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B3 Clinical Application > B3 CPR > Flashcards

B3 CPR Flashcards

1
Q

2 movements of thoracic wall in breathing

A

pump handle (AP dimension increase)
bucket handle (transverse dimension increase)

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2
Q

thoracentesis/needle aspiration

A

remove blood/pus from pleural cavity
need to do in cases of pneumonia
8, 9, 10 intercostal space @ junction of rib & diaphragm lining

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3
Q

Chest tube/thoracostomy tube

A

insert into pleural space for inflation of collapsed lung, draining fluid, deliver meds
create negative pressure

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4
Q

pneumothorax

A

excess air in pleural cavity

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5
Q

hemothorax

A

excess blood in pleural cavity

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6
Q

pleural effusion/hydrothorax

A

excess fluid in pleural cavity

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7
Q

chylothorax

A

excess chyle in pleural cavity

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8
Q

empyema

A

excess pus in pleural cavity

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9
Q

Intercostal nerve block

A

anesthesthetic around intercostal nerves
superior rib first
inferior rib second
will do in times of chest tube insertion

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10
Q

intercostal neurovascular bundle

A

between internal & innermost intercostal muscle in costal groove

Superior to inferior: Vein, Artery, Nerve

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11
Q

Herpes Zoster/Shingles

A

varicella-zoster virus that cause chicken pox
virus reactivate & travel along nerve pathways

lives in dorsal root ganglion and transport along axon
expression along dermatome

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12
Q

Inferior Thoracic Aperture

A

separate thorax from abdomen
wider transverse & oblique slopes down/back
completely closed by diaphragm

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13
Q

structures pass through inferior thoracic aperture

A

Inferior vena cava (caval opening @T8)
esophagus (esophageal hiatus @T10)
Vagus nerve (esophageal hiatus)
aorta (aortic hiatus @T12)
thoracic duct (aortic hiatus)

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14
Q

Thoracic Outlet Syndrome diagnoses

A

Adson’s test (compress subclavian A by scalene & view pulse change)
Roos test (elevate arm stress to see compression neurovasc)
Wright’s test (hyperabduction for compression axillary A & brachial plexus)

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15
Q

Thoracic outlet syndrome

A

compression of any structures between clavicle & rib 1
be from anatomical variations, trauma, repeat use
mostly pain, numb, parethesia hand/arm
swell, pain, cyanosis
cold, numb, pain, dimished pulse

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16
Q

axillary inlet

A

thoracic inlet
neurovasc bundle between clavicle & first rib, exit between scalenes
Clavicle, scapula, first rib form borders

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17
Q

thoracic outlet

A

area above clavicles, between sternum, & T1 & 1st rib
T1, First rib, manubrium form borders

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18
Q

Superior thoracic aperture

A

anterior boundary: posterior border of manubrium
lateral boundary: 1st ribs & costal cartilages
Posterior boundary: T1

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19
Q

structures pass through superior thoracic aperture

A

trachea & esophagus
common carotid arteries, subclavian arteries, internal jugular veins, brachiocephalic veins
vagus nerve, phrenic nerves, recurrent laryngeal nerves, outflow to 3 cervical symoatgetic ganglua
thoracic & right lymphatic duct

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20
Q

transesophageal echocardiography (TEE)

A

probe posterior to L atrium
help diagnose patent foramen ovale & septal defects, valve function
guides interventional procedures, evaluate prosthetic valves, detect intercardiac masses

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21
Q

pericardial effusion

A

too much fluid in sac
from infection, trauma, autoimmune
can cause cardiac tamponade

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22
Q

cardiac tamponade

A

excess compression on heart which results in inability to effectively pump blood
ventricles can not move blood & life threatening

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23
Q

pericardiocentesis

A

drainage of excess fluid from pericardial cavity
left angle
5th/6th intercostal space near sternum

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24
Q

Right ventricle in systole

A

contracts
force blood through the OPEN pulmonary valve
Tricupsid valve is CLOSED, preventing backflow into R atrium

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25
Q

R ventricle in diastole

A

relax
tricupsid valve OPEN blood fill R atrium
pulmonary valve CLOSED prevent backflow into pulmonary trunk

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26
Q

Papillary muscles & MI

A

MI can cause rupture of posteromedial papillary muscle
then cause mitral valve prolapse
occurs up to week after MI

