38
Q

Which of the following depolarizes?

a. sheath cells
b. glomus cells

A

b. glomus cells

(What induces the depolarization? low oxygen, high carbon dioxide, low pH)

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39
Q

What information do glomus cells rely to the brain? Through which nerve does this occur?

A

Changes in the CO2, O2, and H+ concentrations

via glossopharyngeal nerve

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40
Q

Where are baroreceptor-sensory nerve terminals located?

A

in the tunica adventitia

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41
Q

What is the primary pacemaker of the heart? Why?

A

the SA node is the primary pacemaker because it depolarizes at a more rapid pace than the others (60-100bpm)

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42
Q

What’s the intrinsic rate of the AV node?

A

40 to 55 beats/min

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43
Q

What’s the intrinsic rate of Tawara branches & Purkynje?

A

25 to 40 beats/min

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44
Q

Which results from ventricular repolarization?

a. P wave
b. T wave
c. QRS complex

A

b. T wave

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45
Q

Which results from ventricular depolarization?

a. P wave
b. T wave
c. QRS complex

A

c. QRS complex

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46
Q

What’s the electrical connection that links the atria and ventricles?

A

the AV node and AV bundle

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47
Q

What is the last place to be activated in the heart?

A

posterobasal areas of the ventricles (the outflow tracts)

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48
Q

Where does depolarization first take place?

a. endocardium
b. myocardium
c. epicardium

A

a. endocardium

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49
Q

Which results from artrial depolarization?

a. P wave
b. T wave
c. QRS complex

A

a. P wave

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50
Q

Where does repolarization first take place?

a. endocardium
b. myocardium
c. epicardium

A

c. epicardium

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51
Q

Action potentials last shorter in which of the following? Why?

a. endocardium
b. myocardium
c. epicardium

A

c. epicardium

they have stronger Ito current (outward potassium current) which acts to repolarize

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52
Q

Describe the ion flow in stage 2. What causes the plateau

A

Ca influx is balancing K efflux

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53
Q

Does this represent the AP in the antiarrhythmic cells or the AP in cardiac muscle?

A

In cardiac muscle

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54
Q

During stage 4, what is the cell permeable to?

A

Na and K (more to Na; as stage four continues the K movement decreases)

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55
Q

How does the positive chronotropic effect work?

A

opens more HCN-channels and L-type calcium channels to make the depolarization more rapid (so we reach threshold faster-> heart rate increases)

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56
Q

Explain how Parasympathetic stimulation causes a slower heart rate. What mechanisms are used?

A

reduces iHCN and iCa2+ channels (these channels act to depolarize)

opening of the acetylcholine regulated K+-channels (these channels hyperpolarize)

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57
Q

At which stage can another AP form?

A

At the latter part of stage 3, deformed AP can be generated with stronger than normal stimuli

(relative refractory period is end of stage 3)

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58
Q

Describe the action potential that occurred in stage 3

A

They’re abnormal (upstroke is slower, amplitude is lower, duration is shorter)

The sodium channels aren’t fully activated, but the calcium channels are fully activated.

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59
Q

Explain cardiovascular syncope

A

Fear causes a strong activation of the vagus nerve, which hyperpolarizes the AV node. Due to this hyperpolarization, the threshold cannot be reached.

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60
Q

T/F: the smaller the radius, the more vulnerable the nodal cell is to conduction block (AV block)

A

true

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61
Q

Why is the AV-node delay important?

A

ensures that the ventricles are relaxed at the time of atrial contraction and permits optimal ventricular filling during the atrial contraction

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62
Q

What does negative dromotropic intervention cause?

a. increases speed of conduction
b. decreases speed of conduction

A

b. decreases speed of conduction

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63
Q

What determines absolute refractory period?

A

The refractory period lasts as long as the inactivation gates are closed

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64
Q

What does the conduction speed of the AV node depend on?

A

diameter of node

the amplitude

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65
Q

Which of the following does hyperkalemia cause?

a. increases speed of conduction
b. decreases speed of conduction

A

b. decreases speed of conduction

(Negative dromotropic intervention)

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66
Q

Conduction velocity is called

A

dromotropy

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67
Q

How do Sympathetic stimulation & catecholamine speed up dromotropy?

A

phosphorylation of Ca-channels and HCN channels

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68
Q

Which of the following use the sympathomimetic effect to change dromotropy?

a. hyperkaliemia
b. thyroxine
c. ischemia
d. inflammation

A

b. thyroxine

(sensitizes sympathetic receptors)

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69
Q

How does hyperkaliemia effect dromotropy? HOW?

