SHOCK
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Transcript of SHOCK
SHOCK
Presenter:Dr. Joseph John
P.G studentThe Dept Of Oral & Maxillofacial Surgery
Guided By:Dr. Ramdas Balakrishna
Introduction
• Shock is an acute state in which tissue perfusion is inadequate to maintain the supply of oxygen and nutrients necessary for normal cell function which results in widespread hypoxia.
• “As an acute, generalized , inadequate perfusion of the vital organs that, if continued, will produce serious pathophysiologic consequences.”
Classification
Hypovolemic Shock
Traumatic shock
Cardiogenic Shock
Extracardiac obstructive
Shock
Distributive Shock:-
Septic shock
Anaphylactic shock
Neurogenic Shock:-
vasovagal or vasogenic shock
psychogenic shock.
3
Shock?
• Its Progressive• Positive Feedback.• Cell membrane ion pump dysfunction• Intracellular edema• Leakage of intracellular contents into the
extracellular space• Inadequate regulation of intracellular pH.
Why Shock?
• Low SVR.• low contractility.• low preload.
EtiologyDISTRIBUTIVE (VASODILATORY) SHOCK SIRS (Systemic Inflammatory Response Syndrome) Sepsis
PancreatitisExtensive burnsMultiple traumatic injuries
AnaphylaxisToxic ingestions
Insect bitesTransfusion reactionsHeavy metal poisoningNarcoticsBarbituatesAnesthetics
Neurogenic shockSpinal cord injuryCerebral damage
HYPOVOLEMIC SHOCK External blood loss
Trauma GIT bleeding Massive hemoptysis
Internal blood loss Ruptured aortic aneurysm
Hemothorax HemoperitoneumLoss of plasma volume
GI losses Diarrhea/Vomiting
Renal losses Diabetes insipitus Overzealous use of diuretics
Transcutaneous losses Extensive burns
Inadequate repletion of insensible loses
CARDIOGENIC SHOCKMyopathic (reduced contractility)
CardiomyopathyAdvanced septic shockMyocarditisSevere acidosis
ArrhythmogenicTachyarrhythmiasBradyarrythmias
Intracardiac mechanical abnormalitiesPapillary muscle rupture resulting in acute severe mitral regurgitationAcute aortic insufficiency from an aortic dissectionCritical aortic stenosisSeptal rupture
Inadequate diastolic fillingMassive pulmonary embolusTension pneumothoraxSevere pulmonary hypertensionSevere constrictive pericarditisPositive pressure ventilationIntracardiac tumors
Stages Of Shock An initial non progressive phase
Compensatory stage
progressive stage
irreversible stage / Refactory Stage
Cells Deprived of O2
Reduced Production Of ATP
Damage to Cell Membrane
Activation Of Alternate Mechanism, ANAEROBIC
METABOLISM
Production Of Lactic acid, Pyruvic acid
Development of SYSTEMIC MEABOLIC ACIDOSIS
AN INITIAL NON PROGRESSIVE PHASE
Body tries to intervene
Hyperventilation Occurs
Activation of Baroreceptors
Release of Adrenaline & Nor adrenaline
Vasoconstruction
Increase in B.P & heart rate
Blood re routing
Oligourea
COMPENSATORY STAGE
When Compensatory
Mechanism Fails, This Stage Activates
Decreased perfusion
Anaerobic metabolism Continues
Increase in metabolic acidosis
Arteriolar and pre capillary sphincters
construct
Blood trap in these capillaries
Increase in H.P
Histamine release
Leakage of fluid to extra cellular space
Blood Conc. And viscosity increases
Slugging of micro circulation
Further compensate the perfusion to vital organs
PROGRESSIVE STAGE
General Symptoms/Signs
1. Cardiovascular System2. Nervous System3. Pulmonary System4. Skin5. Kidneys6. GI System7. Hematologic System8. Diffuse cellular injury
General Symptoms/Signs
1. Cardiovascular System2. Nervous System3. Pulmonary System4. Skin5. Kidneys6. GI System7. Hematologic System8. Diffuse cellular injury
General Symptoms/Signs
