Hemorrhage

1
Hemorrhage Shock
Terry White, RN
2
Review of Hemorrhage

• Location
• Anatomical Type Timing
• Coagulation
• Fibrinolysis
• Assessment
• Management

3
Review of Hemorrhage

• Location
• External
• Internal
• Traumatic
• Non-Traumatic
• Examples?

4
Review of Hemorrhage

• Anatomical Type
• Arterial
• Venous
• Capillary
• Timing
• Acute
• Chronic

5
Severity of Hemorrhage
Comparison of Adult vs Child
6
Hematocrit

• of RBC in blood (hematocrit)
• Normal
• 37 - 47 (Female)
• 40 - 54 (Male)

7
Thrombocytes

• Platelets
• Form platelet plugs
• contact collagen adhere to injured surface
• activate platelets
• aggregate to form platelet plug

8
Coagulation

• Formation of blood clots
• Prothrombin activator
• Prothrombin ? Thrombin
• Fibrinogen ? Fibrin
• entrap platelets, blood cells plasma
• Clot retraction

9
Fibrinolysis

• Breaking up the clot
• tissue plasminogen activator (tPA)
• plasminogen ? plasmin

10
Assessing Hemorrhage

• Clues
• Bright red blood from wound, mouth, rectum or
  other orifice
• Hematemesis
• Coffee ground appearance of vomitus
• Hematochezia
• Melena
• Orthostatic hypotension
• Dizziness or syncope on sitting or standing
• Signs and symptoms of hypovolemic shock

11
Management of Hemorrhage

• Airway and Ventilatory Support
• Circulatory Support
• From nose or ears after head trauma loose drsg
• Control bleeding
• direct pressure, elevation, pressure points
• tourniquet
• packing of large wounds
• splinting
• PASG
• transport to appropriate facility

12
Shock
A rude unhinging of the machinery of life
A brief pause in the act of dying
13
Shock

• Inadequate peripheral perfusion leading to
  failure of tissue oxygenation
• ? may lead to anaerobic metabolism

14
Shock

• Homeostasis
• cellular state of balance
• perfusion of cells with oxygen is one of its
  cornerstones

15
Shock

• Adequate Cellular Oxygenation
• Red Cell Oxygenation
• Red Cell Delivery To Tissues

Fick Principle
16

• The following variables are measured
• VO2 consumption per minute using a spirometer
  (with the
• subject re-breathing air) and a CO2
  absorber
• Cv, the oxygen content of blood taken from the
• pulmonary artery (representing deoxygenated
  blood
• blood)
• Ca, the oxygen content of blood from a cannula in
  a
• peripheral artery (representing oxygenated
  blood)

From these values, we know that where CO
Cardiac Output, CA Oxygen concentration of
arterial blood and CV Oxygen concentration of
venous blood.
x
CV
)
(
x
CA
)
CO
CO

(
VO2
This allows us to say
VO2
CO

CA
CV
17
Fick Principle

• Airs gotta go in and out.
• Bloods gotta go round and round.
• Any variation of the above is not a good thing!

18
Shock

• Red Cell Oxygenation
• Oxygen delivery to alveoli
• Adequate FiO2
• Patent airways
• Adequate ventilation

19
Shock

• Red Cell Oxygenation
• Oxygen exchange with blood
• Adequate oxygen diffusion into blood
• Adequate RBC flow past alveoli
• Adequate RBC mass/Hgb levels
• Adequate RBC capacity to bind O2
• pH
• Temperature

20
Shock

• Red Cell Delivery To Tissues
• Adequate perfusion
• Blood volume
• Cardiac output
• Heart rate
• Stroke volume (pre-load, contractility,
  after-load)
• Conductance
• Arterial resistance
• Venous capacitance

21
Shock

• Red Cell Delivery To Tissues
• Adequate RBC mass
• Adequate Hgb levels
• Adequate RBC capacity to unbind O2
• pH
• Temperature
• Distance between capillaries and cells

22
Shock

• Inadequate oxygenation or perfusion causes
• Inadequate cellular oxygenation
• Shift from aerobic to anaerobic metabolism

23
AEROBIC METABOLISM
Glycolysis Inefficient source of energy
production 2 ATP for every glucose produces
pyruvic acid Oxidative phosphorylation Each
pyruvic acid is converted into 34 ATP
24
ANAEROBIC METABOLISM
Glycolysis Inefficient source of energy
production 2 ATP for every glucose produces
pyruvic acid
25
Anaerobic Metabolism

• Occurs without oxygen
• oxydative phosphorylation cant occur without
  oxygen
• glycolysis can occur without oxygen
• cellular death leads to tissue and organ death
• can occur even after return of perfusion
• ? organ or organism death

