Hemodynamic

Monitors
Acid + Base
Fluids + Blood
 • What’s going on with my patient?
Goals • What should I do about it?
 The Patient
• 55 y/o male with hx of COPD (no home O2),
non-ischemic cardiomyopathy (EF 40-45%),
atrial fibrillation on warfarin
• Found to have an increased oxygen requirement
in clinic and productive cough. Febrile to 39.7.
• Drove himself to the ER (because of course he
did) and accidentally ran into an ambulance at
25 mph, causing his airbags to go off
• He was distracted trying to text his mom to watch his
dogs (at least he was wearing his seatbelt)
• GCS 13 though seems kinda confused, wheezing
and coarse breath sounds noted, tachycardic,
abdomen soft, but moderately tender in the
epigastrium and LUQ
So, what’s
going on with
this patient?
Let’s take some measurements
Basic Vitals

123 123

This is a good start but he

just looks pretty sick…

etCO2

93/32 (52) 55
A word on placement of invasive lines…
Blood pressure/SVR/Afterload
• Blood pressure
• Noninvasive methods have been
used to measure blood pressure
and therefore estimate flow
• Commonly performed incorrectly

• Art lines
• Direct measurement of the
pressure in a vessel is hard to beat
• This can be affected too by
vasospasm, clotting, size
mismatch, etc (dampening)
Preload
• CVP
• Reported and something
measurable using similar
technique of pressure bag
• SEVERAL things affect the
reading and make it
unreliable
• Best used as a trend, not a
spot measurement
Cardiac Output
• Pulmonary Artery catheters
(Swan-Ganz) can be useful in
determining volume status
and cardiac output through
thermodilution
• Pulls blood from the most
central circulation possible to
assess total body oxygen
extraction
Swan-Ganz Insertion Procedure
Cardiac Output
• Fick Equation
• Technically should be done
with venous sample from a
PA cath
• Can do a bootleg one from a
CVL but you miss the
coronary sinus (blood that
the heart itself took oxygen
from)
Cardiac Output
• FloTrac
• Can provide a pretty good
estimation of cardiac output
• Limited by lack of direct
measurements
• Useful when you don’t want
to put in a PA cath
Preload/Cardiac Output
• Ultrasound anyone?
• Less invasive, readily available
• Used for placing these lines
anyway
• This is a whole series of
lectures itself, 12 in fact
 Ok, this guy is in Shock….but which kind?

Volume

Shock
O2
Supply-
Demand
Mismatch

Output

…and what’s his Acid-Base Status? RT hands you an ABG…

 What if his ABG shows this….

7.15 20 85 9 -12 2

pH pCO2 pO2 HCO3 BE AG

 What if his ABG shows this….

7.15 80 85 29 2 3

pH pCO2 pO2 HCO3 BE AG

 What if his ABG shows this….

7.05 80 62 6 -19 15

pH pCO2 pO2 HCO3 BE AG

How
should we
interpret
these
numbers?
 6 STEP ABG
EVALUATION
Are these numbers valid?

Acidemia or Alkalemia:
What is the pH?
Do these values look like an ABG?
Is this Respiratory or Metabolic process?
We presume yes. (Look at pCO2, HCO3 & Base Excess)

You can check with the Henderson-Hasselbach Is there Compensation?

Equation but this isn’t Gen Chem 1…
For Metabolic Acidosis:
Is there an Anion Gap?

If there is an Anion Gap:

How does it compare to change in HCO3?
 6 STEP ABG
EVALUATION
Are these numbers valid?

Acidemia or Alkalemia:
pH < 7.35 Acidemia What is the pH?
pH > 7.45 Alkalemia
Is this Respiratory or Metabolic process?
(Look at pCO2, HCO3 & Base Excess)
This is usually the primary disorder
Is there Compensation?
Remember: Acidosis or Alkalosis may be
present even if pH is normal (7.35 – 7.45) For Metabolic Acidosis:
Is there an Anion Gap?

You will need to check the pCO2, HCO3 and If there is an Anion Gap:
How does it compare to change in HCO3?
anion gap (AG)
 6 STEP ABG
EVALUATION
Are these numbers valid?

Acidemia or Alkalemia:
What is the pH?
What is the relationship between the direction
Is this Respiratory or Metabolic process?
of change in the pH and the direction of (Look at pCO2, HCO3 & Base Excess)
change in the pCO2?
Is there Compensation?
Primary Respiratory: pH and pCO2 go opposite
Primary Metabolic: pH and pCO2 go same For Metabolic Acidosis:
Is there an Anion Gap?

Respiratory compensation is more immediate If there is an Anion Gap:

How does it compare to change in HCO3?
Metabolic compensation takes days
 6 STEP ABG
EVALUATION
Are these numbers valid?