1. Cardiovascular System2. Nervous System3. Pulmonary System4. Skin5. Kidneys6. GI System7. Hematologic System8. Diffuse cellular injury
General Symptoms/Signs
1. Cardiovascular System2. Nervous System3. Pulmonary System4. Skin5. Kidneys6. GI System7. Hematologic System8. Diffuse cellular injury
General Symptoms/Signs
1. Cardiovascular System2. Nervous System3. Pulmonary System4. Skin5. Kidneys6. GI System7. Hematologic System8. Diffuse cellular injury
General Symptoms/Signs
1. Cardiovascular System2. Nervous System3. Pulmonary System4. Skin5. Kidneys6. GI System7. Hematologic System8. Diffuse cellular injury
General Symptoms/Signs
1. Cardiovascular System2. Nervous System3. Pulmonary System4. Skin5. Kidneys6. GI System7. Hematologic System8. Diffuse cellular injury
General Symptoms/Signs
1. Cardiovascular System2. Nervous System3. Pulmonary System4. Skin5. Kidneys6. GI System7. Hematologic System8. Diffuse cellular injury
General Symptoms/Signs
1. Cardiovascular System2. Nervous System3. Pulmonary System4. Skin5. Kidneys6. GI System7. Hematologic System8. Diffuse cellular injury
Do not wait !
Start the management measures immediately
The Pulmonary Artery Catheter (Swan-Ganz catheter)
1. Central venous, pulmonary artery, and pulmonary capillary pressures.
2. Cardiac output and vascular resistance.
3. Sampling of mixed venous blood.
Categories of Shock
CVP CO SVR SvO2
Hypovolemic ↓ ↓ ↑ ↓
Distributive ↓ / ↔ ↑ ↓ ↑
Cardiogenic ↑ ↓ ↑ ↓
HYPOVOLAEMIC OR HAEMATOSHOCK
• Results from blood loss.• Decreased blood volume causes a decrease in
blood pressure.• Insufficient amounts of O2 is being transported
to body tissues and organs .
HEMORRHAGIC :
• a. Trauma (RTA, interpersonal violence, Sport and athletic . injuries, Industrial accidents)
b. Gastrointestinal bleeding
NON HEMORRHAGIC :
External fluid loss Diarrhoea Vomiting Polyurea Fluid redistribution Burns
Parameter Class I Class II Class III Class IV
% loss of blood volume
< 15% 15-30% 30-40% > 40%
Heart rate < 100 > 100 > 120 > 140
Urine outputMildly
decreasedSeverely
decreasedAnuric
Mental Status Anxious Agitated Confused Lethargic
Classification Of Hemorrhagic Shock By American College Of Surgeons Committee On Trauma
PATHOPHYSIOLOGY
Loss of blood
decreased filling of the right heart( dec. in venous return)
decrease of filling of the pulmonary vasculature
decreases filling of the left atrium and ventricle
left ventricular stroke volume decreases
Drop in arterial pressure which leads to reduced perfusion to vital organs leading to multiple organ failure and finally death if
untreated
Compensatory mechanisms
• Increase in Heart Rate & Vascular Resistance.
• Increase water and Na retention.
Clinical features • Skin: cool, moist, pale skin
• Resp. rate: rate and depth are increased
• Heart rate: pulse is weak and thready, MAP is decreased, pulse pressure is narrow
• Blood pressure: increases then decreases
• Urine output: decreased
• Mentation: Loss of consciousness, restlessness, agitation, mild confusion
Management : A,B,C,D IMMEDIATE MANAGEMENT RESUSCITATION : maintenance of patent airway(A), and
breathing(B) IMMEDIATE CONTROL OF BLEEDING QUICK ASSESSMENT EXTRACELLULAR FLUID REPLACEMENT :-maintenance of
circulation and B.P DRUGS : (D)
SEDATIVES CHRONOTROPIC AGENTS INOTROPIC AGENTS VASODILATORS VASOCONSTRICTORS BETA-BLOCKERS DIURETICS
PHYSICAL EXAMINATION AND MONITORING
Immediate Management : POSITION
Immediate control of bleeding Compression
bandages/pressure packs
Local hemostatic agents
ElectroCautery Ligature of vessels
Quick examination
• The patients clothing is cut away & the whole body is visualized, palpated & examined for other injuries or bleeding sites.
