EKG Exam Flashcards
(117 cards)
1
Q
A
- 2nd degree block: type 2
- some p waves conduct, some don’t
- rhythm regular if conduction ratio is constant; if variable, R-R interval will be irregular
- rate atrial normal; ventricular bradycardic at 1/2, 1/3, or 1/4 of atrial
- p wave upright, uniform, more of these than QRS complexes
- PR interval constant but longer than normal
- QRS normal, 0.12 sec or less
- QT usually normal, less than 1/2 preceding R-R
2
Q
medications for V.Tach
A
- amiodarone 150 mg IV over 10 min
- followed by continuous infusion
- if unstable - cardiovert
- torsades de pointes
- mag sulfate 1-2g IV over 5-60 min
3
Q
what is this rhythm?
A
asystole
4
Q
concerns and treatment with complete heart block
A
- concerns
- hemodynamic compromise
- CHB common PEA
- treatment
- transcutaneous pacing
- atropine - only acts on atria
- dopamine or epi drip - will impact both atria and ventricles
5
Q
clinical presentation of sinus tachycardia
A
- depends on underlying cause and individual’s ability to tolerate rapid HR
- may be symptomatic
- hypotension, chest pain, SOB
6
Q
symptoms of bradycardias
A
- hypotension
- poor peripheral vascular assessment
- change in mental status
- fatigue, lethargy, dizziness, near syncope
- chest pain
- SOB
7
Q
relative refractory period
A
- period of time following absolute refractory period
- heart can respond to strong stimulus, but response will be abnormal
- R on T phenomenon
8
Q
etiology of PVCs
A
- hypokalemia, hypomagnesemia
- hypoxia
- bradycardia
- caffeine, ETOH, tobacco
- MI
- dig toxicity
- exercise
9
Q
morphology of P wave and A:V ration in dysrrhythmia interpretation
A
- are all P waves the same?
- all coming from same source
- do some look different?
- dramatically different morphologies indicate taking different paths from atria to ventricles
- A:V ratio is 1:1?
- atrial activity = p wave
- ventricular activity = QRS complex
10
Q
A
- sinus tachyardia
- rhythm regular
- rate > 100 bpm
- P wave for every QRS; same size and shape
- PR interval normal, 0.10-0.20 sec
- QRS same size and shape; duration normal (0.04-0.12 sec
- QT interval normal (0.36-0.40 sec)
11
Q
causes of first degree heart block
A
- cardiomyopathy
- ischemia or injury to AV node
- valvular disorders, digitalis toxicity
- mechanical injury to AV node or junctional tissue
- common in beta blockers
- slows down AV node
12
Q
treatment for A.fib
A
- rate control: meds with negative chronotropic and/or negative dromotropic properties to slow conduction speed through AV node
- B-blockers, Ca channel blockers, amiodarone, digoxin
- anticoagulation to prevent clot becoming thrombus
- check with echo
- chronic anticoag therapy (coumadin, prodaxa, xarelto)
- cardioversion
- EP procedures to ablate pathologic tissue
- MAZE procedure to carve up atria to prevent abnormal foci from conducting
13
Q
PR Interval
A
- atrial to ventricular conduction time
- time for impulse to travel through atria, through AV node, down to ventricles
- most of delay is located in AV node
14
Q
etiologies of sinus tachycardia
A
- non-physiologic conditions
- exercise, caffeine, smoking, alcohol, emotions, pain, anxiety
- physiologic stressors
- hypovolemia, fever, anemia, early sepsis, hypermetabolic states, heart failure, allergic rxn
- medications
- atropine, epi, dopamine, norepi
15
Q
junctional rhythm overview
A
- rhythm from AV junction below AV node in bundel of His
- if conduction from SA node disrupted d/t SA or AV node damage, no impulses come down from atria in time
- cells in junctional tissue step in has backup pacemaker to preseve life (junctional “escape” rhythm)
- rate is less than that of SA node (40-60)
- impulse conducted down ventricle but up atria, so P wave is late and inverted - QRS is normal
- P waves can be before, during, or after QRS
- lose atrial kick
16
Q
parasympathetic stimulation
A
- occurs through control of vagus nerve
- vagal stimulation slows heart (valsalva maneuver)
- only affects atria (vagal nerve innervates)
- atropine will speed up heart via decreasing vagal suppression
- BUT with heart block, will not conduct down to improve ventricular rate
- atropine lifts vagal suppression and increases HR
17
Q
causes of second degree heart block: type 2
A
- worsening ischemia or injury to AV node or junctional tissue
- cardiomyopathy
- valve disease
- digialis toxicity
18
Q
refractory period
A
period of time after a cell has depolarized during which it cannot depolarize again