26
Ultimate Effects of Anaerobic Metabolism
27
Maintaining perfusion requires

• Volume
• Pump
• Vessels
• Failure of one or more of these causes shock

28
Shock

• Hypovolemic Shock Low Volume

• Trauma
• Non-traumatic blood loss
• Vaginal
• GI
• GU
• Burns
• Diarrhea

• Vomiting
• Diuresis
• Sweating
• Third space losses
• Pancreatitis
• Peritonitis
• Bowel obstruction

29
Shock

• Cardiogenic Shock Pump Failure

• Mechanical obstruction (distributive shock)
• Cardiac tamponade
• Tension pneumothorax
• Pulmonary embolism

• Acute M I
• CHF
• Bradyarrhythmias
• Tachyarrhythmias

30
Shock

• Vasogenic Shock Low Resistance
• Spinal cord trauma
• neurogenic shock
• Depressant drug toxicity
• Simple fainting

31
Shock

• Mixed Shock
• Septic Shock
• Overwhelming infection
• Inflammatory response occurs
• Blood vessels
• Dilate (loss of resistance)
• Leak (loss of volume)

32
Shock

• Mixed Shock
• Septic Shock
• Fever
• Increased O2 demand
• Increased anaerobic metabolism
• Bacterial toxins
• Impaired tissue metabolism

33
Shock

• Mixed Shock
• Anaphylactic Shock
• Severe allergic reaction
• Histamine is released
• Blood vessels
• Dilate (loss of resistance)
• Leak (loss of volume)

34
Shock

• Mixed Shock
• Anaphylactic Shock
• Histamine release
• Extravascular smooth muscle spasm
• Laryngospasm
• Bronchospasm

35
Shock

• Progressive syndrome
• Three phases
• Compensated
• Decompensated
• Irreversible

36
Shock

• Signs and symptoms due to
• Hypoperfusion
• Compensatory responses

37
Compensated Shock

• Baroreceptors detect fall in BP
• Usually 60-80 mm Hg (adult)
• Sympathetic nervous system activates
• What are the primary SNS Neurotransmitters
  their effects?

38
Compensated Shock

• Cardiac effects
• Increased force of contractions
• Increased rate
• Increased cardiac output

39
Compensated Shock

• Peripheral effects
• Arteriolar constriction
• Pre-/post-capillary sphincter contraction
• Increased peripheral resistance
• Shunting of blood to core organs

40
Compensated Shock

• Decreased renal blood flow
• Renin released from kidney arteriole
• Renin Angiotensinogen combine
• Converts to Angiotensin I
• Angiotensin I converts to Angiotensin II
• Peripheral vasoconstriction
• Increased aldosterone release (adrenal cortex)
• promotes reabsorption of sodium water

41
Compensated Shock

• Decreased blood flow to hypothalamus
• Release of antidiuretic hormone (ADH or Arginine
  Vasopressin) from posterior pituitary
• Retention of salt, water
• Peripheral vasoconstriction

42
Compensated Shock

• Insulin
• ? secretion caused by epinephrine
• contributes to hyperglycemia
• Glucagon
• ? release caused by epinephrine
• promotes liver glycogenolysis gluconeogenesis
• ACTH
• stimulates adrenal cortex release of cortisol
• ? glucose production

43
Compensated Shock

• Peripheral capillaries contain minimal blood
• Stagnation
• Aerobic metabolism changes to anaerobic
• Extracellular potassium shifts begin

44
Compensated Shock

• Presentation
• Restlessness, anxiety
• Earliest sign of shock
• Tachycardia
• ?Bradycardia in cardiogenic, neurogenic

45
Compensated Shock

• Presentation
• Normal BP, narrow pulse pressure
• Falling BP late sign of shock
• Mild orthostatic hypotension (15 to 25 mm Hg)
• Possible delay in capillary refill

46
Compensated Shock

• Presentation
• Pale, cool skin
• Cardiogenic
• Hypovolemic
• Flushed skin
• Anaphylactic
• Septic
• Neurogenic

47
Compensated Shock

• Presentation
• Slight tachypnea
• Respiratory compensation for metabolic acidosis

48
Compensated Shock

• Presentation
• Nausea, vomiting
• Thirst
• Decreased body temperature
• Feels cold
• Weakness

49
Decreased Cardiac Output
Catecholamine Release
Aldosterone, ADH Release
Increased Blood Volume
Increased PVR
Increased Cardiac Output
Increased Myocardial Work, O2 Demand
Increased Volume Loss
Compensated Shock Leading to Decompensation
Myocardial Ischemia
50
Decompensated Shock

