SURGERY - SHOCK DRA.

LAHOZ

HEMOSTASIS - REVIEW CAUSES OF BLEEDING

BIOLOGY OF HEMOSTASIS 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

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
4 MAJOR PHYSIOLOGIC EVENTS  Platelet count
 BT, PT, PTT
1. Vascular Constriction
2. Platelet Plug Formation TRANSFUSION - REVIEW
3. Fibrin Formation/ Clot formation? Coagulation 1. Whole Blood – fresh and banked
4. Fibrinolysis 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 I II III IV
Blood loss </= 750 750 - 1500 1500-2000 30% - <40%
(1500-
2000ml)
Blood loss (% </= 15% 15-30% 30-40% >/= 40%
B volume)
Pulse rate <100 >100 >120 >140
BP Normal Normal Decreased Decreased
Pulse pressure Normal or Decreased Decreased Decreased
(mmH) decreased
Capillary refill Normal Positive Positive Positive
test
Respiratory 14-20 20-30 30-40 >35
rate
Urinary >/= 30 20-30 5-15 Negligible
output
(ml/hr)
Mental Status Slightly Mildly Anxious and Confused,
anxious anxious confused lethargic
Fluid Crystalloid Crystalloid Crystalloid + Crystalloid
replacement blood + blood
(3:1 rule)

Stage I Compensated II Mild III moderate IV Severe

Blood <15% 15%-<30% 30% - <40% >40%
loss (750-1000ml) (1000-1500ml) (1500-2000ml) (2000ml or
more)
Heart Normal Tachycardia Tachycardia Tachycardia
rate <100bpm >100bpm >120bpm >14obpm
BP Normal; Orthostatic Markedly Profoundly
Vasoconstriction changes in BP; decreased (SBP decreased
redistributes vasoconstriction <90mmHG); (SBP<80mmHG)
blood flow, intensifies in vasoconstriction Decreased
slight rise in non-critical decreases perfusin affects
diastolic organs (skin, perfusion to the brain and
pressure seen muscles, gut) kidneys, heart
pancreas, liver,
and spleen
Respi- Normal Rate mildly Moderate Marked
ration increase tachypnea tachypnea;
respiratory
collapse
Capillary Normal >2 seconds; Usually >3 seconds;
refill <2 seconds Clammyskin > 3 seconds; Cold, mottled
time pale skin skin
Bowel Present, all four Hypoactive Absent Absent(paralytic
sounds quadrants (paralytic ileus) ileus, mucosal
necrosis)
Urinary >30ml/hr 20-30ml/hr <20ml/hr None (anuria)
output
Mental Normal or Mildly anxious Confused, Obtunded
Status slightly anxious or agitated agitated
SURGERY - SHOCK DRA. LAHOZ

SHOCK PHASES OF SHOCK

1.COMPENSATED PHASE

2.DECOMPENSATED PHASE

3.IRREVERSIBLE PHASE

PATHOPHYSIOLGY OF SHOCK

PHYSIOLOGIC RESPONSES

CLASSES OF SHOCK A. Stretch receptors and Baroreceptors in the Heart and Vasculature
HYPOVOLEMIC Loss of circulating blood volume B. Chemoreceptors
SHOCK C. Cerebral ischemia responses
CARDIOGENIC SHOCK Failure of heart as a pump D. Release of endogenous vasoconstrictors
VASOGENIC SHOCK Decreased resistance within E. Shifting of fluid into the intravascular space
(Septic shock) capacitance vessels, usually in F. Renal reabsorption and conservation of salt and water
infections
PHYSIOLOGIC RESPONSES
NEUROGENIC SHOCK Form of vasogenic shock in which the
spinal cord injury or spinal anesthesia AFFERENT SIGNALS EFFERENT SIGNALS
Baroreceptors (heart) Cardiovascular response
causes vasodilation due to acute loss of
Chemoreceptors Hormonal response
vascular tone (aorta & carotid bodies)
OBSTRUCTIVE SHOCK Form of cardiogenic shock due to (inflammatory mediators)
mechanical impediment to circulation Loss of Circulation Blood Volume
leading to depressed cardiac output Pain
rather than primary cardiac failure Hypoxemia/Hypercarbia
TRAUMATIC Injury leads to activation of Acidosis
inflammatory cells and release of Infection
circulation factors that modulate the Change in Temperature
immune system Emotional arousal
Hypoglycemia
SURGERY - SHOCK DRA. LAHOZ

HEMORRHAGE SHOCK

PITUITARY GLAND (Vasopressin/ADH)

DIMINISHED VENOUS RETURN  Increased water permeability

DECREASED CARDIAC OUTPUT  Decreased water and Sodium loss
 Preserve Intravascular volume
 Potent Mesenteric vasoconstrictor
CARDIOVASCULAR RESPONSE:  Increased Hepatic Gluconeogenesis
 Increased Hepatic Glycolysis
 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
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

BECK’s TRIAD

 hPN
 Muffled heart sounds  Dec BP
 NVE  Bradycardia
DECOMPRESSION  Warm extremities
-pericardiocentesis  Motor and Sensory Deficits
 Radiographic evid of vertebral column Fx

ACUTE SCI
OBSTRUCTIVE SHOCK – TENSION PNEUMOTHORAX
MANAGEMENT
Resp. distress in awake patients
hPN BP control
Dec. BS Oxygenation
Hyper resonance Hemodynamics
JV distention
Mediastinal shift

DECOMPRESSION
-Needle thoracentesis

NEUROGENIC SHOCK

-Loss of vasomotor tone to peripheral arterial beds

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.