19
Q
treatment for asystole
A
- CPR, epi, correct underlying cause
- meds are not rhythm specific and do not improve survival to discharge
- check for DNR
20
Q
sympathetic stimulation
A
- catecholamines
- epi, norepi, dopamine
- affects the atria and ventricles
- can give endogenous substances via exogenous methods as code drugs (epi is #1)
- increases HR, conduction velocity, irritability
21
Q
anticipated interventions for SVT
A
- treat underlying cause
- valsalva maneuvers
- medications
- push adenosine as close to heart as possible and elevate that extremity - will cause chest pain and anxiety
- synchronized cardioversion if there is a pulse
- synced to R wave to avoid R on T
22
Q
etiologies of SVT
A
- stress
- metabolic dx
- medications
- cardiac dx
- anemia
- thyrotoxicosis
- hypoxia
- cardiomyopathy
23
Q
A
- superior level junctional rhythm
- upside down P waves before QRS
- PR interval shorter than normal
24
Q
P wave
A
atrial depolarization as impulse travels through atria
25
etiologies of sinus bradycardia
* normal in athletes
* sleep
* vagal stimulation
* increased parasympathetic tone d/t cerebral edema or subdural hematoma
* decreased sympathetic tone d/t SCI
* decreased metabolic rate d/t hypothyroidism or hypothermia
* inferior wall MI
* drugs such as beta blockers, calcium channel blockers, digoxin, antiarrhythmics
26
PR interval in dysrrhythmia interpretation
* usually between .12-.2 s (120-200 ms)
* how long is it taking impulse to travel from atria through AV node?
* how long is it delayed until getting to ventricle?
27
clinical presentation of normal sinus rhythm
usually does not cause hemodynamic instability
28
R on T phenomenon
* PVC falls on preceding initial down slop of T wave
* may cause deterioration into unstable rhythm
* Vf, VT, torsades de pointes
* due to new electrical stimulus during relative refractory period
29
repolarization
* return of cell's membrane to resting state
* positive and negative charges return to original positions
* cells must repolarize before depolarizing again
* sodium and calcium move out of cell, potassium back in
30
* junctional rhythm
* **rate** 40-60
* **rhythm** regular
* **P wave** inverted; immediately before/after QRS or hidden in QRS
* **PR interval** short - 0.10 sec or less
* **QRS** normal, 0.12 sec or less
* **QT** less than 1/2 preceding R-R
31
* third degree (complete) heart block
* **rhythm** atria regular; ventricle regular - different
* **rate** atrial rate normal; ventriclular rate slower...
* ...if junctional focus - 40-60
* ...if ventricular focus 20-40
* **p wave** upright, uniform, more of these than QRS complexes
* **PR interval** none, no relationship to QRS
* **QRS** = 0.12 sec if junctional focus; \>/= 0.12 if ventricular focus
32
Purkinje Fibers
* bundle branches terminate in this network branching of fibers
* conduction through Purkinje fibers is extremely rapid
* spreads throughout inner surface of both ventricles
* fibers contain pacemaker cells with inherent rate of 20-40 times/minute
33
anticipated interventions for normal sinus rhythm
no treatment is usually necessary
34
* electricity flows from upper right to lower left
* right arm negative; left leg positive
* as electricity flows through heard and down towards left leg
* towards positive lead
* positive ECG deflection
* flow towards negative lead = negative deflection
35
concerns with V.tach
* response varies
* asymptomatic --\> pulseless
* bad CO, bad pumping
* no diastolic filling
* no perfusion of heart b/c no diastole
* why rapid deterioration is imminent - V.fib
36
* accelerated junctional rhythm
* **rate** 60-100; \> 100 = tachycardia
* **P wave** same as junctional escape
* **PR interval** short, if measurable
37
atrioventricular node
* impulse passes from internodal tracts through AV node to reach ventricles
* located at top of interventricular septum in right atrium near coronary sinus
* **cardiac impulse is delayed here to allow for ventricular filling during atrial contraction (atrial kick is 25% of ventricular filling, occurring after diastolic filling)**
* acts as gatekeeper by controlling number of atrial impulses reaching ventricles
* normally no more than 180 impulses/minute
* **AV node does NOT possess pacemaker cells - surrounding junctional tissue does**
38
overview of supraventricular tachycardia
* fast rhythms originating above ventricles
* atria, junctional tissue, sometimes sinus node
