Shock

Dr. TSEGAYE ALEM

7/7/2025 1
Objectives
• Participants are expected to
– understand definition and pathophysiology of
shock
– Understand overview of the different types of
shock
– develop a systematic approach to the detection
and management of shock
 Definition of Shock
• Inadequate perfusion and oxygenation of cells
 Definition of Shock
Inadequate perfusion and oxygenation of cells
(imbalance b/n O2 demand & supply)

Cellular dysfunction and damage

Organ dysfunction and damage

 Why should we care?
• High mortality - 20-90%

• Early in the course , O2 deprived cells are

REVERSIBLE

• Early intervention reduces mortality

 Pathophysiology

• 4 types of shock
– Cardiogenic
– Hypovolemic
– Obstructive
– Distributive
Ok…it’s really not THAT simple

MAP = CO x SVR

HR x Stroke volume

Preload Afterload Contractility

Type of Insult Physio Compen Compensation Compensation
Shock logic sation Heart Rate Contractility
Effect
Cardiogenic Heart fails to ↓CO BaroRc ↑ ↑
pump blood ↑SVR
out
Obstructive Heart pumps ↓CO BaroRc ↑ ↑
well, but the ↑SVR
outflow is
obstructed
Hemorrhagic Heart pumps ↓CO BaroRc ↑ ↑
well, but not ↑SVR
enough blood
volume to
pump
Distributive Heart pumps ↓SVR ↑CO ↑ ↑
well, but
there is No Change - No Change -
peripheral in neurogenic in neurogenic
vasodilation shock shock
Additional Compensatory Mechanisms
• Renin-Angiotensin-Aldosterone Mechanism
– AII components lead to vasoconstriction
– Aldosterone leads to water conservation

• ADH leads to water retention and thirst

• Inflammatory cascade
 Hypovolemic Distributive Cardiogenic Obstructive
Shock Shock Shock Shock

HR Increased Increased May be Increased

(Normal in increased or
Neurogenic decreased
shock)
JVP Low Low High High

BP Low Low Low Low

SKIN Cold Warm (Cold Cold Cold

in severe
shock)
CAP Slow Slow Slow Slow
REFILL
 Stages of Shock

Insult

Preshock
(Compensation) Timeline and progression will
depend on:
Shock -Cause
(Compensation -Patient Characteristics
Overwhelmed) -Intervention
End organ
Damage

Death
 Symptoms and Signs of Pre-
Shock/Shock
• Level of consciousness
– agitation, progresses to confusion or delirium, and
ends in obtundation or coma.
• Initially may show few symptoms
– Continuum starts with
• Anxiety
• Agitation
• Confusion and Delirium
• Obtundation and Coma
 Symptoms and Signs of Shock
• Pulse
– Tachycardia HR > 100 - What are a few exceptions?
– Rapid, weak, thready distal pulses
• “What are a few exceptions to tachycardia?”
– neurogenic shock
– relative tachycardia - e.g. in an athlete HR of 90 is
tachycardia
– bradycardic causes of shock!
– bradycardia in severe shock - an agonal event from any
cause of shock
• Respiration : tachypnea occurs due to
– Chemoreceptors sense hypoxia and compensate by
causing tachypnea
– Compensatory mechanism for metabolic acidosis
(to blow off CO2)
BRADYCARDIA CAUSES OF SHOCK
-high grade AV block
- severe sinus bradycardia
- hypothyroidism
- hypothermia
- neurogenic shock
- Increased ICP
Symptoms and Signs of Shock
• Blood Pressure
– May be normal!
– Definition of hypotension
• Systolic < 90 mmHg
• MAP < 65 mmHg
• 40 mmHg drop systolic BP from baseline
 Symptoms and Signs of Shock
• Skin
– Cold, clammy (Cardiogenic, Obstructive, Hemorrhagic)
– Warm
• Early phase of Distributive shock
• Terminal shock due to failure of compensatory
vasoconstriction
– Mottled appearance in children
– Look for petechia
• Dry Mucous membranes
• Low urine output <0.5 ml/kg/hr
 Empiric Criteria for Shock
4 out of 6 criteria have to be met

