Resuscitation Flashcards
1
Q
factors contributing to likelihood of sudden cardiac death
A
CV pathology: CAD, severe LV dysfunction, cardiomyopathy (hypertrophic, arrhytmogenic RV), congenital heart disease, valvular heart disease, cardiac pacemaker and conducting system disease
hereditary channelopathies: Brugada, early repolarization syndrome (ERS), long QT, short QT, catecholaminergic polymorphic VT
risk factors and triggers:
- long term risk factor mgmt: htn, hyperlipidemia, smoking, diabetes, SES
- unstable atherosclerotic plaque: psychological stress, physical activity
2
Q
who is more likely to survive cardiac arrest (at home or in public)
A
in public
3
Q
what is survival of EMS treated cardiac arrest
A
11.4%
4
Q
what is surivival of all comers -cardiac arrest (includes DOA)
A
6.8%
5
Q
what time of day is AMI and SCD more common
A
in first few hours upon wakening due to increased sympathetic stimulation
6
Q
what medication helps prevent SCD
A
beta blockers especially in patents with CAD with previous MI and low EF
7
Q
initial rhythm of ventricular fibrillation in cardiac arrest consistent with what etioology
A
acute coronary syndrome
8
Q
when to consider ICD in patients with low EF
A
below 35% EF to prevent SCD
9
Q
who to consider for ICD
A
individuals with previous documented cardiac arrest, ventricular fibrillation, hemodynamically significant or nonsustained VT, patients with first degree relative with SCD, one or more recent unexplained syncope, a max LV thickness of 30mm, abnormal BP response to exercise in presence of other SCD risk factors, or high risk children with unexplained syncope, massive LV hypertrophy or family hx of SCD
10
Q
what is arrhythmogenic right ventricular cardiomyopathy
A
hereditary form of cardiac muscle disease that is characterized by right-sided heart failure, ventricular arrhythmias of right ventricular origin (i.e., ventricular tachycardia with a left bundle- branch block morphology), syncope, and sudden cardiac death
11
Q
what ECG changes are seen in arhymogenic RV cardiomyopathy
A
T wave inversion in right precordial leads (V1-V3)
12
Q
which congenital heart defects are often associated with sudden cardiac death
A
aortic stenosis coarctation of aorta Ebsteins anomaly Tetralogy of Fallot transposition of great arteries coronary artery anomalies (anomalous left coronary artery from pulmonary artery) single ventricle
13
Q
what is the pathophysiology of anomalous left coronary artery from pulmonary artery
A
the left coronary artery traversing between the aorta and main pulmonary artery
Ischemic symptoms, ventricular arrhythmias, and sudden death can be triggered during exercise as a result of increasing venous return, which dilates the main pulmonary artery and compresses the anomalous coronary artery in the space between the aorta and main pulmonary artery
14
Q
harsh, late-peaking systolic murmur at the upper-right sternal border with radiation to the neck is found with what lesion
A
hemodynamically significant aortic stenosis
15
Q
what sequelae can occur with significant aortic stenosis
A
effort-induced dyspnea, myocardial ischemia, and ventricular arrhythmias, which can trigger syncope and sudden cardiac death
16
Q
what is the most common cause of aortic stenosis
A
bicuspid aortic valve that typically calcifies and narrows its orifice in mid-adulthood or sclerosis/calcification of a tricuspid aortic valve, which can occur in individuals who are older than 70 or 80 years of age
17
Q
what causes sick sinus syndrome
A
diffuse degenerative disease of the heart’s electrical generation and conduction system
Sick sinus syndrome affects the heart’s primary pacemaker and can cause intermittent lightheadedness, syncope, or sudden cardiac death
18
Q
what is sudden arrhythmic death syndrome
A
udden arrhythmic death syndrome is characterized by sudden cardiac death occurring out of hospital in relatively young adults (mostly men), often during sleep or at rest, usually without any premonitory symptoms (including syncope) and with no anatomic abnormality identified at autopsy.
19
Q
what is the etiology of Brugada syndrome
A
autosomal dominant inheritance that results in total loss of function of the sodium channel or in acceleration of recovery from sodium channel activation
20
Q
what ethnicity most commonly has Brugada
A
SE asian, and males
21
Q
ECG changes in early repolarization syndrome
A
notch-like J wave on the QRS down-slope, followed by upsloping ST-segment elevation, most prominently in the mid to lateral precordium but can also occur just laterally or inferiorly. There is commonly reciprocal ST-segment depression in aVR.
