SURGERY - SHOCK

DRA. LAHOZ
HEMOSTASIS - REVIEW

BIOLOGY OF HEMOSTASIS

CAUSES OF BLEEDING
1. Congenital Factor Deficiencies
Coagulation Factor Deficiencies
Platelet Functional Defects
2. Acquired Hemostatic Defect
Platelet abnormalities
- Quantitative Defects
- Qualitative Defects
Acquired Hypofibrinogenemia
Myoloproliferative Diseases
Coagulopathy of Liver Diseases (Vit K)
Coagulopathy of Trauma
Acquired Coagulation Inhibitors
Anticoagulation & Bleeding (medication)
EVALUATION OF HEMOSTASIS

4 MAJOR PHYSIOLOGIC EVENTS

1. Vascular Constriction
2. Platelet Plug Formation
3. Fibrin Formation/ Clot formation? Coagulation
4. Fibrinolysis

1. HISTORY
Bleeding tendencies toothbrush, menses, dental extraction,
spontaneous bruising
Transfusion
Medical Problems: Liver/ Renal
Family History of bleeding difficulties
Medications
2. PHYSICAL EXAMINATION
Bruises
Other illness jaundice, wounds, renal
3. DIAGNOSTIC PROCEDURES
BLOOD TYPING
Platelet count
BT, PT, PTT
TRANSFUSION - REVIEW
1. Whole Blood fresh and banked
FWB- provides greater coagulation activity than equal units of
component therapy
2. Red blood Cell (PRBC)
3. Platelet Concentrate
4. Fresh Frozen Plasma
5. Tranexamic acid
6. Expanders DEXTRAN
7. Human polymerized hemoglobin
*AUTOTRANSFUSION
TRANSFUSION INDICATIONS
1. Improvement in Oxygen-Carrying Capacity (RBC)
2. Treatment of anemia Hb <10g/L or Hct <30%
3. Volume replacement most common
DAMAGE CONTROL RESUSCITATION (TRAUMA)
Permissive hypotension
Minimize Crystalloid-based resuscitation
Immediate release and admin of pre-defined blood products
(RBC/Plt/Plasma)

SURGERY - SHOCK

DRA. LAHOZ

Class

II

III

IV

Blood loss

</= 750

750 - 1500

1500-2000

Blood loss (%
B volume)
Pulse rate

</= 15%

15-30%

30-40%

30% - <40%
(15002000ml)
>/= 40%

<100

>100

>120

>140

BP

Normal

Normal

Decreased

Decreased

Pulse pressure
(mmH)
Capillary refill
test
Respiratory
rate
Urinary
output
(ml/hr)
Mental Status

Normal or
decreased
Normal

Decreased

Decreased

Decreased

Positive

Positive

Positive

14-20

20-30

30-40

>35

>/= 30

20-30

5-15

Negligible

Slightly
anxious
Crystalloid

Mildly
anxious
Crystalloid

Anxious and
confused
Crystalloid +
blood

Confused,
lethargic
Crystalloid
+ blood

Fluid
replacement
(3:1 rule)

Stage

I Compensated

II Mild

III moderate

IV Severe

Blood
loss

<15%
(750-1000ml)

15%-<30%
(1000-1500ml)

30% - <40%
(1500-2000ml)

Heart
rate
BP

Normal
<100bpm
Normal;
Vasoconstriction
redistributes
blood flow,
slight rise in
diastolic
pressure seen

Tachycardia
>100bpm
Orthostatic
changes in BP;
vasoconstriction
intensifies in
non-critical
organs (skin,
muscles, gut)

Respiration

Normal

Rate mildly
increase

Tachycardia
>120bpm
Markedly
decreased (SBP
<90mmHG);
vasoconstriction
decreases
perfusion to
kidneys,
pancreas, liver,
and spleen
Moderate
tachypnea

