Shock

1
Shock IV Fluids

• Dr. Ahmed Khan SangrasiAssociate Professor,
  Department of Surgery,
• LUMHS Jamshoro

2
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

3
Objectives

• Definition
• Approach to the hypotensive patient
• Types
• Specific treatments

4
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

5
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

6
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

7
Global Tissue Hypoxia

• Endothelial inflammation and disruption
• Inability of O2 delivery to meet demand
• Result
• Lactic acidosis
• Cardiovascular insufficiency
• Increased metabolic demands

8
Multiorgan DysfunctionSyndrome (MODS)

• Progression of physiologic effects as shock
  ensues
• Cardiac depression
• Respiratory distress
• Renal failure
• DIC
• Result is end organ failure

9
1. ANTICIPATION STAGE
10
2. PRE-SHOCK STAGE
11
3. COMENSATED SHOCK STAGE
12
4. DECOMPENSATED SHOCK STAGE (REVERSABLE)
13
5. DECOMPENSATED SHOCK STAGE (IRREVERSABLE)
14
(No Transcript)
15
(No Transcript)
16
(No Transcript)
17
Approach to the Patient in Shock

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

18
Diagnosis

• Physical exam (VS, mental status, skin color,
  temperature, pulses, etc)
• Infectious source
• Labs
• CBC
• Chemistries
• Lactate
• Coagulation studies
• Cultures
• ABG

19
Further Evaluation

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

20
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

21
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 lt110
• Tachycardia

Yes! These are all signs and symptoms of shock
22
Shock

• Do you remember how to quickly estimate blood
  pressure by pulse?

60

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

70
80
90
23
Goals of Treatment

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

24
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

25
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

26
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

27
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 gt 10 g/dL
• Serial lactate levels or central venous oxygen
  saturations to assess tissue oxygen extraction

28
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 gt 0.5 mL/kg/hr
• CVP 8-12 mmHg
• MAP 65 to 90 mmHg
• Central venous oxygen concentration gt 70

29
Persistent Hypotension

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

30
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!

31
Types of Shock

• Hypovolemic
• Cardiogenic
• Septic
• Anaphylactic
• Neurogenic
• Endocrine
• Obstructive

32
What Type of Shock is This?

• Types of Shock
• Hypovolemic
• Septic
• Cardiogenic
• Anaphylactic
• Neurogenic
• Obstructive

• 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
33
Hypovolemic Shock
34
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

35
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

36
Evaluation of Hypovolemic Shock

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

• CBC
• ABG/lactate
• Electrolytes
• BUN, Creatinine
• Coagulation studies
• Type and cross-match

37
Infusion Rates

• Access Gravity Pressure
• 18 g peripheral IV 50 mL/min 150 mL/min
• 16 g peripheral IV 100 mL/min 225 mL/min
• 14 g peripheral IV 150 mL/min 275 mL/min
• 8.5 Fr CV cordis 200 mL/min 450
  mL/min

38
What Type of Shock is This?

• Types of Shock
• Hypovolemic
• Septic
• Cardiogenic
• Anaphylactic
• Neurogenic
• Obstructive

• 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
39
Septic Shock
40
Sepsis

• Two or more of SIRS criteria
• Temp gt 38 or lt 36 C
• HR gt 90
• RR gt 20
• WBC gt 12,000 or lt 4,000
• Plus the presumed existence of infection
• Blood pressure can be normal!

41
Septic Shock

• Sepsis (remember definition?)
• Plus refractory hypotension
• After bolus of 20-40 mL/Kg patient still has one
  of the following
• SBP lt 90 mm Hg
• MAP lt 65 mm Hg
• Decrease of 40 mm Hg from baseline

42
Sepsis
43
Pathogenesis of Sepsis
Nguyen H et al. Severe Sepsis and Septic-Shock
Review of the Literature and Emergency Department
Management Guidelines. Ann Emerg Med.
20064228-54.
44
Septic Shock

• Clinical signs
• Hyperthermia or hypothermia
• Tachycardia
• Wide pulse pressure
• Low blood pressure (SBPlt90)
• Mental status changes
• Beware of compensated shock!
• Blood pressure may be normal

45
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?)

46
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

47
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

48
Persistent Hypotension

• If no response after 2-3 L IVF, start a
  vasopressor (norepinephrine, dopamine, etc) and
  titrate to effect
• Goal MAP gt 60
• Consider adrenal insufficiency hydrocortisone
  100 mg IV

49
Treatment Algorithm

• Rivers E et al. Early goal-directed therapy in
  the treatment of severe sepsis and septic shock N
  Engl J Med. 20013451368-1377.

