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SHOCK

GUIDED BY DR. S. ACHARYA SIR

  

Introduction Types and causes of shock Pathophysiology of shock Stages and clinical features of shock First stage or non-progressive shock Second stage or progressive shock Third stage or refractory shock Treatment of shock with physiological basis Applied

Definition
In 1852, shock was defined as a rude unhinging of the machinery of life. Shock is a clinical syndrome characterized by inadequate tissue perfusion due to low cardiac output ( or acute circulatory failure). The cardinal features of all type of shock is low cardiac activity.

Physiologic causes of shock


Any condition that reduces the cardiac output far below level will lead to shock. Two type of factors a) cardiac abnormalities- That decrease
the ability of heart to pump blood e.g. .Myocardial infarction , severe heart valve dysfunction, arrhythmias . b) factors that decreases the venous return--Diminished blood volume and also b/c of decreased vascular tone or obstruction to blood flow.

Stages of shock
A non progressive stage (compensated stage): normal circulatory compensatory mechanisms eventually cause full recovery without outside therapy. A progressive stage : Without therapy shock becomes steadily worse. An irreversible stage (refractory stage) ;Shock has progressed to such an extent that all the therapies are inadequate to save the life.

FIRST STAGE OR NON PRGORESSIVE SHOCK


A non progressive stage (compensated stage).
o o o

Compensated shock Moderate reduction in CO Compensatory mechanism-

RAPID COMPENSATORY MECHANISM (NEURAL MECHANISM)


BARORECEPTOR REFLEXHemorrhage (Blood loss) Decrease Blood Volume Decrease Venous Pressure Decrease Venous Return Decrease Atrial Pressure Decrease Ventricular end-diastolic volume

Cardiac Muscle Decrease Stroke Volume Decrease Cardiac Output Decrease Arterial Blood pressure

CHEMORECEPTOR REFLEX Acute hemorrhage carrying capacity acidosis loss of RBCs and reduce O2 anemia &stagnant hypoxia , excite

stimulate chemoreceptors

vasomotor centre. Fall in BP below 60mmhg usually initiates chemoreceptor reflex.

CNS ISCHEMIC RESPONSE


Fall in BP <50mmHg initiates response. It causes more powerful sympathetic stimulation. SYMPTOMS AND SIGNS
1. 2. 3. 4. 5. 6.

Pale, cold and moist skin Cyanotic tinge of skin Tachycardia and fall in pulse pressure, thin & thready pulse Increase rate &force of respiration Oliguria Restlessness & apprehension

INTERMEDIATE COMPENSATORY MECHANISM


1.

Renin angiotensin vasoconstrictory mechanism. Reverse stress relaxation. Capillary fluid shift mechanism

2.

3.

RENIN-ANGIOTENSIN-ALDOSTERONE
Decrease in plasma volume / decrease in Na+
Detected by

Kidney (Juxtraglomerular apparatus)


Release

Renin
Converts

Angotensin I
Via ACE

Angiotensin II

Adrenal Cortex Releases Aldosterone Increase Sodium Reabsorption Increase fluid volume Increase BP

Increase Vasoconstriction PVR Increase BP

Increase Thirst Increase fluid volume Increase BP

Increase ADH (Anti Diuretic hormone) Increase fluid volume Increase BP

REVERSE STRESS RELAXATION MECHANISM


Prolong slow bleeding Reverse stress relaxation mechanism Correct upto 15% change in blood volume below normal
Decrease BP Tightening of vessel wall by vascular tone adjustment secondary to less stress on vessel wall Restore BP back to normal

CAPILLARY FLUID SHIFT MECHANISM

Decrease BP

Mean capillary pressure is low Absorption of fluid from interstial fluid compartment to circulation Thus,blood vol. increased restore BP normal

LONG TERM COMPENSATORY MECHANISM


1.

Restoration of plasma volume and protein Restoration of red cell mass

2.

RESTORATION OF PLASMA VOLUME AND PROTEINAfter moderate hemorrhage the plasma volume is restored n in 12-72 hrs bez of increase in plasma water along with electrolyte content. Hemodilution occurs Rapid entry of preformed albumin from extravascular stores Plasma protein loss is restored by hepatic synthesis over a period of 3-4 days.

Restoration of red cell mass


Excessive release of erythropoietin which the rate of cell production in the bone marrow within 10 days.

PROGRESSIVE SHOCK
Occurs after 15-25% loss of total blood volume. In this stage compensatory mechanisms are not able to stop the progression of shock. Intense arteriolar vasoconstriction is inadequate for maintenance of normal BP. Various Positive Feedback mechanism develop.

POSITIVE FEEDBACK CYCLES

1.

Cardiac failure Vasomotor failure Peripheral circulatory failure Septicaemic & toxaemia

2.

3.

4.

