Transcript 2008_08_14-Dowling-Shock

Shock
Shawn Dowling, PGY-5
Objectives
Briefly discuss general pathophysiology
Classification of shock
Review of vasopressors
Lots of cases
We will not talk about septic shock - this
will be discussed in a future set of
rounds
Intro
35M. Pulled from an industrial fire.
Brought in by EMS.
Pt is awake, but clearly altered. Only complaint is a
HA. Prev well.
T37, HR 110, BP 160/70, RR 20/100% c/s 7
The nurses have already drawn a venous gas
CO is 18%, lactate is 13
Is this patient in shock?
What do you think is going on?
Lactate > 10 is highly predictive of cyanide toxicity
with inhalational exposure regardless of CO level
Baud FJ, et al: Elevated blood cyanide concentrations in victims of smoke inhalation. N Engl J Med
2001; 325:1761–1766.
How do you want to treat this patient other than
with O2 +/- hyperbarics? Why?
Only give the sodium thiosulfate portion
of the Cyanide Antidote Kit – if you give
them the nitrite component you induce
more of a functional anemia which they
will not tolerate because of the other
functional anemia – the CO
Definition of shock
Rude unhinging of the machinery of life
Or
The inability of the circulatory
system to adequately supply tissues
with 02 & nutrients and remove
cellular waste
Diagnosis of Shock – Rosen’s
Need 4 of 6
Ill appearance or decreased LOC (as a general
rule MAP< 50 before AMS)
HR > 100
RR > 22 or PC02 < 32
Base deficit <-5 or lactate >4
Urine output < 0.5 ml/kg/hr
Hypotension > 20 minute duration
NOTE - ↓BP not required for Dx
Diagnosing Shock
The more advanced the shock state, the easier
the Dx, but…
Significant tissue hypoxia appears to exist prior to
development of significant signs & symptoms
THE BETTER WE CAN RECOGNIZE SHOCK,
THE EARLIER WE CAN INSTITUTE Tx
TIME IS TISSUE (see RIVERS STUDY)
Can be is shock with “normal” vitals
Normal BP in face of hypovolemia means some organs are
hypoperfused to maintain systemic BP
Shock is the transition between life
and death
Shock unifying features:
Imbalance between cellular O2 demand and
supply
Disrupted cellular homeostasis
Failed aerobic metabolism –> anaerobic
metabolism –> lactic acidosis
Calcium shifts - impairs cardiac contractility
Failed ion gradients and cellular pumps
Cell edema and death
How does our body
compensate?
Counter-regulatory mediators
Catecholamines, glucocorticoids,
angiotensin, vasopressin, insulin
Increased substrates
glucose, TG and FFA
Anaerobic metabolism
incr CO2:02 ratio
Pertinent Critical Care
formulas
CO =
HR x SV
BP =
CO x SVR
O2 content =
1.34 x hgb x O2 saturation + 0.003 x Po2
(02 bound to hgb)
(02 in plasma)
Oxygen delivery is the CO x O2 content
Why is this equation so important to a shock talk?
In which shock scenario do we target the O2 in
plasma for treatment?
CO poisoning
What are some different shock
classifications?
Classification of Shock
Many different ways
Mnemonics
Physiologic
Clinical
It doesn’t matter which you use as long as
You know it cold
It’s exhaustive
Shock
BP = ↓CO x ↓SVR
Hypovolemic
Cardiogenic
Obstructive
Distributive
Shock
Shock
Hypovolemic
Cardiogenic
Bleeding or
Fluid Loss
•Overt
•Occult
•Excessive
Losses
•Vessels
•Rhythm
•Valvular
•Myocardium
•Pericardium
Obstructive
•Intravascular
•Extravascular
Distributive
NASTE
Neurogenic
Anaphylactic
Septic
Toxicologic
Endocrine
Hypovolemic
Overt/Occult losses of blood
5 sources of life threatening hemorrhage in
trauma?