>40%
(2000ml or
more)
Tachycardia
>14obpm
Profoundly
decreased
(SBP<80mmHG)
Decreased
perfusin affects
the brain and
heart

Capillary
refill
time
Bowel
sounds

Normal
<2 seconds

>2 seconds;
Clammyskin

Present, all four

quadrants

Hypoactive

Urinary
output
Mental
Status

>30ml/hr

20-30ml/hr

<20ml/hr

Normal or
slightly anxious

Mildly anxious
or agitated

Confused,
agitated

Usually
> 3 seconds;
pale skin
Absent
(paralytic ileus)

Marked
tachypnea;
respiratory
collapse
>3 seconds;
Cold, mottled
skin
Absent(paralytic
ileus, mucosal
necrosis)
None (anuria)
Obtunded

SURGERY - SHOCK

DRA. LAHOZ

SHOCK

PHASES OF SHOCK

1.COMPENSATED PHASE

2.DECOMPENSATED PHASE
3.IRREVERSIBLE PHASE

PATHOPHYSIOLGY OF SHOCK

PHYSIOLOGIC RESPONSES
HYPOVOLEMIC
SHOCK
CARDIOGENIC SHOCK
VASOGENIC SHOCK
(Septic shock)
NEUROGENIC SHOCK

OBSTRUCTIVE SHOCK

TRAUMATIC

CLASSES OF SHOCK
Loss of circulating blood volume
Failure of heart as a pump
Decreased resistance within
capacitance vessels, usually in
infections
Form of vasogenic shock in which the
spinal cord injury or spinal anesthesia
causes vasodilation due to acute loss of
vascular tone
Form of cardiogenic shock due to
mechanical impediment to circulation
leading to depressed cardiac output
rather than primary cardiac failure
Injury leads to activation of
inflammatory cells and release of
circulation factors that modulate the
immune system

A. Stretch receptors and Baroreceptors in the Heart and Vasculature

B. Chemoreceptors
C. Cerebral ischemia responses
D. Release of endogenous vasoconstrictors
E. Shifting of fluid into the intravascular space
F. Renal reabsorption and conservation of salt and water
PHYSIOLOGIC RESPONSES
AFFERENT SIGNALS
EFFERENT SIGNALS
Baroreceptors (heart)
Chemoreceptors
(aorta & carotid bodies)
(inflammatory mediators)
Loss of Circulation Blood Volume
Pain
Hypoxemia/Hypercarbia
Acidosis
Infection
Change in Temperature
Emotional arousal
Hypoglycemia

Cardiovascular response
Hormonal response

SURGERY - SHOCK

DRA. LAHOZ
HEMORRHAGE

SHOCK
PITUITARY GLAND (Vasopressin/ADH)

DIMINISHED VENOUS RETURN

DECREASED CARDIAC OUTPUT

CARDIOVASCULAR RESPONSE:
Increased Cardiac heart rate and contractility
Venous and arterial vasoconstriction
Redistribution of blood flow (selective vasoconstriction less
essential organs such as intestines, kidney, skin)
Brain & heart preserve blood flow

HEMORRHAGE
SYMPATHETIC RESPONSE (CATHECHOLAMINE EFFECTS)
EPINEPHRINE ADRENAL MEDULLA
NOREPINEPHRINE SYNAPSES OF SYMPATHETIC NERVOUS
SYSTEM
Hepatic glycogenolysis & Gluconeogenesis
(Increased glucose availability to peripheral tissues)
Increased skeletal muscle glycogenolysis
Suppression of insulin release
Increase Glucagon release

HORMONAL RESPONSE
STRESS

HPA AXIS
Hypothalamus Corticotropin releasing hormone
Pituitary gland Adrenocorticotropic Hormone (ACTH)
Adrenal cortex Cortisol
CORTISOL: Acts with Epinephrine & Glucagon
1. Hyperglycemia - Gluconeogenesis
- Insulin resistance
2. Muscle protein breakdown
3. Lipolysis
4. Retention of salt and water by nephrons