22
Q
what is characterized by prolongation of the corrected QT interval (QTc), syncope, and sudden
death caused by torsade de pointes and ventricular fibrillation
A
long QT syndrome
0.35 to 0.44 second is normal
23
Q
how to calculate QTc
A
QTm / square root of (R-R)
QTm is the measured QT interval in seconds, and R-R is the interval
between any two consecutive R waves on the electrocardiogram in seconds. Because the QT interval is heart-rate dependent, the formula “corrects” the measured QT interval to a heart rate of 60 beats/min (at which the R-R interval is 1 second)
24
Q
management of patients of long QT syndrome
A
avoidance of QT prolonging drugs, high-intensity sports, and refer to cardiology/EP
25
hereditary long QT syndromes associated with nerve deafness
autosomal recessive - Jervell and Lange-Neilsen syndrome
26
short QT time
less than 0.34s
27
causes of long QT
hypokalemia, hypomagnesemia, hypocalcemia, anorexia, ischemia, central nervous system pathology,
terfenadine-ketoconazole combinations, or certain antipsychotic or antiarrhythmic drugs
28
causes of short QT
hypercalcemia, hyperkalemia, acidosis, systemic inflammatory syndrome, myocardial ischemia, or increased vagal tone or can be inherited in an autosomal
dominant genetic pattern
29
presentation of catecholaminergic polymorphic VT
Affected individuals have exercise- and stress-related ventricular tachycardia, syncope, and sudden cardiac death, usually in childhood or early adulthood. Although there are no characteristic abnormalities in the electrocardiogram pattern, a significant number of affected individuals have sinus bradycardia that is not otherwise explainable. Almost half of these individuals carry a diagnosis of epilepsy as the cause of their recurrent syncope before the true cause (i.e., catecholaminergic polymorphic ventricular tachycardia) is identified.
30
premonitory symptoms in SCD
most common premonitory symptoms reported by sudden cardiac death survivors or family members of victims are chest discomfort, dyspnea, and "not feeling well
31
what did the Cardiac Arrhythmia Suppression Trial show
potent class I sodium channel–blocking antiarrhythmic drugs (encainide, flecainide, and moricizine) are proarrhythmic and paradoxically increase the odds of developing sudden cardiac death, as compared with placebo, in patients at relatively low risk for death
32
prevention of SCD techniques
The benefits of β-blockade, sotalol, and amiodarone in decreasing mortality from sudden cardiac death pale in comparison with the protective effects of the implantable cardioverter-defibrillator in high-risk patients,36 including those who have been resuscitated from ventricular fibrillation or cardioverted out of sustained ventricular tachycardia.37 Although these devices are expensive to insert, their effectiveness over conventional therapy results in a cost of less than $30,000 per year of life saved, which makes them relatively cost-effective for implantation in high-risk individuals.
33
what did Public Access Defibrillation randomized clinical trial show
laypersons trained and equipped to use automated external defibrillators in public places can double survival to hospital discharge compared with that which can be achieved by layperson rescuers who can only perform CPR while awaiting EMS arrival
34
survival of cardiac arrest if initial rhythm not VF/pulseless VT
<5%
35
define bradyasystole
ventricular rate <60 beats/min or periods of absent heart rhythm (asystole)
36
what is primary vs. secondary bradyasystole
Primary bradyasystole occurs when the heart's electrical system fails to generate and/or propagate an adequate number of ventricular depolarizations per minute to sustain consciousness and other vital functions. Secondary bradyasystole is present when factors external to the heart's electrical system cause it to fail (e.g., hypoxia).
37
causes of bradyasystolic arrest
```
myocardial ischemia or infarct
sick sinus syndrome
hypoxia
hypercarbia
stroke
opiates, B-blockers, CCBs, adenosine, or parasympathetics
```
38
what is the underlying pathophysi of PEA
a marked reduction in cardiac output due to either profound myocardial depression or mechanical factors that reduce venous return or impede the flow of blood through the cardiovascular system
39
conditions that cause PEA
```
hypovolemia
tension pneumothorax
pericardial tamponade
pulmonary embolism
massive myocardial dysfunction due to ischemia or infarction, myocarditis, cardiotoxins, etc.