• Ill appearance or altered mental status

• Heart rate >100
• Respiratory rate > 22 (or PaCO2 < 32 mmHg)
• Urine output < 0.5 ml/kg/hr
• Arterial hypotension > 20 minutes duration
• Lactate > 4
 MANAGEMENT
The ABCDE of shock resuscitation
Establishing Airway
controlling the work of Breathing
Optimizing the Circulation
assuring adequate oxygen Delivery
achieving End points of resuscitation.
 ESTABLISHING THE AIRWAY

• endotracheal intubation
• Sedatives used for intubation may cause arterial
vasodilatation, venodilation, or myocardial suppression and
may result in hypotension
• PPV reduces preload and CO------mhemodynamic collapse
• To avoid this , initiate volume resuscitation and vasoactive
agents before intubation and PPV
• Decompress pneumothorax before initiating PPV
 CONTROL THE WORK OF BREATHING

• Control of breathing is required when

significant tachypnea accompanies shock
• Respiratory muscles are significant consumers
of oxygen and contribute to lactate production
• Mechanical ventilation and sedation allow for
adequate oxygenation, improvement of
hypercapnia
 OPTIMIZING THE CIRCULATION
• Fluids
– Most patients in shock have either an absolute or
relative volume deficit
– The exception is the patient in cardiogenic shock
with pulmonary edema
– Start with crystalloids
– Administer fluid rapidly (over 5 to 20 minutes), in
set quantities of 500 or 1000 mL of NS , and
reassess after each bolus
 ….
• Pts with septic shock may receive 6L of
crystalloid per 24 hours
• If larger volume is needed , use RL to avoid
hyperchloremic metabolic acidosis

• DO NOT WAIT for hypotension

• Vasopressors
– used when there has been an inadequate
response to volume resuscitation or if there are
contraindications to volume infusion
– Vasopressors are most effective when the vascular
space is “full” and least effective when the
vascular space is depleted
– Common agents
• Dopamine , adrenaline , norepinephrine
 ASSURE ADEQUATE O2 DELIVERY
• Factors that increase O2 consumption
– Pain
– Anxiety
– Shivering
• Anagesics , anxiolytics , warming
• Maintain SpO2>91%
• Transfuse with goal Hgb>7
 END POINTS OF RESUSCITATION
• target
– MAP >65 mm Hg
– central venous pressure of 8 to 12 mm Hg
– Scvo2 >70%
– urine output >0.5 mL/kg/h
– Hgb>7
– Lactate<2
– Control of hemorrhage , loss and infecton
 USG in Shock…
• RUSH protocol
 Pump
 Tank RUSH PROTOCOL(rapid ultrasound for shock &hypotension)
- HI-MAP
H........heart
 Pipes I..........IVC
M.......morrison's pouch
A....... Aorta
P......... pneumothorax/pulmonary
~_Heart-----pump
Ξ IVC/Lungs/Abdomen-------tank
k Large arteries & veins------pipe
 Cardiogenic Shock: Causes
↓MAP = ↓ CO (HR x Stroke Volume) x ↑SVR

• Decreased Contractility (Myocardial Infarction, myocarditis,

cardiomyopathy, Post resuscitation syndrome following cardiac arrest)

• Mechanical Dysfunction – (Papillary muscle rupture post-MI, Severe

Aortic Stenosis, rupture of ventricular aneurysms etc)

• Arrhythmia – (Heart block, ventricular tachycardia, SVT, atrial fibrillation

etc.)