A

decrease it by inactivating calcium channels (-> inhibit AP generation and block conduction)

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70
Q

How does Parasympathetic stimulation slow down the conduction velocity?

A

hyperpolarization via opening of acetylcholine regulated K-channels

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71
Q

The heart tube is derived from what structure?

A

angioblastic cords

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72
Q

Initially, before the three folds occur, the heart tube is in which relation to the pericardial cavity?

a. dorsal
b. ventral

A

b. ventral

(becomes dorsal after the folds)

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73
Q

What gives rise to the pericardium?

A

mesoderm

(also gives rise to the heart)

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74
Q

Whats the origin of heart muscles?

A

cardiac jelly

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75
Q

What structure develops to become the ascending aorta and the pulmonary trunks?

A

truncus arteriosus

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76
Q

What allows communication between the primordial atrium and ventricle?

A

atrioventricular canal

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77
Q

Which early structure is absorbed and becomes the right atrium (smooth part of R atrium)?

A

sinus venosus

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78
Q

What two things does the sinoatrial valve separate?

A

sinus venosus and primordial atrium

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79
Q

During the folding of the heart tube, which structure is dorsal?

a. atria
b. ventricles

A

a. atria

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80
Q

Where does the septum perimum grow towards?

A

fused endocardial cushions

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81
Q

foramen primum allows the communication between what two structures?

A

the right and left atrium

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82
Q

Which end of the heart tube is located dorsally?

a. atrial end
b. venous end
b. out flow end

A

b. venous end

(its the tail end and is the inflow region)

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83
Q

Which structure splits the atrioventricular canal into right and left sections?

A

endocardial cushions that grow towards each other and fuse to form “fused endocardial cushion”

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84
Q

After birth, increased blood return from the lungs closes foramen ovale. Which is true about this mechanism?

a. the blood pressure pushes the upper limb of the septum primum
b. the blood pressure pushes the lower limb of the septum primum
c. the blood pressure pushes the upper limb of the septum secundum
d. the blood pressure pushes the lower limb of the septum secundum

A

b. the blood pressure pushes the lower limb of the septum primum

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85
Q

T/F: foramen secondum is formed due to perforations in septum secondum

A

false, it’s formed due to perforations in septum primum

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86
Q

Which of the following veins bring blood from the body of the embryo?

a. Umbilical vein
b. Viteline veins
c. Cardinal veins

A

c. Cardinal veins

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87
Q

What’s the origin of the smooth part of right vs smooth part of left atrium

A

Right= Sinus venarum

Left= pulmonary vein

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88
Q

What’s the origin of the rough part of right vs smooth part of left atrium

A

Both develop from the primordial atrium

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89
Q

Which of the following veins bring blood from the yolk sac?

a. Umbilical vein
b. Viteline veins
c. Cardinal veins

A

b. Viteline veins

(Umbilical vein brings from placenta)

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90
Q

What’s the most common type of congenital heart disease?

A

Ostium secundum types of septal defects

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91
Q

What type of defect is located in the superior part of the interatrial septum?

A

sinus venosus defect

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92
Q

What occurs if both the septum primum and septum secundum fail to develop?

A

The interatrial septum is absent and a common atrium is formed

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93
Q

How does AV canal/ AV septal defect occur?

A

Endocardial cushions fail to fuse with each other

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94
Q

How does the patent foramen primum defect occur?

A

Failure of fusion of septum primum with endocardial cushions

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95
Q

What are the three things that fuse together to form the membranous part of the interventricular septum?

A

left bulbar ridge

+

right bulbar ridge

+

downward projection of the endocardial cushion

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96
Q

Both the right and left ventricles have smooth outflow parts. Where are these regions derived from?

A

Bulbus cordis

right ventricle = conus arteriosus / Infundibulum

left ventricle = aortic vestibule

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97
Q

The ascending aorta and pulmonary trunk develop from…

A

trucus arterious

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98
Q

Which of the following is used to bypass the liver in fetal circulation?

a. ductus venosus
b. foramen ovale
c. ductus arteriosus

A

a. ductus venosus

(the rest are used to bypass the pulmonary circulation)

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99
Q

Which of the following forms ligamentum teres after birth?

a. ductus venosus
b. foramen ovale
c. ductus arteriosus
d. umbilical veins

A

d. umbilical veins

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100
Q

After birth what do these structures develop into?

ductus venosus

ductus arteriosus

A

ductus venosus-> ligamentum venosum

ductus arteriosus-> ligamentum arteriosum

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101
Q

What will the incomplete closure of interventricular foramen cause?

