Shock.pdf

Definition of shock
• Shock is a state in which there is inadequate blood flow to the tissues to
meet demand.
• Shock and hypotension often co-exist, BUT a normal blood pressure DOES
NOT exclude the diagnosis of shock
• Imbalance between tissue supply and demand →Anaerobic Metabolism
→Lactic Acid Production
• The acute circulatory failure if prolonged, results in irreversible organ
failure.
• Mortality is high without early diagnosis and treatment.
Department of Anaesthesia and Intensive Care, the Chinese Universityof Hong Kong July 2015
Medical Guidelines Medicins Sans Fronteires on Shock

Clinical features-- Signs common to most forms of
shock
– Pallor, mottled skin, cold extremities, sweating and thirst.
– Rapid and weak pulse often only detected on major arteries (femoral or
carotid).
– Low blood pressure (BP), narrow pulse pressure, BP sometimes
undetectable.
– Capillary refill time (CRT) > 3 seconds.
– Cyanosis, dyspnoea, tachypnoea are often present in varying degrees
depending on the mechanism.
– Consciousness usually maintained, but anxiety, confusion, agitation or
apathy are common.
– Oliguria or anuria.

Different types of Shock
1. Hypovolaemic
2. Cardiogenic
3. Distributive
4. Obstructive
Department of Anaesthesia and Intensive Care, the Chinese Universityof Hong Kong
July 2015

Signs specific to the mechanism of shock --
Hypovolaemic shock
• The common signs of shock listed above are typical of hypovolaemic
shock.
• Do not underestimate hypovolaemia. Signs of shock may not become
evident until a 50% loss of blood volume in adults.

Distributive Shock
• Caused by maldistribution of blood flow from peripheral
vasodilatation and decrease in systemic vascular resistance (SVR)
(decreased afterload)
• Sepsis
• Anaphylaxis
• Neurogenic

Signs specific to the mechanism of shock - Septic
shock
– High fever or hypothermia (< 36 °C), rigors, confusion
– BP may be initially maintained, but rapidly, same pattern as for
hypovolaemic shock.

Signs specific to the mechanism of shock -
Anaphylactic shock
– Significant and sudden drop in BP
– Tachycardia
– Frequent cutaneous signs: rash, urticaria, angioedema
– Respiratory signs: dyspnoea, bronchospasm

Signs specific to the mechanism of shock -
Cardiogenic shock
– Respiratory signs of left ventricular failure (acute pulmonary oedema)
are dominant: tachypnoea, crepitations on auscultation.
– Signs of right ventricular failure: raised jugular venous pressure,
hepatojugular reflux, sometimes alone, more often associated with
signs of left ventricular failure.

Causes of
Cardiogenic
Shock
Hollenberg SM, Kavinsky CJ, ParrilloJE. Cardiogenic shock. Ann Intern Med. 1999;131(1):47-59.

Trauma Patients
Can Present with A
Combination of
Different Types of
Shock
Jeremy Richards et al. Diagnosis And Management Of Shock In The
EmergencyDepartment. EmergencyMedicine Practice 2014, 16:3

The aetiological diagnosis is oriented by:
– The context: trauma, insect bite, ongoing medical treatment, etc.
– The clinical examination:
• fever
• skin pinch consistent with dehydration
• thoracic pain from a myocardial infarction or pulmonary embolus
• abdominal pain or rigidity of the abdominal wall from peritonitis,
abdominal distension from intestinal obstruction
• blood in stools, vomiting blood in intestinal haemorrhage
• subcutaneous crepitations, likely anaerobic infection

Characteristics of different types of shock
Type of shock JVP/CVP Cardiac output (CO) Systemic vascular
resistance (SVR)
Clinically
Hypovolemic ↓ ↓ ↑ Cold and shut down
Cardiogenic ↑ ↓ ↑ Cold and shut down
Distributive ↓ ↓/-/↑ ↓ Warm and dilated
Obstructive ↑ ↓ ↑ Cold and shut down
July 2015

Lab studies
• FBC
• RP
• LFT
• Amylase
• Cardiac biomarkers
• ABG
• Cultures
• Lactate

Imaging
• USS
• Maximal inferior vena cava diameter was better able to differentiate a central venous
pressure <10mmHg from a central venous pressure >10mmHg
• Abdominal aortic aneurysm
• Echo
• Cardiac ejection fraction to determine etiology of shock – depressed in cardiogenic shock
• Cardiac tamponade
• Aortic dissection
• Pulmonary embolism
• CXR
• Heart size, presence/absence of pulmonary edema/infiltrates/effusion/ pneumothorax
• CT scan
• Only if USS is inconclusive

Management of Shock (General)
• Definitive treatment for patients in shock depends on the specific
etiology; however, this may not be immediately clear on initial
presentation
• Thus initiation of therapy and patient stabilization may occur
simultaneously with evaluation.
• The goals in treating patients in shock are restoring adequate organ
perfusion and oxygen delivery while considering/treating the possible
cause(s) of shock

