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Shock (Classification (Hypovolemic (Haemodynamics (low (CVP), low (PCWP),…
Shock
Classification
Hypovolemic
loss in circulatory volume, which results in decreased venous return, decreased filling of the cardiac chambers, and hence a decreased cardiac output
Haemodynamics
low (CVP), low (PCWP), low (CO) and cardiac index (CI), high SVR
causes
• Hemorrhagic
• Fluid depletion (nonhemorrhagic)
External fluid loss: Dehydration, Vomiting, Diarrhea, Polyuria
Interstitial fluid redistribution
Thermal injury
Trauma
Cardiogenic
• due to acute failure of left ventricular pump function
• high PCWP, low CO and CI, and generally a high SVR
Myopathic
MI, Myocarditis, Cardiomyopathy
Septic myocardial depression, Pharmacologic (Anthracycline, Calcium channel blockers)
Mechanical
Valvular failure, Hypertropic cardiomyopathy, Ventricular septal defect
Arrhythmic
Bradycardia, Sinus,AV Block,
Tachycardia
Distributive or Vasogenic
• poor vascular tone in the peripheral circulation,
• maldistribution of blood flow to organs within the body also
• CO varies - usually raised, low or normal PCWP, high CO, low arterial blood pressure, and a low SVR
• Septic (bacterial, fungal, viral, rickettsial)
• Toxic shock syndrome
• Anaphylactic, anaphylactoid
• Neurogenic (spinal shock)
• Endocrinologic(Adrenal crisis)
• Toxic (e.g., nitroprusside, bretyllium)
Extracardiac obstructive
impairment of circulatory flow involving mechanisms different than primary myocardial or valvular dysfunction
Impaired diastolic filling
Direct venous obstruction
tumors
Increased intrathoracic pressure(Tension pneumothorax,PEEP, autoPEEP, Asthma
Decreased cardiac compliance (Constrictive pericarditis, Cardiac tamponade
Impaired systolic contraction
Right ventricle(Pulmonary embolus, Acute pulmonary hypertension
Left Ventricle(Saddle embolus, Aortic dissection)
Diagnosis
Clinical
Tachycardia, tachypnea, cyanosis, oliguria, confusion, peripheral hypoperfusion, hypotension
Laboratory
Hemoglobin, WBC, platelets, PT/PTT,
Electrolytes, arterial blood gases,
Ca, MgBUN, creatinine, Serum lactate, ECG
Imaging
Chest radiograph, Radiographs of abdomen, CT scan,
Echocardiogram Pulmonary perfusion scan USG
Monitoring
• ECG and respiratory
• Arterial pressure catheter
• Central venous pressure monitor
• Pulmonary artery flotation catheter
• Cardiac output
• Pulmonary wedge pressure
• Mixed venous oxygen saturation
• Oxygen delivery (Do2) and oxygen consumption(VO2)
• Oximetry
• Transcutaneous oxygen tension
• Gastric intramucosal pH
• Echocardiogram
Pathophysiology
Cellular ischemia
hypoperfusion → diminished ATP→ problem with maintenance of transmembrane potential,mitochondrial function and other energy-dependent enzyme reactions→ lysosomal disruption→ death
Inflammatory mediators
Free radical injury
• induced by reperfusion or neutrophil activity
The availability of O2 generates superoxide (O2-) by xanthine oxidase which isconverted to hydrogen peroxide (H2O2) which further reacts to produce the highly reactive tissue damaging hydroxyl radicals
Therapy
1) specific therapy
• Airway menagement
• Acid base Balance
• Fluids
• Vasopressor agents
a) inotropes(dobutamine, Milrinone
b) vasoconstrictors (phenylephrine, vasopressin)
c)mixed pressors(dopamine, epinephrine, norepinephrine)
• Vasodilatators(nitroglycerin, sodium nitroprusside, hydralazine hydrochloride, ACE inhibitors and fenoldopam)
• Steroids – controversial; when no response to therapy after 24h or adrenal insufficiency, hypothyroidism, in patients with impaired adrenal pituitary axis,
Hypovolemic
• permissive hypotension, minimal crystalloid resuscitation, earlier blood transfusion, and higher plasma and platelet-to-red cell ratios
• Hemostatic adjuncts: tranexamic acid and prothrombin complex
Cardiogenic
• revascularization, valvular repair,
• Oxygenation and ventilation
• Adequate inotropic therapy
• Mechanical support devices, ev ECMO
• Transplant
Septic
• Control of the infectious source (guidline)
• Goals during the first 6 hrs of resuscitation:
a) Central venous pressure (CVP) 8–12 mm Hg
b) Mean arterial pressure (MAP) ≥ 65 mm Hg
c) Urine output ≥ 0.5 mL/kg/hr
d) Central venous (superior vena cava) or mixed venous oxygen saturation 70% or 65%, respectively
fluids
• Cristaloids ev albumin, no HES
Vasopressors
• target (MAP)
• norepinephrine as the first choice, epinephrine as second
• Vasopressin 0.03 units/minute to ↗ MAP or to ↘norepinephrine
• Dopamine
• Arterial catheter
Inotropes
dobutamine infusion up to 200 micrograms/kg/min in the presence of myocardial dysfunction as suggested by elevated cardiac filling pressures and low cardiac output,
Corticosteroids
hydrocortisone only if adequate fluid resuscitation and vasopressor therapy are unable to restore hemodynamic stability
2)
• Hemodynamic: MAP, PWP, CI
• Optimization of oxygen delivery Hb, SpO2, Svo
• Reverse organ dysfunction: urine output
Microvascular function in shock
Mechanisms
(a) tissue acidosis
(b) catecholamine depletion
(c) release of arachidonic acid metabolites
(d) nitric oxide generation
(e) decreased sympathetic tone
Compensatory Responses to Shock
(a) Maintenance of mean circulatory pressure(fluid and pressure)
(b) Maximizing cardiac function(sympathetic, adrenergic)
(c) Redistributing perfusion to vital organs
(d) Optimizing unloading of oxygen at tissues
insufficient tissue perfusion in relation to cellular function