A

membrane ventricular septal defects

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Not at all
2
3
4
5
Perfectly
102
Q

excessive cavitation of myocardial tissue during development of the ventricular walls leads to

A

Muscular ventricular septal defects

103
Q

What defect leads to the development of a single ventricle?

A

failure of interventricular septum formation

104
Q

Which conditon occurs when truncus arteriosus is not divided? Which other condition is associated with it

A

Persistent truncus arteriosus (PTA)

associated with ventricular septal defects

105
Q

An aortic window is an opening between which two structures? What is this defect called?

A

opening between aorta and pulmonary trunk near the arotic valve

Aorticopulmonary septal defect

106
Q

What causes pulmonary atresia?

A

unequal division of truncus arteriosus

(pulmonary trunk has no lumen or orifice at the level of pulmonary valve.)

107
Q

What causes aortic atresia?

A

edges of the valve are usually fuse

108
Q

What’s the most common cause of cyanosis?

a. tetralogy
b. patent ductus arteriosus

A

b. patent ductus arteriosus

109
Q

T/F: the heart in Ectopia Cordis is developed normally

A

true, the only problem is its location

110
Q

What’s Dextrocardia?

A

developing heart tube bends to the left side instead of right side (can be a part of part of situ in-versus)

111
Q

T/F: all class 1 antiarrhythmic drugs increase refractory period

A

false; class 1a increases it, 1b decreases, and 1c doesn’t change it

112
Q

Which two phases do class 1 antiarrhythmic drugs affect and how?

A

reduced rate of phase 0 and phase 4 depolarization

they do this by blocking Na channels

113
Q

Which has no effect on duration of the action potential?

a. Mexiletine
b. Disopyramide
c. Procainamide
d. Flecainide
e. Quinidine
f. Lidocaine

A

d. Flecainide

114
Q

Which of the following causes cinchonism as an adverse effect?

a. Mexiletine
b. Disopyramide
c. Procainamide
d. Flecainide
e. Quinidine
f. Lidocaine

A

e. Quinidine

115
Q

In which location(s) do class 1B antiarrhythmic agents reduce the duration of AP?

A

Shortens the duration of AP in Purkinje fibers and ventricular muscle.

(No difference in AP of atrial fibers)

116
Q

Which of the following is mainly used for ventricular arrhythmias in unresponsive patients?

a. Mexiletine
b. Disopyramide
c. Procainamide
d. Flecainide
e. Quinidine
f. Lidocaine

A

b. Disopyramide

117
Q

Which phase do class 2 and 3 antiarrhythmic drugs affect and how?

A

Reduce slope of phase 4-depolarization

118
Q

How is Quinidine taken? Where is it found in the body? Where is it metabolized and excreted?

A

taken orally, 90% found in plasma proteins, metabolized in liver and excreted in urine

119
Q

Why does Quinidine cause hypotension?

A

because it blocks alpha-adrenergic receptors, which vasoconstrict vessels

120
Q

Which has the highest anticholinergic effect?

a. Quinidine
b. Disopyramide
c. Procainamide

A

b. Disopyramide

121
Q

Which is mostly used to treat long-term treatment of ventricular arrhythmias associated with previous myocardial infarction?

a. Mexiletine
b. Disopyramide
c. Phenytoin
d. Flecainide
e. Quinidine
f. Lidocaine

A

a. Mexiletine

122
Q

Which antiarrhythmic drugs are used to stimulate uterine activity?

A

Quinidine

(Acts as oxytocic agent=stimulate uterine activity)

123
Q

Which of the following is used for re-entry arrhythmias and acute ventricular tachycardia?

a. Mexiletine
b. Disopyramide
c. Procainamide
d. Flecainide
e. Quinidine
f. Lidocaine

A

c. Procainamide

124
Q

Which is used to treat ventricular arrhythmias in children?

a. Mexiletine
b. Disopyramide
c. Phenytoin
d. Flecainide
e. Quinidine
f. Lidocaine

A

c. Phenytoin

125
Q

Which has an adverse effect of bone marrow depression?

a. Mexiletine
b. Disopyramide
c. Phenytoin
d. Flecainide
e. Quinidine
f. Lidocaine

A

f. Lidocaine

126
Q

Which of the following is mainly used with other drugs?

a. Mexiletine
b. Disopyramide
c. Phenytoin
d. Flecainide
e. Quinidine
f. Lidocaine

A

a. Mexiletine

127
Q

Which class of antiarrhythmic drugs increases threshold potential? What does this result in?

a. class 1A
b. class 1B
c. class 1C

A

c. class 1C

increasing threshold potential reduces automaticity

128
Q

Which drug leads to the development of lupus-like syndrome when you stop prolonged treatment?