50
What Type of Shock is This?

• Types of Shock
• Hypovolemic
• Septic
• Cardiogenic
• Anaphylactic
• Neurogenic
• Obstructive

• A 55 yo M with hx of HTN, DM presents with
  crushing substernal CP, diaphoresis,
  hypotension, tachycardia and cool, clammy
  extremities

Cardiogenic
51
Cardiogenic Shock
52
Cardiogenic Shock

• Signs
• Cool, mottled skin
• Tachypnea
• Hypotension
• Altered mental status
• Narrowed pulse pressure
• Rales, murmur

• Defined as
• SBP lt 90 mmHg
• CI lt 2.2 L/m/m2
• PCWP gt 18 mmHg

53
Etiologies

• What are some causes of cardiogenic shock?

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

54
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

55
Ancillary Tests

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

56
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

57
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)

58
What Type of Shock is This?

• Types of Shock
• Hypovolemic
• Septic
• Cardiogenic
• Anaphylactic
• Neurogenic
• Obstructive

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

Anaphalactic
59
Anaphalactic Shock
60
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

61
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

62
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

63
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
  life-threatening laryngeal edema

64
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

65
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

66
Anaphylactic Shock- Treatment

• Epinephrine
• 0.3 mg IM of 11000 (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 110,000
• If refractory, start IV drip

67
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

68
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

69
What Type of Shock is This?

• Types of Shock
• Hypovolemic
• Septic
• Cardiogenic
• Anaphylactic
• Neurogenic
• Obstructive

• A 41 yo M presents to the ER after an MVC
  complaining of decreased sensation below his
  waist and is now hypotensive, bradycardic, with
  warm extremities

Neurogenic
70
Neurogenic Shock
71
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)

72
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

73
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

74
Neurogenic Shock- Treatment

• 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

75
What Type of Shock is This?

• Types of Shock
• Hypovolemic
• Septic
• Cardiogenic
• Anaphylactic
• Neurogenic
• Obstructive

• 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
76
Obstructive Shock
77
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

78
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

79
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

80
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

81
FLUID Therapy
82
Fluid and electrolyte balance is an extremely
complicated thing.
83
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 gt 100gms

84

• 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

85
Kinds of IV Fluid solutions

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

86
Crystalloid vs ColloidType 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.

87

• There are two components to fluid therapy
• Maintenance therapy replaces normal ongoing
  losses, and
• Replacement therapy corrects any existing water
  and electrolyte deficits.

88
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
  enteralnutrition.

89

• Maintenance Requirements can be broken
• into water and electrolyte requirements

90
Water

• Two liters of water per day are generally
  sufficient for adults
• Most of this minimum intake is usually derived
  from the water contentof 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.

91

• 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.

92
Several formulas can be used to calculate
maintenance fluid rates.
93
4/2/1 rule a.k.a Weight40

• I prefer the 4/2/1 rule (with a 120 mL/h limit)
  because it is the same as for pediatrics.

94

• 4/2/1 rule4 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
  thatThis always gives 60ml/hr for first 20
  kgthen 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

95
What to put in the fluids

96
Start D5 1/2NS20 meq K _at_ Wt40/hr

• a reasonable approach is to start 1/2 normal
  saline to which 20 meq of potassium chloride is
  added per liter. (1/2NS20 K _at_ Wt40/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 1/2NS20 meq K
• at a rate equal to their weight 40ml/hr, but
  no greater than 120ml/hr.
• then adjust as needed, see next page.

97
Start D5 1/2NS20 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.

98
Usually kidneys regulate well, butAltered
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.

99
(No Transcript)
100
(No Transcript)
101
(No Transcript)
102
(No Transcript)
103

• Now onto Part 2 of the presentation

104
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

105
Causes of FVDhypovolemia

• Gastrointestinal losses N/V/D
• Renal losses diuretics
• Skin or respiratory losses burns
• Third-spacing intestinal obstruction,
  pancreatitis

106
Replacement therapy.
107

• 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.

108

• 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.

109
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

110
Basic signs of hypovolemia

• Urine output, less than 30ml/hr
• Decreased BP, Increase pulse

111
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.

112
SIGNS SYMPTOMS OF Fluid Volume Excess

• SOB orthopnea
• Edema weight gain
• Distended neck veins tachycardia
• Increased blood pressure
• Crackles wheezes
• pleural effusion

113
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.

114
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

115
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.)

116
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.

117
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

118
IV Modes of administration

• Peripheral IV
• PICC
• Central Line
• Intraosseous

119
IV ProblemExtravasation / 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

120
Thank you