Chest, Abdo, Pelvis, Long bones, Street (from
skin)
Excessive Fluid loss
3rd spacing (burns, pancreatitis, dermatologic,
ascites)
Excessive sweating/vomiting/diarrhea/urine
output(diuretics, DI)
Cardiogenic
Vessels
AMI or acute or chronic–
usually need to infarct
40% to cause shock
AoD
Rhythm
Brady
Tachydysthrythmias
Valvular
Stenosis
Regurgitation
Myocardium
Rupture (FW or VSD)
Myocarditis
Cardiomyopathy
RV involvement
Pericardium
Tamponade
Obstructive
Intravascular
PE
Amniotic Fluid Embolism
Air embolism
Fat embolism
Extravascular
Tension PTX
Cardiac tamponade
SVC syndrome
Distributive
Neurogenic
Anaphylactic
Septic
Toxicologic
(CaCB, BB), CO, cyanide, iron, ASA, etc
Endocrine
Adrenal insufficiency, thyroid storm, electrolytes
(hyperK)
Top three causes of shock in infants
Sepsis
Hypovolemic
Cardiac
SHOCK in a neonate
Sepsis
Cardiac
non-Accidental Trauma
Metabolic
Surgical
Physical Exam
Two purposes
1. Try to determine if the patients is in shock
– Look for evidence of end organ damage
2. Determine the cause of the shock
– JVP & perfusion status is VERY helpful
Thanks to ICU Crash Course
Match the shock with the appropriate
vasopressor and why
Sepsis
Neurogenic Shock
Anaphylactic Shock
Epinephrine
Ephedrine
Phenylephrine
Norepinephrine
Dopamine
Milrinone
Direct vs indirect vasopressors
Direct agents stimulate the
receptor directly
Indirect agents have their
effect by stimulating the
adrenals to release
catecholamines
:. If stressor has been ongoing
for a period of time -> body’s
catecholamine reserve is likely
deplete and the indirect agents
will have less effect
Direct
Norepi
Epi
Phenylephrine
Indirect
Dopamine
Dobutamine
Ephedrine
Receptor
Primary location
Primary fx
α
ß1
ß2
D
D=Dopaminergic
Receptor
Primary location
Primary fx
α
Vessel walls
Peripheral Arterial Constriction
ß1
Heart
Inotropy/Chronotropy
ß2
Lungs/Skeletal muscle
Dilatation of smooth muscle
(skeletal and bronchial)
D
Kidneys
Increase renal blood flow
D=Dopaminergic
Cochrane Review:
(updated) Feb. 11, 2005.


For all kinds of shock
RCTs



Levo + dob vs epi (2 studies, N=52)


Levo vs Dop (3 studies, N=62)
RR death 0.88 (0.57,1.36)
RR death 0.98 (0.57,1.67)
Unfortunately, these studies are too small to
definitively answer the question but better data to
support that norepi achieves HD endpoints better
and since it’s a direct agent likely better for septic
patients
Case 1
PP: 8yo F with known allergy to wasps
PMHx: Healthy and no meds
HPI:
At day camp and “forgot” her epi-pen
Stung by 2 hornets after accidentally running into a
nest
Presents by personal vehicle to ED
Given PO Benadryl by family member
Case 1
Generally
Appears unwell and flushed
HR=128, RR=38, T=37.8, BP=85/40, Sat 89% RA
CVS
Tachy, warm extremities
Resp
Significant indrawing
Audible wheeze throughout
No stridor noted
Derm
Urticarial rash and diffuse flushing
ENT
Lip swelling noted and uvula swollen on exam
Case 1
1) Name the general category of shock
2) Describe the pathophysiology
3) Name the management goals
4) Define the best interventions to obtain
the above goals
5) Name potential pitfalls
Case 1
The pediatric nurse is panicked…..
He wants to know how much
Epinephrine you want to give this child
and by what route…..
Case 1
The patient is not responding to your IM
epinephrine
The pressure is 60 systolic and the
patient has become obtunded…..
