Shock Corrected
Shock Corrected
Shock Corrected
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.
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.
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
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
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
Renin
Converts
Angotensin I
Via ACE
Angiotensin II
Adrenal Cortex Releases Aldosterone Increase Sodium Reabsorption Increase fluid volume Increase BP
Decrease BP
Mean capillary pressure is low Absorption of fluid from interstial fluid compartment to circulation Thus,blood vol. increased restore BP normal
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.
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.
1.
Cardiac failure Vasomotor failure Peripheral circulatory failure Septicaemic & toxaemia
2.
3.
4.
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.
TYPES OF SHOCK
1.
Hypovolaemic shock Low-resist or distributive or vasogenic shock Cardiogenic shock Obstructive shock
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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
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.
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
Vital sign unstable or acidosis worsen Cardiac Index <3.5 PCWP < 15 Administered crystalloid blood
Insert PAC
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.
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.
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:
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
Acute pulmonary edema O2 and intubation as needed NTG Furosemide IV 0.5 to 1 mg / kg Morphine IV 2 to 4 mg
Pump problem
Rate problem
Bradycardia or trachycardia
Blood Pressure
NTG if SBP > 100 mmhg Dopamine if SBP 70-100 Dobutamine if SBP < 100
Identify & treat reversible causes PAC IABP Angiography & PCI
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
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.
Sepsis, Anaphylaxis
Hemorrhage
Na/H2O loss