Lecture presentation for Clinical 1 Students

Outline
• Overview of circulatory system
• Definition
• Pathophysiology
• Stages of shock
• Classification
• Clinical features.
• Management of shock
• All cells require energy to function
• Energy is mainly extracted from the catabolism of glucose.
• Energy is stored and dispensed within the cell in the form of
adenosine triphosphate (ATP) molecules
• Aerobic metabolism
• Oxygen is required for efficient production of ATP (energy)
• The end product is CO2
• Anaerobic metabolism
• Inadequate oxygen results in decreased energy (ATP) production
• The end accumulation of lactic acid
• A functioning circulatory system requires:
– Adequate amount of blood (fluid) to fill the
vascular compartment (intravascular space)
– functional intravascular volume
– A heart that pumps adequately
– filling, propelling
– Intact blood vessels to conduct the blood being
pumped
– closed intravascular space
– dynamic physiological resistance
Shock:
• a life-threatening circulatory disorder that
leads to tissue hypoxia and a disturbance in
microcirculation.
• the very commonly encountered clinical
condition.
• the most common cause of death in
surgical patients
Definition
Shock is a state of inadequate tissue perfusion
marked by
•decreased delivery of required metabolic
substrates (O2 and glucose)
•decrease cellular energy (ATP) production
•inadequate removal of cellular waste products.
Pathophysiology
Tissue perfusion requires:
• Adequate fluid (blood) volume 5 Lt
• Pump (functioning heart)
• COP = HR × SV 5 lit/min
• Vessels - intact vessels, vascular tone (SVR )
• MAP= COP × SVR
Decrease in tissue perfusion results from:
• Loss of intravascular fluid → hypovolemic shock
• Inability of the heart to pump the blood
→ cardiogenic shock
• Redistribution of body fluid → distributive shock
Clinical clues for tissue hypoperfusion
• SBP ≤90 mmHg (or a decrease in SBP ≥20 % from
baseline);
• increase in heart rate (HR) ≥10 % from baseline;
• Cold clammy skin
• urinary output < 0.5 ml/kg/min for more than 2 h;
• hyperlactatemia (>2 mmol/L)
•Tissue hypoxia can result in
• organ damage such as
• kidney failure,
• DIC (disseminated intravascular coagulation),
• ARDS (acute respiratory distress syndrome),
• circulatory collapse.
• complex metabolic disorders such
• metabolic acidosis
Stage of compensation: Non-
progressive phase
• “Reversible stage during which compensatory
mechanisms are effective and homeostasis is
maintained”
• Clinical presentation begins to reflect the body’s
response to the imbalance of oxygen supply and
demand
• The baroreceptors in the carotid and aortic bodies
activating the sympathetic nervous system (SNS).
• Sympathetic vasoconstriction
• Release of epinephrine and norepinephrine (potent
vasconstrictors)
• Blood flow to the vital organs, such as the heart and
brain, are maintained,
• Blood flow to other organs such as, the kidneys, liver,
skin, GI tract and the lungs, is shunted.
 Decreased blood flow to the kidneys
activates the renin-angiotensin system.
 Renin is released, which activates
angiotensinogen to produce angiotensin I,
which is then converted to antiotesnsin II.
 Angiotensin II causes vasoconstriction in
both the arteries and venous system
• activation of compensatory neurohumoral reflexes in
order to maintain vital organ perfusion →
Peripheral vasoconstriction → cold, clammy
extremities and sluggish capillary refill
• Decreased capillary hydrostatic pressure → increases
absorption of interstitial fluids into intravascular space
to help maintain blood pressure
• Tachycardia
• Oliguria
• At this stage, the body is able to compensate for
the changes in tissue perfusion.
• If the underlying cause is corrected, the patient
will recover with little to no residual effects.