A

Procainamide

129
Q

Which had the shortest half-life?

a. Mexiletine
b. Disopyramide
c. Procainamide
d. Flecainide
e. Quinidine
f. Lidocaine

A

f. Lidocaine

(1.5-2hrs)

130
Q

Which class of antiarrhythmic drugs are the most potent Na channel blockers? Describe dissociation rate.

a. class 1A
b. class 1B
c. class 1C

A

c. class 1C

they have a high affinity to the Na channels and dissociate very slowly, prolonging their effect

131
Q

How is Flecainide taken? Where is it found in the body? Where is it metabolized and excreted?

A

taken IV or oral, no first-pass metabolism. 75% found on plasma proteins and highly concentrated in cardiac tissue. partly metabolizes and partly unchanged (slow renal excretion)

132
Q

Which type of antiarrhythmic drugs act by blocking K channels?

a. class I drugs
b. class II drugs
c. class III drugs
d. class IV drugs

A

c. class III drugs

(depolarization affected)

133
Q

Which type of antiarrhythmic drugs decreases conduction across AV node at high concentrations only?

a. class I drugs
b. class II drugs
c. class III drugs
d. class IV drugs

A

b. class II drugs
(d. class IV drugs do this also…)

134
Q

Which is the drug of choice in paroxysmal supraventricular tachycardia?

a. class I drugs
b. class II drugs
c. class III drugs
d. class IV drugs

A

d. class IV drugs

135
Q

Which has an adverse effect of decreased hearing and disorientation?

a. Mexiletine
b. Disopyramide
c. Phenytoin
d. Flecainide
e. Quinidine
f. Lidocaine

A

f. Lidocaine

(CNS symptoms in high concentrations ex/drowsiness)

136
Q

Which type of antiarrhythmic drugs has withdrawal symptoms when the patient stops taking it after long term use?

a. class I drugs
b. class II drugs
c. class III drugs
d. class IV drugs

A

class II drugs (beta adrenergic agnoists)

137
Q

What type of antiarrhythmic drug is Amiodarone? How is the half-life of the drug?

A

type 3, but it hals actions of all the other classes. half life is very high (days or months) so toxicity is more likely

138
Q

Which type of antiarrhythmic drugs act by blocking Ca channels?

a. class I drugs
b. class II drugs
c. class III drugs
d. class IV drugs

A

d. class IV drugs

139
Q

Which type of calcium channel is most used?

A

L type Ca channel

140
Q

Which of the following is best for a hypertensive patient? How about a patient with an arrhythmia or angina?

a. diltiazem
b. nifedipine
c. verapamil

A

hypertensive—> b. nifedipine

arrhythmia or angina—> c. verapamil

141
Q

The ECG line is made by comparing which of the following?

a. inside and outside of cell
b. outside of cells from different locations

A

b. outside of cells from different locations

142
Q

During Lead III, we use two electrodes- a negative one on the left arm and a positive one the left leg. From which angle are we monitoring the heart?

a. upper angle
b. lower angle
c. side angle

A

b. lower angle

the positive electrode is the one recording

143
Q

During Lead I, we use two electrodes- a negative one on the righ arm and a positive one the left arm. From which angle are we monitoring the heart?

a. upper angle
b. lower angle
c. right side angle
d. left side angle

A

d. left side angle

144
Q

Describe a depolarization wave if we are viewing it from a perpendicular view

A

biphasic wave

145
Q

The green arrow is the sum of all dipoles of a normal patient. Your patient’s arrow is red, which is the most likely diagnosis?

a. hypertension
b. right ventricular hypertrophy
c. myocardial infarction

A

b. right ventricular hypertrophy

146
Q

The green arrow is the sum of all dipoles of a normal patient. Your patient’s arrow is red, which is the most likely diagnosis?

a. hypertension
b. right ventricular hypertrophy
c. myocardial infarction

A

a. hypertension

147
Q

In which direction is the septum of the heart depolarized?

A

from left to right

148
Q

Which ECG wave represents septal depolarization?

A

Q wave

149
Q

Which ECG wave represents depolarization of the ventricular base?

A

S wave

150
Q

What is occuring in the heart if the PR segment (also called PQ segment) is elongated?

A

AV block

151
Q

What does the U wave of an ECG represent?

A

repolarization of purkinje fiber remnants

152
Q

What does the ST segment of an ECG represent?

A

plateau phase of AP

153
Q

What is the amplitude of the QRS complex?

A

0.7mV

(7 tiny boxes X 0.1 mV per box= 0.7mV)

154
Q

Calculate the PR interval.