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27
Q

tricupsid valve dysfunction

A

stenosis (narrow) restrict flow from R atrium to R ventricle
Regurgitation (not close well) backflow blood from R ventricle to R atrium

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28
Q

Mitral valve prolapse/regurgitation

A

valve no longer closes properly
backflow from L ventricle to L atrium
symptoms of fatigue, SOB, palpitations

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29
Q

semilunar valves diastole

A

Aortic & Pulmonary
CLOSED prevent backflow from aorta/pulmonary artery to ventricles

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30
Q

semilunar valves systole

A

aortic & pulmonary
OPEN bloood flow into aorta & pulmonary artery

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31
Q

semilunar valves sound

A

aortic & pulmonary valves
make second heart sound (S2)

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32
Q

location & sound of aortic valve

A

in second intercostal space, R of sternal border
LUB in systole

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33
Q

location & sound Pulmonic valve

A

in second intercostal space, L of sternal border
DUB in diastole

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34
Q

location & sound of tricupsid valve

A

fourth intercostal space, near L sternal border
hard to hear as lower intensity

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35
Q

location & sound of mitral valve

A

5th intercostal space, near L midclavicular line
Easiest to hear

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36
Q

Systolic murmur

A

turbulent blood flow through narrowed valve or improper closure of valve
when blood contract blood out of ventricles

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37
Q

diastolic murmur

A

turbulent blood flow through improperly closed valve
when heart fill from atria

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38
Q

sound of murmur from narrowing of valve

A

high-pitch, harsh sound
hear in diastole or systole

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39
Q

sound of murmur from valve incompetence

A

soft, blowing sound
hear in diastole or systole

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40
Q

Right Dominant Heart

A

70% of people
posterior interventricular artery is pranch of right coronary artery
need to know for bypass or grafting procedures

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41
Q

causes of coronary artery disease

A

collateral circulation
myocardial ischemia/infarction
artherosclerosis

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42
Q

artherosclerosis

A

build up of lipid in lining of coronary artery
restrict flow to myocardium

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43
Q

collateral circulation

A

when coronary arteries blocked, compensate by using collateral blood vessels
insufficient to meet heart demand in activity

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44
Q

myocardial ischemia

A

mismatch blood supply & myocardial oxygen demand

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45
Q

cardiac referred pain

A

perceive as arising somatic structures like chest wall & arm as visceral & somatic afferent fibers merge

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46
Q

visceral heart pain

A

by visceral afferent fibers (T1-4)
accompany by sympathetic efferent fibers
Refers to dermatomes T1-4

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47
Q

anginal heart pain

A

radiate from substernal & Left pec region to left shoulder & medial L arm
T1-4

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48
Q

Most common sites of coronary artery occlusion

A

Left anterior descending artery
Right coronary artery
left circumflex artery
obtuse marginal artery
diagonal artery
posterior descending artery

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49
Q

percutaneous transluminal cornary angioplasty

A

open blockage via iunflated balloon or thrombokinase enzyme
stent placed to prevent re-narrow
new blood clots can form

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50
Q

coronary bypass graft

A

saphenous vein, internal thoracic artery or radial artery grafts
connect one end to aorta & other to coronary artery that then bypass blocked area

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51
Q

Infective endocarditis

A

bacterial or fungal infections that affect mitral & aortic valves mostly
Microorganisms, white blood cells, platelets, and fibrin form vegetations. These enlarge/dislodged, causing
embolism to vital organs like the brain and coronary arteries
Valves can be impair by vegetation

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52
Q

pulmonary artery hypertenstion

A

persistent increase mean arterial presure above 25mmHGat rest
more work on R ventricle & causes hypertrophy which eventually R side heart failure
Can also cause dilation to coronary sinus which impacts blood supply not just flow

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53
Q

3 main layers of large/elastic arteries

A

tunica intima
tunica media
tunica adventitia
*Travel along surface

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54
Q

tunica intima (large/elastic arteries)

A

endothelial cells

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55
Q

tunica media (large/elastic arteries)

A

many layers smooth musc
lots elastic fibers

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56
Q

tunica adventitia (large/elastic arteries)

A

connective tissue, blood vessels, nerves, macrophages

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57
Q

main layers of medium/muscular arteries

A

tunica intima
tunica media (different contents)
tunica adventitia
*travel along surface

