Basics of Hemodynamic Monitoring
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Transcript Basics of Hemodynamic Monitoring
Cardiovascular
Dysfunction
Arrythmias in the Critically Ill
S. Mountain
Sept. 25, 2008
For each case, please answer the following 4
questions:
1. What is the rhythm? Why do you think so? What
is your approach to the diagnosis of this rhythm?
2. What are some likely causes/risk factors?
3. What is the potential impact of this rhythm in the
ICU patient? What are the risks of not treating this
rhythm?
4. How do you treat this rhythm? What are some of
the risks of treating? How efficacious are the various
treatments?
Case 1. (Todd) * Difficulty rating. See EKG
1, below. You are called to see a 78 year old
man in emerg. regarding hypotension and
tachycardia. His wife noted he had a fever and
was more difficult to rouse this morning. You
quickly interpret the EKG, and for the benefit
of your med student, you delineate the answers
to the 4 questions above.
Sinus Tachycardia
…With 1st-degree bock and left atrial
enlargement
Why? It’s a regular rhythm at about 100 bpm,
with a narrow QRS, prolonged PRI (driven by
wide P wave, but that’s the way it goes), normal
axis, and no evidence of intraventricular
conduction delay. There are no ST or T-wave
abnormalities, nor Q waves.
Approach is systematic, or something will be
missed. The computer on the ECG cannot be
trusted.
Sinus Tachycardia
Likely cause?
Sinus tachycardia is the heart’s response to
stress. In this case, an elderly gentleman with a
likely clinical presentation of sepsis may have
sinus tachycardia for several reasons:
–
–
–
–
–
Fever
Vasodilation
Intravascular volume depletion
Acidosis
Anxiety/fear/discomfort
Sinus Tachycardia
Why might this be bad? What’s the worst that
can happen?
– Increased myocardial oxygen demand
Degeneration into other arrhythmias, including
interventricular conduction delays
CHF (tachycardia-mediated cardiomyopathy)
– Hypotension (decreased diastolic filling time, although
this is rare with sinus rhythm, as atrial component is
preserved, and rate is usually slow enough)
– On the plus side, it is a diagnostic clue (i.e. SIRS
criteria, Wells criteria, early sign of hemorrhage, etc)
Treatment: Underlying cause.
Case 2. (Neil)* * Difficulty rating. While your junior
medicine resident is writing up the E.R. patient, you are paged
back to the ICU to see one of your patients. She is a 79-yearold woman who is admitted to the unit with heart failure, and
was intubated yesterday. She was stable until a few minutes
ago when her EKG tracing changed, and her sats dropped.
Previous physical exam had revealed a systolic murmur
loudest at the apex radiating to the axilla. An EKG was done
while you were on the way up from the E.R. and is available
for your interpretation. Your med student wonders what the
diagnosis is, and what it’s significance is to your patient.
Atrial Fibrillation w/ rapid
Ventricular response
NO P waves
Usually Narrow complex
Irregularly irregular ventricular response
Fibrillary waves of irregular atrial
activation may be seen (inferior or V1)
Causes/Risk Factors
Ischemic Heart Disease
Valvular disease (esp. Mitral)
Pericarditis
Sick Sinus
Myocardial contusion
Hypertensive Heart disease
Cardiomyopathy
Cardiac Surgery
CHF
Accessory pathway (WPW)
PE
Catecholamine excess
Acute Ethanol ingestion (Holiday heart)
Idiopathic
Hyperthyroidism
SAH
Potential Impact of this rhythm
Can cause hemodynamic instability
– Worsens NYHA class
– Especially MS or HOCM
– Loss of atrial systole can decrease LVEDP by
20-35%
AF in the ICU
– Increase in stroke, heart failure, all cause
mortality
– W>M
Risks
CHADS2 score
Treatment
Stable vs. Unstable
– Hemodynamically
– Pulm edema
– Chest pain
DC Cardioversion vs. Chemical
Electrical
– Conversion rates reported high(67-94%), but
one reported 35% in surgical ICU patients
– Recommended for AF 50-100J
When is it safe to cardiovert?
HD stable
AHA Class I
– <48 hours
– Anticoagulated > 3 weeks (INR 2-3)
– No atrial clot on TEE
Which drug to use?
AFFIRM (2002)
– Rate control = rhythm control in mortality
– Less ADR’s in rate control
– Not our population (ie. Not stressed or
hypotensive)
Which drug to use?
Rate control
AHA Class I
– B-blockers
– Calcium channel blockers
AHA Class I in Heart Failure
– Digoxin
– Amioderone
Which drug to use?
Rhythm control
AHA Class I
– Flecanide
– Propafenone
– Dofetilide
– ibutilide
AHA Class IIb
– amioderone
Which drug to use?
Rhythm control
Case 3. (Todd) * * Difficulty rating . See EKG 3.
Just as you have finished making your diagnosis
and educating your student about the last
patient, the alarm goes off on the patient’s
monitor across the hall. He is an 80 year old
man with a remote history of an MI. He is in the
ICU post abdominal surgery, and has been
recovering from intra-abdominal sepsis, but is
nearly ready for the ward. His BP has dropped
with this new rhythm. You call for an EKG,
interpret it, and make a diagnosis and
management plan. What are they?