A

0.12sec

(3 tiny boxes X 0.04 sec per box= 0.12sec)

155
Q

Calculate the heart rate

A

60bpm

300/5=60bpm

156
Q

How long is a normal PR segment?

A

0.12 -> 0.21 s

157
Q

Diagnose this patients ECG. Does he have any symptoms? (if yes, list them)

A

The PR segment is prolonged, but no QRS complexes are missing, this means first degree AV block.

*First-degree heart block often does not cause symptoms*

158
Q

Is this Atrial flutter or atrial fibrillation? What is the difference between the two conditions?

A

atrial fibrillation

both conditions are abnormal heart rhythms. In atrial fibrillation, the atria beat irregularly. In atrial flutter, the atria beat regularly, but faster than usual and more often than the ventricles, so you may have four atrial beats to every one ventricular beat.

159
Q

diagnose

A

ventricular fibrillation

160
Q

diagnose

A

independent atrial and ventricular rhythms, so complete (third degree) AV block

161
Q

What is this ECG describes as? Diagnose it.

A

Sawtooth appearance

atrial flutter (regular but fast)

162
Q

diagnose

A

Sinus tachycardia

163
Q

diagnose. Is the pause compensatory or noncompensatory? Is the SA node affected?

A

Premature ventricular complex (PVC)

The pause is compensatory and SA nose not affected (beat time didn’t change)

164
Q

How many ectopic foci are present?

A

one (atrial flutter)

165
Q

How many ectopic foci are present?

A

many foci in the atrium

166
Q

diagnose

A

Second degree heart block Type II, Mobitz II

(PR interval constant + a QRS missing)

167
Q

diagnose

A

Second degree heart block type I, Mobitz I

(PR interval prolonging + QRS missing)

168
Q

diagnose

A

2:1 block, second degree AV block

(2p waves then one QRS complex)

169
Q

diagnose

A

Third degree complete heart block

170
Q

How many ectopic foci are present?

A

one ventricular foci

(Monomorphic ventricular tachycardia)

171
Q

How many ectopic foci are present?

A

many ventricular foci

Polymorphic ventricular tachycardia

AKA Torsades de pointes

172
Q

diagnose. How many ectopic foci are present?

A

Ventricular fibrillation

many ventricular foci

173
Q

diagnose. How many ectopic foci are present?

A

Ventricular flutter

one ventricular ectopic focus

174
Q

diagnose. Is there an ectopic foci? if yes, where is it located?

A

Premature atrial complex (PAC)

ectopic foci is next to the SA node (R atrium), if it was in any other place the extra beat would be inverted

175
Q
A

couplet

176
Q
A

trigeminy

177
Q
A

bigeminy

178
Q

What is the normal resting potential of myocardial cells? What occurs to the cells when it increases to -60mV? how about -50mV?

A

normal resting potential is -85mV, the more positive the resting potential becomes the less functional the cell gets. Thats because channels get blocked.

resting potential→ -60 = less Na channel available

resting potential→ -50 = all Na channels unavailable

179
Q

Why do patients with heart disease experience arrhythmias more often?

A

Heart conditions can cause myocardial death. When the cell dies, it releases all its contents, including the potassium. That leads to a region that’s hyperkalemic, which causes the nearby myocytes to contract- thus cause arrhythmias.

(when the K increases extracellularly, the gradient between K inside and outside decreases, that causes less K from leaving the cell- and that makes it more + = partial depolarization)

180
Q

A 30 year old cannot get his heart rate to 160. What is this called?

A

Chronotropic incompetence = sinus rate does not adequately increase in response to stress or exertion (< 85% of age appropriate HR during exercise testing)

His maximum should be 190. 85% of that is 161.5

181
Q

How do you calculate the age appropriate heart rate?

A

220 - age

(if patient is 20, maximum heart rate is 200)

182
Q

What are Escape rhythms and how are they activated?

A

Normally, overdrive suppression occurs and all cells besides the SA are suppressed from exhibiting normal spontaneous depolarization. However, when the SA node is defective these cells are released from this suppression and we will get “Escape rhythms”.

(it’s a protective mechanism; ex/ Atrial escape and ventricular escape)

183
Q

What is it called when the SA node stops generating electrical impulses. How would it present in an ECG?

A

sinus arrest

No P wave in ECG

184
Q

What occurs to QRS complex when the pacemaker is in the ventricles? Why?

A

wide QRS

it’s wide because its not going through the fast Purkinje fibers

(supraventricular/arterial orgin= narrow QRS because Purkinje fibers are fast)

185
Q

When the SA node stops pacing the heart, junctional escape beats take over. Where is the focus located?