drug toxicity (BBs, CCBs, TCAs)
profound shock
hypoxia
acidosis
severe hypercarbia
auto PEEP
hypothermia
hyperkalemia
pseudo-PEA
```
40
4 main mechanisms of shock
hypovolemic
obstructive
distributive
cardiogenic
41
cardiac output determined by
CO= HR x SV
42
MAP is determined by
MAP = CO X SVR
43
oxygen delivery is determined by
oxygen delivery = cardiac output x arterial oxygen content
Do2 = CO × [(1.39 × Hb × Sao2) + (Pao2 × 0.0031)]
Do2 is the amount of O2 delivered to the tissues per minute. A normal value is 1000 mL O2 per minute
44
how to calculate arterial oxygen content
Arterial Oxygen Content = Amount of Oxygen in the Blood
| Cao2 = (1.39 × Hb × Sao2 ) + (Pao2 × 0.0031)
45
how to calculate oxygen consumption
Oxygen Consumption = Cardiac Output × (Arterial O2 Content – Venous O2 Content) V̇o2 = CO × (Cao2 – Cvo2)
46
how to calculate shock index
SI = HR/ SBP
A normal value is 0.5–0.7. A persistent elevation of the shock index (>1.0) indicates an impaired left ventricular function (as a result of blood loss or cardiac depression) and carries a high mortality rate.
47
hemodynamic changes seen in hypovolemic shock
decreased preload
increased SVR
decreased CO
48
etiologies of hypovolemic shock
hemorrhage
capillary leak
GI losses
burns
49
hemodynamic changes seen in cardiogenic shock
increased preload
increased afterload
increased SVR
decreased CO
50
aetiologies of cardiogenic shock
MI, dysrhythmia, heart failure, valvular heart disease
51
hemodynamic changes in obstructive shock
decreased preload
increased SVR
decreased CO
52
aetiologies of obstructive shock
tension pneumothorax, PE, pericardial tamponade
53
hemodynamic changes in distributive shock
decreased preload
decreased SVR
mixed CO
54
aetiologies of distributive shock
sepsis, anaphylaxis, neurogenic
55
physical examination findings in shock
temp: hyper or hypothermia may be present
HR: usually elevated, can be bradycardic due to hypogylemic, BB use or pre-existing cardiac dz.
SBP: may increase slightly initially when cardiac contractility increases,then decreases as shock progresses
DBP: may rise early in shock and then fall when cardiovascular compensation fails
pulse pressure: increases in early shock, then decreases before SBP begins to drop
MAP: often low <65
CNS: acute delirium, restlessness, disorientation, confusion, and coma secondary to decreased CPP
skin: pale, dusky, cyanosis, swearing, altered temp, increased cap refill time of > 2-3s
CV: may have flat or distended JVP based on type of shock, tachycardia and arrhythmia, S3 in high output states, decreased coronary perfusion can lead to ischemia, decreased ventricular compliance, increased left ventricular diastolic pressure, and pulmonary edema
resp: Tachypnea, increased minute ventilation, increased dead space, bronchospasm, and hyper- or hypocapnia with progression to respiratory failure
splanchnic organs: Ileus, GI bleeding, pancreatitis, acalculous cholecystitis, and mesenteric ischemia can occur due to low flow states
renal: decreased GFR
metabolic: Hyperglycemia, hypoglycemia, and hyperkalemia; as shock progresses metabolic acidosis occurs with resp. compensation
56
initial investigations in shock
```
CBC, lytes, urea/Cr, lactate, glucose, coags, ABG, transaminases/LFTs
ECG
UA
CXR
blood cultures; other appropriate cultures
pregnancy test
cortisol level
imaging if indicated
```
57
use of POCUS in shock
Cardiac Evaluation with Sonography in Shock protocol looks at cardiac function, inferior vena cava dynamics, pulmonary congestion, sliding and consolidation, abdominal free fluid, abdominal aortic aneurysm, and leg venous thrombosis to assist in differential diagnosis generation or narrowing
58
end points of resuscitation in ED
goal- directed approach of MAP >65 mm Hg, central venous pressure of 8 to 12 mm Hg, Scvo2 >70%, and urine output >0.5 mL/kg/h during ED resuscitation of septic shock
59
questions to ask if patient has persistent shock or hypotension despite resuscitation
is patient monitored properly?
equipment malfunction? ie. dampening of art line
is the IV tubing connected and running well
are the vasopressor infusion pumps working
are the vasopressors mixed adequately and in correct dose
does mentation/clinical appearance match degree of hypotension
is pt. adequately volume resuscitated
did the pt get a pneumo after placement of central venous access
has pt been assess for occult penetrating injury
is there hidden bleeding from a ruptured spleen, large vessel aneurysm, or ectopic pregnancy
does the pt have adrenal insufficiency ?
is the pt allergic to medication given or taken before arrival?
is there cardiac tamponade in the dialysis or cancer pt?
is there associated AMI, dissection, or PE
60
when to use bicarb in shock
In settings of a low pH and when evidence of decreased contractility (despite ongoing resuscitative efforts) or development of a dysrhythmia, partially correct the metabolic acidosis, either with sodium bicarbonate boluses or a drip.
