B3 CPR Flashcards
1
Q
2 movements of thoracic wall in breathing
A
pump handle (AP dimension increase)
bucket handle (transverse dimension increase)
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
3
Q
Chest tube/thoracostomy tube
A
insert into pleural space for inflation of collapsed lung, draining fluid, deliver meds
create negative pressure
4
Q
pneumothorax
A
excess air in pleural cavity
5
Q
hemothorax
A
excess blood in pleural cavity
6
Q
pleural effusion/hydrothorax
A
excess fluid in pleural cavity
7
Q
chylothorax
A
excess chyle in pleural cavity
8
Q
empyema
A
excess pus in pleural cavity
9
Q
Intercostal nerve block
A
anesthesthetic around intercostal nerves
superior rib first
inferior rib second
will do in times of chest tube insertion
10
Q
intercostal neurovascular bundle
A
between internal & innermost intercostal muscle in costal groove
Superior to inferior: Vein, Artery, Nerve
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
12
Q
Inferior Thoracic Aperture
A
separate thorax from abdomen
wider transverse & oblique slopes down/back
completely closed by diaphragm
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)
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)
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
16
Q
axillary inlet
A
thoracic inlet
neurovasc bundle between clavicle & first rib, exit between scalenes
Clavicle, scapula, first rib form borders
17
Q
thoracic outlet
A
area above clavicles, between sternum, & T1 & 1st rib
T1, First rib, manubrium form borders
18
Q
Superior thoracic aperture
A
anterior boundary: posterior border of manubrium
lateral boundary: 1st ribs & costal cartilages
Posterior boundary: T1
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
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
21
Q
pericardial effusion
A
too much fluid in sac
from infection, trauma, autoimmune
can cause cardiac tamponade
22
Q
cardiac tamponade
A
excess compression on heart which results in inability to effectively pump blood
ventricles can not move blood & life threatening
23
Q
pericardiocentesis
A
drainage of excess fluid from pericardial cavity
left angle
5th/6th intercostal space near sternum
24
Q
Right ventricle in systole
A
contracts
force blood through the OPEN pulmonary valve
Tricupsid valve is CLOSED, preventing backflow into R atrium
25
R ventricle in diastole
relax
tricupsid valve OPEN blood fill R atrium
pulmonary valve CLOSED prevent backflow into pulmonary trunk
26
Papillary muscles & MI
MI can cause rupture of posteromedial papillary muscle
then cause mitral valve prolapse
occurs up to week after MI
27
tricupsid valve dysfunction
stenosis (narrow) restrict flow from R atrium to R ventricle
Regurgitation (not close well) backflow blood from R ventricle to R atrium
28
Mitral valve prolapse/regurgitation
valve no longer closes properly
backflow from L ventricle to L atrium
symptoms of fatigue, SOB, palpitations
29
semilunar valves diastole
Aortic & Pulmonary
CLOSED prevent backflow from aorta/pulmonary artery to ventricles
30
semilunar valves systole
aortic & pulmonary
OPEN bloood flow into aorta & pulmonary artery
31
semilunar valves sound
aortic & pulmonary valves
make second heart sound (S2)
32
location & sound of aortic valve
in second intercostal space, R of sternal border
LUB in systole
33
location & sound Pulmonic valve
in second intercostal space, L of sternal border
DUB in diastole
34
location & sound of tricupsid valve
fourth intercostal space, near L sternal border
hard to hear as lower intensity
35
location & sound of mitral valve
5th intercostal space, near L midclavicular line
Easiest to hear
36
Systolic murmur
turbulent blood flow through narrowed valve or improper closure of valve
when blood contract blood out of ventricles
37
diastolic murmur
turbulent blood flow through improperly closed valve
when heart fill from atria
38
sound of murmur from narrowing of valve
high-pitch, harsh sound
hear in diastole or systole
39
sound of murmur from valve incompetence
soft, blowing sound
hear in diastole or systole
40
Right Dominant Heart
70% of people
posterior interventricular artery is pranch of right coronary artery