Case 2
PP:
58yo Male with known shrimp allergy
PMHX
MI 2 years ago
NIDDM
HTN
HPI:
Ate the “egg roll special” at a Thai restaurant
Immediate throat swelling
EMS called and IM epinephrine given on route
Case 2
Generally
Appears flushed and unwell with marked work of breathing and
distress
HR 62, RR 28, BP 80/46, Sat 89% on mask, T37.4
CVS
Normal heart sounds, normal cap refill
Resp
Diffuse wheeze throughout
Abdomen
Soft but mildly tender
Neuro
Starting to appear somnolent
Case 2
You repeat another IM injection of 0.3cc
of 1:1000 epi and give H1 and H2
blockers intravenously
There is no improvement and the
patient remains hypotensive and
relatively bradycardic…..
Case 2
1) Name the general category of shock
2) Describe the pathophysiology
• Difference between anaphylaxis and
anaphylactoid?
3) Name the management goals
4) Define the best interventions to obtain
the above goals
5) Name potential pitfalls
Management
Fluids
Meds
Epi is the first line Tx for anaphylaxis
IV (1:10,000)
1 mL (100ug) aliquot – repeat q60sec until desired effect
Infusion - 1ug/min-4ug/min
If pt not in shock – IM (why not SC?)
Ventolin nebs
Benadryl 50mg IV
Zantac 50mg IV
Solu-medrol 125mg IV
Glucagon (for pts on ßß, ?ACE-I)
1-2mg IV
Then 5-15mcg/min infusion
Inotropic/chronotropic/vasoactive
properties beyond the b-receptor
Case 3
80M. Hx of COPD.
Presents with productive cough and feels unwell.
T-40, RR28, sats 85% on NRB, HR-120, BP 90/50
Working Dx – Pneumonia + Sepsis
You decide you going to intubate this patient because
of failure to oxygenate
Any concerns? How are you going to prepare?
Induction agent? Other meds?
Sepsis and airway
management
Sepsis significantly increases you O2
requirements – therefore these patients can
desaturate quite rapidly – :. Optimize the
conditions (i.e. positioning, pre-oxygenate,
best-intubator, etc)
Use of accessory muscles can ↑O2 consumption
by 50-100%!
Another reason to manage their airway early or if
you are not meeting your physiologic end points
Any other concerns
Post-intubation hypotension
Septic patients are very catecholamine driven
– intubating can remove that stimuli and they
can drop their pressures precipitously
Also, the agents we give for intubation may
play a role
↑ intra-thoracic pressure (from mechanical
ventilation) can drop the preload :. causing
hypotension)
Intubating a septic patient
Pre-oxygenate as much as possible
Pretreat with fluids +/- bicarb if you thing they are really acidotic (no
evidence)
Careful choice of induction agent
Ketamine or ½ dose etomidate (0.15mg/kg) are likely best options, AVOID
propofol
Have some pressors drawn up (phenyl/norepi)
Why not dopamine or ephedrine?
phenylephrine
How do you mix this?
10mg in 100mL bag – draw up 10cc and give 1cc(100Ug)/dose
RSI if no CI (gives you the best look)
http://ca.youtube.com/watch?v=pY8jaG
s7xJ0
Case 3
PP: 38yo Male transfer by STARS
PmHx: Asthma but otherwise healthy
Meds: Ventolin and Flovent PRN
HPI:
Patient riding QUAD in kananaskis country and flipped
+ Helmet and no LOC
Trapped under bike for 10 minutes extrication by friends
STARS scene call
No major blood loss noted on scene
Case 3
Generally
GCS 12/15 patient confused and aggitated
HR 120, BP 81/40, RR 15, Temp 37.2, Sats 92%
CVS
Tachycardic, normal HS, Cap refill 4 seconds, weak thready pulse
Resp
Clear bilaterally but poor inspiratory effort
Abdomen
Diffusely tender to palpation
Soft and not distended
MSK
Pelvis is grossly unstable to palpation
Perineal hematoma noted
Femurs and hips normal to exam
Neuro
PEARL, No signs of depressed skull or basal skull injury
No signs of head trauma
Case 3
1) Name the general category of shock
2) Describe the pathophysiology
3) Name the management goals
4) Define the best interventions to obtain
the above goals
5) Name potential pitfalls
Case 3
You do a ED FAST and it is negative for
free fluid in the abdomen
What do you want to do now?
