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SHOCK & IV FLUIDS

Dr. Ahmed Khan Sangrasi


Associate Professor, Department of
Surgery,
LUMHS Jamshoro

Shock

Shock is a life threatening medical


condition that occurs due to inadequate
substrate for aerobic cellular respiration.
Shock is a common end point of many
medical conditions and one of the most
common causes of death for critically ill
people

Objectives

Definition
Approach to the hypotensive patient
Types
Specific treatments

Definition of Shock

Inadequate oxygen delivery to meet


metabolic demands
Results in global tissue
hypoperfusion and metabolic
acidosis
Shock can occur with a normal blood
pressure and hypotension can occur
without shock

Understanding Shock

Inadequate systemic oxygen delivery


activates autonomic responses to
maintain systemic oxygen delivery

Sympathetic nervous system

NE, epinephrine, dopamine, and cortisol release

Causes vasoconstriction, increase in HR, and increase of


cardiac contractility (cardiac output)

Renin-angiotensin axis

Water and sodium conservation and


vasoconstriction
Increase in blood volume and blood pressure

Understanding Shock

Cellular responses to decreased systemic


oxygen delivery
ATP depletion ion pump dysfunction
Cellular edema
Hydrolysis of cellular membranes and cellular
death
Goal is to maintain cerebral and cardiac
perfusion
Vasoconstriction of splanchnic,
musculoskeletal, and renal blood flow
Leads to systemic metabolic lactic acidosis that
overcomes the bodys compensatory
mechanisms

Global Tissue Hypoxia

Endothelial inflammation and disruption


Inability of O2 delivery to meet demand
Result:

Lactic acidosis
Cardiovascular insufficiency
Increased metabolic demands

Multiorgan Dysfunction
Syndrome (MODS)

Progression of physiologic effects as


shock ensues

Cardiac depression
Respiratory distress
Renal failure
DIC

Result is end organ failure

1. ANTICIPATION STAGE

2. PRE-SHOCK STAGE

3. COMENSATED SHOCK STAGE

4. DECOMPENSATED SHOCK STAGE (REVERSABLE)

5. DECOMPENSATED SHOCK STAGE (IRREVERSABLE)

Approach to the Patient in


Shock

ABCs

Cardiorespiratory monitor
Pulse oximetry
Supplemental oxygen
IV access
ABG, labs
Foley catheter
Vital signs including rectal temperature

Diagnosis

Physical exam (VS, mental status, skin color,


temperature, pulses, etc)
Infectious source
Labs:

CBC
Chemistries
Lactate
Coagulation studies
Cultures
ABG

Further Evaluation

CT of head/sinuses
Lumbar puncture
Wound cultures
Acute abdominal series
Abdominal/pelvic CT or US
Cortisol level
Fibrinogen, FDPs, D-dimer

Approach to the Patient in


Shock

History

Recent illness
Fever
Chest pain, SOB
Abdominal pain
Comorbidities
Medications
Toxins/Ingestions
Recent hospitalization
or surgery
Baseline mental status

Physical
examination

Vital Signs
CNS mental status
Skin color, temp,
rashes, sores
CV JVD, heart sounds
Resp lung sounds,
RR, oxygen sat, ABG
GI abd pain, rigidity,
guarding, rebound
Renal urine output

Is This Patient in Shock?

Patient looks ill


Altered mental status
Skin cool and
mottled or hot and
flushed
Yes!
Weak or absent
These are all signs
peripheral pulses
and symptoms of
SBP <110
shock
Tachycardia

Shock

Do you remember how to


quickly estimate blood
pressure by pulse?