A

located in the AV junction

186
Q

The SA node of a patient stopped pacing the heart, but his heart rate is 100. How is this possible?

A

Accelerated idioventricular rhythm, a ventricular rhythm with a rate of between 40 and 120 beats per minute.

Idioventricular = ventricle alone

187
Q

suppression of all pacemaker activity occurs during

A

cardiac arrest

188
Q

Early afterdepolarizations occur due to which of the following?

a. Na/Ca exchanger
b. Ca-channels

A

b. Ca-channels

(delayed afterdepolarizations -> because of Na/Ca exchanger)

189
Q

Describe the relationship between heart rate and QT interval. What does it mean if the QT interval is too long?

A

inversely proportional

If QT is too long, means repolarization is not coming in the correct time, myocytes remain depolarized for longer time.

190
Q

How does the Na/Ca exchanger cause delayed afterdepolarization?

A

The calcium is high in the cell so the Na/Ca exchanger on plasma membrane will bring in Na and take Ca out. This exchanger is electrogenic, that is they will take 3 Na in and 2 Ca out, and this will lead to cell becoming more positive and lead to depolarization, causing the condition.

191
Q

Which gene mutation causes long QT syndrome?

A

LQT 1-17

192
Q

What is the direction of a reentry impulse coming from the atria to the ventricles via accessory pathways (bundle of Kent)? What does this type of reentry result in?

A

It moves in a counter-clockwise direction

This type of reentry results in supraventricular
tachyarrhythmia

193
Q

What is the most important thing that allows reentry impulses to occur?

A

Retrograde conduction must be slow enough to allow for the recovery of excites regions (1st degree block)

194
Q

Which of the following AV node electrical pathways has a longer refractory period?

a. fast pathway
b. slow pathway

A

a. fast pathway

195
Q

Which of the following AV node electrical pathways conducts normal sinus beats?

a. fast pathway
b. slow pathway

A

a. fast pathway

196
Q

How can an atrial premature atrial beat use to create a sustained reentrant supraventricular tachycardia?

A

The impulse cannot go through the fast pathway because its still in the refractory period, so it goes to the slow pathway. It then reenters the fast pathway after the refractory period ended and retrogradely activates it.

197
Q

How do we prevent reentrant supraventricular tachycardia?

A

increase refractory period

(or restore the accessory bypass tract)

198
Q

Which are objective?

a. palpitations
b. arrhythmias

A

b. arrhythmias

they’re measurable and not based on feelings. palpitations are subjective.

199
Q

What’s the first organ to develop?

A

the heart

200
Q

Which increases contractility?

a. Positive chronotropic effect
b. Positive inotropic effect

A

b. Positive inotropic effect

201
Q

What maintains the polarity of myocardial cells?

A

voltage gated channels

(insures appropriate ion distribution)

202
Q

What’s the AV guard?

A

the maximum amount ventricles can pump per minute

250bpm

203
Q

What does mapping and tracing the R’s in an ECG do?

A

insures the R-R intervals are the same, if its a regular heart rate

204
Q

What does it mean to be hemodynamically unstable?

A

insufficient oxygen to vital organs

205
Q

T/F: we apply an electrical shock to hemodynamically unstable patients no matter what type of arrhythmias they have

A

true

206
Q

How do you treat pathologically bradycardic patients?

A

pacemaker

207
Q

How do you treat a hemodynamically stable patient with ventricular tachycardia?

A

shock them- because this condition has a tendency to destabilize quickly

208
Q

How do you treat a hemodynamically stable patient with arrhythmia?

A

if hemodynamically stable, treat with pharmacotherapy!

(except if ventricular tachycardia, then shock them even if they’re stable- because they become unstable quick)

209
Q

T/F: all class 1 antiarrhythmic drugs are used for septal defects of the heart

A

false, they’re only used in normally structured hearts

210
Q

all class 1 antiarrythmatic drugs block which ion channel?

A

Na+

211
Q

Which of the following class 1 antiarrhythmic drugs are pure Na+ blockers? What are two examples of them?

a. 1a
b. 1b
c. 1c

A

c. 1c

Flecainide
Propafenone

212
Q

Which of the following antiarrhythmic drugs block N and K channels? What are two examples?

a. 1a
b. 1b
c. 1c

A

a. 1a

Procainamide IV

Quinidine

213
Q

Which is given for a slow supraventricular pulse?

a. Amiodarone
b. Adenosine
c. Atropine
d. Sotalol

A

c. Atropine

214
Q

Patient comes in with supraventricular tachycardia. Which medications can be used to treat this condition?