Case 4
68yo Male with known small cell lung Ca
Meds:
Undergoing outpatient chemotherapy and radiotherapy at
TBCC for last 2 months
HPI:
3 day history of dyspnea, apprehension and mild chest
pain
Presents today feeling very unwell, presyncopal and
markedly short of breath on minimal exertion
Case 4
Generally
Appears unwell and dyspneic, markedly diphoretic
HR 119, RR 24, BP 90/55, Sat 98% RA, Temp 36.9
CVS
Faint HS appreciated, normal S1S2 and no EHS
Extremities cool and cap refill 3-4 seconds, +mottled
Peripheral edema is noted
JVP = 6cm above sternal angle and pulsus paradoxus =
22mmHg
Resp
Chest clear throughout but shallow breaths
Abd
Soft but tender to palpation diffusely
Neuro
Alert but confused and disorientated
DDX of pulsus paradoxus
Cardiac:
pericardial effusion
Tamponade
PE
Cardiogenic shock
Pulmonary:
Asthma
COPD
Tension pneumothorax
Other:
Anaphylaxis
SVC syndrome
EKG
EDUS
Case 4
1) Name the general category of shock
2) Describe the pathophysiology
3) Name the management goals
4) Define the best interventions to obtain
the above goals
5) Name potential pitfalls
Management of Tamponade
Maximize preload
Fluids to ↑ filling pressure
Pressors
(dialysis)
Temporizing
Measures
Uremic pce is an indication
Pericardiocentesis
See remergs.com for how to
(thoracotomy)
If post-traumatic
Definitive
Measures
Case 5
PP: 26yo Female
PMHx: Healthy
HPI:
Involved in motorcycle accident at highway speeds +
Helmet
+ LOC on scene and now GCS 9
STARS transfer and advised hypotensive on route
unresponsive to fluids
Case 5
Generally
GCS 6, collared, not responding to pain
No obvious sites of external bleeding
HR 57, RR 16, BP 79/40, Sats 98% 3L NP, T37.8
CVS
Heart sounds normal, no pedal edema, JVP normal
Warm and dry skin
Resp
Normal
Abdomen
Soft and non-distended
MSK
Pelvis stable
Neuro
PEARL, no signs of depressed or basal skull fracture
Reflexes absent
Poor rectal tone
C-spine xray
Case 5
What is the difference between spinal
shock and neurogenic shock?
Spinal Shock
Concussive injury to the spinal cord
Causes total neurological dysfunction
distal to the site of injury
Usually lasts <24hrs
May persist for several days
The end of spinal shock is heralded by
the return of…..
Bulbocavernousus reflex
Neurogenic Shock
Disruption of sympathetic autonomic
ganglia resulting in loss of vasomotor
tone and lack of reflex tachycardia
Results in hypotension (low SVR)
Bradycardia: can be absolute or relative
Due to unopposed vagal tone to heart
Usually only occurs is lesion is at/above T4
DDx for hypotension & bradycardia
Medications (CaCB, BB, digoxin)
Neurogenic Shock
Adrenal insufficiency
++ vagal tone (yng, intra-abdominal issue)
Case 5
1) Name the general category of shock
2) Describe the pathophysiology
3) Name the management goals
4) Define the best interventions to obtain
the above goals
5) Name potential pitfalls
Management of neurogenic
shock
Fluids – they have relative hypovolemia
Atropine 0.5 mg – 1.0 mg iv
Can try to help with their pressure transiently
Have ready for intubation as they may brady down
2ndary to the vagal response
Pressors
Phenylephrine: 100mcg aliquots is a good
temporizer
Ephedrine is an alternative
Case 6
53yo M
1400 golfing and severe central CP
radiating to R shoulder and SOB
Within minutes was unresponsive and
EMS called
Nitro given and BP ↓↓
Palpable pressure on route
Case 6
Generally
Appears very unwell, pale diaphoretic and cool periphery.