If you palpate a
pulse,
you know SBP is at
least this number

60

70
80

90

Goals of Treatment

ABCDE

Airway
control work of Breathing
optimize Circulation
assure adequate oxygen Delivery
achieve End points of resuscitation

Airway

Determine need for intubation but


remember: intubation can worsen
hypotension

Sedatives can lower blood pressure


Positive pressure ventilation decreases preload

May need volume resuscitation prior to


intubation to avoid hemodynamic collapse

Control Work of Breathing

Respiratory muscles consume a


significant amount of oxygen
Tachypnea can contribute to lactic
acidosis
Mechanical ventilation and sedation
decrease WOB and improves survival

Optimizing Circulation

Isotonic crystalloids
Titrated to:

CVP 8-12 mm Hg
Urine output 0.5 ml/kg/hr (30 ml/hr)
Improving heart rate

May require 4-6 L of fluids


No outcome benefit from colloids

Maintaining Oxygen
Delivery

Decrease oxygen demands

Maintain arterial oxygen saturation/content

Provide analgesia and anxiolytics to relax


muscles and avoid shivering
Give supplemental oxygen
Maintain Hemoglobin > 10 g/dL

Serial lactate levels or central venous


oxygen saturations to assess tissue oxygen
extraction

End Points of Resuscitation

Goal of resuscitation is to maximize


survival and minimize morbidity
Use objective hemodynamic and
physiologic values to guide therapy
Goal directed approach

Urine output > 0.5 mL/kg/hr


CVP 8-12 mmHg
MAP 65 to 90 mmHg
Central venous oxygen concentration > 70%

Persistent Hypotension

Inadequate volume
resuscitation
Pneumothorax
Cardiac tamponade
Hidden bleeding
Adrenal insufficiency
Medication allergy

Practically Speaking.

Keep one eye on these patients


Frequent vitals signs:

Monitor success of therapies


Watch for decompensated shock

Let your nurses know that these patients


are sick!

Types of Shock

Hypovolemic
Cardiogenic
Septic
Anaphylactic
Neurogenic
Endocrine
Obstructive

What Type of Shock is This?


Types of Shock
68 yo M with hx of HTN and
Hypovolemic
DM presents to the ER with
abrupt onset of diffuse
Septic
abdominal pain with radiation
to his low back. The pt is
Cardiogenic
hypotensive, tachycardic,
afebrile, with cool but dry skin Anaphylactic
Neurogenic
Obstructive
Hypovolemic Shock

Hypovolemic Shock

Hypovolemic Shock

Non-hemorrhagic

Vomiting
Diarrhea
Bowel obstruction, pancreatitis
Burns
Neglect, environmental (dehydration)

Hemorrhagic

GI bleed
Trauma
Massive hemoptysis
AAA rupture
Ectopic pregnancy, post-partum bleeding

Hypovolemic Shock

ABCs
Establish 2 large bore IVs or a central line
Crystalloids

PRBCs

Normal Saline or Lactate Ringers


Up to 3 liters
O negative or cross matched

Control any bleeding


Arrange definitive treatment

Evaluation of Hypovolemic
Shock

CBC
ABG/lactate
Electrolytes
BUN, Creatinine
Coagulation
studies
Type and crossmatch

As indicated

CXR
Pelvic x-ray
Abd/pelvis CT
Chest CT
GI endoscopy
Bronchoscopy
Vascular radiology

Infusion Rates
Access
18 g peripheral IV
16 g peripheral IV
14 g peripheral IV
8.5 Fr CV cordis
mL/min

Gravity

Pressure

50 mL/min
150 mL/min
100 mL/min 225 mL/min
150 mL/min 275 mL/min
200 mL/min
450

What Type of Shock is This?

An 81 yo F resident of a
nursing home presents to the
ED with altered mental status.
She is febrile to 39.4,
hypotensive with a widened
pulse pressure, tachycardic,
with warm extremities

Septic

Types of Shock
Hypovolemic
Septic
Cardiogenic
Anaphylactic
Neurogenic
Obstructive

Septic Shock

Sepsis

Two or more of SIRS criteria

Temp > 38 or < 36 C


HR > 90
RR > 20
WBC > 12,000 or < 4,000

Plus the presumed existence of infection


Blood pressure can be normal!