Supraventricular tachycardia;
AVRT
How do we know what it is? It’s a rapid,
regular rhythm with a narrow QRS. There are
small P waves before every QRS (best seen in
lead II here, but look also in II, aVF and V1),
with a short PR interval.
The R wave has a slight slur to it (delta
wave), indicating a bypass tract (classically
associated with Wolff Parkinson White
Syndrome, but not pathognomonic)and
ventricular preexcitation
– WPW: short PR, wide QRS, secondary
repolarization abnormalities, and PSVT
Accessory Pathway
QuickTime™ and a
TIFF (Uncompressed) decompressor
are needed to see this picture.
Differential diagnosis includes:
Atrial flutter. The ventricular rate is often a factor
of 300 (“classic” is 150 bpm), indicating 2:1
conduction of…
– Flutter waves. These are the “sawtooth” waves
between the QRS complexes, which often look like Twaves. 250-350 bpm.
– A reentry circuit in the right atrium, which usually
runs counterclockwise, with a well-known path
between the IVC and TV annulus
– Classic flutter: negative F waves in II, III, aVF,
positive in V1. Clockwise flutter is the opposite.
Atrial Flutter
Likely cause?
Usually associated with organic heart
disease, and is most commonly seen in
post-bypass patients. Like atrial fibrillation,
may be associated with physiologic stress,
including sepsis, myocardial ischemia,
fever, etc.
Atypical (clockwise) atrial flutter may be a
transition between sinus rhytm and atrial
fibrillation, according to animal models.
Supraventricular Tachycardia
Why might this be bad? What’s the worst that
can happen?
– Ventricular rate of 150 leaves little time for diastolic
filling for patients who need it…
– Hypotension
– Stroke risk thought to be similar to that of atrial
fibrillation
– In case of atrial flutter, 1:1 conduction is rare, but the
resulting HR would be 250-300 bpm.
May degenerate to a-fib, as evidenced by common
presentation of atrial fib/flutter on rhythm strips.
Supraventricular arrhythmias in
the ICU
Very common between 03:00 and 07:30…
Goodman, Shirov, et al Critical Care and Trauma
104 (4) 2007:
– Patients with new-onset supraventricular arrhythmia
(SVA) had higher APACHE II scores, sepsis/SIRS, ARF,
catecholamine infusions, and longer LOS (ICU and
hosp) compared to those without SVA.
– Risk factors for new-onset supraventricular
arrhythmia:
Sepsis/SIRS (OR 50), (LD) dopamine or other
catecholamines, hypothyroidism, pulmonary disease
In ICU, ischemia, ARF and hemorrhagic shock in the setting
of new-onset SVA were associated with in-hospital mortality
SVA: bottom line
According to this paper, mortality in
hospital, ICU and after discharge was
statistically significantly higher (38%,
36%, 16%) in the new onset SVA group
compared to those who had no SVA
– SVA included atrial fibrillation, atrial flutter,
“other”/paroxysmal supraventricular
tachycardias
SVA: Treatment
If hemodynamically unstable: synchronized
cardioversion (often responds to lower energy
than VT, i.e. 120 J biphasic ); 95% effective
– Save the patient now, chin-scratch over the ECG later
If diagnosis is in doubt, may try to slow A-V
conduction to either diagnose the origin or
terminate the rhythm, whichever occurs first
– Vagal maneuver
– Adenosine
Rapid atrial pacing, usually done with
endocardial electrodes (such as those left in post
CABG)
SVA: Pharmacologic Treatment
Adenosine (6 mg, proceed to 12 mg if
unsuccessful, rapid IV push with saline chaser)
Diltiazem or verapamil may also be used UNLESS
a bypass tract (AVRT) is suspected
– They may accelerate conduction over the bypass
tract!
Beta blockers, amiodarone
Procainamide (long infusion time), propafenone,
flecanide
Ibutilide (Class III antiarrhythmic. Takes about
30 minutes, may cause Torsades de Pointes)
Case 4. (Yoan)* * Difficulty rating. See EKG
4. Just as you finish with the man in case 3,
you are paged back to emerg. You are asked to
see a 23 year old woman, who has presented
with a rapid heart rate, and is complaining of
shortness of breath. Please diagnose the
arrhythmia, and answer the 4 questions.
Case 5
Naisan “not a cardiologist”
Garraway
The case
As you are finishing in the E.R. you are
called back to see the man from case 3
(above). He has gone into a new rhythm,
and his blood pressure has dropped
significantly. He is complaining of chest
pain. What do you make of his EKG now?
VT or not?
In 1991 the Brugada Criteria were
published
4 criteria established by the authors, which
were prospectively analyzed in a total of 554
tachycardias with a widened QRS complex
(384 ventricular and 170 supraventricular).
The sensitivity of the four consecutive steps
as 0.987, and the specificity was 0.965.
– Pedro Brugada,et al. Circulation 1991;83:16491659
Step 1: Lack of RS Complex
An RS complex was present in at least one
precordial lead in all SVTs with aberrant
conduction
But only 26% of VTs did not have an RS
complex in any precordial lead.