A

Adenosine/Amiodarone

Beta Blockers

Calcium Blockers (Verapamil, Diltiazem)

Digoxin

(ABCD)

215
Q

Which of the following antiarrhythmic drugs only block Na in a depolarized state? What are two examples?

a. 1a
b. 1b
c. 1c

A

b. 1b

Lidocaine IV

Mexilitine

216
Q

Patient comes in with ventricular tachycardia. Which medications can be used to treat this condition?

A

Beta Blockers

Amiodarone

Lidocaine

Sotalol

(BALS)

217
Q

appropriate vs inappropriate sinus tachycardia

A

appropriate = due to a secondary reason ex/ exercise

inappropriate = no cause

218
Q

Whats the difference between Supraventricular Tachycardia (SVT) and Sinus Tachycardia?

A

Supraventricular Tachycardia (SVT) also known as paroxysmal supraventricular tachycardia (PSVT) occurs suddenly and stops suddenly. While Sinus Tachycardia occurs slowly and fades slowly.

219
Q

AVRT versus AVNRT

AVRT = Atrioventricular reentrant tachycardia

AVNRT = AV-nodal reentrant tachycardia

A

AVRT→ anatomical reentry because of extra conducting tissue that ain’t the AV node (bundle of Kent is the conductor)

AVNRT→ functional reentry that occurs in the structurally normal AV node (the impulse is premature and it causes a circuit- activating the atria and ventricles at the same time + at a faster rate then SA)

220
Q

paroxysmal supraventricular tachycardia (PSVT) occurs most commonly in…

A

young patients

221
Q

Diagnose

A

Paroxysmal supraventricular tachycardia (PSVT)

no P waves, narrow QRS complex, ST depression, and regular but high heart rate

(AVNRT is the most common form of PSVT)

222
Q

What is Wolff-Parkinson-White (WPW) Syndrome?

A

A condition in which there is an extra electrical pathway in the heart.The most common mechanism of tachycardia in patients with WPW is called atrioventricular reentrant tachycardia (AVRT)

223
Q

Diagnose

A

WPW syndrome/AVRT

When an accessory pathway is present, the sinus node action potential can pass through the bypass tract before the AV node, resulting in the ventricles becoming rapidly depolarized. This is termed “pre-excitation” and results in a shortened PR interval on the ECG.

The typical ECG finding of WPW is a short PR interval and a “delta wave.“ A delta wave is slurring of the upstroke of the QRS complex. This occurs because the action potential from the sinoatrial node is able to conduct to the ventricles very quickly through the accessory pathway, and thus the QRS occurs immediately after the P wave, making the delta wave.

224
Q

What is a Delta wave? What does it look like? Why does it occur? When?

A

Delta wave is a slurred upstroke in the QRS complex often associated with a short PR interval. It is most commonly associated with (due to) pre-excitation syndrome such as Wolff-Parkinson-White syndrome.

225
Q

ST depressions are indicators of which pathology?

A

myocardial ischemia/ coronary artery disease

(but when its a young patient check PSVT because it also causes ST depression)

226
Q

What’s the first line treatment of Paroxysmal supraventricular tachycardia (PSVT)?

A

carotid massage (because its a vegal maneuver that slows down the AV node)

+

adenosine (if no difference)

227
Q

What’s the second line treatment of Paroxysmal supraventricular tachycardia (PSVT)?

A

IV Beta Blocker

IV Diltiazem (ca channel blocker)

IV Verapamil

(the goal is to interrupt the circuit at the AV node; Digoxin is also used because it has important parasympathetic effects, on the AV node)

228
Q

What’s the definitive treatment of Paroxysmal supraventricular tachycardia (PSVT)/AVRT?

A

Radiofrequency​ Ablation therapy (aka rhizotomy) which is a type of minimally invasive procedure that uses heat to destroy abnormal tissue

229
Q

What is the most common abnormal heart rhythm?

A

Atrial fibrillation

(more common as age increases)

230
Q

What are some causes of atrial fibrillation (AF)?

A

all cardiac diseases can lead to AF

non-cardiac reasons = drugs, alcohol, acute respiratory infections, hyperthyroidism, hormonal diseases

231
Q

How many foci cause Atrial Fibrillation? Where are they located?

A

many supraventricular foci, especially at the junction of pulmonary veins

232
Q

PSVT and Atrial fibrillation both don’t present P waves on ECG’s. Explain the mechanism of each.

A

PSVT doesn’t show the P waves because the QRS complex covers them due to the atrial and ventricles contracting simultaneously. (there technically IS a P wave)

Atrial fibrillation doesn’t have P waves because the atrial doesn’t contract (no atrial depolarization), it vibrates instead because of the many activations foci.