* usually paroxysmal, but may sustain in some cases
* rhythms that cannot be identified as atrial tachycardia, junctional tachycardia, sinus tachycardia, or atrial flutter are all grouped into this classification
39
* sinus bradycardia
* **rhythm** regular
* **rate** \< 60 bpm
* **P wave** for every QRS; all same size and shape
* **PR interval** normal, 0.10-0.20 sec
* **QRS** all same size and shape; duration normal - 0.04-0.12 sec
* **QT** interval normal: 0.36-0.40 sec
40
causes of asystole
* untreated Vtach or Vfib
* electrocution
* profound electrolyte or acid-base imbalance
* MI
41
* asystole
* **rate** none
* **rhythm** none
* **p wave** none
* **PR interval** none
* **QRS** none
* **QT interval** none
42
internodal tracts & Bachman's bundle
* carry cardiac impulse from SA node
* 3 tracts
* anterior
* middle (Wenkebach)
* posterior (Thorel's)
* Bachman's bundle
* interatrial pathway facilitating transmission from the right to left atrium
43
* normal sinus rhythm originating from SA node
* **regular** atrial and ventricular rhythm
* **60-100** bpm
* **p wave** for every QRS; p waves same size and shape
* **PR interval** normal: 0.10-0.20 sec
* **QRS** waves same size and shape; duration normal - 0.04-0.12 sec
* **QT interval** normal: 0.36-0.40 sec
44
etiologies of atrial fibrillation
* hypoxia
* ischemia/infarction
* electrolyte disturbances
* cardiac surgery
* excessive adrenergic stimulation
* catecholamine surge from stress, surgery
* cardiomyopathy
* CHF
* pericarditis
* alcohol withdrawal
* hyperthyroidism
45
etiology, causes, and treatment of ventricular escape rhythm
* etiology: failure of SA and AV nodes to pacemake
* causes:
* ischemia, infarction
* severe acid-base disturbances
* cardiomyopathy
* dig toxicity
* treatment
* transcutaneous pacing
* dopamine or epi drip
* DO NOT SUPPRESS VENT ESCAPE RHYTHM
46
causes of third degree heart block
* untreated digitalis toxicity
* worsening ischemia/injury
* cardiomyopathy
* valvular disease
* mechanical trauma to AV node
47
QT interval
time from start of depolarization of the ventricles to end of the relative refractory period
beginning of QRS complex to end of T wave
48
sinoatrial node
* posterior wall of the right atrium
* "natural pacemaker" of the heart
* inrinsic rate of 60-100 times/minute
49
* mid-level junctional rhythm
* P waves during QRS - drowned out by much bigger QRS
50
what is pulseless electrical activity?
* any rhythm w/o pulse
* except asystole, VF, VT
* dissociation between the electrical and mechanical functions of heart
* always ask: is there a pulse?
* CPR if no pulse
* large bore IV access (better for circulation)
* epi 1mg IVP q3-5 min
51
what are PVCs?
* early beats from ventricle
* make ventricular rhythm irregular
* can be in individual complexes, pairs, triplets
* bigeminy, trigeminy, quadrageminy
* unifocal or multifocal
* conduction from cell to cell instead of rapidly across tissue
* precursors to V.tach and V.fib
52
treatment for VTach
* pulseless - defibrillate
* pulse with serious S/Sx - synchronized cardioversion
* pusle without serious S/Sx - medication trials
53
treatment of bradycardias
* treated only when symptomatic
* atropine 0.5 mg q3-5 min (total 0.03-0.04 mg/kg)
* transcutaneous pacing as bridge therapy
* dopamine infusion 2-10 ug/kg/min
* epi infusion 2-10 ug/min
* epi and dopamine have more general response if atropine not working
54
overview of ventricular escape rhythm
* potentially lethal - requires immediate assessment and appropriate intervention
* presentations very from asymptomatic to complete cardiac arrest
* likely to result in decreased CO, decreased perfusion
* discomfort, anxiety, fear
55
* low-level junctional rhythm
* upside down P waves after QRS
* sort of hidden in T wave
56
causes of V.fib
* untreated V.tach
* MI
* electrolyte imbalances
* acid-base disturbances
* hypoxia
* cardiac trauma
* electrical shock
57
* ventricular escape rhythm
* **rhythm** regular
* **rate** below 40 bpm
* **PR interval** immeasurable
* **QRS** greater than .12 sec, uniform morphology
* **QT interval** difficult to discern from T-wave - less than 1/2 R-R if measurable
58
anticipated interventions for sinus tachycardia
* beta-blockers, calcium channel blockers
* if HR exceeds 150bpm with serious S/Sx
* tachycardia should be cardioverted
* sinus tachycardia will not respond to cardioversion
* need to treat underlying problem
59
what type of PVC is this?