100% specific for the diagnosis of
ventricular tachycardia.
Step 2: Whether the R to S interval in
any precordial lead is greater than 100
ms
RS interval greater than 100 msec was not
observed in any SVT with aberrant
conduction.
Half of the VTs which did have an RS
complex in at least one precordial lead had
an RS interval less than 100 msec
RS interval of more than 100 msec in any
precordial lead when an RS complex was
present were each 100% specific for the
diagnosis of VT
Step 3: AV Dissociation
When looking at an EKG of a wide
complex tachycardia it is always nice to
see AV dissociation because it is 100%
specific for the diagnosis of VT
Step 4: Morphology Criteria
the morphology criteria are analyzed in
leads V1 and V6
If both leads have a morphology
compatible with the diagnosis of VT, the
diagnosis of VT is made
Tachycardia with a right
bundle branch block-like QRS
Lead V1
Monophasic R or QR or RS favors VT
Triphasic RSR' favors SVT
Lead V6
R to S ratio <1 (R wave smaller than S wave)
favors VT
QS or QR favors VT
Monophasic R favors VT
Triphasic favors SVT
R to S ratio >1 (R wave larger than S wave)favors
SVT
Tachycardia with a left bundle
branch block-like QRS
Lead V1 or V2
Any of following R >30 msec, >60 msec to
nadir S, notched S favors VT
Lead V6
Presence of any Q wave, QR or QS favors
VT
The absence of a Q wave in lead V6 favors
SVT
So lets see…..Step 1
Step 2
110 MS V1
For Fun Step 3
Not sinus, looks like
afib
Afib
Step 4 Morphology
Tachycardia with a left bundle branch
block-like QRS
Lead V1 or V2
– Any of following R >30 msec, >60 msec to
nadir S, notched S favors VT
– R is 40 msec, 70 msec to nadir S
Lead V6
Presence of any Q wave, QR or QS favors
VT
The absence of a Q wave in lead V6 favors
SVT
Another Algorythm
Fusion Beats
Initiation and Termination
The numbers game
Other causes Wide Complex
Causes of VT
Risk Factors
Risk factors included age, past medical
history of cardiovascular or endocrine
diseases, and severity of illness as
assessed by SAPS II and the need for
mechanical ventilation or vasopressor
therapy
– Annane et al, Am J Respir Crit Care Med Vol 178. pp 20–25, 2008
Impact of VT in ICU
A large, prospective, multicenter inception
cohort study showed Ventricular
arrhythmias increased the risk of inhospital mortality and the risk of
neurological sequelae
Annane et al, Am J Respir Crit Care Med Vol 178. pp 20–25, 2008
Survival
In adult ICU patients, ventricular
tachycardia/fibrillation was more common
than pulseless electrical activity. Survival
was highest (39%) with pulseless
electrical activity and lower with
ventricular arrhythmias (33%) and
asystole (24%)
Enohumah et al. Outcome of cardiopulmonary resuscitation
in intensive care units in a university hospital. Resuscitation
2006; 71:161–170.
Treatment
ABC
If unstable Shock/Cardiovert! …….ACLS
If stable determine if VT or not
Multiple medication options
– Amiodarone most common now
– Procainamide 80-90% effective in VT related
to MI
20 min infusion and hypotension common
– Lidocaine generally inefective (Gorgels et al, Am J Cardiol,
1996)
Case 6. (Yoan) * * Difficulty rating. See
EKG 6. You have finally sorted everybody
out, and are leaving the unit for lunch.
However, as you pass by bed 2, the nurse
says the monitor has been spewing out
strips for a while, and she has gotten an
EKG. She asks you to take a quick look.
What do you think of the EKG from this 81
year old woman?
You have finally made it to lunch. As you
eat your chicken stir fry, your med student
notes that every patient you saw this
morning had some kind of arrhythmia.
She wonders if this is typical of all critically
ill patients. You fill her in with answers to
the following questions (Scot)
1. What is the frequency of sustained arrhythmia (i.e.
>30s) in the ICU?
2. Which patients, in general, are most likely to suffer
an arrhythmia?
3. What is the most common arrhythmia in the ICU?
4. What impact does a sustained arrhythmia have on
a patient’s outcome? I.e. is there an impact on
mortality? How about other outcomes?
Incidence of Clinically Significant
Arrhythmias
Annane, 2008; 26 general ICUs over 1
month.
Recorded new, sustained arrhythmias in
1,341 patients, and broke them down as
to type, and risk factors.
Overall, 12% had new onset arrhythmia
during their ICU stay.
Median time to arryhthmia is day 1-2 (as
in post-op patients).
Risk Factors
Patients with arrhythmias were:
– older
– more likely to have past medical history of
cardiovascular, pulmonary, or endocrine
diseases
– were more likely to present with sepsis/septic
shock or other acute cardiovascular disorder
– had higher SAPS II score
– were more likely to be on ventilator or on
vasopressors.
5.3% SVT in non-cardiac diagnoses or chronic arrhythmia (mainly AF)
When adjusting for age and SAPS, SVT not associated with poorer 90
day survival.