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58
Q

tunica media of medium/muscular arteries

A

litttle elastic fibers, prominent elastic membranes at boundaries

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59
Q

layers of arterioles

A

tunica intima
tunica media (differnt)
tunica adventitia (different)
*inside organs/tissues

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60
Q

tunica media in arterioles

A

few layers of smooth muscles, normally 2 layers max

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61
Q

what makes tunica adventitia differnt in arterioles

A

connective tissue aspect is continuous with connective tissye of surrounding system

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62
Q

Passive & active regulatioijn of arteries/arterioles

A

stretch/recoil due to hemodynamic forces
contract/relax via humoral factors, biochem influences, autonomic innervation

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63
Q

autonomic innervation receptors for arteries/arterioles

A

coronary arteries only one by both sympathetic & parasympathetic
alpha 1 (symp) cause contraction - vasoconstriction
beta (symp) cause realxation - vasodfilation
alpha 2 (symp) are pre-synaptic auto-receptors
Adrenal NE/E similar as direct sympathetic

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64
Q

cardiac conducting cells

A

have processes of bundles & Purkinje fibers that from nodes to cardiac tissue
use mostly fatty acids

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65
Q

modification of spontaneous rhythm contraction

A

neuronal input by ANS
sympathetic increase rhythm/force of contract
parasympathetic decrease rhythm/force

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66
Q

Detection of MI

A

increased troponin levels
tissue damage where loss cardiac m,uscle replace by connective tissue

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67
Q

True aneurysm

A

Weakening of Tunica MEDIA
form @ branching points of arteries
when can’t hold shape, especially recoil
Saccular (one side of artery wall stretch)
fusiform (both side artery wall stretch)

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68
Q

Hematoma (fake aneurysm)

A

rupture of artery wall, but bleeding self-contained
false aneurysm - form visible hemotoma between artery wall & extravasc connective tissue
Dissection - tear in intima & blood pools there

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69
Q

Sequelae of aneurysm

A

potential for rupture/bleed
remain intact but compress neighbor area of artery, decrease blood flow

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70
Q

arteriovenous malformations

A

failure form capillary bed
artery/ateriole entagle with vein
no blood-brain exchange
can rupture & bleed
form gradual = other vessels supply capillaries
form fast = no compensation = ischemia

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71
Q

artery disease (artherosclerosis & plaques)

A

breach in endothelium
WBC cross over to respond to chage
microphages bloat (foam cell)
smooth muscle cells proliferate to surround & reduce chance of rupture
narrow diameter
plaque activate clot cascade
cclot can rupture & cause embolism

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72
Q

Cardiac muscle action potential

A

Ventricular action potential
Phase 0 - rapid depolarization (Na influx)
Phase 1 - early depolarization ( Na gate close, K start reflux)
Phase 2 - Plateau (Ca leak in, k eflux continue but now balanced)
Phase 3 - late repolarization (ccs closes, K continue effluent)
Phase 4 - Rest membrane potential - Na/K pump

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73
Q

What calcium receptor/channel are opened during phase 2 of Cardiac AP?

A

DHPR

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74
Q

What are some DHPR blocking drugs?

A

Nitrendipine, nimodipine, nifedipine
Stop muscle contraction completely as no calcium release

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75
Q

What is unique about calcium sources in cardiac ventricle AP

A

Initial calcium from extracellular solution increases calcium content by DHPR
this influx triggers more calcium to release from sarcoplasmic reticulum

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76
Q

What happens to ventricle during phase 2?

A

Ventricle fills with blood so ready to eject when has energy to

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77
Q

Role of t tubule in cardiac muscle contraction large

A

Calcium stores in cardiac muscle contraction large t tubule diameter
Mucopolysaccharode bind to store calcium ions
The more calcium the stronger muscle contraction

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78
Q

What happens to impulse as increase dose of calcium channel blockers

A

Bigger the dose, smaller impulse effect becomes
Creates a sever decease in contraction

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79
Q

Main receptor for increasing HR/force contraction &mechanism

A

B1 (sympathetic)
Stimulatory, activates adenylate cyclase
Causes increase cAMP from ATP
This activates PKA and in turn increases calcium concentration

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80
Q

Main receptor for increasing HR/force contraction &mechanism

A

B1 (sympathetic)
Stimulatory, activates adenylate cyclase
Causes increase cAMP from ATP
This activates PKA and in turn increases calcium concentration

