Download Shock & IV Fluids

SHOCK & IV FLUIDS
Dr. Ahmed Khan Sangrasi
Associate Professor, Department of Surgery,
LUMHS Jamshoro
Shock
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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
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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 body’s 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
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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
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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:
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CBC
Chemistries
Lactate
Coagulation studies
Cultures
ABG
Further Evaluation
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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
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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
• Weak or absent
peripheral pulses
• SBP <110
• Tachycardia
Yes!
These are all signs and
symptoms of shock
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
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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
• Provide analgesia and anxiolytics to relax muscles and
avoid shivering
• Maintain arterial oxygen saturation/content
• 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
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Urine output > 0.5 mL/kg/hr
CVP 8-12 mmHg
MAP 65 to 90 mmHg
Central venous oxygen concentration > 70%
Persistent Hypotension
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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
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Hypovolemic
Cardiogenic
Septic
Anaphylactic
Neurogenic
Endocrine
Obstructive
What Type of Shock is This?
• 68 yo M with hx of HTN and DM
presents to the ER with abrupt onset
of diffuse abdominal pain with
radiation to his low back. The pt is
hypotensive, tachycardic, afebrile,
with cool but dry skin
Hypovolemic Shock
Types of Shock
• Hypovolemic
• Septic
• Cardiogenic
• Anaphylactic
• Neurogenic
• Obstructive
Hypovolemic Shock
Hypovolemic Shock
• Non-hemorrhagic
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Vomiting
Diarrhea
Bowel obstruction, pancreatitis
Burns
Neglect, environmental (dehydration)
• Hemorrhagic
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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
• Normal Saline or Lactate Ringers
• Up to 3 liters
• PRBCs
• O negative or cross matched
• Control any bleeding
• Arrange definitive treatment
Evaluation of Hypovolemic Shock
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CBC
ABG/lactate
Electrolytes
BUN, Creatinine
Coagulation studies
Type and cross-match
• As indicated
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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
Gravity
50 mL/min
100 mL/min
150 mL/min
200 mL/min
Pressure
150 mL/min
225 mL/min
275 mL/min
450 mL/min
What Type of Shock is This?
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Types of Shock
An 81 yo F resident of a nursing home
presents to the ED with altered mental • Hypovolemic
status. She is febrile to 39.4,
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Septic
hypotensive with a widened pulse
pressure, tachycardic, with warm
• Cardiogenic
extremities
• Anaphylactic
• Neurogenic
Septic
• Obstructive
Septic Shock
Sepsis
• Two or more of SIRS criteria
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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. 2006;42:28-54.
Septic Shock
• Clinical signs:
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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
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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 infections- Clindamycin 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. 2001:345:1368-1377.
What Type of Shock is This?
• A 55 yo M with hx of HTN, DM
presents with “crushing”
substernal CP, diaphoresis,
hypotension, tachycardia and
cool, clammy extremities
Cardiogenic
Types of Shock
• Hypovolemic
• Septic
• Cardiogenic
• Anaphylactic
• Neurogenic
• Obstructive
Cardiogenic Shock
Cardiogenic Shock
• Defined as:
• SBP < 90 mmHg
• CI < 2.2 L/m/m2
• PCWP > 18 mmHg
• Signs:
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Cool, mottled skin
Tachypnea
Hypotension
Altered mental status
Narrowed pulse pressure
Rales, murmur
Etiologies
• What are some causes of cardiogenic shock?
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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
• 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
• RV infarct
• Fluids and Dobutamine (no NTG)
• Acute mitral regurgitation or VSD
• Pressors (Dobutamine and Nitroprusside)
What Type of Shock is This?
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Types of Shock
A 34 yo F presents to the ER after dining • Hypovolemic
at a restaurant where shortly after eating
the first few bites of her meal, became • Septic
anxious, diaphoretic, began wheezing,
noted diffuse pruritic rash, nausea, and a • Cardiogenic
sensation of her “throat closing off”. She
is currently hypotensive, tachycardic and • Anaphylactic
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
• Poorly controlled asthma
• Previous anaphylaxis
• Reoccurrence rates
• 40-60% for insect stings
• 20-40% for radiocontrast agents
• 10-20% for penicillin
• Most common causes
• Antibiotics
• Insects
• Food
Anaphylactic Shock
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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 Shock- Diagnosis
• 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
• ABC’s
• Angioedema and respiratory compromise require
immediate intubation
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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
• Methylprednisolone 125 mg IV
• Prednisone 60 mg PO
• Antihistamines
• H1 blocker- Diphenhydramine 25-50 mg IV
• H2 blocker- Ranitidine 50 mg IV
• Bronchodilators
• 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?
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Types of Shock
A 41 yo M presents to the ER after
an MVC complaining of decreased • Hypovolemic
sensation below his waist and is now
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Septic
hypotensive, bradycardic, with warm
extremities
• Cardiogenic
• Anaphylactic
• Neurogenic
• Obstructive
Neurogenic
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 Shock- Treatment
• A,B,Cs
• Remember c-spine precautions
• Fluid resuscitation
• 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 Shock- Treatment
• Methylprednisolone
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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
• Beck’s triad: hypotension, muffled heart sounds, JVD
• Diagnosis: large heart CXR, echo
• Rx: Pericardiocentisis
Obstructive Shock
• Pulmonary embolism
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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
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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
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Kinds of IV Fluid solutions
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Hypotonic - 1/2NS
Isotonic - NS, LR, albumen
Hypertonic – Hypertonic saline.
Crystalloid
Colloid
Crystalloid vs Colloid
Type of particles (large or small)
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Fluids with small “crystalizable” particles like NaCl
are called crystalloids
Fluids with large particles like albumin are called
colloids, these don’t (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.
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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
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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 won’t 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 —
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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.
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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
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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.
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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
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Start: D5 1/2NS+20 meq K @ Wt+40/hr
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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)
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Glucose in the form of dextrose (D5) can be added to provide some calories while the
patient is NPO.
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The normal kidney can maintain sodium and potassium balance over a wide range of
intakes.
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So,start:
D5 1/2NS+20 meq K
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at a rate equal to their weight + 40ml/hr, but no greater than 120ml/hr.
then adjust as needed, see next page.
Start D5
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1/2NS+20 meq K, then adjust:
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
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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
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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:
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Gastrointestinal losses: N/V/D
Renal losses: diuretics
Skin or respiratory losses: burns
Third-spacing: intestinal obstruction, pancreatitis
Replacement therapy.
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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.
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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
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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
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Urine output, less than 30ml/hr
Decreased BP, Increase pulse
Physical exam for assessing volume
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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
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SOB & orthopnea
Edema & weight gain
Distended neck veins & tachycardia
Increased blood pressure
Crackles & wheezes
pleural effusion
Which brings us to:
Labnormalities seen with hypovolemia
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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
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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

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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

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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