Acidemia or Alkalemia:
What is the pH?
Is there appropriate compensation for the
primary disturbance? Usually, compensation Is this Respiratory or Metabolic process?
(Look at pCO2, HCO3 & Base Excess)
does not return the pH to normal (7.35 – 7.45)
Is there Compensation?
Metab. Acidosis: PaCO2 = (1.5 x [HCO3-]) +8 +2
For Metabolic Acidosis:
Acute Resp. Acidosis: HCO3- = (∆ PaCO2 /10) +3 Is there an Anion Gap?

If there is an Anion Gap:

(There are other formulas for other situations, but these are the How does it compare to change in HCO3?
most commonly used)
 6 STEP ABG
EVALUATION
Are these numbers valid?

Acidemia or Alkalemia:
What is the pH?
Calculate the anion gap
Is this Respiratory or Metabolic process?
(if a metabolic acidosis exists): (Look at pCO2, HCO3 & Base Excess)
AG= [Na+]-( [Cl-] + [HCO3-] )-12 ± 2
Is there Compensation?
Note: Epic does this part for you on BMPs
For Metabolic Acidosis:
Is there an Anion Gap?
Normal AG= 12
(2.5 meq/L lower for each 1g/dL in Albumin If there is an Anion Gap:
How does it compare to change in HCO3?
 6 STEP ABG
EVALUATION
Are these numbers valid?

If an increased anion gap is present, compare the Acidemia or Alkalemia:

What is the pH?
increase in the anion gap and the decrease in HCO3
Is this Respiratory or Metabolic process?
<1.0 means another, non-gap acidosis is present (Look at pCO2, HCO3 & Base Excess)

1.0-2.0 means uncomplicated AG acidosis

Is there Compensation?
>2.0 means a metabolic alkalosis is present
For Metabolic Acidosis:
Delta:Delta: ∆ HCO3 : (∆ AG /[∆ HCO3-]) Is there an Anion Gap?

If there is an Anion Gap:

(∆ AG /[∆ HCO3-]) = (12 - AG / HCO3 - 24) How does it compare to change in HCO3?
12 and 24 being the assumed normal values
 What if his ABG shows this….

7.15 20 85 9 -12 2

pH pCO2 pO2 HCO3 BE AG

Metab. Acidosis: PaCO2 = (1.5 x [HCO3-]) +8 +2

 What if his ABG shows this….

7.15 80 85 29 2 3

pH pCO2 pO2 HCO3 BE AG

Acute Resp. Acidosis: HCO3- = (∆ PaCO2 /10) +3

 What if his ABG shows this….

7.05 80 62 6 -19 15

pH pCO2 pO2 HCO3 BE AG

Metab. Acidosis: PaCO2 = (1.5 x [HCO3-]) +8 +2
Acute Resp. Acidosis: HCO3- = (∆ PaCO2 /10) +3
Delta:Delta: ∆ HCO3- : = (∆ AG /[∆ HCO3-])
 What his ABG actually shows is….

7.05 80 62 6 -19 3

pH pCO2 pO2 HCO3 BE AG

Metab. Acidosis: PaCO2 = (1.5 x [HCO3-]) +8 +2

Acute Resp. Acidosis: HCO3- = (∆ PaCO2 /10) +3
Ok, so mixed metabolic and Volume

respiratory acidosis
Shock

Could be a COPD
O2
Supply-
Demand
Mismatch

exacerbation plus
hypovolemic/distributive
components from sepsis Output

and possible trauma

Now, what
are we going
to do about
this?
Let’s start with some BiPAP and
volume resuscitation
“Which fluid
do you want
me to pull,
Doc?”
- Trusty, RN
 History of IV fluid therapy

US Civil War Hamburger’s Penicillin first PlasmaLyte FDA

0.9% NS used in patients Approved

O’Shoughnessy’s Ringer’s Tap Lactate added to Disco, baby! SALT-ED/SMART

Solution for Cholera Water for Frog Ringer’s trials
& Bloodletting victims Hearts
(Ab)Normal Saline
• pH: 5.6!
• Composition:
• Na – 154 meq/L
• Cl – 154 meq/L
• mOsm - 308
Lactated Ringer’s
• pH: 6.5
• Composition:
• Na – 130 meq/L
• Cl – 154 meq/L
• K - 4 meq/L
• Ca – 2.7 meq/L
• Lactate – 28 meq/L
• mOsm – 308
Plasmalyte
• pH: 7.4
• Composition:
• Na – 140 meq/L
• Cl – 93 meq/L
• K - 5 meq/L
• Mg – 3 meq/L
• Acetate – 27 meq/L
• Gluconate – 23 meq/L
• mOsm – 294
What about Albumin?
• pH: 6.4-7.4
• Composition:
• Na – 130-160 meq/L meq/L
• Albumin – 12.5g in a 250 5% bottle
• The variable sodium content can
really add up over time
No mortality benefit to albumin > CXL Fewer adverse kidney events with Reduced mortality AND kidney events
balanced crystalloids in hypovolemic ICU patients