Septic Shock

Sepsis (remember definition?)


Plus refractory hypotension

After bolus of 20-40 mL/Kg patient still has


one of the following:
SBP

< 90 mm Hg
MAP < 65 mm Hg
Decrease of 40 mm Hg from baseline

Sepsis

Pathogenesis of Sepsis

Nguyen H et al. Severe Sepsis and Septic-Shock: Review of the Literature and Emergency Department Management Guidelines. Ann Emerg Med.

Septic Shock

Clinical signs:

Hyperthermia or hypothermia
Tachycardia
Wide pulse pressure
Low blood pressure (SBP<90)
Mental status changes

Beware of compensated shock!

Blood pressure may be normal

Ancillary Studies

Cardiac monitor
Pulse oximetry
CBC, Chem 7, coags, LFTs, lipase, UA
ABG with lactate
Blood culture x 2, urine culture
CXR
Foley catheter (why do you need this?)

Treatment of Septic Shock

2 large bore IVs

NS IVF bolus- 1-2 L wide open (if no


contraindications)

Supplemental oxygen
Empiric antibiotics, based on suspected
source, as soon as possible

Treatment of Sepsis

Antibiotics- Survival correlates with how


quickly the correct drug was given
Cover gram positive and gram negative
bacteria

Zosyn 3.375 grams IV and ceftriaxone 1 gram IV or


Imipenem 1 gram IV

Add additional coverage as indicated

Pseudomonas- Gentamicin or Cefepime


MRSA- Vancomycin
Intra-abdominal or head/neck anaerobic infectionsClindamycin or Metronidazole
Asplenic- Ceftriaxone for N. meningitidis, H. infuenzae
Neutropenic Cefepime or Imipenem

Persistent Hypotension

If no response after 2-3 L IVF, start a


vasopressor (norepinephrine,
dopamine, etc) and titrate to effect
Goal: MAP > 60
Consider adrenal insufficiency:
hydrocortisone 100 mg IV

Treatment
Algorithm

Rivers E et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock N Engl J Med.

What Type of Shock is This?

Types of Shock
A 55 yo M with hx of HTN,
Hypovolemic
DM presents with
crushing substernal CP,
Septic
diaphoresis, hypotension,
Cardiogenic
tachycardia and cool,
clammy extremities
Anaphylactic
Neurogenic
Cardiogenic Obstructive

Cardiogenic Shock

Cardiogenic Shock

Defined as:

SBP < 90 mmHg


CI < 2.2 L/m/m2
PCWP > 18
mmHg

Signs:

Cool, mottled skin


Tachypnea
Hypotension
Altered mental
status
Narrowed pulse
pressure
Rales, murmur

Etiologies

What are some causes of cardiogenic shock?


AMI
Sepsis
Myocarditis
Myocardial contusion
Aortic or mitral stenosis, HCM
Acute aortic insufficiency

Pathophysiology of Cardiogenic
Shock

Often after ischemia, loss of LV


function

Lose 40% of LV

clinical shock ensues

CO reduction = lactic acidosis, hypoxia


Stroke volume is reduced

Tachycardia develops as compensation


Ischemia and infarction worsens

Ancillary Tests

EKG
CXR
CBC, Chem 10, cardiac enzymes,
coagulation studies
Echocardiogram

Treatment of Cardiogenic
Shock

Goals- Airway stability and improving


myocardial pump function
Cardiac monitor, pulse oximetry
Supplemental oxygen, IV access
Intubation will decrease preload and
result in hypotension

Be prepared to give fluid bolus

Treatment of Cardiogenic
Shock

AMI

RV infarct

Aspirin, beta blocker, morphine, heparin


If no pulmonary edema, IV fluid challenge
If pulmonary edema
Dopamine will HR and thus cardiac work
Dobutamine May drop blood pressure
Combination therapy may be more effective
PCI or thrombolytics
Fluids and Dobutamine (no NTG)

Acute mitral regurgitation or VSD

Pressors (Dobutamine and Nitroprusside)

What Type of Shock is This?