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81
Q

Main receptor decreasing HR & mechanism

A

M2, parasympathetic
Inhibits adenylate cyclase, cause decrease cAMP
In turn no PKA activation, inhibit myosin light chain kinase
No work on smooth muscle

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82
Q

Hyperkalemia phase 3

A

Raise resting potential
Keep potassium in extra cellular , makes it faster to get back to resting
Shorten phases 2 & 3 to promote efflux
Reduces conduction velocity

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83
Q

Hypokalemia

A

Lowers resting potential
Lengthen phases 2 & 3
Reduces potassium efflux
Take longer get back to resting state

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84
Q

Effective refractory period

A

Can make AP but will not conduct
Includes absolute refractory & is longer than
Na channel begins to recover

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85
Q

Relative refractory period

A

Can’t generate 2 AP
Need greater than normal stimulus

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86
Q

Supranormal period

A

Na channels are recovered, can fire
Increased excitability as closer to threshold
Less na needed

87
Q

SA node rate

A

60-100 bpm

88
Q

AV node rate

A

40-60 bpm
Impulse delayed

89
Q

Bundle of His rate

A

20-40 bpm
Right & left bundle branches

90
Q

Purkinje fibers rate

A

<20 bpm
Impulse all ventricles

91
Q

Sinus node & AV node phases

A

4, 0, 3
Phase 0 - upstroke that open ca
Phase 3 - repolarization inactivate Ca channel, increase a activation K to efflux
Phase 4 - funny current mixes Na/K inward current

92
Q

Sympathetic impact SA/AV nodes

A

B1 receptors
Increase chance they are open
Increase HR

93
Q

Sympathetic impact SA/AV nodes

A

B1 receptors
Increase chance they are open
Increase HR

94
Q

Parasympathetic I,pact SA/AV node

A

M2 receptor
Decrease diastolic depolarization
Increase HR

95
Q

Parasympathetic I,pact SA/AV node

A

M2 receptor
Decrease diastolic depolarization
Increase HR

96
Q

What determine arrhythmia susceptibility

A

Refractory news
Shorter refractory facilitate response heart
If not enough relax time then mnnp blood pushing out to tissues

97
Q

AV node delay

A

Delay cardiac impulse
Most delay in AV node (0..09)
AV bundle (0.04)

98
Q

AV bundles

A

One way conduction
Only one between atria & ventricles
Transmit time is 0.p6 seconds
QRS

99
Q

Purkinje system

A

fastest conduction
fibers from AV node through AV bundle into ventricles
many gap junctions @ intercalated disks

100
Q

what happen as cycle length diminoishes?

A

duration of AP decreases
greater the outward K current becomes

101
Q

What do positive dromotropic effects do?

A

increase conduction velocity (AV node)
sympathetic system increasing calciumw

102
Q

what do negative dromotropic effects do?

A

decrease conduction velocity (AV node)
parasympathetic system decreasing callcium, increasing K out
Causes more negative inward flow

103
Q

Heart block

A

conduction velocity slowed through AV node so no AP
mild: AP from atria to ventricles just slowed
sever: AP from atria to ventricles not conducted atall

104
Q

Ectopic Pacemaker

A

surpass SA node as other part more rapid discharge
sA node block then switch next fasatest
delay in heartbeat creates lack of blood to brain - syncope

105
Q

increase blood volume one area corresponds to

A

decrease blood somewhere else

106
Q

what is MAP

A

mean arterial pressure
state of resistance vessels (arterioles)
increases cause increase blood flow ijn forwards direction

107
Q

how is blood distribution determined

A

output L ventricle (cardaic output)
contractile state of resistance vessels (MAP)

108
Q

what are the main resistance vessels?

