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ShockMUDr. Tomas Hitka
II.KAIM LFUK
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Definition
Failure to meet tissue demand for oxygen
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Other definitions
• Clinical state with characteristic symptoms and signs
occurring due to an imbalance between O2 supply and demand which
leads to tissue hypoxia
• Condition, in which circulation fails to meet the metabolic
need of the tissue and the same time fails to remove the metabolic
waste products.
• CO inadequate to tissue needs
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Classification
• Hypovolemic- due to absolute hypovolemia• Hemorrhagic•
Non-hemorrhagic
• Cardiogenic-due to primary pump failure• Ventricular (MI,
cardiomyopathy)• Non-ventricular (valves, malignant
arrhythmias)
• Obstructive- due to extra-cardiac flow impediment • Venous
return (tension PNO, T)• Arterial outflow (PE)
• Distributive-due to relative hypovolemia secondary to loss of
vascular tone and permeability (anaphylaxis, sepsis, neurogenic
shock)
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Pathophysiology
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Stages of shock
1. Initial- hypoperfusion-hypoxia-cell damage-rising lactate
2. Compensating- hyperventilation, increased adrenaline,
noradrenaline, renine angiotensine
3. Progressive- further damage to cells
4. Refractory- failure of vital organs
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Clinical manifestation
• CNS: confused, drowsy, comatose
• CVS: tachycardic ,hypotensive
• Resp: tachypnoeic
• Renal: oliguric
• GIT: ileus, submucosal bleeding
• Skin:• Hypodynamic: cold, pale, clammy
• Hyperdynamic: warm, bounding pulse
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Management
• A,B,C
• Optimize O2 delivery
• Optimize CO and BP
• Treat underlying pathology
• Support any organ failure
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Haemorrhagic shock
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Cardiogenic shock
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Cardiogenic shock
• Inotropic support
• Intra aortic balloon pump
• V-A ECMO
• Treat the cause• Revascularization
• Transplant
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Pulmonary embolism
• obstruction of the pulmonary artery or one of its branches by
material (eg, thrombus, tumor, air, or fat)
• acute PE
• chronic PE
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Risk factors
•Virchow’s triad:• Venous stasis• Vein wall injury•
Hypercoagulability of blood
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Patophysiology
• PA obstruction =>elevated pulmonary vascular resistance and
acute pulmonary HTN=> RV dilatation =>RV systolic failure
• PA obstruction=> V/Q mismatch- dead space• Hypoxaemia
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Clinical presentation
• Symptoms:• Breathlessness 73%
• Pleuritic chest pain 44%
• Cough 34%
• Haemoptysis
• Syncope
• Signs: can be absent• Tachypnoea 54%
• Tachycardia 24%
• Fever
• RV dysfunction
• Shock 8%
• Signs of DVT
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Investigations
• ABG, ECG, CXR
• D-dimer- useful for exclusion
• CT PA- 91% accuracy
• ECHO- RV assessment
• Doppler ultrasound- search for DVT
• Leg venography- more sensitive but invasive
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Management
• Mild PE- low risk of death and recurence- prevention of
futherembolization- LMWH
• Submassive PE-higher mortality and recurrence -
LMWH+strongconsideration for thrombolysis
• Massive PE- 25-30%mortality- urgent removal of clot+
haemodynamic support
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Prevention of further embolisation
• Oral anticoagulation
• IVC filter
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Anaphylaxis
• Type I hypersensitivity reaction- IgE mediated
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Presentation
• Cardiovascular collapse 88%
• Erythema 45%
• Bronchospasm 36%
• Angio-edema 24%
• Rash 13%
• Urticaria 8.5%
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Initial treatment
• Check A,B,C
• Stop any potential triggers
• Call for help
• Maintain the airway, give 100% O2
• Lay the patient flat with the legs elevated
• Adrenaline 50 ug i.v. until pressure or bronchospasm
improves
• 0.5-1mg i.m. repeat after 10 min if needed
• Crystalloids i.v.
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Secondary treatment
• Antihistamines: chlorpheniramine 10-20mg i.v.
• Corticosteroids: HCT 100-300mg i.v.
• Adrenaline infusion if more than 3 boluses required
• Add noradrenaline or vasopressine
• ABG- if acidosis consider bicarbonate 0.5-1mmol/kg
• Bronchdilators
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Follow up
• All patients with life threatening reaction must be admitted
to the hospital for 24 h monitoring
• Take blood 1 h after reaction for a tryptase assay
• Immunology referral
• Pt chart label
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Any questions?