Consider situations, such as end-stage renal disease and renal tubular acidosis, that cannot reclaim bicarbonate through normal renal processes and whether bicarbonate may be indicated.
61
adverse effects of bicarb
Bicarbonate administration shifts the oxygen-hemoglobin dissociation curve to the left, impairs tissue unloading of hemoglobin-bound oxygen, and may worsen intracellular acidosis.
62
etiology of trauma-induced coagulopathy
combination of factors beginning with loss of coagulation factors from hemorrhage, followed by hemodilution from crystalloid resuscitation, and then exacerbated by acidosis (evidenced by a base deficit) and hypothermia that occur during the course of ongoing hemorrhage and resuscitation.
63
define anaphylaxis
1. Urticaria, generalized itching or flushing, or edema of lips, tongue, uvula, or skin developing over minutes to hours and associated with at least one of the following:
Respiratory distress or hypoxia
or
Hypotension or cardiovascular collapse
or
Associated symptoms of organ dysfunction (e.g., hypotonia, syncope, incontinence)
2.Two or more signs or symptoms that occur minutes to hours after allergen exposure:
Skin and/or mucosal involvement Respiratory compromise
Hypotension or associated symptoms Persistent GI cramps or vomiting
3.Consider anaphylaxis when patients are exposed to a known allergen and develop hypotension
64
treatment of anaphylaxis
epinephrine 0.3-0.5mg (1:1000) IM
diphenhydramine 50mg IV
ranitidine 50mg IV
methylprednisolone 80-125mg IV
65
what to use for ongoing hypotension in pt with anaphylaxis on a beta blockers
glucagon 1mg IV q 5 min until hypotension resolves then 5-15mcg/min infusion
66
discharge planning for patients with anaphylaxis
```
ID inciting allergen
instruct about use of meds and epipen
rx for current rxn: diphenhydramine 25-50mg po q6-8h x 3-5 days, prednisone 40-60mg po daily for 3-5days
rx for epipen
refer to allergist
```
67
treatment of angioedema
airway management
C1 esterase inhibitor 1000IU IV for ACE, 20U/kg for hereditary
Icartibant,30mg SC- a bradykinin-2 antagonist, is effective agent to reduce swelling and shorten time to complete resolution
68
screening test for hereditary angioedema
C4 level < 30% of normal
69
what is the difference in O2 delivery between nasal cannula, O2 face mask and NRB mask
nasal- each liter /min increases 4% FiO2, max 4L/min therefore max FiO2 = 37%
face mask- 10-15L/min - 35-60% FiO2
nonrebreather - 10-12L/min- 95% FiO2
70
indicator of instability in patient with dysrhythmia
```
hypotension
altered mental status
respiratory distress
ischemic chest pain
signs of hypo perfusion
extremely rapid ventricular rate > 200
```
71
when do you need urgent treatment of bradycardia
if rate below 50 with hypotension or hypoperfusion (needs resuscitation)
if caused by structural infra nodal disease (needs pacer)
72
medications to increase HR in symptomatic bradycardia
atropine, B-agonist, glucagon
73
narrow, regular tachycardia
```
sinus tachycardia
atrial flutter
AVRT
AVnRT
atrial tachycardia
junctional tachycardia
```
74
narrow, irregular tachycardia
atrial fibrillation
multifocal atrial tachycardia
atrial flutter with variable block
75
wide, regular tachycardia
ventricular tachycardia
any SVT with abberrancy
antidromic AVRT
76
wide, irregular tachycardia
polymorphic VT
| any SVT with aberrancy
77
treatment of stable, regular narrow complex tachycardia
attempt vagal maneuvers
give 6mg adenosine IV push, followed by 12mg IV push if does not convert
can repeat 12mg dose once
78
which narrow regular complex tachycardia likely diagnosis when converts with adenosine
likely AVRT or AVnRT
79
which narrow regular complex tachycardia more likely diagnoses when does not convert with adenosine
atrial flutter, ectopic atrial tachycardia, junctional tachycardia
80
next step in mgmt of pt with regular narrow complex tachycardia who responds to adenosine
observe and monitor
repeat adenosine if returns
control rate with AV nodal blocking agents (diltaizem or B-blcokers)
81
next step in mgmt of pt with regular narrow complex tachycardia who does not respond to adenosine
control rate with diltaizem or B-blockers (avoid BB in pulmonary disease or CHF)
treat underlying cause of rhythm
consider expert consultation
82
management of irregular, stable, narrow-complex tachycardia
```