• Presentation
• Cardiac Effects
• Decreased RBC oxygenation
• Decreased coronary blood flow
• Myocardial ischemia
• Decreased force of contraction

51
Decompensated Shock

• Presentation
• Peripheral effects
• Relaxation of precapillary sphincters
• Continued contraction of postcapillary sphincters
• Peripheral pooling of blood
• Plasma leakage into interstitial spaces

52
Decompensated Shock

• Presentation
• Peripheral effects
• Continued anaerobic metabolism
• Continued increase in extracellular potassium
• Rouleaux formations of RBCs
• pile up like coins
• Cold, gray, waxy skin

53
Decompensated Shock

• Presentation
• Listlessness, confusion, apathy, slow speech
• Tachycardia weak, thready pulse
• Decreased blood pressure
• Moderate to severe orthostatic hypotension
• Decreased body temperature
• Tachypnea

54
Irreversible Shock

• Post-capillary sphincter relaxation
• Loss of peripheral vascular resistance

55
Irreversible Shock

• Washout of accumulated products
• Hydrogen ion
• Potassium
• Rouleaux formations
• Carbon dioxide
• Rouleaux formations microembolize in lungs
• Systemic metabolic acidosis occurs
• Cardiac Output decreases further

56
Irreversible Shock

• Presentation
• Confusion, slurred speech, unconscious
• Slow, irregular, thready pulse
• Falling BP diastolic goes to zero
• Cold, clammy, cyanotic skin
• Slow, shallow, irregular respirations
• Dilated, sluggish pupils
• Severely decreased body temperature

57
Irreversible Shock

• Irreversible shock leads to
• Renal failure
• Hepatic failure
• Disseminated intravascular coagulation (DIC)
• Multiple organ systems failure
• Adult respiratory distress syndrome (ARDS)
• Death

58
Disseminated Intravascular Coagulation (DIC)

• Decreased perfusion causes tissue damage/necrosis
• Tissue necrosis triggers diffuse clotting
• Diffuse clotting consumes clotting factors
• Fibrinolysis begins
• Severe, uncontrolled systemic hemorrhage occurs

59
Adult Respiratory Distress Syndrome (ARDS)

• AKA Shock Lung, Da Nang Lung
• Decreased perfusion damages alveolar and
  capillary walls
• Surfactant production decreases
• Fluid leaks into interstitial spaces and alveoli
• Gas exchange impaired
• Work of breathing increases

60
Shock Classifications

• Hypovolemic
• Cardiogenic
• Vasogenic (Distributive)
• Neurogenic

61
Shock Classifications

• Hypovolemic Causes
• Hemorrhage
• Plasma
• Fluid Electrolytes
• Endocrine

62
Shock Classifications

• Cardiogenic Causes
• Contractility
• Rate
• Obstructive (Preload/Afterload)
• Tension pneumothorax
• Pericardial tamponade
• Pulmonary embolism
• Severe Hypertension

63
Shock Classifications

• Vasogenic (distributive)
• Increased venous capacitance
• low resistance, vasodilation
• anaphylaxis
• sepsis

64
Shock Classifications

• Neurogenic (spinal shock)
• loss of spinal cord function below site of injury
• loss of sympathetic tone
• cutaneous vasodilation
• relative bradycardia

65
Key Issues In Shock

• Tissue ischemic sensitivity
• Heart, brain, lung 4 to 6 minutes
• GI tract, liver, kidney 45 to 60 minutes
• Muscle, skin 2 to 3 hours

Resuscitate Critical Tissues First!
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Key Issues In Shock

• Recognize Treat during compensatory phase

Restlessness, anxiety, combativeness Earliest
signs of shock
Best indicator of resuscitation effectiveness
Level of Consciousness
67
Key Issues In Shock

• Falling BP LATE sign of shock
• BP is NOT same thing as perfusion
• Pallor, tachycardia, slow capillary refill
  Shock, until proven otherwise

68
Key Issues In Shock

• Isolated head trauma does NOT cause shock
• (possible in peds)

69
General Shock Management

• Airway
• Open, Clear, Maintained
• Consider Intubation

70
General Shock Management

• High concentration oxygen
• Oxygen Most Important Drug in Shock
• Assist ventilation as needed
• When in Doubt, Ventilate
• BVM
• Decompress Tension Pneumothorax

71
General Shock Management

• Establish venous access
• Replace fluid
• Give drugs, as appropriate
• Dont delay definitive therapy
• Maintain body temperature
• Cover patient with blanket if needed
• Avoid cold IV fluids