need to know for bypass or grafting procedures
41
causes of coronary artery disease
collateral circulation
myocardial ischemia/infarction
artherosclerosis
42
artherosclerosis
build up of lipid in lining of coronary artery
restrict flow to myocardium
43
collateral circulation
when coronary arteries blocked, compensate by using collateral blood vessels
insufficient to meet heart demand in activity
44
myocardial ischemia
mismatch blood supply & myocardial oxygen demand
45
cardiac referred pain
perceive as arising somatic structures like chest wall & arm as visceral & somatic afferent fibers merge
46
visceral heart pain
by visceral afferent fibers (T1-4)
accompany by sympathetic efferent fibers
Refers to dermatomes T1-4
47
anginal heart pain
radiate from substernal & Left pec region to left shoulder & medial L arm
T1-4
48
Most common sites of coronary artery occlusion
Left anterior descending artery
Right coronary artery
left circumflex artery
obtuse marginal artery
diagonal artery
posterior descending artery
49
percutaneous transluminal cornary angioplasty
open blockage via iunflated balloon or thrombokinase enzyme
stent placed to prevent re-narrow
new blood clots can form
50
coronary bypass graft
saphenous vein, internal thoracic artery or radial artery grafts
connect one end to aorta & other to coronary artery that then bypass blocked area
51
Infective endocarditis
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
52
pulmonary artery hypertenstion
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
53
3 main layers of large/elastic arteries
tunica intima
tunica media
tunica adventitia
*Travel along surface
54
tunica intima (large/elastic arteries)
endothelial cells
55
tunica media (large/elastic arteries)
many layers smooth musc
lots elastic fibers
56
tunica adventitia (large/elastic arteries)
connective tissue, blood vessels, nerves, macrophages
57
main layers of medium/muscular arteries
tunica intima
tunica media (different contents)
tunica adventitia
*travel along surface
58
tunica media of medium/muscular arteries
litttle elastic fibers, prominent elastic membranes at boundaries
59
layers of arterioles
tunica intima
tunica media (differnt)
tunica adventitia (different)
*inside organs/tissues
60
tunica media in arterioles
few layers of smooth muscles, normally 2 layers max
61
what makes tunica adventitia differnt in arterioles
connective tissue aspect is continuous with connective tissye of surrounding system
62
Passive & active regulatioijn of arteries/arterioles
stretch/recoil due to hemodynamic forces
contract/relax via humoral factors, biochem influences, autonomic innervation
63
autonomic innervation receptors for arteries/arterioles
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
64
cardiac conducting cells
have processes of bundles & Purkinje fibers that from nodes to cardiac tissue
use mostly fatty acids
65
modification of spontaneous rhythm contraction
neuronal input by ANS
sympathetic increase rhythm/force of contract
parasympathetic decrease rhythm/force
66
Detection of MI
increased troponin levels
tissue damage where loss cardiac m,uscle replace by connective tissue
67
True aneurysm
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)
68
Hematoma (fake aneurysm)
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
69
Sequelae of aneurysm
potential for rupture/bleed
remain intact but compress neighbor area of artery, decrease blood flow
70
arteriovenous malformations
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
71
artery disease (artherosclerosis & plaques)
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
72
Cardiac muscle action potential
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
73
What calcium receptor/channel are opened during phase 2 of Cardiac AP?
DHPR
74
What are some DHPR blocking drugs?
Nitrendipine, nimodipine, nifedipine
Stop muscle contraction completely as no calcium release
75
What is unique about calcium sources in cardiac ventricle AP
Initial calcium from extracellular solution increases calcium content by DHPR
this influx triggers more calcium to release from sarcoplasmic reticulum
76
What happens to ventricle during phase 2?