couplet - two PVCs in a row (uniform or multiform)
also known as "pair"
60
* atrial fibrillation
* **rhythm:** atrial - chaotic; ventricular - irregularly irregular
* **rate:** atrial 350-700 bpm; ventricular \> 100 bpm if uncontrolled; \< 100 bpm if controlled
* **P waves:** fibrillatory waves or "f" waves (coarse or fine)
* **PR interval:** unable to measure
* **QRS:** narrow, should be same: 0.04-0.12 sec
61
why is there a pause after a PAC?
compensatory pause - occurs b/c heart is expecting to go back to underlying rhythm
62
what is this rhythm?
V-fib
63
clinical presentation of SVT
* palpitations, angina
* dyspnea, anxiety
* not enough passive diastolic fill time of ventricles
64
concerns for second degree heart block: type 1
* hemodynamic implications based on HR
* individual symptoms vary
* watch for progression of block
65
treatments for accelerated junctional rhythms
* remove underlying cause
* control HR
* meds to limit automaticity of junction
* B blockers
* amiodarone
* Ca channel blockers
66
T wave
ventricular repolarization as ventricules return to resting electrical state
67
treatment for atrial flutter
* similar to A.fib
* rate control - med with negative chronotropic and/or negative dromotropic properties to slow conduction speed through A/V
* B-adrenergic blockers
* calcium channel blockers
* amiodarone
* digoxin
* anticoagulation - coumadin, prodaxa, xarelto
* often cardioversion
* EP procedures - tissue ablation
* MAZE - carve up atria to prevent abnormal conduction
68
concerns and treatments for 1st degree heart block
* concerns:
* nothing major
* hemodynamically stable if asymptomatic
* watch for progression to further block
* treatment
* not required
69
etiologies of junctional rhythms
* infarction, ischemia
* drug toxicity
* digoxin, digitalis, CA channel blockers, beta blockers
70
causes of 2nd degree heart block: Type 1
* inferior MI
* cardiomyopathies
* digitalis toxicity
* valvular disease
71
what type of PVC is this?
ventricular bigeminy - ever other beat is a PVC
72
* first-degree block
* conduction thru SA node delayed, lengthening PR interval
* **rhythm** regular
* **rate** underlying rhythm, atrial and ventricular usually same
* **P wave** sinus, normal, upright
* **P interval** prolonged, greater than 0.20 sec and constant
* **QRS** normal, 0.12 sec or less
* **QT interval** usually normal
73
treatment for V.fib
* CPR when pulselessness is established
* defibrillate ASAP
* first meds:
* epi 1mg IVP q3-5 min
* antiarrhythmic med - amiodarone
74
treatment of PVCs
* treat underlying cause
* limited to those with severe Sx
* meds to suppress ventricular ectopy suppress protective vent escape rhythms
* pro-arrhythmic properties
* treatment is cost-benefit anaysis
75
* PVCs
* **rhythm** may interrupt underlying rhythm
* **rate** at any HR and with any underlying rhythm
* **P wave** may not be present or immediately after; unrelated to PVCs
* **PR interval** immeasurable
* **QRS** wide, bizarre, 0.12 sec or longer
* **T wave** frequently extends in opposite direction of QRS
76
absolute refractory period
immediately following depolarization - heart cannot respond to another stimulus regardless of stimulus strength
77
etiologies of PAC's
* stress, fatigue
* caffeine, alcohol, tobacco
* may be associated with:
* MI, CHF
* infection
* hypoxia
* hypokalemia, hypomagnesemia
* may precede deterioration into A-f or AFc
78
clinical presentation of complete heart block
* serious and life-threatening
* not tolerated d/t low heart rate (decreased CO)
* hemodyanmic instability
* dyspnea, HF, hypotension, syncope, chest pain
* can progress to ventricular standstill with little/no warning
79
P wave/QRS complex in dysrrhythmia interpretation
* P wave in front of every QRS complex?
* every QRS complex with a preceding P wave?