233
Q

T/F: Atrial fibrillation (AF) is always paired up with tachycardia due to many impulses generated by the foci

A

False, the condition has varying heart rates. In AF young patients the AV node may conduct many impulses and cause tachycardia, but in AF older patients, the conductivity is reduced and the heart rate may be normal or reduced.

(so the only things that confirm AF is irregular R-R’s and no P waves, heart rate doesn’t play a factor)

234
Q

What’s the major complication of Atrial Fibrillation?

A

blood clots forming in the atria (because they don’t contract) that can cause infractions or strokes

235
Q

What is Valvular Atrial Fibrillation? How do you treat patients who have it?

A

Valvular Atrial Fibrillation is when a patient who has Atrial Fibrillation as well as Mitral valve stenosis. (both those conditions cause blood to stay in the atria- very high risk of stroke) Give anticoagulants

236
Q

A patient has both atrial fibrillation and aortic stenosis, which does he classify into?

a. Valvular Atrial Fibrillation
b. Nonvalvular Atrial Fibrillation

A

b. Nonvalvular Atrial Fibrillation

237
Q

In Which do you use the “CHA2DS2-VASc score” system to decide if he needs anticoagulants?

a. Valvular Atrial Fibrillation
b. Nonvalvular Atrial Fibrillation

A

b. Nonvalvular Atrial Fibrillation

(in Valvular you immediately give anticoagulants)

238
Q

A male has a CHA2DS2-VASc score of 2, do you give anticoagulants?

A

yes, in males if above 1 then you give

239
Q

How do you treat atrial fibrillation?

A

Control Rate with Beta Blockers, Calcium Channel Blockers, Digoxin

Control Rhythm (AF to Sinus rhythm) with either Electrical or Pharmacological methods.
pharma= Propafenone, Flecanide, Amiodarone

Or treat permanently with Ablation therapy

240
Q

reentry circuit of atrial flutter is 300 and it has a 3 to 1 AV block, what is the heart rate?

A

100bpm

241
Q

What is a common atrial flutter rate?

A

150bpm (300 atrial circuit rate and 2:1 AV physiological block)

242
Q

A female has a CHA2DS2-VASc score of 2, do you give anticoagulants?

A

no, for women it should be above 2 to administer anticoagulants

243
Q

T/F: Atrial flutter can be diagnosed due to its regularity

A

false, it is regular but the AV node may very in its conductivity. So it can conduct 2 to 1 then change to 4 to 1, which would make the rate appear irregular- that’s why we can’t use it.

(diagnose because of saw tooth appearance only, and it’s commonly 150bpm)

244
Q

Diagnose. (What is that wave that’s different than the rest?)

A

Ventricular Tachycardia, with a capture beat (a normal looking SA beat). The ventricles are causing SA suppression, and the capture beat is evidence that the SA node is still functioning and can depolarize the heart.

245
Q

Which is more sensitive to shock?

a. atrial flutter
b. atrial fibrillation

A

a. atrial flutter

(that’s why they give 50J initially)

246
Q

What are the three basic findings in an ECG that points to ventricular tachycardia?

A

wide QRS

no P waves

tachycardia

247
Q

Sustained vs non-sustained ventricular tachycardia

A

sustained= 30 secs or more

non-sustained= less than 30 seconds

248
Q

Diagnose. Explain the activity in the circle.

A

ventricular tachycardia, the circles indicate P waves when the SA node was able to depolarize the atria (but it wasn’t able to continue down the pathway to the AV node and bundle)

249
Q

How many ventricular complexes must be present for the diagnosis of ventricular tachycardia?

A

3 or more

250
Q

Diagnose. Is this monomorphic or polymorphic?

A

polymorphic ventricular tachycardia, also called torsades de pointes

251
Q

diagnose

A

ventricular fibrillation

252
Q

Who is most likely to have ventricular tachycardia?

A

people with structural heart disease (ex/ ischemic heart disease- most likely) and cardiomyopathy patients

253
Q

Treatment of ventricular tachycardia

A
  1. shock ‘em with 100J
  2. pharmacological therapy (Procainamide, Sotalol, Lidocaine, Amiodarone)
  3. give magnesium sulfate if polymorphic VT
  4. correct contributing conditions
254
Q

Mobitz I vs Mobitz II

A

both second degree heart blocks

Mobitz I= (PR interval prolonging + QRS missing)

Mobitz II= (PR interval constant + a QRS missing)

Cardiovascular System - 3rd year (23 decks)

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