Ventricle fills with blood so ready to eject when has energy to
77
Role of t tubule in cardiac muscle contraction large
Calcium stores in cardiac muscle contraction large t tubule diameter
Mucopolysaccharode bind to store calcium ions
The more calcium the stronger muscle contraction
78
What happens to impulse as increase dose of calcium channel blockers
Bigger the dose, smaller impulse effect becomes
Creates a sever decease in contraction
79
Main receptor for increasing HR/force contraction &mechanism
B1 (sympathetic)
Stimulatory, activates adenylate cyclase
Causes increase cAMP from ATP
This activates PKA and in turn increases calcium concentration
80
Main receptor for increasing HR/force contraction &mechanism
B1 (sympathetic)
Stimulatory, activates adenylate cyclase
Causes increase cAMP from ATP
This activates PKA and in turn increases calcium concentration
81
Main receptor decreasing HR & mechanism
M2, parasympathetic
Inhibits adenylate cyclase, cause decrease cAMP
In turn no PKA activation, inhibit myosin light chain kinase
No work on smooth muscle
82
Hyperkalemia phase 3
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
83
Hypokalemia
Lowers resting potential
Lengthen phases 2 & 3
Reduces potassium efflux
Take longer get back to resting state
84
Effective refractory period
Can make AP but will not conduct
Includes absolute refractory & is longer than
Na channel begins to recover
85
Relative refractory period
Can’t generate 2 AP
Need greater than normal stimulus
86
Supranormal period
Na channels are recovered, can fire
Increased excitability as closer to threshold
Less na needed
87
SA node rate
60-100 bpm
88
AV node rate
40-60 bpm
Impulse delayed
89
Bundle of His rate
20-40 bpm
Right & left bundle branches
90
Purkinje fibers rate
<20 bpm
Impulse all ventricles
91
Sinus node & AV node phases
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
Sympathetic impact SA/AV nodes
B1 receptors
Increase chance they are open
Increase HR
93
Sympathetic impact SA/AV nodes
B1 receptors
Increase chance they are open
Increase HR
94
Parasympathetic I,pact SA/AV node
M2 receptor
Decrease diastolic depolarization
Increase HR
95
Parasympathetic I,pact SA/AV node
M2 receptor
Decrease diastolic depolarization
Increase HR
96
What determine arrhythmia susceptibility
Refractory news
Shorter refractory facilitate response heart
If not enough relax time then mnnp blood pushing out to tissues
97
AV node delay
Delay cardiac impulse
Most delay in AV node (0..09)
AV bundle (0.04)
98
AV bundles
One way conduction
Only one between atria & ventricles
Transmit time is 0.p6 seconds
QRS
99
Purkinje system
fastest conduction
fibers from AV node through AV bundle into ventricles
many gap junctions @ intercalated disks
100
what happen as cycle length diminoishes?
duration of AP decreases
greater the outward K current becomes
101
What do positive dromotropic effects do?
increase conduction velocity (AV node)
sympathetic system increasing calciumw
102
what do negative dromotropic effects do?
decrease conduction velocity (AV node)
parasympathetic system decreasing callcium, increasing K out
Causes more negative inward flow
103
Heart block
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
Ectopic Pacemaker
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
increase blood volume one area corresponds to
decrease blood somewhere else
106
what is MAP
mean arterial pressure
state of resistance vessels (arterioles)
increases cause increase blood flow ijn forwards direction
107
how is blood distribution determined
output L ventricle (cardaic output)
contractile state of resistance vessels (MAP)
108
what are the main resistance vessels?
Arterioles
resistance reaches maximum level
109
where is pressure drop greatest
terminal segment of small arteries/arterioles
110
arterioles receptors
alpha 1 adrenergic receptors cause contraction (constrict) blood vessels of heart
beta 2 adrenergic receptors dilate (relax) blood vessels
111
venules/veins receptors
large capitance alpha 1 receptors
112
Norepinephrine receptors
alpha 1, alpha 2, beta 1
113
epinephrine receptors
alpha 1, alpha 2, beta 1, beta 2
114
Cardiac output
rate at which blood pumped out
resistance parallels add inverse together
resistance series add together
L side equals R side
115
factors determine cardiac output
heart rate & myocardial contractility (cardiac factors)
preload & afterload (coupling factors)
Preload - volume at start before contraction
afterload - volume at end after contraction
116
Major determinents of blood flow
pressure difference between 2 ends of vessel
resistance of vessel
117
turbulent blood flow causes
high velocities
sharp turns
rough surfaces
rapid narrow vessls
118
turbulent flow produces
murmur/bruit
119
palpable murmus
thrill
120
What are normal vs abnormal heart sounds
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
types of systolic murmurs
Aortic stenosis
Mitral/tricupsid regurgitation
mitral valve prolapse
ventricular septal defect
122
aortic stenosis
left ventricle has greater pressure than aorta
crescedo-decresendo ejection murmure
Syncope, Angia, Dyspnea (SAD)
123
mitral/tricupsid regurgitation
high pitch, blowing mumur
mitral radiate toward axilla (ischemic disease, mitral prolapse, left ventricle dilation)
Tricupsid from rigth ventricle dilation