Initial Stabilization
• Airway
• Breathing
• Circulation

Management of Shock (General)
• Early recognition and prompt treatment of the underlying cause of
shock
• Ensure oxygenation and maintain perfusion
• Usually aim for:
• Mean Arterial Pressure (MAP) ≥ 65mmHg .…. formula MAP = SBP + 2(DBP)
3
• Urine output ≥ 0.5ml/kg/hr
July 2015

Treatment – Monitoring
• Cardiovascular monitoring
• Cardiac monitoring, BP cuffs automated

Treatment -- Fluid resuscitation
• Only approximately 50% of hypotensive patients are volume responsive
• Passive leg raise can rapidly, noninvasively and easily as a reversible tool to
assess volume responsiveness
• Leg is raised from horizontal to vertical position and then assess volume
responsiveness
• Crystalloid is usually used for the initial treatment of undifferentiated shock

Management -- Vasopressor
• Once patient is euvolemic but there is still ineffective oxygen delivery,
vasoactive medications are likely required
• Vasopressor medications used to support mean arterial pressure by
increasing systemic vascular resistance and/or cardiac output
• Noradrenaline is a strong alpha agonist with some beta 1 activity and is a
recommended initial choice for most categories of shock
• Metaanalysis of 11 trials showed there is a statistically significant increased
risk of death associated with dopamine. Thus should not be used as a first
line pressor agent

Treating Shock – Vasopressors
Activity at Receptors
Agent α1 α2 𝛽1 𝛽2 Dopaminergic
Dobutamine + + ++++ ++ 0
Adrenaline ++++ ++++ ++++ +++ 0
Noradrenaline +++ +++ +++ +/++ 0

Restoring Blood Pressure
• Mean arterial pressure is the preferred blood pressure to target during resuscitation
• The recommended initial goal is 65 mm Hg. A higher goal of 80 to 85 mm Hg may help patients
with chronic hypertension, while a lower target may be better tolerated in patients with reduced
systolic function, older patients, and patients with end-stage liver disease
• After blood pressure falls below a critical threshold, tissue perfusion decreases linearly. That
critical threshold can vary between organ systems and individuals, and the target can later be
personalized based on global and regional perfusion as assessed with urine output, mental status,
or lactate clearance
• Decisions to titrate vasopressors to achieve mean arterial pressure goals should be balanced
against potential adverse effects, including arrhythmias, cardiovascular events, and ischemia
Siddharth Dugar et al Sepsis and septic shock: Guideline-based managementCLEVELAND CLINIC JOURNAL OF
MEDICINE VOLUME 87 • NUMBER 1 JANUARY 2020

Restoring Blood Pressure
• Norepinephrine is the first line vasopressor agent
• A second vasopressor is routinely added when norepinephrine doses
exceed 40 or 50 μg/min
• Epinephrine or vasopressin as second line vasopressor agent

Hypovolaemic shock
- Due to inadequate circulating fluid volume
Causes:
- divided to haemorrhagic or non-haemorrhagic (major burns;
gastrointestinal losses: vomiting, fistulas; urinary losses: diabetes,
diabetes insipidus; evaporative losses with fever, abdominal surgery)
Management:
- fluid resuscitation
- haemorrhagic cause: transfusion of red cells and blood products.
- review source of bleeding and stop bleeding promptly
- use of hemostatic agent
July 2015

Cardiogenic shock
- due to cardiac pump failure resulting from myocardial or valvular failure
Causes:
- commonest: acute coronary syndrome
- other causes: arrhythmia, myocardial contusions post-trauma; myocarditis; acute valvular dysfunction;
cardiomyopathy
- echo is very useful in reviewing the cause and monitor the progress
Management:
- Acute Coronary Syndrome (ACS): reperfusion by fibrinolytics or Per Cutaneous Intervention (angiogram ±
angioplasty ± stenting)
- control arrhythmia: pharmacological, electrical: pacing/ cardioversion
- optimise preload by fluid: a trial of small bolus of fluid with close observation of CVP/BP trend
- inotropic support: augment myocardial contractility. Increasing diastolic blood pressure to increase coronary
perfusion pressure and flow
- afterload: vasodilator will cause further hypotension, use with caution in normotensive patients
- mechanical device: Intraaortic Ballon Pump (IABP), Extracorporeal Membrane Oxygenation (ECMO)
July 2015

Distributive shock
Due to peripheral vascular dilatation causes a fall in peripheral resistance. The
cardiac output is often increased but the perfusion of vital organs is comprised
because the body loses its ability to distribute blood properly (vasoplegia)
Causes:
- septic shock; anaphylaxis; neurogenic shock
Management:
- Fluid resus
- Septic shock: prompt antibiotics, source control
- Inotropic support: start when BP is refractory to fluid. Usually noradrenaline for
septic shock
- Anaphylaxis: SC/ IV/ IM adrenaline
July 2015

Anaphylactic Shock
• Mainstay of treatment is rapid administration of adrenaline
• Adrenaline should be administered immediately if anaphylaxis is
suspected.
• Adrenaline should be given intramuscularly if intravenous access is
not available; treatment should not be delayed by attempting to place
an intravenous line.
• The standard intramuscular dose of adrenaline is 0.3 mg to 0.5 mg in
a 1:1000 dilution, and dosing may be repeated every 3 to 5 minutes
as clinically indicated.