• If the body is unable to compensate the body
will enter the progressive stage of shock
• Progressive phase
• Worsening hypotension
• Hypoperfusion of peripheral tissues → generalized
tissue hypoxia → anaerobic metabolism in the
underperfused organs → lactic acidosis →
• Worsening tachypnea
• Precapillary dilation and postcapillary constriction of the blood
vessels → pooling and stasis of blood in the capillary bed →
decreased cardiac output and formation of microthrombi in the
capillaries → DIC and further hypoxic injury to tissues
• Acidosis, cerebral hypoperfusion → altered mental status
• Irreversible phase (stage of decompensation): irreversible
tissue damage sets in
• Cerebral hypoxia → autonomic dysfunction → worsening of shock
• Myocardial ischemia → acute coronary syndrome → decreased
cardiac output → worsening of shock
• Widespread cell necrosis →
• Release of lysosomal enzymes → further tissue injury → worsening of
shock
• Activation of the immune system → release of cytokines → DIC, further
tissue damage → worsening of shock
• Bowel ischemia → bacteremic sepsis → worsening of shock
• The end result of these vicious cycles is a downward spiral from
which there is no recovery (multiple organ failure)
Classification of Shock
Three categories
• Hypovolemic shock
• Cardiogenic shock
• Distributive shock
Causes of hypovolemic shock
• Hemorrhagic shock
• Trauma - revealed / concealed bleeding,
• External bleeding from avulsed/ severed major vessels
• intra abdominal solid organ injury/ femoral/pelvic fracture,
• Gynecologic and obstetric causes –
• APH, uterine rupture, PPH, ruptured ectopic pregnancy.
• GI bleeding – upper/lower GI
• Hemorrhagic pancreatitis
• Ruptured aneurysm
• Fluid losses
• Diarrhea/ Vomiting
• Burns
• Third space fluid loss
• Renal fluid loss: adrenal insufficiency and other salt
wasting nephropathies, osmotic/drug-induced diuresis
Pathophysiology of hypovolemic shock
• Caused by decreased preload due
to intravascular volume loss (20% of
blood volume)
• preload is one of the determinants
of stroke volume
•  preload   stroke volume  
cardiac output
• Systemic vascular resistance is
typically increased in an effort to
compensate
Clinical manifestations
• tachycardia, weak or absent peripheral pulses
• Hypotensive
• tachypnea
• flat neck veins
• clear lungs
• cool, clammy, cyanotic extremities
• evidence of bleeding?
• Anticoagulant use
• trauma, bruising
• oliguria
• agitation,
 Classification of hemorrhagic shock
Class I II III IV
Blood loss < 15% 15–30% 30–40% > 40%
Heart rate < 100 100–120 120–140 > 140
Systolic blood
Normal Normal ↓ ↓
pressure
Pulse pressure Normal or ↑ ↓ ↓ ↓
Respiratory
14–20 20–30 30–40 > 35
rate
Urine output > 30 mL/hr 20–30 mL/hr 5–15 mL/hr Absent
Mental status Anxious, Confused,
Anxious Mildly anxious
confused lethargic
Initial laboratory investigation
• blood group and x-match
• CBC , (WBC, Hct, platelets)
• Blood chemistry
• electrolyte levels
• BUN, creatinine
• RBS
• Serum lactate,
• prothrombin time, activated partial thromboplastin time
• urinalysis (in patients with trauma)
• urine HCG-childbearing aged women
Imaging studies
• Radiography – hemothorax, fracture
• ABDOMINAL UITRASOUND
• focused abdominal sonography for trauma (FAST) looks for free
fluid in abdominal cavity
• ENDOSCOPY-UGIB
Management of hypovolemic shock
Three goals exist in the emergency department
treatment of the patient with hypovolemic shock:
(1)maximize oxygen delivery
(2)control further blood loss
(3)restoring blood volume
Maximize oxygen delivery –
• ABCD of life
• ensuring adequacy of ventilation,
• endotracheal intubation and mechanical
support if needed
• increasing oxygen saturation of the blood,
• high flow oxygen with nasal prong
• Address underlying chest problems
• Tension pneumothorax, hemothorax, pain
from rib fractures, flail chest,
Control further blood loss
• Tourniquet, ligating , packing, compressing dressing
• Splint long bone fracture
• Surgical intervention for internal bleeding
• restoring intravascular volume