EFFECT ON BODY TISSUE IN PROGRESSIVE SHOCK


Widespread cellular degeneration (liver,lung&heart). active transport of Na and K through cell membrane resulting in accumulation of sodium in the cells and loss of K from the cell so cell begins to swell Mitochondrial activity in liver cells &other cells Metabolism of glucose is depressed in last stages of shock. Poor delivery of O2 to tissue oxidative metabolism the cells switch to anaerobic glycolysis of lactic acid in the blood Accumulation of CO2 leading to Acidosis vasodilatation aggravates shock vicious cycle starts

REFRACTORY SHOCK
In this stage all the therapeutic interventions are usually ineffective and eventually the patient dies. Causes of refractiveness of shockDepletion of high energy phosphate compounds Slow necrosis of cells esp near venous end of capillary, patchy necrosis first appears in cells of liver, kidney tubules ,lungs ,heart . Kidney acute tubular necrosis acute renal failure uraemic death. Deterioration of the lungs respiratory distress shock lung syndrome.

 

Khurana book of human physiology

TYPES OF SHOCK

1.

Hypovolaemic shock Low-resist or distributive or vasogenic shock Cardiogenic shock Obstructive shock

2.

3.

4.

HYPOVOLEMIC SHOCK
Hypovolemia volume Haemorrhage is the most common cause Cardiac output and arterial pressure falls to Zero when 35-45 % of total blood volume removed. means diminished blood

CAUSES
Hemorrhagic GI Bleed Trauma Massive hemoptysis Post partum bleeding Non hemorrhagic Vomiting Diarrhoea Bowel obstruction/ Pancreatitis Burns

CLINICAL FEATURES
Hypotension Tachycardia Rapid shallow breathing Cold, pale, clammy skin Intense thirst

Hypovolemic shock is further subdivided in following categories on basis of causes.


   

Hemorrhagic Traumatic Surgical Dehydration shock

Most common type is hemorrhagic shock

HEMORRHAGIC SHOCK
If the blood loss is upto 10-30% compensatory changes take place and normal condition is restore. If the blood loss is severe upto 40% of blood volume then condition progresses leading to circulatory collapse and death.

Ctd.

MECHANISM OF DEVELOPMENT OF SHOCK:


Haemorrhage Circulating blood volume Tissue perfusion Anaerobic glycolysis Lactic-acidosis i) Depresses the myocardium ii) Decreases peripheral vascular responsiveness to catecholamines, Coma

Sympathetatic reflexes (Baro receptor) becomes activated within 30 sec to 1 min after hemorrhage. Angotension and vasopressing mechanism and reverse stress relaxation mechanism required 10min to 1hr to respond. Finally absorption of fluid for intestinal tract and intestinal spaces may take 1hr to 48hrs.

HYPOVOLEMIC SHOCK

APPROACH TO PATIENT OF HYPOVOLEMIC SHOCK


Hypotension / Tachycardia VS unstable (Heart rate > 120 and / or SBP <90) Central monitoring CVP <15 Administered crystalloid blood CVP > 15 Airway control Assure ventilation Augment circulation (Crystalloid Blood) VS normalized Definative W/u CVP > 15 Consider Cardiac dysfunction Tamponade Treat appropriately

Vital sign unstable or acidosis worsen Cardiac Index <3.5 PCWP < 15 Administered crystalloid blood

Insert PAC

Cardiac Index < 3.5 PCWP 15-25

Cardiac Index <3.5 PCWP > 25 Inotropes as indicated

Distributive or vasogenic shock


There is no loss of blood instead there is increase in vascular capacity. This is due to decrease in vascular tone. Three types- a) Neurogenic shock. b) Anaphylactic shock. c) Septic shock.

NEUROGENIC SHOCK
There is generalized vasodilatation caused by decrease vasomotor tone. Also known as fainting /syncope Reduction in vasomotor tone can occur at the level of vasomotor tone (neurogenic) Or at the level of blood vessels (vasogenic)

Causes
Spinal anesthesia. Direct damage to vasomotor centre of the medulla. Altered function of the vasomotor centre in response to low blood glucose level (insulin shock)

Types
Vasovagal syncope. Postural syncope. Micturation syncope. Carotid sinus syncope. Cough syncope.

Mechanism
Decrease sympthatic tone or increase parasympthatic tone Decrease vascular tone Massive vasodilatation Decrease SVR and preload Decrease cardiac output Decrease tissue perfusion

Treatment
Fluid resuscitation - to keep MAP at 85-90 mmhg for first 7 days. - if crystalloid are insufficent vasopressors can be used. - Bradycardia Atropine - pacemaker - methyl prednisolone must be started within 8 hrs.

ANAPHYLACTIC SHOCK
ANAPHYLAXIS- a severe systematic hypersensitivity reaction characterized by multisystem involvement. It is IgE mediated. ANAPHYLACTOID REACTION- clinically indistiquishable from anaphylaxis. Do not require sensitizing exposure. Not IgE mediated.

Mechanism
Acute allergic reaction Large quantity of histamine like substance released Mark vasodilatation Reduced peripheral resistance Increase in capillary permeability Fluid loss and hypovolemia

Symptoms
Pruritis , flushing , urticaria. Throat fullness. Anxiety Chest tightness Shortness of breath Altered mental status. Respiratory distress.