72
General Shock Management

• Monitor
• Mental Status
• Pulse
• Respirations
• Blood Pressure
• ECG

73
Hypovolemic Shock

• Control severe external bleeding
• Elevate lower extremities
• Avoid Trendelenburg
• Pneumatic anti-shock garment

74
Hypovolemic Shock

• Two large bore IV lines
• Infuse Lactated Ringers solution
• Titrate BP to 90-100 mm Hg

75
Hypovolemic Shock

• Do NOT delay transport
• Start IVs enroute to hospital

Where does stabilization of critical trauma occur?
76
Cardiogenic Shock

• Supine, or head and shoulders slightly elevated
• Do NOT elevate lower extremities

77
Cardiogenic Shock

• Keep open line, micro-drip set
• Fluid challenge based on cardiovascular mechanism
  and history
• Titrate to BP 90 mm Hg

78
Cardiogenic Shock

• Treat the underlying cause if possible
• Treat rate, then rhythm, then BP
• Correct bradycardia or tachycardia
• Correct irregular rhythms
• Treat BP
• Cardiac contractility
• Dobutamine, Dopamine
• Peripheral resistance
• Dopamine, Norepinephrine

79
Cardiogenic Shock

• Obstructive Shock
• Treat the underlying cause
• Tension Pneumothorax
• Pericardial Tamponade
• Isotonic fluids titrated to BP w/o pulmonary
  edema
• Control airway
• Intubation

80
Shock Management

• Avoid vasopressors until hypovolemia ruled out,
  or corrected

81
Shock Management
Squeezing partially empty tank can cause
ischemia, necrosis of kidney and bowel
82
Vasogenic Shock

• Consider need to assist ventilations
• Patient supine lower extremities elevated
• Avoid Trendelenburg

83
Vasogenic Shock

• Infuse isotonic crystalloid
• Top off tank
• Consider PASG
• Consider possible hypovolemia
• Consider vasopressors

84
Vasogenic Shock

• Maintain body temperature
• Hypothermia may occur

85
Vasogenic Shock

• Anaphylaxis
• Suppress inflammatory response
• Antihistamines
• Corticosteroids
• Oppose histamine response
• Epinephrine
• bronchospasm vasodilation
• Replace intravascular fluid
• Isotonic fluid titrated to BP 90 mm

86
Pneumatic AntiShock Garment (PASG)

• Function
• Primary effect is increased PVR
• Hemorrhage control through
• Direct pressure
• Fracture stabilization
• Increased intra-abdominal pressure
• Little effect from autotransfusion

87
Pneumatic AntiShock Garment

• Indications
• Multiple lower extremity fractures
• Pelvic fractures
• Abdominal injuries
• Abdominal aortic aneurysm
• Refractory decompensated shock

88
Pneumatic Antishock Garment

• Contraindications
• Absolute
• Pulmonary edema

89
Pneumatic Antishock Garment

• Contraindications
• Relative
• Closed head injury
• Thoracic hemorrhage
• Impaled object (abdomen, chest?)
• Pregnancy (abdominal section)
• Evisceration
• Ruptured diaphragm
• Cardiogenic shock

90
Shock in Children

• Small blood volume
• Increased hypovolemia risk
• Very efficient compensatory mechanisms
• Failure may cause sudden shock
• Pallor, altered LOC, cool skin shock UPO

91
Shock in Children

• Avoid massive fluid infusion
• Use 20 cc/kg boluses
• High surface to volume ratio
• Increased hypothermia risk

92
Shock in the Elderly

• Poor cardiovascular condition
• Rapid decompensation
• Sepsis more likely
• Hypoperfusion can cause
• CVA
• AMI
• Seizures
• Bowel Infarctions
• Renal failure

93
Shock in the Elderly

• Assessment more difficult
• Peripheral vascular disease
• Weak pulses
• Altered sensorium
• Hypertension masking hypoperfusion
• Beta-blockers masking hypoperfusion
• Fluid infusion may produce volume overload/CHF

94
Shock in OB Patients

• Pulse increases 10 to 15 bpm
• BP lower than in non-pregnant patient
• Blood volume increased by 45
• Slower onset of shock signs/ symptoms
• Fluid resuscitation requires greater volume

95
Shock in OB Patients

• Oxygen requirement increased 10 to 20
• Pregnant uterus may compress vena cava,
  decreasing venous return to heart
• Place women in late-term pregnancy on left-side
• Fetus can be in trouble even though mother looks
  well-perfused

96
Transport Considerations

• Indications for Rapid Transport
• Indications for Trauma Center Transport
• Considerations for Air Medical Transport