• Secure wide bore IV cannula – two (bilateral)
• Crystalloid fluid resuscitation –
• 2L bolus fast for adults (30 ml per kg for adults) assess pt
condition
• For children 20 ml / kg bolus
• transfusion of blood products –
• Whole blood
• RBC concentrate
• Fresh frozen plasma
• platelet
Cardiogenic shock
• Results from pump failure and
• manifested as decreased cardiac output
• Causes:
• Mechanical
• Cardiomyopathies • Valvular stenoses
• Myocardial infarction
• Valve insufficiencies
• Dilated cardiomyopathy
• Obstructive/extracardiac
• Arrhythmias • Pulmonary embolism
• Both tachycardia and bradycardic
• Tension pneumothorax
• Pericardial tamponade
• Clinical features
• Weak pulse, tachycardia
• Cold, clammy extremities, poor capillary refill
• Dyspnea, fine basal crepitations
• Elevated JVP and distended neck veins
• Hypotension with a narrow pulse pressure in the
decompensated stage
• Other clinical features related to the underlying
disease: chest pain, abnormal auscultatory
findings (e.g., S3, S4)
• Diagnostics
• Identifying the cause
• Cardiac markers (↑ troponin I, troponin T): to
identify acute coronary syndrome
• ECG: to identify myocardial infarction, cardiac
arrhythmias
• Echocardiography: to identify valvular lesions, cardiac
tamponade
• Pulmonary artery catheterization: to monitor
hemodynamic parameters as a guide to therapy
Treatment of cardiogenic shock
• Cardiopulmonary resuscitation if necessary
• Myocardial infarction
• sBP < 70 mm Hg: norepinephrine
• sBP 70–100 mm Hg: dopamine
• Reperfusion therapy (thrombolysis, PTCA )
• If pulmonary congestion: diuretics
• Vasodilators to
decrease afterload (e.g., hydralazine, isosorbide dinitrate)
Treatment cont…
• Cardiac tamponade: pericardiocentesis
• Tension pneumothorax: needle
decompression followed by chest
tube insertion
• Pulmonary embolus: thrombolysis
Distributive shock
• AKA vasodilatory shock
• Results from a severe decrease in systemic vascular
resistance
• Examples:
• septic shock
• neurogenic shock (spinal shock, sympatholytic drugs)
• anaphylaxis
• Addisonian crisis
Septic shock
• The extreme of SIRS spectrum
• Defined as abnormal host response to infection with circulatory,
metabolic, and cellular abnormalities → capillary leakage,
systemic vasodilation → acute and life-threatening organ dysfunction
Clinical features
• Patients typically present with a poor overall condition and
generalized edema (capillary leak).
• Fever , chills, and diaphoresis or hypothermic
• Tachycardia- with bounding pulse or weak / inpalpable
pulses
• Tachypnea
• Severe hypotension (< 65 mmHg)
• Initially warm skin and normal capillary refill time
(warm shock) → cold cyanotic, pale, or mottled skin with
prolonged capillary refill time (cold shock)
• Features of the primary infection
Causes of sepsis and septic shock
• Soft tissue infection (necrotizing fasciitis, burn sepsit)
• GI onset infection (septicemia
• Peritonitis with bowl necrosis, or rupture
• Genito Urinary infection (pyelonephritis, cyctitis)
• Chest infection (lung abcess,
• Features of organ dysfunction
• CNS impairment: altered mental status
• Cardiovascular failure: hypotension
• Coagulopathy → disseminated intravascular coagulation
→ petechiae, purpura
• Liver failure: jaundice
• Kidney failure: oliguria
• Respiratory failure: symptoms of acute respiratory distress
syndrome (ARDS)
• Diagnostics
• CBC - Leukocytosis or leukocytopenia, anemia
• Organ function tests - RFT, LFT
• Positive blood cultures
• Imaging (US, CT scan)
Treatment
• Immediate resuscitation (respiratory and circulatory
support)
• Intubation and mechanical ventilation may be required if the
following is present: respiratory insufficiency, dyspnea,
persistent hypotension, or poor peripheral perfusion
• Fluid resuscitation (hypotension and hypoperfusion)
• Vasopressors (catecholamines) may be necessary when
patients remain hypotensive despite fluid resuscitation
• Empiric antibiotic treatment: begin immediately after blood
cultures have been drawn, preferably within 1 hour after
recognition