SALT-ED, SMART, & CRISTAL Trials

Hetastarch
• A nice thought experiment
• In fact, actively more harmful in Sepsis
• Increased renal failure 
• Increased mortality 
The Patient

• We fixed him! BP is now 150/91

• But then….our patient takes a downturn
• He appears significantly more pale,
arterial line pressures have dropped and
his abdomen is more distended
• FAST exam positive for free fluid in the
LUQ
• Diagnosis? On top of his sepsis and COPD
exacerbation? Presumed splenic
rupture…oh, dear…
 OK, so what about bleeding?
Well, blood is technically a fluid too Dr Smarty-pants, so I was planning to talk
about this all along - Ha!
 History of blood product replacement

Halstead transfuses Charles Drew

own blood into Blood 1:1 ratio from
appointed to US Military
American sister then operates American Red fractionation “Crystalloid
Revolution on her standardized Convenience” experience
Cross

Post-partum ABO groups Disco, baby! RCT of permissive RCT of DCR

Lower gives
bleeding identified strategy in
sheep blood hypotension
to a mentally treated with spousal Trauma
ill man Blood donor blood
transfusions
banned!
• Minimize crystalloid
• Causes capillary leak
• Makes endothelium less efficient
• Lowers pH
• Dilutes coag. factors
• COLD!
• Permissive hypotension
(palpable or SBP 90)
• Otherwise clots CAN break loose
• 1:1:1 ratio
• They are bleeding whole blood, so give
that back
CRASH Trials and other blood adjuncts
• Transaxemic acid (TXA) is an antifibrinolytic that supposedly prevents
what clots you do have from breaking up
• Cheap, available worldwide and nebulizable

“Effects of tranexamic acid on death, disability, vascular occlusive

events and other morbidities in patients with _____________”
• significant haemorrhage (CRASH-2)
• Helpful if given to bleeding people within 3 hrs of injury
• acute traumatic brain injury (CRASH-3)
• No real mortality benefit in head trauma
Hemoglobin-based O2 Carriers
• What about cow hemoglobin
in little spheres?
• Typeless and pathogen free
• OK with most JW patients
• This is great, right?
• All trials halted for increased
adverse events/mortality 
• Some design flaws though…
• Approved in South Africa and
only for “compassionate use”
in USA
Perfluorocarbons
• What about a totally non-biologic
oxygen carrying fluid?
• Doesn’t do much for volume
expansion
• Has been shown to reduce
ischemic injury in several models
• Stroke
• CAD/STEMI
• Asphyxia
• Spinal cord injury
• Cardiac arrest
OK, so what about a lot of
bleeding?
…..like, really, really bleeding
…like, wow they’re still bleeding…
HELP!
REBOA
• Indications
• PEA arrest (<10 minutes) secondary to
exsanguination from sub-diaphragmatic
haemorrhage and femoral vessels immediately
identifiable on ultrasound (if not identifiable
consider emergency thoracotomy), or
• severe hypovolaemic shock and a systolic
blood pressure <70mmHg, or
• those in an agonal state due to non-
compressible exsanguinating haemorrhage,
who are non/partial responders to rapid
volume resuscitation and have had causes of
obstructive shock excluded, and:
• suspected or diagnosed intra-abdominal
haemorrhage due to blunt trauma or
penetrating torso injuries (Zone I REBOA), or
• blunt trauma patients with suspected pelvic
fracture and isolated pelvic haemorrhage (Zone
III REBOA), or
• patients with penetrating injury to the pelvic or
groin area with uncontrolled haemorrhage from
a junctional vascular injury (iliac or common
femoral vessels) (Zone III REBOA)
REBOA
• Contraindications
• Age >70y
• PEA arrest (<10 minutes) secondary
to exsanguination from sub-
diaphragmatic haemorrhage and
femoral vessels not immediately
identifiable on ultrasound
• Cardiac arrest due to causes other
than exsanguination due to severe
subdiaphragmatic trauma
• PEA arrest >10 minutes
• High clinical/radiological suspicion
of proximal traumatic aortic
dissection
• Pre-existing terminal illness or
significant comorbidities
REBOA insertion
We have Resuscitation!
Patient is temporized and Trauma is really rather impressed by our efforts to
stop this bleeding while the patient is rushed to the OR for emergent ex-lap,
packing and splenectomy and everyone high-fives at the end of the case