A

Arterioles
resistance reaches maximum level

109
Q

where is pressure drop greatest

A

terminal segment of small arteries/arterioles

110
Q

arterioles receptors

A

alpha 1 adrenergic receptors cause contraction (constrict) blood vessels of heart
beta 2 adrenergic receptors dilate (relax) blood vessels

111
Q

venules/veins receptors

A

large capitance alpha 1 receptors

112
Q

Norepinephrine receptors

A

alpha 1, alpha 2, beta 1

113
Q

epinephrine receptors

A

alpha 1, alpha 2, beta 1, beta 2

114
Q

Cardiac output

A

rate at which blood pumped out
resistance parallels add inverse together
resistance series add together
L side equals R side

115
Q

factors determine cardiac output

A

heart rate & myocardial contractility (cardiac factors)
preload & afterload (coupling factors)
Preload - volume at start before contraction
afterload - volume at end after contraction

116
Q

Major determinents of blood flow

A

pressure difference between 2 ends of vessel
resistance of vessel

117
Q

turbulent blood flow causes

A

high velocities
sharp turns
rough surfaces
rapid narrow vessls

118
Q

turbulent flow produces

A

murmur/bruit

119
Q

palpable murmus

A

thrill

120
Q

What are normal vs abnormal heart sounds

A

Normal S1 & S2
S1 - closure of mitral & tricupsid valves
S2 - closure of Aortic & pulmonary valves

Abnormal S3 & S4
S3 - Rapid ventricular filling
S4 - tubulent flow from stiff left ventricle

121
Q

types of systolic murmurs

A

Aortic stenosis
Mitral/tricupsid regurgitation
mitral valve prolapse
ventricular septal defect

122
Q

aortic stenosis

A

left ventricle has greater pressure than aorta
crescedo-decresendo ejection murmure
Syncope, Angia, Dyspnea (SAD)

123
Q

mitral/tricupsid regurgitation

A

high pitch, blowing mumur
mitral radiate toward axilla (ischemic disease, mitral prolapse, left ventricle dilation)
Tricupsid from rigth ventricle dilation

124
Q

mitral valve prolapse

A

late systolic crescendo murmur with click
sudden tensing chordae tendinae
prolapse into left atrium
can predispose to infective endocarditis but otherwise benign

125
Q

ventricular septal defect

A

harsh sounding
loudest @ tricupsid area

126
Q

Diastolic murmurs

A

aortic regurgitation
mitral stenosis

127
Q

continuous murmur

A

patent duct arteriosus

128
Q

aortic regurgitation

A

high pitch, blowing early descendo
due to Bicuspid aortic valve, Endocarditis, Aortic root dilation, Rheumatic fever (BEAR)
often progress to L heart fail

129
Q

mitral stenosis

A

opening snap, delayed rumble
late sympmtom of rheumatic fever, pulmonary congestion/hypertension, left aorta dilation, a-fib

130
Q

patent duct arteriosus

A

machine like murmur (continuous)
from congenital rubella/prematurity

131
Q

factors that influence resistance of blood vessels

A

blood viscosity (direct proportional)
length (direct proportional)
fourth power of radius (inversely proportional)

132
Q

hematocrit change affect blood flow

A

increase hematocrit causes increase viscosity, causes increase in vascular resistance (Polycythemia)

decrease in hematocrit causes decrease in viscosity, causes decrease in vascular resistance (anemia)

133
Q

vascular conductance & affect on blood flow

A

measure of blood flow through vessel
conductance increases are due to increase of diameter

134
Q

blood pressure & pulse pressure

A

BP - force exert by blood against any unit area of vessel wall
PP - difference between systolic/diastolic (want about 40)

135
Q

Pressure of R atrium

A

less than 5
makes blood easy to return to heart from veins

136
Q

Pressure of R ventricle

A

25/5

137
Q

Pressure of pulmonary trunk/branches

A

25/10

138
Q

Pressure of L atrium

A

<12

139
Q

Pressure of L ventricle

A

130/10

140
Q

Pressure of aorta

A

130/90

141
Q

vascular distensibility

A

increase in volume for each decrease in mmHG
veins are 8x more distensible than arteries

142
Q

vascular compliance/capitance

A

how much blbood can be stored in given part of circulation for each mmHg, relate to distensibility
Veins have higher capitantce/compliance than arteries
aged arteries have lowest compliance/capitance

143
Q

how does age influence blood vessel compliance

A

Become less compliant
walls become stiffer, less distensible, less compliant
decrease arterial compliance increases arterial pressures

144
Q

compliance vs elastance

A

compliance is stretchiness of vaculature
elastance is pressure change from volume change

145
Q

factores affect pulse pressure

A

stroke volume (larger stroke volume, makes larger difference pulse pressure)
arterial compiance (less compliant means greater pulse pressure diference)