124
mitral valve prolapse
late systolic crescendo murmur with click
sudden tensing chordae tendinae
prolapse into left atrium
can predispose to infective endocarditis but otherwise benign
125
ventricular septal defect
harsh sounding
loudest @ tricupsid area
126
Diastolic murmurs
aortic regurgitation
mitral stenosis
127
continuous murmur
patent duct arteriosus
128
aortic regurgitation
high pitch, blowing early descendo
due to Bicuspid aortic valve, Endocarditis, Aortic root dilation, Rheumatic fever (BEAR)
often progress to L heart fail
129
mitral stenosis
opening snap, delayed rumble
late sympmtom of rheumatic fever, pulmonary congestion/hypertension, left aorta dilation, a-fib
130
patent duct arteriosus
machine like murmur (continuous)
from congenital rubella/prematurity
131
factors that influence resistance of blood vessels
blood viscosity (direct proportional)
length (direct proportional)
fourth power of radius (inversely proportional)
132
hematocrit change affect blood flow
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
vascular conductance & affect on blood flow
measure of blood flow through vessel
conductance increases are due to increase of diameter
134
blood pressure & pulse pressure
BP - force exert by blood against any unit area of vessel wall
PP - difference between systolic/diastolic (want about 40)
135
Pressure of R atrium
less than 5
makes blood easy to return to heart from veins
136
Pressure of R ventricle
25/5
137
Pressure of pulmonary trunk/branches
25/10
138
Pressure of L atrium
<12
139
Pressure of L ventricle
130/10
140
Pressure of aorta
130/90
141
vascular distensibility
increase in volume for each decrease in mmHG
veins are 8x more distensible than arteries
142
vascular compliance/capitance
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
how does age influence blood vessel compliance
Become less compliant
walls become stiffer, less distensible, less compliant
decrease arterial compliance increases arterial pressures
144
compliance vs elastance
compliance is stretchiness of vaculature
elastance is pressure change from volume change
145
factores affect pulse pressure
stroke volume (larger stroke volume, makes larger difference pulse pressure)
arterial compiance (less compliant means greater pulse pressure diference)
146
arteriosclerosis
make walls of arteries stiffer/less compliant, stroke volume make greater change in arterial pressure than nomral arteries
increases pulse pressure
147
aortic stenosis
aortic lumen reduced, decreasing stoke volume, systolic pressure and pulse pressure, low flow thriough aortic valve
low pulse pressure
148
pulse pressure in patent ductus arteriosus
low diastolic pressure, high systolic pressyre
high pulse pressure
no closure between pulmonary artery and aortic output
149
aortic regurgitation pulse pressure
back flow through aortic valve
low diastolic, high systilic, high pulse pressure
150
factors affect central venous pressure
R atrial pressure
increased blood volume
increased venous tone
arteriole dilation
decreased cardiac function
151
increase venous pressures
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
gravitational pressure on venous pressure
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
What germ layer become primordial heart
sphlanic mesoderm
154
5 tube dilations
sinus venous
primitive atrium
primitive ventricle
bulbus cordis
truncus arteriosus
155
What does coronary sinus develop from?
Sinus Venosus
156
incomplete adhesion between septum primum & septum secundum after birth
atrial septal defect
157
what pharyngeal arch artery changes course of recurrent laryngeal nerves differ R and L
sixth arch
158
ductus arteriosus
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
ligamentum teres hepatis
from the umbilical vein after birth
takes a couple of moths to develop anatomically
160
congenital heart disease @18-22 weeks
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
Dextrocardia with situs inversus
heart point down to R side chest
all other organs mirror normal
more common, lowers incidence of accompanied cardiac defects
162
Isolated dextrocardia with situs solitus
heart point to R side chest & only heart
complication with severe cardiac anomalies
163
atrial septal defect
10-15% congenital heart disease
probe patent oval foramen from incomplete adhesion sseptum primum & septume secundum after birth
164
membranous ventricular septal defect
most common
fail membranous part of IV septum to develop
165
muscular ventriucular septal defect
less common
anywhere of muscular IV septum
excess cavitation of myocardial tissue
166
transposition of great arteries
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
Tetralogy of Fallot (PROV)
Classic group of 4 cardiac defects
Pulmonary stenosis
R ventricular hypertrophy
Overriding Aorta
Ventricular septal defect
168
Pharyngeal arch arterial anomalies
mostly from persistence of parts that should disappear
disappear of parts that should persist
169
Coarctation of Aorta
postductal allow develop of collateral circulation in fetal to allow blod iunferior body
often see differential BP
170
ductus venosus
becomes the L umbilical vein
bypass lliver and lungs
171
foramen ovale
take blood R to L aatrium
bypass liver & lungs
172
what do septum primum & secundum form?