Types of Shock
A 34 yo F presents to the ER after
Hypovolemic
dining at a restaurant where shortly
after eating the first few bites of her
Septic
meal, became anxious, diaphoretic,
began wheezing, noted diffuse
Cardiogenic
pruritic rash, nausea, and a
sensation of her throat closing off. Anaphylactic
She is currently hypotensive,
tachycardic and ill appearing.
Neurogenic
Obstructive

Anaphalactic

Anaphalactic Shock

Anaphylactic Shock

Anaphylaxis a severe systemic


hypersensitivity reaction characterized
by multisystem involvement

IgE mediated

Anaphylactoid reaction clinically


indistinguishable from anaphylaxis, do
not require a sensitizing exposure

Not IgE mediated

Anaphylactic Shock

What are some symptoms of anaphylaxis?


First- Pruritus, flushing, urticaria appear

Next- Throat fullness, anxiety, chest


tightness,
shortness of breath
and lightheadedness
Finally- Altered mental status, respiratory
distress and circulatory collapse

Anaphylactic Shock

Risk factors for fatal anaphylaxis

Reoccurrence rates

Poorly controlled asthma


Previous anaphylaxis
40-60% for insect stings
20-40% for radiocontrast agents
10-20% for penicillin

Most common causes

Antibiotics
Insects
Food

Anaphylactic Shock

Mild, localized urticaria can progress to full


anaphylaxis
Symptoms usually begin within 60 minutes of
exposure
Faster the onset of symptoms = more severe reaction
Biphasic phenomenon occurs in up to 20% of patients

Symptoms return 3-4 hours after initial reaction has cleared

A lump in my throat and hoarseness heralds lifethreatening laryngeal edema

Anaphylactic ShockDiagnosis

Clinical diagnosis

Defined by airway compromise,


hypotension, or involvement of
cutaneous, respiratory, or GI systems

Look for exposure to drug, food, or


insect
Labs have no role

Anaphylactic Shock- Treatment

ABCs

Angioedema and respiratory compromise


require immediate intubation

IV, cardiac monitor, pulse oximetry


IVFs, oxygen
Epinephrine
Second line

Corticosteriods
H1 and H2 blockers

Anaphylactic Shock- Treatment

Epinephrine

0.3 mg IM of 1:1000 (epi-pen)


Repeat every 5-10 min as needed
Caution with patients taking beta blockers- can cause
severe hypertension due to unopposed alpha
stimulation
For CV collapse, 1 mg IV of 1:10,000
If refractory, start IV drip

Anaphylactic Shock Treatment

Corticosteroids

Antihistamines

H1 blocker- Diphenhydramine 25-50 mg IV


H2 blocker- Ranitidine 50 mg IV

Bronchodilators

Methylprednisolone 125 mg IV
Prednisone 60 mg PO

Albuterol nebulizer
Atrovent nebulizer
Magnesium sulfate 2 g IV over 20 minutes

Glucagon

For patients taking beta blockers and with refractory hypotension


1 mg IV q5 minutes until hypotension resolves

Anaphylactic Shock Disposition

All patients who receive epinephrine


should be observed for 4-6 hours
If symptom free, discharge home
If on beta blockers or h/o severe reaction
in past, consider admission

What Type of Shock is This?