control rate (BB or dilt)
treat underlying cause of rhythm (a.fib, MAT, or flutter with variable block)
consider consult
```
83
potential pharmacologic agents used to terminate stable wide-complex tachycardia
procainamide, amiodarone, lidocaine, magnesium
84
evidence for pharmacologic agent choice in stable wide complex tachcardia
```
procamio trial - procainamide higher efficacy - 67% va. 38% for amiodarone at tachycardia termination at 40mins
side effects (major cardiac events) lower for procainamide - 9 vs. 41% with amio
```
doses compared
IV procainamide 10mg/kg over 20 min
IV amiodarone 5mg/kg over 20 min
85
current algorithm mgmt of stable, wide-complex regular tachycardia
give amio 150mg IV over 10 min, repeat if necessary to max 2.2g/24h, prep for sync cardio version
if known SVT with aberrancy, then give adenosien
86
current algorithm mgmt of stable, wide-complex, irregular tachycardia
if pre-excitation with AF (ie. AF + WPW) - avoid AV nodal agents (Eg. diltiazem or BB), consider antiarrhytmics (amiodarone or procainamide)
if torsades de pointes - give MgSO4 2g IV
if polymorphic VT - prep for sync cardio version
if AF with aberrancy - follow narrow-complex irregular protocol
87
ECG features of sinus arrhythmia
variation in SA node discharge rate greater than 120ms between longest and shortest P-P
consistent P wave morphology from beat to beat
upright P waves in lead I, II, III
consistent P wave, QRS complex relationship
88
what is Bainbridge reflex
changes in vagal tone occurring with respiration, causing sinus arrhytmia
89
what is first degree SA block
impulse is delayed in its conduction from SA node to atria, diagnosed with EP studies, nothing on ECG
90
what is secondary degree SA block
some impulses from SA node go through and some are blocked, suspected on ECG when expected P wave and corresponding QRS complex are absent, interval between normal P waves encompassing the missing beat is a simple multiple of the existing P to P rate
91
what is third degree SA block
sinus node discharge is completely blocked and no P wave originating from the sinus is seen
92
DDX for absence of P wave on ECG
third degree SA block
sinus node failure
sinus node stimulus inadequate to activate the atria
atrial unresponiveness
93
causes of SA block
myocardial disease (acute rheumatic fever, acute eifnerior MI, or other causes of myocarditis), drug toxicity ( digoxin, quinidine, salicylate, B-Blockers, CCBs), vagal stimulation
94
treatment of SA block
atropine , however schema may result from a rhyme that is accelearted
cardiac pacing is indicated for recurrent or persistent symptomatic bradyacardia
95
define sinus pause on ECG
failure of impulse formation in the SA node; P to P wave interval encompassing the missing beat has no relation tot he underlying SA node discharge rate
96
define sick sinus syndrome
abnormalitites of supra ventricular impulse generation and conduction that produce a wide variety of intermittent supra ventricular tachycardia and bradydysrhythmias
97
ECG features of sick sinus syndrome
intermittent combination of bradydysrhythmias and tachydysrhymthmias
bradys: sinus bradycardia, sinus arrest, SA block
tachys: AF, a. flutter, paroxysmal SVT
98
ECG features of premature atrial contractions
P waves appear sooner than expected sinus beat
ectopic P waves : with different shape and axis than the SA node-initiated P wave, may or may not be conducted throughout he AV node
interval between normal P waves encompassing the PAC is less than twice the existing P=P cycle length
99
PACs seen more commonly in
seen in normal its
patients with chronic heart or lung disease
chemical agents that enhance SNSS tone (coke, amphetamines, caffeine, nicotine), PNS tone (eg. digoxin)
100
PACs could precipitate
atrial tachycardia, flutter, or fibrillation
101
ECG features of premature junctional contractions
ectopic P wave - with different shape, axis or amplitude from SA node-initiated P waves, may occur before or after QRScomplex
QRS complex with similar morphology to SA node-initiated QRS complex
102
premature junctional contractions
uncommon in healthy hearst
| typically seen in patients with heart failure, dig toxicity, ischemic heart disease, and myocardial ischemia
103
ECG features of PVCs
absence of P wave prior to QRS complex
occasional retrograde P wave following QRS