• Cardiotoxicity (B blocker and CCBs Overdose)

 Obstructive Shock:
Pathophysiology
• Heart pumps well, but the output is decreased due
to an obstruction (in or out of the heart)

MAP = CO x SVR

HR x Stroke volume
 Obstructive Shock:
Pathophysiology
Normal Obstructive

MAP = CO x SVR MAP = ↓CO x SVR

MAP = ↓CO x ↑ SVR
↓MAP = ↓↓CO x ↑ SVR
 Obstructive Shock: Causes
↓MAP = ↓ CO (HR x Stroke Volume) x ↑SVR

• Heart is working but there is a block to the outflow

– Massive pulmonary embolism
– Aortic dissection
– Cardiac tamponade
– Tension pneumothorax

• Obstruction of venous return to heart

– Vena cava syndrome - eg. neoplasms, granulomatous disease
– Sickle cell splenic sequestration
 Hypovolemic Shock:
Pathophysiology
• Heart pumps well, but not enough blood volume to
pump

MAP = CO x SVR

HR x Stroke volume
 Hypovolemic Shock:
Pathophysiology
Normal Hypovolemic

MAP = CO x SVR MAP = ↓CO x SVR

MAP = ↓CO x ↑ SVR
↓MAP = ↓↓CO x ↑ SVR
 Hypovolemic Shock: Causes
↓MAP = ↓ CO (HR x Stroke Volume) x ↑SVR

• Decreased Intravascular volume (Preload) leads to Decreased Stroke

Volume
– Hemorrhagic - trauma, GI bleed, AAA rupture, ectopic pregnancy
– Hypovolemic - burns, GI losses, dehydration, third spacing (e.g. pancreatitis,
bowel obstruction), Adesonian crisis, Diabetic Ketoacidosis
 Distributive Shock:
Pathophysiology
• Heart pumps well. There is peripheral
vasodilation due to loss of vessel tone

MAP = CO x SVR

HR x Stroke volume
 Distributive Shock:
Pathophysiology
Normal Distributive
MAP = co x ↓ SVR
MAP = CO x SVR
MAP = ↑co x ↓ SVR

↓MAP = ↑co x ↓↓ SVR

 Distributive Shock: Causes
↓MAP = ↑CO (HR x SV) x ↓ SVR

• Loss of Vessel tone

– Inflammatory cascade
• Sepsis and Toxic Shock Syndrome
• Anaphylaxis
• Post resuscitation syndrome following cardiac arrest
– Decreased sympathetic nervous system function
• Neurogenic - C spine or upper thoracic cord injuries
– Toxins
• Due to cellular poisons -Carbon monoxide,
methemoglobinemia, cyanide
• Drug overdose (a1 antagonists)
 Septic shock
Sepsis
Life threatening organ dysfunction caused by dys-regulated host
response to infection.
• Infection: the invasion of normally sterile tissue by organism
resulting in infectious pathology.
– Signs & symptoms of infection
– Radiologic & microbiologic evidence
– Response to therapy

• Organ dysfunction: an increase of ≥2 points in SOFA score or >=2 of the

qSOFA criteria are met

7/7/2025 37
 qSOFA===quick sequential organ failure assessment

Cont…. RC LCCR mnemonics

R--respiratory [PaO2]
C---coagulopaty (platelet)
L---liver (bilirubin)
C---CVS (MAP)
qSOFA C----CNS (GCS)
R----SCr or UOP
Altered mental status-GCS
systolic blood pressure < 100mHg
Respiratory rate > 22/min
• Score >=2 indicates high risk for poor outcome.
• good for rapid identification of high risk patients in ED
• Poor sensitive (doesn't identify those at risk of later disease
progression) and higher specifity (for short term mortality)

7/7/2025 38
• Septic shock is defined by the need for a vasopressor to
maintain a patient’s mean arterial pressure (MAP) ≥ 65 mmHg
and serum lactate level ≥ 2 mmol/L
SIRS
• Systemic Inflammatory Response Syndrome
– A constellation of abnormal signs
– The presence of at least two of the ff clinical
criteria
• HR>90/min
• RR>20 /min or Low pCO2 <32mmhg
• T > 38 c or < 36 c
• Abnormal WBC count Wbc<4000/mm3 or >12000/mm3
or 10% bands
• Most frequently isolated pathogens in sepsis/septic shock:
 Gram-positive bacteria
o Staphylococcus aureus and Streptococcus pneumoniae,
 Gram-negative bacteria
o Escherichia coli, Klebsiella, and Pseudomonas spp.
 fungal infections
o Predominant role is played by Candida spp.