146
Q

arteriosclerosis

A

make walls of arteries stiffer/less compliant, stroke volume make greater change in arterial pressure than nomral arteries

increases pulse pressure

147
Q

aortic stenosis

A

aortic lumen reduced, decreasing stoke volume, systolic pressure and pulse pressure, low flow thriough aortic valve

low pulse pressure

148
Q

pulse pressure in patent ductus arteriosus

A

low diastolic pressure, high systolic pressyre
high pulse pressure
no closure between pulmonary artery and aortic output

149
Q

aortic regurgitation pulse pressure

A

back flow through aortic valve
low diastolic, high systilic, high pulse pressure

150
Q

factors affect central venous pressure

A

R atrial pressure

increased blood volume
increased venous tone
arteriole dilation
decreased cardiac function

151
Q

increase venous pressures

A

compressional factors, cause resistance in large peripheral veins
increase R atrial pressure cause blood back up into venous system
abdominal pressures increase venous pressure uin legs

152
Q

gravitational pressure on venous pressure

A

weight blood in vessels cause 90mmHg of venous pressyure

have muscle pumpos that maintain low venous pressure when moving/using muscles
creates low pressure ofn <20mmHg
as soon as stop using muscles for extended period, no pump and so noi venous return - high venous pressure

153
Q

What germ layer become primordial heart

A

sphlanic mesoderm

154
Q

5 tube dilations

A

sinus venous
primitive atrium
primitive ventricle
bulbus cordis
truncus arteriosus

155
Q

What does coronary sinus develop from?

A

Sinus Venosus

156
Q

incomplete adhesion between septum primum & septum secundum after birth

A

atrial septal defect

157
Q

what pharyngeal arch artery changes course of recurrent laryngeal nerves differ R and L

A

sixth arch

158
Q

ductus arteriosus

A

fetal vascular that shunt blood from R ventricle to L aorta
connect pulmonary artery to aorta
Bypasses the lungs
all oxygen comes from the mom

159
Q

ligamentum teres hepatis

A

from the umbilical vein after birth
takes a couple of moths to develop anatomically

160
Q

congenital heart disease @18-22 weeks

A

range of birth defects
ventral septal defects most common

Normal:
heart is 1/3 chest
R/L side structures equal
patent foramen ovale
intact cardiac crux (septum, AV valves)
Right ventricle w moderator band

161
Q

Dextrocardia with situs inversus

A

heart point down to R side chest
all other organs mirror normal
more common, lowers incidence of accompanied cardiac defects

162
Q

Isolated dextrocardia with situs solitus

A

heart point to R side chest & only heart
complication with severe cardiac anomalies

163
Q

atrial septal defect

A

10-15% congenital heart disease
probe patent oval foramen from incomplete adhesion sseptum primum & septume secundum after birth

164
Q

membranous ventricular septal defect

A

most common
fail membranous part of IV septum to develop

165
Q

muscular ventriucular septal defect

A

less common
anywhere of muscular IV septum
excess cavitation of myocardial tissue

166
Q

transposition of great arteries

A

common cause cyanotic heart disease
often assoc with other cardiac defects
causes anterior aorta from R ventricle & pulmonary trunk arise from L ventricle
other defect permit interchange of pulmonary/systemic that lower blood oxygen level

likely the AP septum fail pursue spiral as bulbous cordis don’t incorporate correctly
Defect migration of neural crest

167
Q

Tetralogy of Fallot (PROV)

A

Classic group of 4 cardiac defects
Pulmonary stenosis
R ventricular hypertrophy
Overriding Aorta
Ventricular septal defect

168
Q

Pharyngeal arch arterial anomalies

A

mostly from persistence of parts that should disappear
disappear of parts that should persist

169
Q

Coarctation of Aorta

A

postductal allow develop of collateral circulation in fetal to allow blod iunferior body
often see differential BP

170
Q

ductus venosus

A

becomes the L umbilical vein
bypass lliver and lungs

171
Q

foramen ovale

A

take blood R to L aatrium
bypass liver & lungs

172
Q

what do septum primum & secundum form?