* if YES - electrical activity coming from atria
* but NOT necessarily the SA node
* if NO - QRS complex w/o preceding P wave
* electrical activity originated in ventricle
80
* wandering atrial pacer
* **rate** usually 60-100, if over 100 - multiple atrial tachycardia
* **rhythm** regular or irregular
* **P wave** 3+ morphologies, A:V ratio 1:1
* **PR interval** varies on location of ecotpic atrial sites (some may be less than .12sec)
* **QRS** less than 0.12 sec
* **QT interval** less than 1/2 preceding R-R interval
81
regular or irregular HR in dysrrhythmia interpretation
* regular, regularly irregular, or irregularly irregular?
* ex: a.fib is irregularly irregular
* does the abnormality appear on a regular basis or irregular basis?
* pattern in the abnormality or abnormalities?
82
what type of PVC is this?
ventricular trigeminy - every third beat is a PVC
83
* ventricular fibrillation
* **rate** immeasurable
* **rhythm** chaotic
* **p wave** chaotic, no AV ratio
* **PR interval** immeasurable
* **QRS** absent
* **QT interval** absent
* will NEVER be a perfusing rhythm
84
atrial fibrillation overview
* chaotic electrical activity originating from irritable atrial tissue
* cause atrial muscle to quiver ineffectively, losing atrial kick
* only some of atrial impulse conduct thru AV junctional tissue thru ventricular conduction system
* CO can be compromised by 5-30%
* gatekeeping fxn of AV node important
* only lets the strongest of the 300+ atrial impulses thru/minute
85
etiology of normal sinus rhythm
normal pacemaker rate
86
* 2nd degree heart block: type 1 (Wenckebach)
* **rhythm** irregular
* **rate** atrial normal; ventricular slower b/c not all beats conduct
* **P wave** upright, uniform, some now followed by QRS
* **PR interval** progressively longer until no conduction
* **QRS** normal, 0.12 sec or less
* **QT** usually normal, less than 1/2 preceeding R-R
87
causes of PEA
88
depolarization
* electrical excitation across the myocardial cell membrane
* spreads from cell to cell through conduction system and muscle cells
* sodium and calcium move into cell, potasssium out
* provides stimulus for ocntraction
89
* sinus arrhythmia - from SA node irregularly in relation to respiration
* variations in breathing d/t fluctuations in parasympathetic vagal tone
* **rhythm** irregular
* **rate** speeds up during inspiration, slows during expiration
* **P wave** for every QRS, same size and shape
* **PR interval** normal, 0.10-0.20 sec
* **QRS** same size and shape; normal duration (0.04-0.12 sec)
90
what is this rhythm?
V-tach
91
* supraventricular tachycardia (SVT)
* **rhythm** may be regular
* **rate** 150-250 bpm
* **p wave** usually hidden in preceding T wave
* **PR interval** immeasurable d/t hidden P waves
* **QRS** narrow, less than 0.12, all the same
92
overview of atrioventricular conductiondisorders (aka blocks)
* delay through bundle of His = PR interval
* time to allow atria to complete contract and impart "kick" in pressurizing ventricles to prepare (stretch) them for power of stroke contraction (Starling's Law)
* problems arise when conduction through AV node is slowed (1st), delayed to prevention (2nd T1), intermittent (2nd T2), completely blocked (3rd)
* reaches a point where more passive filling of RA won't impact CO (too much delay)
* dysfxn, fewer ventricular complexes, fewer ventricular contractions, negative impact on CO
93
conduction system of the heart
94
QRS interval in dysrrhythmia interpretation
* less than .12 s (120 ms)
* QT normally less than 1/2 of proceeding R-R interval
95
concerns and treatments with 2nd degree heart block: type 2
* concerns
* bradycardia common
* often progresses to complete heart block
* treatment
* transcutaneous pacing
96
QRS wave
* ventricular depolarization as impulse travels through both ventricles
* width of QRS wave indicates intraventricular conduction time
97
etiologies of atrial flutter
* after open heart surgery
* MI
* mitral or tricuspid valvular disease
* PE
* chronic atrial flutter d/t organic heart dx
* ischemia
98
EKG
graphic recording of the electrical current produced by depolarization and repolarization of the heart
99
overview of third degree (complete) heart block
* total block at AV node, so no conduction of SA node impulses through AV node
* atria and ventricles dissociated from each other
* funtion independently, using intrinsic mechanisms to pace themselves
100
causes of ventricular tachycardia
* MI, CHF, cardiomyopathy
* electrolyte disturbances
* acid-base disturbances
* R on T
* direct stimulation of myocardium
* profound hypokalemia
101
isoelectric line
* EKG machine's stylus producing a straight line on the paper when unconnected from the patient's electrodes
* all electrical forces are equal
* also asystole - no electrical activity
* flow towards positive electrode = upright waveform
* flow towards negative electrode = downward waveform
102
HR in dysrrhythmia interpretation
* normal = 60-100
* origin likely from SA node
* dramatic changes in HR without changes in SV will change CO
103
* ventricular tachycardia
* **rate** 140-250 bpm
* **rhythm** regular
* **p wave** no discernable p waves
* **QRS** \>0.12 sec, morphology can be identical or vary
* **QT interval** usually immeasurable
* subcategory of VT called polymorphic, prolonged QT, ventricular tachycardia b/c of QT of underlying rhythm
* can be brief/nonsustained (30 sec or less) or sustained (\>30 sec)
104
what type of PVC is this?