• The main sites of infection related to sepsis:

 Respiratory tract/pulmonary parenchyma (43%)
 Urinary system (16%)
 Abdomen (14%)
 Head, which is associated with a fever of unknown origin (FUO) (14%); and
 Other sites/causes (13%)
Management

• The cornerstones of the initial treatment of sepsis or

sepsis shock
– Early recognition

– Early reversal of hemodynamic compromise

– Early infection control

I. Initial resuscitative therapy
• Initial rresuscitation should be started immediately

• Resuscitate 30ml/kg over 3hrs of presentation with crystalloids

– Further fluid should be based on clinical and hemodynamic response

– Presence or absence of pulmonary edema

• Current literature does not provide clear guidance about the best fluid
strategy following the initial resuscitation bolus of fluids

• Some patients may require higher volume

-Indicators of fluid responsiveness (clinical & hemodynamic)
-Albumin for patients who received large volumes of crystalloids
II. TREAT INFECTION
• Broad-spectrum antibiotics should be started as early as
possible of sepsis recognition

• Initiated within one hour of presentation, preferably after

cultures have been obtained.

• Linear increase in mortality with each hour delay of

antibiotics.

• antimicrobial treatment duration of 7 to 10 days is adequate.

Source control: includes removal of the potential source of
ongoing microbial contamination

• Drainage of abscess
• Debridement of infected necrotic tissue
• Peritoneal wash and closing GI perforation

A time lag of no more than 6 to 12 hrs after diagnosis should be

targeted for source control after initial resuscitation
III. Vasopressors
• An integral component of the management of septic shock.
• Used in those
 Remain hypotensive despite adequate fluid resuscitation
 Develop cardiogenic pulmonary edema.
• Sepsis campaign 2021 recommend using norepinephrine (at a dose of
0.1–1.2 µg/kg/min) as the first-line agent over other vasopressors
/Strong recommendation/

• Start vasopressin when NE dose is in the range of 0.25-0.5 μg/kg/min at fixed

dose

• In settings where norepinephrine is not available, epinephrine or dopamine

can be used as an alternative, but Experts encourage efforts to improve the
availability of norepinephrine.

• Target MAP>65mmhg
IV.Glucocorticoids
• Using IV corticosteroids suggested for adults with septic shock
and an ongoing requirement for vaso-pressor therapy. /Weak
recommendation/

• It is suggested that this is commenced at a dose of

norepinephrine or epinephrine ≥0.25 mcg/kg/min at least 4 h
after initiation to maintain MAP>60

• hydrocortisone 200 mg IV/day is recommended, 50 mg IV

every 6 h or as a continuous infusion.

• Duration of corticosteroids remain uncertain. But usually

administered for 5-7 days.
Additional therapies
• RBC transfusion
-Hg ≤ 7 g/dl. However,
RBC transfusion should not be guided by
hemoglobin concentration alone.
-No mortality benefit with liberal strategy

• Stress ulcer prophylaxis

-Suggested for adults with sepsis or septic shock, and who have risk
factors for GI bleeding /Weak recommendation/

• Venous thromboembolism (VTE) prophylaxis

-Using pharmacologic VTE prophylaxis is recommended for adults
with sepsis or septic shock unless a contraindication to such
therapy exists /Strong recommendation/
-Preferably using LMWH (rather than UFH).

• Glucose control
-Initiating insulin therapy is recommended at a glucose level
of≥180 mg/dL (10 mmol/L). /Strong recommendation/
Case discussion ………