Risk factors for fatal anaphylaxis


Poor controlled asthma. Previous h/o anaphylaxis. Causes - a) antibiotics b) insects c) food ( fish , groundnuts)

Mild localized urticaria can progress to fatal anaphylaxis. Symptoms usually begin within 60 sec of exposure. Faster the onset of symptoms = more severe is reaction. BIPHASIC PHENOMANON- occurs in sever anaphylaxis. a) symptoms return 3-4 hrs after initial reaction has cleared. 40- 60% for insect stings 20- 40 % for radio contrast agent. 10-20 % for drug.

Treatment
Epinephrine 0.3mg IM of 1:1000 - repeat every 5 -10 mins as needed. -caution with patients on beta blocker ( causes severe hypertension due to unopposed alpha stimulation.) - if refractory start IV drip 2-8 ugm min.

Corticosteroids a) prednisolone 50 mg od b) Methylprednisolone 125 mg IV od Antihistaminic a) H1 blocker diphenhydramine b) H2 blocker ranitidine. Bronchodilators albuterol . Glucagon for pt taking beta blocker and with refractory hypotension. 1 mg IV in 5 divided doses.

SEPTIC SHOCK
Bactremia:
Presence of bacteria in blood, as evidenced by positive blood cultures.

Septicemia: Presence of microbes & their toxins in


blood

SIRS:

Two or more of the following conditions: 1) Fever (oral temperature >380C) or Hypothermia (<360C), 2) Tachypnea (>24 breaths/min), 3) Tachycardia (heart rate >90 beats/min), 4) Leukocytosis (>12,000/l), or >10% band forms or Leukopenia (<4000/l) SIRS that has a proven or suspected microbial etiology.

Sepsis:

Severe sepsis: Sepsis with one or more signs of organ dysfunction Septic shock: Sepsis with hypotension arterial blood pressure
<90 mmHg systolic for at least 1 hr despite adequate fluid resuscitation. (CVP 8 or PCWP 12 mmHg) Or Need for vasopressors to maintain systolic BP 90 mmHg or MAP 70 mmHg

Refractory septic shock: Septic shock that lasts for > 1 h and
does not respond to fluid or pressor administration

MODS:

Dysfunction of more than one organ requiring intervention to maintain homeostasis.

ETIOLOGY

CARDIOGENIC SHOCK
DEFINED ASA) SBP < 90 mmhg. B) CI < 2.2 l/m2. C) PCWP > 18 mmhg.

Decrease pumping ability of the heart because of cardiac abnormality. Severe depression of the systolic cardiac performance is key factor in causing this type of shock. Inadequate pumping of venous return congestion of lung and viscera (congested shock).

Causes
Anterior wall MI. LVF Ventricular septal rupture. Severe MR HOCM with severe outflow obstruction. Aortic dissection Severe valvular heart disease.

Signs cool mottled skin - tachypnoea - hypotension - Altered mental status - narrowed pulse pressure

Approach to a patient of cardiogenic shock


Shock

Acute pulmonary edema O2 and intubation as needed NTG Furosemide IV 0.5 to 1 mg / kg Morphine IV 2 to 4 mg

Volume problem Administer fluids Blood transfusion Consider vasopressor

Pump problem

Rate problem

Bradycardia or trachycardia

Blood Pressure

Systolic BP defines 2nd line of action

SBP > 100

SBP 70-100 no signs of shock

SBP 70-100 signs of shock

SBP < 70 sings of shock

NTG if SBP > 100 mmhg Dopamine if SBP 70-100 Dobutamine if SBP < 100

NTG 1020 mug / min

Dobutami ne 2 to 20 mug kg / min

Dopamin e 2-20 mug/kg/ min

Norepinepri ne 0.5 to 30 mug/min

Identify & treat reversible causes PAC IABP Angiography & PCI

Intra aortic balloon pump (IABP)


-

Augments coronary blood flow in diastole. Balloon collapse in systole creates a vacuum effect.---- decrease afterload. Decrease myocardial o2 demand.

Indication
Class 1- evidence that an IABP should be used in acute MI with
- hypotension - low output states -cardiogenic shock not quickly recovered with pharmacologic therapy. haemodynamic

Class 2 the e/o is in favour of benefit from IABP in pt with ac MI.


- refractory polymorphic VTAC in an attempt to diminish myocardial ischemia. - Refractory pulmonary congestion.

Contraindication
Significant AR Abdominal aortic aneurysm Uncontrolled sepsis Uncontrolled bleeding disorder Peripheral vascular disease

Complication
Cerebro vascular episode Sepsis Ballon rupture Thrombocytopenia Peripheral neuropathy

OBSTRUCTIVE SHOCK
Impairment of ventricular filling during diastole due to external pressure on heart. ventricular filling & stroke volume cardiac output circulatory shock. causes Peripheral cardiac temponade Tension pneumathorax Constrictive pericarditis Pulmonary embolism

1. 2. 3. 4.

Diagnostic approach to shock

MI, PTE, Sepsis Tension Pneumothorax, Cardiac Tamponade, Sepsis

Sepsis, Anaphylaxis

Hemorrhage

Na/H2O loss