abnormally widened QRS complex with different morphology from SA node- initiated QRS complex
commonly a compensatory postectopic pause following the PVC
ST segments and T waves that are directed opposite the major QRS complex deflection
104
consequence of PVCs
infrequent or rare PVCs seen in patients without any evidence of heart disease
PVCs can trigger sustained runs of VT
105
in patient with ACS who has PVCs, what is implication
PVC indicates underlying electrical instability to the heart, but not reliable predictor of VF
106
treatment of patient with PVC
review ECG for evidence of schema or infant, chamber enlargement, QT prolongation or Brugada syndrome
assess for reversible conditions (hypoxia, drug effect, or electrolyte abnormalities)
107
ECG features of sinus bradycardia
normal SA node-initiated P waves: consistent morphology among all P waves with upright amplitude in leads I, II, and III
normal PR interval (120-200ms)
1:1 AV conduction: a QRS complex for each P wave consistent association
rate <60beats/min and regular
108
ECG features of junctional rhythm
absence of normal P waves with normal PR interval
rare retrograde P wave (usually an inverted P wave immediately adjacent to QRS complex, pre or post)
narrow QRS complex
regular rate
ventricular rate: 40-60 for junctional rhythm, 60-100 for accelerated junctional rhythm, > 100 fr junctional tachycardia
109
causes of sinus bradycardia
physiologic (in well-condiitonaed athletes, during sleep or with vagal stimulation)
pharmacologic (BB, digoxin, opioids, CCBs)
pathologic: hypoxia, acute inferior MII, increased ICP, carotid sinus hypersensitivity, hypothyroidism
110
treatment of sinus bradycardia with hypoperfusion
correct underlying causes
atropine in unstable patient, followed with transcutaneous cardiac pacing and infusions of dopamine or epinephrine if there is no response to atropine
111
define idioventricular rhythm
ventricular origin, regular widened QRS complexes without evidence of atrial activity, rate of 30-50, accelerated idioventricualr rhythm rate or 50-75
typically begins with a fusion beat
112
ECG features of idioventricular rhythm
widened QRS complex
QRS complexes occurring regularly
no evidence of atrial activity: no P waves
ventricular rate: 30-50 or 50-75 accelerated
often in non sustained fashion with runs of short duration: 3-30 consecutive beats
113
when are idioventricular rhythms most commonly seen
in setting of STEMI
when occurs after fibrinolysis - called repercussion dysrhythmia
114
treatment of idioventricular rhythm producing hypo perfusion
atropine
transcutaneous pacing
NB: if accelerated idioventricular rhythm treated with antiarrhtymic and it is only functioning pacemaker may cause asystole; most don't need tx. , pace if necessary
115
first degree AV block
PR interval > 200ms
| consistent relationship between P wave and QRS complex
116
second degree AV block - Mobitz I
Wenckebach
longer longer longer drop
PR lengthens until dropped beat (P wave with no QRS)
after nonconducting beat cycle repeats
117
second degree AV block - Mobitz II
dropped beat without warning
PR interval is constant
when more than one consecutive beat non conducted = high grade AV block
118
third degree AV block
complete dissociation of atria and ventricular contractions
P-P distance constant, R-R distance constant
QRS can be wide or narrow depending on origin
119
difference between nodal and infra nodal AV blocks
nodal blockade usually due to reversible depression of conduction, is often self-limited, and generally has a stable infranodal escape pacemaker pacing the ventricles
infra nodal AV blockade usually are due to organic disease of the His bundle or bundle branches; often the damage is irreversible. They generally have a slow and unstable ventricular escape rhythm pacing the ventricles, and they frequently have a bad prognosis.
120
significance of 1st degree AV block
occasionally is found in normal hearts
-increased vagal tone of any cause, medication toxicity, inferior myocardial infarction, and myocarditis.
in ACS- can indicate an increased chance of progression to complete heart block.
Patients with first-degree AV block without evidence of organic heart disease appear to have no difference in mortality compared with matched controls
121
when can you not tell the difference between Type 1 and Type II Mobitz ?
