Shock

Daniel Eshetu

Objectives Understand the pathogenesis of shock Classify different categories of shock Be able to assess different categories

of shock Will understand management principles

of shock

Why do we learn shock repeatedly?

Shock one of the commonest EM problems in all disciplines(Imed,surgery,Oby-GY,Pediatrics,etc)

If Not promptly handled it is a killer(Prompt diagnoses, management and monitoring is vital)

Frequently delay in diagnoses, delay in decision, inappropriate management and referral kills patients.

Case scenerio A 32 years old woman presented with

profuse watery diarrhea and becomes agitated(resless/anxious).

BP is 60/40 Pulse weak/120/min RR 30/min.

What is your approach/How do you manage?

What is your order in the order sheet?

EM Evaluation of Pts(ABCD/VS)

A –Air way opening B-Breathing or function of respiration C-circulation D-Disability-neurologic functions(AVPU

or Glasow coma scale-alert,respond to verbal stimuli,respond to noxious stimuli,unresponsive)

V/S-BP,PR,RR,Temp

Approach/Management1. The ABCD/ primaryassessement and

stabilization of the patient is priority.2. Frequent monitoring and

reassessment and adjustment of management .

3. Detailed HX,P/E,and workup for identification of the cause and manage accordingly.

Order sheet=in the first 20min then revise after 20’

1. N/S 1000CC fast to go in 20/min(bolus or 1000/20=50ml/min=not count in drops,2 veins may be neeed)

2. Oxygen with face mask with flow of 10l/min3. Keep warm in shock position4. Reassure5. Monitor BP,PR,RR,SaO2 every 15min6. Catheterize and monitor urine output every

hour

DefinitionSHOCK: inadequate organ perfusion to meet

the tissue’s oxygenation demand. Organ perfusion depends on blood flow which depends on arterial blood pressure(ABP).

(Pressure is low )

Cardiac arrest :Sudden stoppage of the heart to pump blood and as a result no circulation to the brain.

(Pressure is 0)

Physiology of ABP ABP cardiac out put(CO) and peripheral vascular resistance

CO= Stroke volume(SV) * heart rate(HR)

SV EDV(depends on venous return) , myocardial contractility and the after load.

Systemic Vascular Resistance (SVR) Vessel length, Blood viscosity, Vessel diameter

Hypotension

• In Adults:– systolic BP ≤ 90 mm Hg– mean arterial pressure ≤ 60 mm Hg– Reduction of systolic BP > 40 mm Hg from the patient’s

baseline pressure– Hypotension causes inadequate transport and delivery of

oxygen and Glucose.– Hypotension(shock) affects the biochemistry of

cells(Aerobic to anaerobic) and cellular dysfunction occurs.

Cellular Requirements Oxygen Glucose

C6H12O6 (s) + 6 O2 (g) → 6 CO2 (g) + 6 H2O (l) + heat

Glycolysis-first pathway in glucose metabolism and Krebs Cycle

1

Pathophysiology Shock affects mitochondria first Oxidative Phosphorylation impaired & anaerobic

metabolism begins leading to lactic acid production. Without oxygen mitochondria convert pyruvate/fuels

to lactate → lactic acid(LDH) Failure of the Krebs cycle

Oxygen is the final electron accepter to form water

Pathophysiology-cellular dysfunction ATP production falls, the Na+/K+ pump fails resulting in

the inability to correct the cell electronic potential.

-Cell swelling occurs leading to rupture and death.

ATP + H2O ⇒ ADP + Pi + H+ + Energy Acidosis results from the accumulation of acid during

anaerobic metabolism.

H+ shift extracellularly and a metabolic acidosis develops

Effects of shock on the body/systems serum pH is lowered(acidoses) lead to tachypnea. endothelial dysfunction-endothelial leak and coagulation

cascade stimulated(DIC). Kidney-tubular necrosis and acute renal failure. stimulation of inflammatory and anti-inflammatory cascades Heart-hypoxia causes reduced contractility and interstitial

edema causes poor diastolic compliance. compensatory catecholamine release causing tachycardia Lung-capillary leak with acute respiratory distress

syndrome may occur.

Compensation in shock baroreceptor reflexesbaroreceptor reflexes → sympathetic

stimulation → constrict arteriols in most parts of the body and venous reservoirs → protection of coronary and protection of coronary and

cerebral blood flowcerebral blood flowangiotensinangiotensin aldosteron, ADH aldosteron, ADH → vasoconstriction,water and salt retention by the kidneys

Stages Pre-shock Shock End-organ dysfunction

Stages: Pre-shock(compensated) Warm or compensated shock Compensatory mechanisms are able to

compensate for diminished perfusion. Tachycardia, peripheral vasoconstriction,

and either a modest increase or decrease in BP may be the only sign.

Stages: shock• Compensatory mechanisms become

overwhelmed, resulting in:– Tachycardia– Tachypnea ,Metabolic acidosis– Oilguria– Cool, clammy skin

• Usually occur with Loss of 20-25% of effective blood volume

• Eventually irreversible shock or multiple end organ damage happens.

Etiologic classification(HDCO)

HYPOVOLEMIC

DISTRIBUTIVE

CARDIOGENIC

OBSTRUCTIVE

Hypovolemic Shock Causes

hemorrhage vomiting diarrhea dehydration third-space loss burns

Signs cardiac

output PAOP SVR

Classes of Hypovolemic Shock

Distributive Shock• Types

– Sepsis– Anaphylactic– Acute adrenal insufficiency– Neurogenic

• Signs– ± cardiac output– SVR

Case scenerio 60 years old type 2 DM patient presented to ED with

new onset of cough,shortness of breath ,fever and left sided pleuritic chest pain of 3 days duration.The patient was taking predinisolone for rheumatoid arthritis but discontinued a month before.