Types of Shock
A 41 yo M presents to the ER
Hypovolemic
after an MVC complaining of
decreased sensation below
Septic
his waist and is now
Cardiogenic
hypotensive, bradycardic,
with warm extremities
Anaphylactic
Neurogenic
Neurogenic Obstructive

Neurogenic Shock

Neurogenic Shock

Occurs after acute spinal cord injury


Sympathetic outflow is disrupted leaving
unopposed vagal tone
Results in hypotension and bradycardia
Spinal shock- temporary loss of spinal
reflex activity below a total or near total
spinal cord injury (not the same as
neurogenic shock, the terms are not
interchangeable)

Neurogenic Shock

Loss of sympathetic tone results in warm


and dry skin
Shock usually lasts from 1 to 3 weeks
Any injury above T1 can disrupt the
entire sympathetic system

Higher injuries = worse paralysis

Neurogenic ShockTreatment

A,B,Cs

Fluid resuscitation

Remember c-spine precautions


Keep MAP at 85-90 mm Hg for first 7 days
Thought to minimize secondary cord injury
If crystalloid is insufficient use vasopressors

Search for other causes of hypotension


For bradycardia

Atropine
Pacemaker

Neurogenic ShockTreatment

Methylprednisolone

Used only for blunt spinal cord injury


High dose therapy for 23 hours
Must be started within 8 hours
Controversial- Risk for infection, GI bleed

What Type of Shock is This?

A 24 yo M presents to the
ED after an MVC c/o chest
pain and difficulty breathing.
On PE, you note the pt to be
tachycardic, hypotensive,
hypoxic, and with decreased
breath sounds on left

Obstructive

Types of Shock
Hypovolemic
Septic
Cardiogenic
Anaphylactic
Neurogenic
Obstructive

Obstructive Shock

Obstructive Shock

Tension pneumothorax

Air trapped in pleural space with 1 way


valve, air/pressure builds up
Mediastinum shifted impeding venous
return
Chest pain, SOB, decreased breath sounds
No tests needed!
Rx: Needle decompression, chest tube

Obstructive Shock

Cardiac tamponade

Blood in pericardial sac prevents venous


return to and contraction of heart
Related to trauma, pericarditis, MI
Becks triad: hypotension, muffled heart
sounds, JVD
Diagnosis: large heart CXR, echo
Rx: Pericardiocentisis

Obstructive Shock

Pulmonary embolism

Virscow triad: hypercoaguable, venous


injury, venostasis
Signs: Tachypnea, tachycardia, hypoxia
Low risk: D-dimer
Higher risk: CT chest or VQ scan
Rx: Heparin, consider thrombolytics

Obstructive Shock

Aortic stenosis

Resistance to systolic ejection causes


decreased cardiac function
Chest pain with syncope
Systolic ejection murmur
Diagnosed with echo
Vasodilators (NTG) will drop pressure!
Rx: Valve surgery

FLUID THERAPY

Fluid and
electrolyte
balance is an
extremely
complicated
thing.

Importance

Need to make a decision regarding fluids


in pretty much every hospitalized patient.
Aggressive IV fluids are recommended in
most types of shock eg. 1-2 litres of NS
bolus over 10mins or 20ml/kg in a child
Can be life-saving in certain conditions
Choice of IV fluid whether crystalloid or
colloid is superior: remains undetermined
For persistent shock after initial
resuscitation, packed RBCs should be
given to keep Hb% > 100gms

loss of body water, whether acute or chronic,


can cause a range of problems from mild
lightheadedness to convulsions, coma, and in
some cases, death.
Though fluid therapy can be a lifesaver, it's
never innocuous, and can be very harmful.
Permissive hypotension: For haemorrhagic
shock current evidence supports that, limiting
the use of fluids for penetrating thorax and
abdominal injuries allowing mild hypotension.
(Target: MAP of 60mmHg, SBP: 70-90 mmHg

Kinds of IV Fluid solutions

Hypotonic - 1/2NS
Isotonic - NS, LR, albumen
Hypertonic Hypertonic saline.
Crystalloid
Colloid

Crystalloid vs Colloid
Type of particles (large or small)

Fluids with small crystalizable particles


like NaCl are called crystalloids
Fluids with large particles like albumin are
called colloids, these dont (quickly) fit
through vascular pores, so they stay in the
circulation and much smaller amounts can
be used for same volume expansion.
(250ml Albumin = 4 L NS)

Edema resulting from these also tends to stick


around longer for same reason.
Albumin can also trigger anaphylaxis.