if Type II has 2:1 conduction cannot tell if Mobitz I or II
122
clinical significance of Type II Mobitz
indicates infra nodal disease and has potential to deteriorate to complete heart block suddenly
123
treatment of Type II Mobitz
apply pacing pads in ED in case they need them
atropine rarely effective
most end up needing transvenous pacing
124
treatment of patients with complete heart block
asymptomatic -> admit for monitoring
| symptomatic -> atropine, pacing
125
ECG features of sinus tachycardia
normal sinus P waves and PR interval
1:1 AV conduction
atrial rate usually 100-160
126
ECg features of atrial fibrillation
absence of discernible P waves with flat or chaotic isoelectric baseline
QRS complexes narrow unless preexisting BBB
irregularly irregular rhythm
127
narrow complex regular tachycardia with rate of ~150 suggests
atrial flutter with 2:1 conduction
128
ECG features of atrial flutter
identifiable P waves: single morphology, negative amplitude (flutter waves best seen in V1 and inferior leads), atrial rate is regular usually 300 ppm
QRS complex narrow unless pre-existed BBB
ventricular rate regular although occasional irregularity can be seen
ventricular rate often 150 bpm
129
causes of atrial fibrillation
```
ischemic or valvular heart disease
CHF
myocarditis
EtOh binge (holiday heart)
thyrotoxicosis
blunt chest trauma
```
130
different types of atrial fibrillation
paroxysmal- lasting less than 7 days, terminating either spontaneously or with treatment
persistent - sustained longer than 7 days or requiring treatment to termination
long-standing persistent - eating continuously longer than 1 year
permanent - long-standing where decision has been made not to try to restore NSR
new or recent onset = symptomatic pateitsn presenting to ED without prior history of atrial fbirillation
131
what is risk of conversion of new onset a fib
if present less than 12 hours- 0.3% risk of arterial embolism
1% if present 12-48 hours
for patients with heart failure or DM, conversion under 48 hours carries risk of thromboembolic events as high as 9.8%; with neither risk factors < 0.2%
>48 hours - risk increased for all groups
132
approach of treatment of a.fib in ED
ventricular rate control:
rhythm conversion
anticoagulation to prevent arterial embolism
133
components of CHA2DS2-VASc
```
CHF- 1
HTN- 1
AGE > 75 - 2
DM - 1
stroke, TIA or VTE- 2
vasc dz. (CAD, PAD) -1
age 65-74- 1
sex (female)
```
134
treatment of patient with recent-onset afib and a rapid ventricular response producing hypotension, myocardial schema or pulmonary edema
urgent electrical cardioversion
if possible, check old records to determine if longstanding --> if it is, then unlikely for cardio version to succeed, and instead initiate ventricular control treatment
consider anticoagulation with heparin before or immediately after electrical cardio version and continue as bridge to oral anticoagulants in patens are increased risk of embolic complications 9CHADS > 1, mechcanil heart valve, rheumatic valvular disease)
135
treatment of stable low-risk patients in the ED with new-onset afib
rate control: start AV node blocking agents to control ventricular response, initiate oral anticoagulants to prevent thromboelmboislm and re-aelvatue after 3-4 weeks for elective cardioversion
rhythm-conversion approach: electrical or pharmacologic methods to convert patients back into sinus rhythm
136
doses for rate control agents in atrial fib/flutter
diltiazem 15-20mg IV bolus over 2 mins, may repeat bolus if inadequate rate response
once satisfactory response ,begin IV infusion 5-10mg/hr
transition to oral diltiazem, 60-90mg po for 5 or 10 mg drip rate respectively
stop IV infusion 2 hours after oral dose
metoprolol 5mg IV, may repeat q 5 mins to max of 15mg
once satisfactory response, give as 12.5mg po per 5mg IV
137
electrical cardioversion energy requirements
atrial flutter - may require as little as 25-50J
| atrial fib 150-200J
138
next step if BB or CCB are ineffective in controlling rate in atrial fib
IV procainadmie or amiodarone
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discharge steps for pt with new afib/flutter
ensure that pt breathing comfortable on room air with SpO2 > 95%, and BP is at baseline
ventricular rate has been controlled to a rate less than 100bpm at rest
for nonvavluvalr AF not converted to sinus rhythm, determine risk for embolic event with CHADSVASC score- 0, no oral AC, 1 - either no AC or oral AC acceptable, 2 - oral anticoagulants recommended, f/u with consultant
consult with internist for med choice
arrange outpatient echo for new AF
D/C pt with rx for rate and/or rhythm control, and AC if indicated - enough until f/u appt
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ECG features of paroxysmal SVT
absence of normal P waves with normal PR interval
rare retrograde P wave
narrow QRs complex
ventricular rate usually 170-180bpm (can be 130-300)
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ECG features of multifocal atrial tachycardia
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at least 3 distinct P wave morphologies
no consistent P-P, PR or R-R intervals
irregularly irregular rhythm (usually 100-180)
normal QRS
frequently confused with afib/flutter
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treatment of multifocal atrial tachycardia
treat underlying disorder, ie. in chronic lung disease - oxygen and bronchodilators improve pulmonary function and arterial oxygenation and decrease atrial ectopy. Antidysrhythmic treatment is not indicated, and cardioversion has no effect.