2016 Sepsis-3 committee – Sepsis Definition
• Sepsis—A life-threatening condition caused by a dysregulated host
response to infection, resulting in organ dysfunction
• Septic shock—Circulatory, cellular, and metabolic abnormalities in
septic patients, presenting as fluid-refractory hypotension requiring
vasopressor therapy with associated tissue hypoperfusion (lactate > 2
mmol/L
Singer M, Deutschman CS, Seymour CW, et al. The Third International Consensus Defi nitions for
Sepsis and Septic Shock (Sepsis-3). JAMA 2016; 315(8):801–810. doi:10.1001/jama.2016.0287

Septic Shock
• Starting with broad-spectrum antimicrobials, particularly in the setting of
hypotension, and then rapidly de-escalating to an antimicrobial with the
narrowest spectrum based on local sensitivity patterns.
• If the clinical course suggests the illness is not actually due to infection, the
antibiotics should be stopped immediately
• Antibiotics de-escalation should be discussed daily. A 7- to 10-day course or
even shorter may be appropriate for most infections, although a longer
course may be needed if source control cannot be achieved, in
immunocompromised hosts, and in S aureusbacteremia, endocarditis, or
fungal infections

Sepsis and Death – Delay in Antibiotics
• Retrospective study of 35,000 randomly
selected inpatients with sepsis treated at 21
emergency departments between 2010 and
2013 in Northern California
• The primary exposure was antibiotics given
within 6 hours of emergency department
registration
• Primary outcome was adjusted in-hospital
mortality
Even a 6 hour delay will increase
death rates by 2 fold
Liu, Fielding-Singh, Greene, et al.: Timing of Early Antibiotics in Sepsis American Journal of
Respiratory and Critical Care MedicineVolume 196 Number 7 | October 1 2017, 856-863

Septic Shock – Fluid Resuscitation
• Rescue: During the initial minutes to hours, fluid boluses (a 1- to 2-L fluid
bolus of crystalloid/balanced crystalloid solution) are required to reverse
hypoperfusion and shock
• Optimization: During the second phase, the benefits of giving additional
fluid to improve cardiac output and tissue perfusion should be weighed
against potential harms
• Stabilization: During the third phase, usually 24 to 48 hours after the onset
of septic shock, an attempt should be made to achieve a net-neutral or a
slightly negative fluid balance
• De-escalation: The fourth phase, marked by shock resolution and organ
recovery, should trigger aggressive fluid removal strategies

Septic Shock – Fluid resuscitation
• Within the first 3 hours patients have a lactate level checked, blood
cultures drawn prior to antibiotics, broad-spectrum antibiotics given, and
30mL/kg of crystalloid/balanced crystalloid given for hypotension or lactate
≥ 4 mmol/L.
• Within 6 hours, vasopressors should be started for hypotension that does
not respond to fluid resuscitation to maintain a mean arterial pressure ≥ 65
mm Hg.
• Measuring the lactate level is an objective way to assess response to
resuscitation, better than other clinical markers, and it continues to be an
integral part of sepsis definitions and the Surviving Sepsis Campaign care
bundle
Jeremy Richards et al. Diagnosis And Management Of Shock In The Emergency Department. Emergency
Medicine Practice2014, 16:3

Septic Shock – Source Control
• Source control can range from removal of infected intravascular
devices to a chest tube for empyema to percutaneous or surgical
intervention in cases of cholecystitis and pyelonephritis

Septic Shock – Role of corticosteroids
• In septic shock, they have a vasopressor-sparing role and reduce the duration of
shock, ventilator use, and ICU stay
• However, the evidence is not conclusive that giving corticosteroids for sepsis
improves clinical outcomes or survival
• They can be added as adjunctive therapy for patients requiring higher doses of
vasopressors
• If corticosteroids are used in septic shock, current guidelines recommend
hydrocortisone 200 mg per day intravenously as a continuous drip or 50 mg bolus
in 4 divided doses for at least 3 days

Septic Shock – Biomarkers
• C-reactive protein and erythrocyte sedimentation rate have been
used in the past, but with limited success
• Procalcitonin has emerged as a method to help detect bacterial
infections early and to guide de-escalation or discontinuation of
antibiotics.
• Galactomannan and beta-D-glucan can be used to detect infections
with fungi, specially Aspergillus. Beta-d-glucan is more sensitive for
invasive Aspergillus, while galactomannan is more specific

Obstructive shock
Due to obstruction of great vessels or heart that impedes the blood flow
Causes:
- cardiac tamponade; tension pneumothorax; pulmonary or air embolism
Mangement:
- Prompt relief of obstruction: e.g. pericardiocentesis for tamponade,
chest drain for tension pneumothorax
- Fluid and inotrope are for temporary support
July 2015

Pitfalls

Shock.pdf

Recommended

Recommended

More Related Content

Similar to Shock.pdf

Similar to Shock.pdf (20)

Recently uploaded

Recently uploaded (20)

Shock.pdf