• Assessment of blood loss :
• Blood loss with fractures considered as :- 1,000 to 2,000 mL for pelvic fractures, 500 to 1,000 mL for femur fractures,
250 to 500 mL for tibia or humerus fractures,
125 to 250 mL for fractures of smaller bones.
• A hematoma the size of an apple usually contains at least 500 mL of blood.
Neurological examination :
– Glasgow coma scale
Fluid replacement• Crystalloids : Fluid replacement should be started with a crystalloid
• 3 ltrs. Over a time of 45 min is sufficient or depends on the vital signs(pulse, b.p, CVP,urine output)
• In the mean time blood should be sent for cross matching
• Colloids: (ex: albumin) – Will increase osmotic pressure, watch for pulmonary
oedema – Remains in vascular space longer (several hrs)
How much Fluid?
1. Calculate total blood volume2. Determine the % of blood loss3. Multiple total blood volume by the % loss4. Replacement by:5. Colloid fluids, 1.5 times the result in step 3.6. Crystalloid fluids, 4 times the result in step 3.
• Blood: – 500 ml whole blood increases Hct 2-3%, 250ml
Packed RBC’s increases Hct 3-4%
Drugs (common in all types)
• Sedatives : to reduce pain– Morphine : 10 mg i.m– Pethidine : 100 mg i.m
• Chronotropic agents : increases H.R– Adrenaline : 1-8 mcg/min
• Ionotropic agents : inc. cardiac contractility– Dopamine : 3-10 mcg/min
• Vasoconstrictors– Phenylephrine : 20 mcg/min
Central Venous Pressure Normal value : 10-15 mm of Hg In hypovolemic shock, the blood volume is decreased, so is
the CVP is also decreased. In cardiogenic shock there is no depletion of blood volume
and the CVP remains normal.
Urine
Urine output is a good indication of severity of shock. Urine output is affected quite early even in moderate shock. It is also a good index of adequacy of replacement therapy.
Normal output : 60-70 ml/hr. In shock : <30 ml/hr
Septic ShockResults due to a severe infections Usually a bacterial
infection(gram-negative bacteria)
Definitions:• SIRS (Systemic inflammatory response syndrome• Severe SIRS• Sepsis• Severe Sepsis• Septic Shock
Venn diagram displaying the various terminology surrounding sepsis and SIRS:
(Adapted from: Marini JJ, et al. Critical Care Medicine, 2nd ed. 1997.)
Diagnostic Criteria
SIRSRequires 2 of the following:
Severe SIRSMust meet criteria for SIRS, plus 1 of the
following:a. Temp >38.3° or <36.0° Cb. Tachypnea (RR>20 )c. Tachycardia (HR>90, in the
absence of intrinsic heart disease)
d. WBC > 10,000/mm3
a. Altered mental statusb. SBP<90mmHg or fall of >40mmHg from
baselinec. Impaired gas exchanged. Lactic acidosis (pH<7.30 & lactate > 1.5 x
upper limit of normal)e. Oliguria or renal failure (<0.5mL/kg/hr)f. Hyperbilirubinemiag. Coagulopathy (platelets < 80,000-100,000/mm3, INR >2.0, PTT >1.5 x control, or elevated fibrin degredation products)
Etiology
The most frequent causative organisms are gram-negative bacteria, though any agent capable of producing infection (including viruses, parasites and fungi) may cause septic shock.