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ECG features of monomorphic VT
no P wavs associated with QRS
rapid and regular rhythm
rate usually 140-180 (range 120-300)
wide QRS with consistent beat-to-beat morphology
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ECG features of polymorphic VT
no P waves associated with QRS
rapid anorrregular rhythm
rate 140-180, range 120-300
widened QRS with inconsistent beat-to beat moprhlology
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causes of VT
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most common are ichronic ischemic heart disease andAMI
dilated or hypertrophic cardiomyopathy
valvular heart diease
inherited ion channel abnormalities
drug toxicity
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hypoxia, alkalosis, and lyte abnormalities especially hyper exacerbate propensity for ventricular ectopy and tachycardia
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five ECG features helpful in differentiating VT from SVT with aberrant conduction
irregularity: VT is usually regular or only minimally irreg
AV dissociation: P wave visualized with no associated to QRS
fusion and capture beats: independent atrial impulse may occasionally cause ventricular depolarization via normal conducting system (ie. see different QRS morphology)
QRS duration: VT usually has wider QRS, therefore QRS > 160 favours VT
QRS complex concordance: negative concordance (all QRS's pointing down) favours VT
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Vereckei criteria favouring VT over SVT with aberrancy
notch present on the initial descending limb of a predominantly negative QRS
slow conduction at beginning of QRS: rtio of vertical distance travelled in voltage during the initial 40ms and terminal 40ms: ration of Vi/Vt < 1
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Pava criteria favouring VT over SVT with aberrancy
VT diagnosed if time from isoelectric to peak of R wave in lead II is >50ms
149
what to do if successful treatment of VF arrest
restore dysthrythmi triggers like acute ishcemia, metabolic derangements or toxicologic insults
150
treatment of VF
electrical defibrillation + chest compressions + epinephrine + ACLS
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ECG findings in WPW
shortened PR interval <120ms
delta wave
widened QRS
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treatment of narrow complex SVT in WPW
the first intervention is vagal maneuver (Table 18-3). If this intervention fails, the next step would be intravenous adenosine (Table 18-2). If adenosine fails, then longer acting AV nodal blocking agents, such as β-blockers and calcium channel blockers are indicated. In refractory cases, procainamide is an effective agent that blocks conduction in the accessory conduction pathway and can terminate this reentrant tachycardia. If all medications are unsuccessful, the patient can be electrically cardioverted with appropriate sedation.
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treatment of wide complex tachycardia in WPW
procainamide should be administered
If unsuccessful, electrical cardioversion with
appropriate sedation should be considered
agents that can enhance conduction in the accessory tract and/or block conduction in the AV node should be avoided in WPW patients with wide-complex irregular
tachycardias; these include adenosine, amiodarone, β-blockers, and calcium channel blockers
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disposition of WPW patient
After conversion, observe the patient with continuous cardiac rhythm monitoring and a repeat ECG. In general, patients who have rare episodes of tachydysrhythmias and who are stable after conversion can be discharged home with routine follow-up. Patients with frequent tachydysrhythmia episodes or who have an episode of atrial fibrillation with a very rapid ventricular response should be promptly referred for ablation of the accessory pathway. Patients who experience loss of consciousness during a known or possible tachydysrhythmia should be kept for observation due to the potential for repeat episode or cardiac arrest. Asymptomatic patients in whom WPW appears as an incidental finding should be referred to a
cardiologist for further evaluation
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types of Brugada
Type 1: coved-shaped ST elevation >2mm + T wave inversion
Type 2: ST elevation >2mm with trough of 1mm
saddleback appearance, biphasic T wave
Type 3: either pattern with 1-2mm elevation
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risk stratification of person with Brugada features on ECG
personal hx: near or complete syncope, seizure, nocturnal atonal respiration, polymorphous VT
aborted SCD: VF,
Fam hx: of SCD, of Type 1 ECG pattern
EP study: indelibility of VT or VF with programmed stimulation
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mamangement of pt with Brugada ECG findings
a kid use of meds with have sodium channel blockade
educate patient on importance of treating fever, even with minor infections
only way to prevent malignant ventricular arrhythmia's = ICD
refer for follow up
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managemnt of pt with long QT in ED
; do not use medications that possess channel blockade effects, impair cardiac repolarization, prolong the QT interval, and provoke tachydysrhythmias
Correct underlying electrolyte abnormalities, especially those of potassium and magnesium. β-Blockers are the initial treatment for symptomatic patients with congenital long QT syndrome.90 Propranolol and nadolol are the most effective β-blockers, and patients with congenital long QT syndrome type 1 are the most responsive.
Lifestyle modifications are beneficial in congenital long QT syndrome.91 Exercise is a trigger for lethal dysrhythmic events, especially in patients with congenital long QT syndrome type 1, where swimming is notably dangerous. Patients with congenital long QT syndrome type 2 are sensitive to decreased serum potassium and are at risk for lethal cardiac events triggered by emotions or being startled, as being roughly aroused from rest or sleep.