1 & 3 SUBSTRATE FOR HEPATIC GLUCONEOGENESIS

SHOCK
RAA SYSTEM
Angiotensin II -Vasoconstrictor ( Splanchnic & Peripheral Vasc)
-Secretion of Aldosterone
-ACTH
-Antidiuretic hormone
Aldosterone promotes reabsorption of sodium and water
- Potassium & Hydrogen ions are lost

Increased water permeability

Decreased water and Sodium loss
Preserve Intravascular volume
Potent Mesenteric vasoconstrictor
Increased Hepatic Gluconeogenesis
Increased Hepatic Glycolysis

SURGERY - SHOCK

DRA. LAHOZ

HEMORRHAGIC/HYPOVOLEMIC SHOCK

MANAGEMENT PRIORITIES
Secure Airway
Control Source of Blood Loss
Volume Resuscitation

SURGERY - SHOCK

DRA. LAHOZ

DAMAGE CONTROL RESUSCITATION

*BLOOD PRODUCTS (TRANSFUSSION)

SEPTIC SHOCK
SEPTIC SHOCK (VASODILATORY SHOCK)
INFECTION + INFLAMMATION
Fever
Tachycardia
Tachypnea
Confusion
Malaise
Oliguria
Hypotension

SURGERY - SHOCK

DRA. LAHOZ

TREATMENT PROTOCOLS
Insulin
Ventilatory Support
Corticosteroids
Immunoglobulin Modulation
CARDIOGENIC SHOCK
-Circulatory pump failure
Hemodynamic Criteria
Sustained hypotension (SBP <90mmHg for at least 30 minutes)
Reduced cardiac index (<2.2l/min per sq m)
Elevated Pulmo artery wedge pressure (>15mmHg)

OBSTRUCTIVE SHOCK

SURGERY - SHOCK

DRA. LAHOZ
ACUTE SCI
-Vascular compromise to the SC
loss of autoregulation,
vasospasm and thrombosis
-Loss of cellular membrane
integrity and impaired energy
metabolism
-Neurotransmitter accumulation
and release of free radicals

OBSTRUCTIVE SHOCK CARDIAC TAMPONADE

BECKs TRIAD
hPN
Muffled heart sounds
NVE
DECOMPRESSION
-pericardiocentesis

Dec BP
Bradycardia
Warm extremities
Motor and Sensory Deficits
Radiographic evid of vertebral column Fx

ACUTE SCI
OBSTRUCTIVE SHOCK TENSION PNEUMOTHORAX
Resp. distress in awake patients
hPN
Dec. BS
Hyper resonance
JV distention
Mediastinal shift
DECOMPRESSION
-Needle thoracentesis

NEUROGENIC SHOCK
-Loss of vasomotor tone to peripheral arterial beds

MANAGEMENT
BP control
Oxygenation
Hemodynamics

SURGERY - SHOCK

DRA. LAHOZ
KEY POINTS

1. Definition of SHOCK failure to meet the metabolic demands of

cells and tissues
2. DECREASED TISSUE PERFUSSION Central component of shock
(etiology)
HYPOVOLEMIC/HEMORRHAGIC
CARDIOGENIC
NEUROGENIC
SEPTIC SHOCK (release of molecules)
TRAUMATIC

3. AFFERENT AND EFFERENT RESPONSES

NEUROENDOCRINE
METABOLIC
IMMUNE/INFLAMMATORY
4. MANAGEMENT: VOLUME RESUSCITATION
HEMORRHAGIC BLOOD PRODUCTS
5. PREVENTION OF HYPOTHERMIA, ACIDEMIA, AND COAGULOPATHY

6. SEPTIC SHOCK ANTIBIOTIC TX, CONTROL OF SOURCE OF

INFECTION
7. PHYSIOLOGIC AND MARKERS OF ORGAN/TISSUE PERFUSION
MONITOR PROGRESS

JL D.