Minimally responsive
HR 108, BP 88/65, Sats 84% non-rebreather, RR 30
CVS
Tachy with no obvious murmur
Cool peripheries and thready pulse
Resp
Diffuse crackles throughout
Pink froth at the mouth
Significant respiratory distress
EKG
Case 6
1) Name the general category of shock
2) Describe the pathophysiology
3) Name the management goals
4) Define the best interventions to obtain
the above goals
5) Name potential pitfall
Shock Post-MI
DDx
Myocardium: pump failure,VSD, FWR, RV infarct
Valvular: acute MR
Rhythm: brady/tachycardia
Other (later): PE, pericardial effusion, stroke,
bleed (from a/c)
Cardiogenic shock
approach
AMI +shock?
RV infarct?
YES
Volume resuscitate
NO
Response adequate
NO
NO
Pulmonary congestion present?
YES
Pressor
YES
Revascularize
Response adequate
YES
NO
IABP and PTCA
Thanks Phil
How does a IABP
work?
Cardiogenic Shock:
Approach
Stabilize the ABCs
Identify etiology of cardiogenic shock
Small fluid bolus (250cc)
Don’t be shy on fluids if RV infarct
Ionotropic/vasopressor support
Manage infarct (avoid ßß & nitrates)
Cath vs lytics
MI + Cardiogenic shock:
How to manage the MI?
Options
Thrombolysis
Get BP up with ionotropes then
thrombolyse
Stabilize with IABP then thrombolyse
Early Revascularization (PTCA or CABG)
What does the literature tell us?
MI + Cardiogenic shock:
How to manage the MI?
Thrombolysis in cardiogenic shock
GISSI (N=280)
streptokinase
medical mx
30 day MR
70.1%
69.6%
NO trial has shown reduction mortality with
cardiogenic shock with thrombolysis
Thanks Rob
SHOCK trial
RCT of AMI + cardiogenic shock
152 early revascularization (PTCA or CABG) or
150 initial medical mx only (lysis initially, some had
PTCA/CABG after 52hrs)
End Point early revasc. Med Mx
stats
30d MR
46.7%
56%
p=.11
6mth MR
50.3%
63.1%
p=.027
Cardiogenic Shock:
the SHOCK trial
Hochman JS. One year survival following
early revascularization for cardiogenic shock.
JAMA 2001.
End Point
early revasc. Med Mx
1yr survival
46.7%
33.6%
stats
p=.03
MI + Cardiogenic shock:
How to manage the MI?
Conclusions …….
Patients with AMI complicated by
cardiogenic shock, especially those <
75yo, should undergo emergent
revascularization (PTCA or CABG)
Bonus Case
78F.
Presents with SOB, hypoxia + hypotension
PMHX: CAD, CHF
VS:HR 110 BP 80/50, RR28, sats 88%RA
JVP up, lungs are clear, no peripheral edema –
poorly perfused
You order a portable CXR
N CXR
What do you think?
What do you want to do?
Which can help you make the Dx?
Empiric heparin
STAT ECHO
while investigating
CT
(if no CI)
– but this patient is not stable enough for CT
As the pCXR is being done the patient finally
stops pestering you with questions about
what you think is going on.
You’re enjoying the silence until you see the
monitor…
What do you want to do know?
Jerjes-Sanchez C. et al. Streptokinase and Heparin versus
Heparin Alone in Massive Pulmonary Embolism: A
Randomised Controlled Trial. Journal of Thrombosis and
Thrombolysis. 1995.
Prospective and randomised trial, N=8
all had “massive” PE and in cardiogenic shock
high prob. V/Q, with abnormal RH on echo or >9
obstructed segments on V/Q
100% survival in streptokinase plus heparin group
100% mortality in heparin group
Small study, lots of limitations BUT one of the few
studies on this
tPA in PE
The role for tPA in submassive PE is debatable – not
a decision for us to make
If the patient is in shock & they have a PE – give tPA
(likely in consultation with ICU)
In the mean time intubate, heparinize + fluids PRN +/pressors
If the patient has a cardiac arrest – give it
tPA dosing
1mg/kg over 2-5 mins if in CA
Over 30mins if perfusing
If stable 100mg over 2 H & ask yourself why you’re giving it in
emerg