A

Primum form oval fossa floor
Secundum form border of oval fossa

173
Q

what does umbilical vein become

A

ligamentum teres hepatis
Round ligament of liver
brought oxygenated blood to fetus

174
Q

what does ductus venosus become

A

legamentum venosum
thgrough liveer from left branch of portal vein to inferior vena cavae

175
Q

what do distal umbilical arteries become

A

medial umbilical ligaments
proximal continue post-birth help with bladder

176
Q

what does ductus arteriosus become

A

ligamentum arteriosum
from L pulmonary artery to aortic arch

177
Q

patent ductus arteriosus

A

create shunt that make too much blood to lungs/heart

creates rise in partial pressure of oxygen (pulmonary hypertension)

decline in prostaglandin concentration (cardiac hypertrophy of L side/failure)

178
Q

truncus arteriosus becomes what

A

split into pulmonary artery & aorta

179
Q

bulbous cordis become what

A

Right ventricle
Conus cordis (ooutflow tract of ventricle)

180
Q

primitive ventricle become what

A

Left ventricle
has trabeculated walls too

181
Q

primitive atrium become what

A

R & L auricles
anterior sides of R & L atriums

182
Q

path of impulse from cardiac pacemaker through heart

A

originate in SA node spread through internodal pathways, cause atria contract, to the AV node which has delay as the atria need finish contract before ventricle fill, then bundle of His which travels to Purkinje fibers, this allow impulse to to spread rapidly through ventricular contraction

183
Q

what happens in each EKG waveform

A

P Wave: atrial depolarization
QRS Complex: ventricular depolarization
T wave: Ventricular repolarization
U Wave: Purkinje repolarizes
ST segment: isoelectric, both ventricles completely depolarized

184
Q

PR interval

A

initial depolarization of atria to initial depolarization of ventricles

Increase conduction velocity decreases PR interval

185
Q

QT interval

A

first to last ventricular depolarization

186
Q

PR interval length

A

0.12-0.20 s

187
Q

QRS interval length

A

0.06-0.11s

188
Q

QT interval length

A

0.36-0.44s
elongation of this predisposes person to arrythmia

189
Q

what must be there for normal sinus rhythm

A

1- Pwave, P precede QRS, Twave
2 - R-R interval always regular
3 - Normal HR of 60-100bpm

190
Q

Up/down deflection

A

upward always positive
downward always negative

191
Q

when is vector largest

A

if half of ventricle is depolarized
Normal average QRS vector is 60 degrees

192
Q

Inferior leads & what measure

A

II, III, aVF
vectors to/from apex

193
Q

lateral leads & what measure

A

I, aVL, V5, V6
vectors to/from left ventricular free wall

194
Q

Right sided lead & what measure

A

aVR, V1
vectors to/from right side

195
Q

anterior lead & what measure

A

V2, V3, V4
vectors to/from anterior & posterior heart

196
Q

precordial leads give what view

A

horizontal plane through heart

197
Q

P wave in leads

A

R atrium depolarize first
lead I positive wave, aVR negative wave, lead II biphasic wave, V1 biphasic wave, V6 positive wave

198
Q

Q wave in leads

A

small Q waves normal
deeper Q waves leads III & aVR
not normally see in V1-3

199
Q

what leads see ventricular depolarization

A

I, II, aVR

200
Q

EKG hyperkalemia

A

peak T wave, wide PR interval, flat/absence P wave, widen QRS complex

201
Q

EKG hypokalemia

A

QT prolongation, T wave flatten

202
Q

Wolff Parkinson White syndrome

A

ventricular pre-excitation
abnormal fast atria-ventricle bypass delay AV node
partial depolarization of ventricles earlier
delta wave between P & wide QRS
supraventricular tachycardia

203
Q

atrial fibrillation ekg

A

no P wave
abnormal R-R

204
Q

atrial flutter ekg

A

flutter P waves
skips beats

205
Q

ventricular fibrillation ekg

A

no identifiable waves

206
Q

first degree AV block

A

long PR
over 0.2s of QRS complex

207
Q

second degree AV block TI

A

Wenckebach
elongation of P wave
drop beat
vary RR

208
Q

second degree AV block TII

A

Mobitz 11
interval of P-R same
drop beat

209
Q

third degree AV block/complete heart block

A

AV dissociation
HR <30 bpm

210
Q

Torsade de pointes ekg

A

wave flip from positive deflection to negative deflection

211
Q

ECG paper horizontal box

A

small box - 0.04s
large box 0.20s

212
Q

ECG paper vertical box

A

large box 0.5mV

213
Q

estimate heart rate from EKG paper

A

count QRS in 6 second strip x 10

B3 Clinical Application (5 decks)

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