On P/E 60/30 RR 36/min Temp 390c PR 120/min He is confused. Analyze this case and how do you manage?

Order sheet=in the first 20min then revise after 20’1. N/S 1000CC fast to go in 20/min(bolus or

1000/20=50ml/min=not count in drops,2 veins may be needed)

2. Oxygen with face mask with flow of 10l/min3. Immediate broad-spectrum antibiotics4. Keep warm in shock position5. Reassure6. Monitor BP,PR,RR,SaO2 every 15min7. Catheterize and monitor urine output every hour8. If no response with fluid-innotropes

Case scenerio A 32 years old woman presented with

sudden collapse after TAT was administered. Intern in ED immediately evaluated a patient who had labored breathing and weak and fast pulse.

What is your approach/How do you manage?

Case A 40 years old man after spinal

developed hypotension and confusion and BP=6/40 and PR=120/min.What is your diagnoses?

Cardiogenic shock Results from pump failure and decreased

cardiac output Main categories:

Myopathies Arrythimia Mechanical Extracardiac/obstructive small amount of Fluids first, then cautious

pressers

Obstructive Shock Causes

Cardiac Tamponade Tension Pneumothorax Massive Pulmonary Embolus

Signs cardiac output SVR

General Assessment and V/S BP is decreased PR increase due to compensatory sympathetic

discharge RR increase: as a result of inadequate perfusion of

the organs including the brain.Hypoxia is a drive to stimulate respiratory center and respiratory compensation metabolic acidosis also can occur due to tissue hypoxia

General AssessmentCirculation: The patient may have mottled or pale,

diaphoretic skin due to increased peripheral vascular resistance secondary to increased sympathetic discharge.

In severe cases cyanosis may be seen

Assessment-CirculationConduct a thorough evaluation of the

circulation, including both: Cardiovascular function assessment –

heart rate, blood pressure, pulse pressure, and capillary refill time

End-organ function assessment- skin, brain, and renal perfusion

Assessment-PR and Pulse pressure Tachycardia is an important early sign of shock because

of compensatory mechanisms that help to maintain cardiac output during shock

The pulse should be carefully palpated for volume and pressure.

The palpable pulse volume(strength of the pulse) is normally relate to stroke volume and pulse pressure (the difference between systolic and diastolic pressures)

Assessment-Pulse volume/pressure

Narrowing pulse pressure with “thready “ pulses in shock with low cardiac output

Wide pulse pressure with bounding pulses(due to normal or increased stroke volume and low systemic vascular resistance) are seen in septic shock

Discrepancy in volume between peripheral and central pulses is an important sign of decreased cardiac output

Loss of peripheral and central pulses indicates cardiac arrest

Assessment-Circulation(BP) At first compensatory mechanisms may maintain BP

by increasing systemic vascular resistance Hypotension is a late and often sudden sign of

cardiovascular decompensation, therefore even mild hypotension should be treated quickly and aggressively

25% of blood volume must be lost before a drop in blood pressure occurs.

Hypotension may occur early in septic shock

Assessment- Capillary Refill Time Sluggish, delayed, or

prolonged capillary refill time of > 2-3 seconds can be a sign of shock, fever, or cold temperature

Brisk capillary refill may be present in septic shock

End organ function assessment

Skin Perfusion Cool extremities and pale, diaphoretic skin are early

signs of shock.Brain Perfusion Altered mental status is one of the most important

clinical indicators of deteriorating shock.Renal Perfusion Urine output of < 1ml/kg per hour in an infant or young

child, and < 30ml/hr in adolescents can be an important sign of decreased systemic cardiovascular perfusion

Management of ShockThe fundamentals of shock management are : Optimizing oxygen content of the blood Improving volume and distribution of cardiac output Reducing oxygen demand Correcting metabolic derangements: hypoglycemia,

hypocalcemia, hyperkalemia, metabolic acidosis

Management of ShockTherapeutic end points of shock

management are: Normal pulses (central & peripheral) Capillary refill < 2 seconds Warm extremities Normal mental status Normal BP Urine output >0.5-1ml/kg/hr Decreased serum lactate

General Management of Shock Positioning Oxygen administration Obtain vascular access Fluid resuscitation Monitoring Frequent Assessment Pharmacologic support consultation

Fluid Administration

crystalloids are cheaper and main choice(NS or RL) 2-3litres in 20-30minutes or in children start fluid

resuscitation for hypovolemic and distributive shock with 20ml/kg isotonic crystalloid (NS or RL) administered as a bolus over 5-20 minutes

Fluid is given more slowly in cardiogenic shock. Repeat dose if no improvement with in 10-20’ blood must supplement in hemorrhage. One big vein, or two smaller veins with large canulla. Pressors?

Blood Products Therapy Blood and blood products are not the first

choice for immediate volume expansion in shock

Blood is recommended for volume loss in trauma patients with inadequate perfusion despite administration of 2-3 boluses of isotonic crystalloid

Packed red blood cells 10ml/kg is recommended.

Monitoring

continuous assessment of the physiologic status is necessary.

Blood pressure, pulse, and respiratory rate should be monitored continuously

a Foley catheter should be inserted to follow urine flow

and mental status should be assessed frequently.

Oxygen saturation

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SHOCK

THE END.