There are two components to fluid


therapy:
Maintenance therapy replaces normal
ongoing losses, and
Replacement therapy corrects any
existing water and electrolyte deficits.

Maintenance therapy

Maintenance therapy is usually undertaken


when the individual is not expected to eat
or drink normally for a longer time (eg,
perioperatively or on a ventilator).
Big picture: Most people are NPO for 12
hours each day.
Patients who wont eat for one to two
weeks should be considered for parenteral
or enteral
nutrition.

Maintenance Requirements can be broken


into water and electrolyte requirements:

Water

Two liters of water per day are generally


sufficient for adults;
Most of this minimum intake is usually derived
from the water content
of food and the water of oxidation, therefore
it has been estimated that only 500ml of water
needs be imbibed given normal diet and no
increased losses.
These sources of water are markedly reduced in
patients who are not eating and so must be
replaced by maintenance fluids.

water requirements increase with:


fever, sweating, burns, tachypnea,
surgical drains, polyuria, or ongoing
significant
gastrointestinal losses.
For example, water requirements increase
by 100 to 150 mL/day for each C degree
of body temperature elevation.

Several formulas can be used to calculate maintenance fluid


rates.

4/2/1 rule a.k.a


Weight+40

I prefer the 4/2/1 rule (with a 120 mL/h


limit) because it is the same as for
pediatrics.

4/2/1 rule
4 ml/kg/hr for first 10 kg (=40ml/hr)
then 2 ml/kg/hr for next 10 kg (=20ml/hr)
then 1 ml/kg/hr for any kgs over that
This always gives 60ml/hr for first 20 kg
then you add 1 ml/kg/hr for each kg over 20 kg

This boils down to: Weight in kg + 40 = Maintenance IV


rate/hour.
For any person weighing more than 20kg

What to put in the fluids

Start: D5 1/2NS+20 meq K @


Wt+40/hr

a reasonable approach is to start 1/2 normal saline to which 20 meq


of potassium chloride is added per liter.
(1/2NS+20 K @ Wt+40/hr)

Glucose in the form of dextrose (D5) can be added to provide some


calories while the patient is NPO.

The normal kidney can maintain sodium and potassium balance over
a wide range of intakes.

So,start:
D5 1/2NS+20 meq K

at a rate equal to their weight + 40ml/hr, but no greater than


120ml/hr.
then adjust as needed, see next page.

Start D5
adjust:

1/2NS+20 meq K, then

If sodium falls, increase the


concentration (eg, to NS)
If sodium rises, decrease the
concentration (eg, 1/4NS)
If the plasma potassium starts to fall,
add more potassium.
If things are good, leave things alone.

Usually kidneys regulate well, but:


Altered homeostasis in the
hospital
In the hospital, stress, pain, surgery can

alter the normal mechanisms.


Increased aldosterone, Increased ADH
They generally make patients retain
more water and salt, increase tendency
for edema, and become hypokalemic.

Now onto Part 2 of the presentation:

Hypovolemia

Hypovolemia or FVD is result of water &


electrolyte loss
Compensatory mechanisms include:
Increased sympathetic nervous system
stimulation with an increase in heart
rate & cardiac contraction; thirst;
plus release of ADH & aldosterone
Severe case may result in hypovolemic
shock or prolonged case may cause renal
failure

Causes of
FVD=hypovolemia:

Gastrointestinal losses: N/V/D


Renal losses: diuretics
Skin or respiratory losses: burns
Third-spacing: intestinal obstruction,
pancreatitis

Replacement therapy.

A variety of disorders lead to fluid losses


that deplete the extracellular fluid .
This can lead to a potentially fatal
decrease in tissue perfusion.
Fortunately, early diagnosis and
treatment can restore normovolemia in
almost all cases.