This type of shock is usually caused by dissemination of a potent endotoxin liberated from gram-negative bacteria without evidence of bacteraemia
44
Pathopysiology Infections Release of toxins
Vasodialatation
Decreased B.P,C.O
Shock
Hypoxic injury to endothelium
Coagulation cascade
Formation of micro thrombi
D.I.C
Infarction of organs and bleeding
Worsening of shock
Multi organ failure
Death
Treatments
• Fluid resuscitation• Vasopressors• Antibiotics initially : empirical antibiotics later : specific antibiotics(based on appropriate culture
and sensitivity test) Empirical therapy Cephalothin (6 to 8 Gm/day I.V. in 4 to 6 divided doses), Gentamicin ( 5 mg/Kg./,day ), Clindamycin (particularly when infecting organism is
Bacteroids)
• Respiratory Support• Transfusions• Recombinant Activated Protein C• Corticosteroids• Glycemic Control
• Respiratory Support• Transfusions• Recombinant Activated Protein C• Corticosteroids• Glycemic Control
Anaphylactic Shock
Pathopysiology
Anaphylaxis is the type I hypersensitivity reaction — (immediate, antigen induced or antibody mediated.)
The resultant antigen - antibody reaction causes degranulation of mast cells, which in turn releases vasoactive amines known as anaphylatoxins.
they cause increase in capillary permeability & widespread dilatation of arterioles & capillaries.
Etiological agents:
These include drugs, insect venom or antisera (serum containing antibodies)
Drugs:1. Antibiotics — Penicillin, Tetracycline2. Analgesics — Acetyl salicylic acid, NSAIDS, Morphine3. Antianxiety drugs — Barbiturates4. Local anesthetics (methyl paraben preservative)5. Methyl methacrylate
Management 1. Epinephrine: 0.5- 1 ml of 1:1000 epinephrine s.c or i.m & repeated every 15 minutes
until improvement. If IV, 1:10000 conc.
2. Histamine (H1) antagonists: 10—20mg chlorpheniramine may be given slowly I.V. & repeated if
required for 24 hours. It counteracts the effects of histamine . It is particularly effective in the management of angioedema, pruritis &
urticaria
3. Corticosteroids: 200 mg of hydrocortisone hemisuccinate I.V.
4. Miscellaneous: Bronchodilators: Aminophyline, salbutamol or terbutaline –
for bronchospasm. Oxygen with assisted ventilation. Emergency tracheostomy for laryngeal oedema or
respiratory obstruction
Cardiogenic Shock
Results due to the inability of the heart to pump enough blood to the body
It is usually due to primary dysfunction of one ventricle : myocardial infarction chronic congestive heart failure cardiac arrhythmia pulmonary embolism systemic arterial hypertension.
Pathophysiology
Clinical features
• Pale & Cool Skin.• Reduced cardiac output: <2.2L/min.• Fall in B.P.• Stagnation of Blood in Atrium… pulmonary oedema.• Increased CVP• Low urine output.
Treatment
Can be divide into 2: Treatment of shock : Treatment of underlying cause
In case of right sided failure . pain in cases of left sided failure : morphin should be prescribed. Fulminant pulmonary oedema : diuretics.
Obstructive shock The symptoms are those of shock plus
congestion of the lungs and viscera because the heart fails to put out all the venous blood returned to it.
• Chest wall trauma : Inability to ventilate adequately
• Tension pneumothorax : Compression of lung tissue and kinking of vena cava
• Pulmonary embolus : Obstruction of the pulmonary artery & inefficient loading of RBC at the lungs
Metabolic Shock
Results due to a severe illness that goes untreatedE.g. : untreated diabetes
Results due to an extreme loss of bodily fluidE.g. excessive urination, diarrhea, or vomiting
References • Review of medical physiology by William F. Ganong – 22nd
edition.• Text book of medical physiology by Guyton & Hall – 11th
edition• Robbins, Pathological basis of diseases – 6th edition, by
Cotran, Kumar, Collins.• Baileys and Love’s Short Practice of Surgery, 23rd edition,
edited by- R.C.G. Russell, Norman S. Williams & Christopher J.K. Bulstrode, Arnold International students edition
• Oral and Maxillofacial trauma; Fonseca Walker; volume 1.• Peterson’s principles of oral and maxillofacial surgery vol. I • J Oral Maxillofac Surg. 54:292-295, 1996.• Oral Maxillofacial Surg Clin N Am 18 (2006) 261 – 273.