Primum form oval fossa floor
Secundum form border of oval fossa
173
what does umbilical vein become
ligamentum teres hepatis
Round ligament of liver
brought oxygenated blood to fetus
174
what does ductus venosus become
legamentum venosum
thgrough liveer from left branch of portal vein to inferior vena cavae
175
what do distal umbilical arteries become
medial umbilical ligaments
proximal continue post-birth help with bladder
176
what does ductus arteriosus become
ligamentum arteriosum
from L pulmonary artery to aortic arch
177
patent ductus arteriosus
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
truncus arteriosus becomes what
split into pulmonary artery & aorta
179
bulbous cordis become what
Right ventricle
Conus cordis (ooutflow tract of ventricle)
180
primitive ventricle become what
Left ventricle
has trabeculated walls too
181
primitive atrium become what
R & L auricles
anterior sides of R & L atriums
182
path of impulse from cardiac pacemaker through heart
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
what happens in each EKG waveform
P Wave: atrial depolarization
QRS Complex: ventricular depolarization
T wave: Ventricular repolarization
U Wave: Purkinje repolarizes
ST segment: isoelectric, both ventricles completely depolarized
184
PR interval
initial depolarization of atria to initial depolarization of ventricles
Increase conduction velocity decreases PR interval
185
QT interval
first to last ventricular depolarization
186
PR interval length
0.12-0.20 s
187
QRS interval length
0.06-0.11s
188
QT interval length
0.36-0.44s
elongation of this predisposes person to arrythmia
189
what must be there for normal sinus rhythm
1- Pwave, P precede QRS, Twave
2 - R-R interval always regular
3 - Normal HR of 60-100bpm
190
Up/down deflection
upward always positive
downward always negative
191
when is vector largest
if half of ventricle is depolarized
Normal average QRS vector is 60 degrees
192
Inferior leads & what measure
II, III, aVF
vectors to/from apex
193
lateral leads & what measure
I, aVL, V5, V6
vectors to/from left ventricular free wall
194
Right sided lead & what measure
aVR, V1
vectors to/from right side
195
anterior lead & what measure
V2, V3, V4
vectors to/from anterior & posterior heart
196
precordial leads give what view
horizontal plane through heart
197
P wave in leads
R atrium depolarize first
lead I positive wave, aVR negative wave, lead II biphasic wave, V1 biphasic wave, V6 positive wave
198
Q wave in leads
small Q waves normal
deeper Q waves leads III & aVR
not normally see in V1-3
199
what leads see ventricular depolarization
I, II, aVR
200
EKG hyperkalemia
peak T wave, wide PR interval, flat/absence P wave, widen QRS complex
201
EKG hypokalemia
QT prolongation, T wave flatten
202
Wolff Parkinson White syndrome
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
atrial fibrillation ekg
no P wave
abnormal R-R
204
atrial flutter ekg
flutter P waves
skips beats
205
ventricular fibrillation ekg
no identifiable waves
206
first degree AV block
long PR
over 0.2s of QRS complex
207
second degree AV block TI
Wenckebach
elongation of P wave
drop beat
vary RR
208
second degree AV block TII
Mobitz 11
interval of P-R same
drop beat
209
third degree AV block/complete heart block
AV dissociation
HR <30 bpm
210
Torsade de pointes ekg
wave flip from positive deflection to negative deflection
211
ECG paper horizontal box
small box - 0.04s
large box 0.20s
212
ECG paper vertical box
large box 0.5mV
213
estimate heart rate from EKG paper
count QRS in 6 second strip x 10