There is no easy formula for assessing the degree


of hypovolemia.
Hypovolemic Shock, the most severe form of
hypolemia, is characterized by tachycardia, cold,
clammy extremities, cyanosis, a low urine output
(usually less than 15 mL/h), and agitation and
confusion due to reduced cerebral blood flow.
This needs rapid treatment with isotonic fluid
boluses (1-2L NS), and assessment and
treatment of the underlying cause.
But hypovolemia that is less severe and therefore
well compensated is more difficult to accurately
assess.

History for assessing


hypovolemia

The history can help to determine the presence and etiology of


volume depletion.
Weight loss!
Early complaints include lassitude, easy fatiguability, thirst,
muscle cramps, and postural dizziness.
More severe fluid loss can lead to abdominal pain, chest pain, or
lethargy and confusion due to ischemia of the mesenteric,
coronary, or cerebral vascular beds, respectively.
Nausea and malaise are the earliest findings of hyponatremia, and
may be seen when the plasma sodium concentration falls below
125 to 130 meq/L. This may be followed by headache, lethargy,
and obtundation
Muscle weakness due to hypokalemia or hyperkalemia
Polyuria and polydipsia due to hyperglycemia or severe
hypokalemia
Lethargy, confusion, seizures, and coma due to hyponatremia,
hypernatremia, or hyperglycemia

Basic signs of hypovolemia

Urine output, less than 30ml/hr


Decreased BP, Increase pulse

Physical exam for assessing


volume

physical exam in general is not sensitive or specific


acute weight loss; however, obtaining an accurate weight over
time may be difficult
decreased skin turgor - if you pinch it it stays put
dry skin, particularly axilla
dry mucus membranes
low arterial blood pressure (or relative to patient's usual BP)
orthostatic hypotension can occur with significant hypovolemia;
but it is also common in euvolemic elderly subjects.
decreased intensity of both the Korotkoff sounds (when the blood
pressure is being measured with a sphygmomanometer) and the
radial pulse ("thready") due to peripheral vasoconstriction.
decreased Jugular Venous Pressure
The normal venous pressure is 1 to 8 cmH2O, thus, a low value
alone may be normal and does not establish the diagnosis of
hypovolemia.

SIGNS & SYMPTOMS OF Fluid


Volume Excess

SOB & orthopnea


Edema & weight gain
Distended neck veins & tachycardia
Increased blood pressure
Crackles & wheezes
pleural effusion

Which brings us to:


Labnormalities seen with
hypovolemia
a variety of changes in urine and blood
often accompany extracellular volume
depletion.
In addition to confirming the presence of
volume depletion, these changes may
provide important clues to the etiology.

BUN/Cr

BUN/Cr ratio normally around 10


Increase above 20 suggestive of prerenal
state
(rise in BUN without rise in Cr called
prerenal azotemia.)
This happens because with a low pressure
head proximal to kidney, because urea
(BUN) is resorbed somewhat, and
creatinine is secreted somewhat as well

Hgb/Hct

Acute loss of EC fluid volume causes


hemoconcentration (if not due to blood
loss)
Acute gain of fluid will cause
hemodilution of about 1g of hemoglobin
(this happens very often.)

Plasma Na

Decrease in Intravascular volume leads


to greater avidity for Na (through
aldosterone) AND water (through ADH),
So overall, Plasma Na concentration
tends to decrease from 140 when
hypovolemia present.

Urine Na

Urine Na goes down in prerenal states


as body tries to hold onto water.
Getting a FENa helps correct for urine
concentration.
Screwed up by lasix.
Calculator on PDA or medcalc.com

IV Modes of administration

Peripheral IV
PICC
Central Line
Intraosseous

IV Problem:
Extravasation / Infiltrated

The most sensitive indicator of


extravasated fluid or "infiltration" is to
transilluminate the skin with a small
penlight and look for the enhanced halo
of light diffusion in the fluid filled area.
Checking flow of infusion does not tell
you where the fluid is going

Thank you