triplet - three PVCs in a row (uniform or multiform)
105
* premature atrial contractions
* impulse from atria that is earlier than next expected sinus beat d/t irritable, ectopic focus in atrial tissue
* **rhythm** underlying may be regular, overall irregular d/t PAC
* **rate** of underlying rhythm
* **P wave** different morphology from SA node p wave; may be hidden in preceding T wave
* **PR interval** between .10 and .20 seconds - different fro the ectopic beat
* **QRS** narrow, same, less than .12 sec
* **QT interval** less than 1/2 preceding R-R
106
overview of second degree heart block: type 1
* aka Wenckebach
* SA node impulses progressively delayed until one impulse is not conducted
* then cycle repeats
* longer, longer, longer drop. Now I know my Wenkebach
107
six questions for dysrrhythmias interpretation
1. HR: fast, slow, normal?
2. regular or irregular?
3. morphology of p waves and A:V ratio
4. PR interval
5. QRS measurement
6. P wave for every QRS?
1. QRS after every P wave?
108
treatments for second degree heart block: type 1
* based on symptoms of bradycardia
* transcutaneous pacing
* atropine
* dopamine or epi drip
* permanent pacemaker may be indicated if Wenckebach persists
109
polarized
* resting cell's electrical charges are balanced
* cell is ready for action
110
atrial rhythms - overview
* result of electrical impulse originating from atrial tissue that is NOT SA node - ectopic impulse
* occurs when atrial rate faster than sinus rate and overrides SA node to generate depolarization
* unusual P waves - notched, flattened, peaked or biphasic
* d/t slower, atypical impulse conduction thru atria
* impulse travels thru AV junctional tissue and ventricular conduction pathways terminating in Purkinje fibers
* supraventricular rhythms create narrow (normal) QRS wave - no problem in ventricle
111
etiologies of accelerated junctional rhythms
* usually transient
* enhanced autorhythmicity of junction
* digitalis or theophylline toxicity
* catecholamien surge from stress, stimulants
* acid base imbalances
112
digitalis
* increases contractility of heart indirectly by actingon AV node to make it less irritable and slow conduction
* allows for more ventricular filling
* rate control in A.fib
* things to check
* therapeutic levels - narrow therapeutic range (renally cleared)
* apical HR
113
Bundle of His and Bundle branches
* divides into right and left Bundle branches which descends on either side of interventricular septum
* left bundle branch divides into 2 fascicles (anterior and posterior)
* conduction speed in left bundle is faster than right
* Bundle of His is a pacemaker site with inherent rate of 40-60 times/minute
114
what type of PVC is this?
ventricular quadrigeminy - every fourth beat is a PVC
115
basic electrophysiology of EKG
* electrocardiography cannot detect mechanical performance of the heart
* beware of pulseless electrical activity (PEA)
* aka electromechanical dissociation
* expert level dysrhythmia interpretation does not replace expert level patient assessment
116
concerns with atrial fibrillation
* most common dysrhythmia - patients can live with it chronically
1. rate control
2. prevent clot formation
3. loss of CO from atrial kick
117
* atrial flutter
* **rhythm** atrial regular, ventricular variable (depends on A:V)
* **rate** atrial 250-400, ventricular variable
* **P wave** fast "saw tooth" or "picket fence" flutter waves that are uniform; AV ratio can be fixed w/ regular ventricular rhythm or variable
* **PR interval** immeasurable
* **QRS duration** less tahn 0.12 sec, identical morphology
* **QT interval** less than 1/2 preceding R-R interval (normal)
