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• The definition of shock is a maldistribution of blood flow such that delivery of oxygen and nutrients is inadequate to organs (essentially a state of inadequate tissue oxygenation ). 
•  The purpose of tissue oxygenation is to facilitate ATP production.  Make 38 ATP from one molecule of glucose w/O2 and only 2 ATP w/ anaerobic glycolosis, with lactic acid as a by-product.
• Hemodynamic events during shock contribute to poor cardiac output, hypovolemia, and altered distribution of blood flow, which results in multiple organ failure. 
• Hypotension is the clinical hallmark of shock, although hypertension can be seen in the early stages of septic shock.

• Loss of 15% of circulating blood volume will cause tachycardia. 
• Loss of 15-35% causes hypovolemic shock that can be corrected with vasoconstriction and aggressive fluid replacement. 
• Loss of 35-45% loss can sometimes be reversed but prognosis is very guarded. 
• Loss of over 50% is irreversible and always results in death.

• Blood loss-  internal/external bleeding, trauma, tumor
• Plasma loss – burns, severe exudative dermatitis, peritonitis, pancreatitis, HGE
• Ascites
• Fluid and electrolyte loss – vomiting, diarrhea, dehydration, hypoadrenocorticism, hyperthermia
• Diuresis – hypoadrenocorticism, diabetes insipidus and mellitus

• Occurs when there is maldistribution of blood away from vital organs,  ie venous pooling of blood in peripheral vessels
• Cardiac output (CO) can be low, normal or high
• Blood pressure can be hypo, normo or hypertensive

• Trauma, Surgical Trauma
• Anesthetic overdose
• Endotoxemia
• Metabolic – renal and hepatic failure, severe alkalosis or acidosis
• Endocrine – Hypoadrenocorticism, diabetic ketoacidosis
• Anaphylaxis
• Neurogenic – spinal or cerebral – Sudden loss of sympathetic tone causes vasodilation and bradycardia.
• Sepsis – induced by bacterial endotoxins or cytokines.  Can be caused by Gram-positive, gram-negative, viral, protozoal and fungi.  Inflammatory mediators (cytokines) include: histamine, kinins, interleukins, eicosanoids, complement, b-endorphins and tumor necrosis factor. Most result in moderate to severe vasodilatation.  Common causes: peritonitis, pyometra, pyothorax, prostatic or liver abscess, intestinal strangulation or volvulus, HGE, and wound infection.

• Severe cardiac insufficiency and decreased cardiac output
• Only shock which results in increased central venous pressure.

• Cardiomyopathy – includes thyrotoxic cardiomyopathy
• Valvular disease
• Heartworm disease
• Arrhythmias
• Congenital heart disease
• Cardiac drug overdose
• Pericardial tamponade
• Pulmonary hypertension
• Intracardiac neoplasia

• Cardiac output (CO) = heart rate (HR) x stroke volume (SV)
•  Delivery of oxygen (DO2) = CO x oxygen content in the arterioles (CaO2)
• CaO2 = (1.34 x Hb x SpO2) + (0.003 x PaO2)
• VO2 = CaO2 - CvO2
• BP = CO x SVR

• Pre-load – when decreased will decrease stroke volume, diastolic filling

• Very early HV shock – decreased venous return will decrease CO which then causes hypotension and hypoperfusion.

• Baroreceptors – in aortic arch and internal and external carotid arteries – when BP is adequate, they send inhibitory impulses to brain and stim cardioinhibitory center which prevents further vasoconstriction.

• With hypotension, baroreceptors decrease their inhibitory impulses >> stim of SNS >> adrenal medulla >> catacholamines >> alpha 1 and 2 and Beta 1 and 2 receptors. >> increased HR, vasoconstriction of arteries and veins and contractility >> increased CO, BP, and venous return ( by constricting large veins ).  Splenic contraction can increase circulating blood volume by 20 %.

• The goal of the SNS is to maintain cerebral and coronary blood flow with less vasoconstriction to these areas at the expense of the rest of the body.

• CNS Ischemic response  - severe SNS stimulation when BP < 50 mmHg ( usually when < 20 mmHg)

• SNS - is maximally activated within 30 seconds after hemorrhage

• RAAS and ADH are activated within 10-30 mins

• Cushings Reaction - w/ increased CO2, you get increased BP to maintain CBF.

• Local tissue hypoxia also causes catacholamine (CAT) release from adrenal medulla (AM) and this also increases CO.

• Clinically see- increased HR, normal or increased BP, bounding pulses, hyperemic MM, rapid CRT.  This can be easily overlooked since the patient may appear normal, but HR is the key. 

• Tx is still needed at this time

• If fluid loss continues, get increased stimulation of SNS >> reduces blood to skin, muscles, viscera and kidneys in order to save blood for brain and heart.
• Uneven blood flow is the key to middle shock
• Opiods and neuropeptides are released due to stress >> peripheral vasodilation
• Hypoxia worsens – ATP and glucose are depleted >> FFA are metabolized – arachidonic acid >> toxic by-products (prostaglandins [PG], thromboxane A2 and leukotriene) >> can get vasoconstriction, vasodilation, platelet aggregation, lysosomal membrane leakage, cardiac depression and chemotaxis of WBC’s.

• Hypoxic tissues release – kinins, adenosine, PO4, lactate, K, histamine, CO2, serotonin and proteolytic enzymes

  • Vasoactive substances cause vasodilation, increased capillary permeability, myocardial depression and initiation of the clotting cascade

• Decreased arterial tone >> capillary stasis, sludging >> lactic acidosis, DIC

• As hypoxia persists > get cell death. 

  • As ATP decreases, intracellular Ca increases >> lysosomes rupture >> osmolarity changes and cell membrane leaks and ruptures. - need ATP to maintain the Na-K pump > so get ­ Na and Ca   intracellularly.  Na pulls water in, causing swelling > cell ruptures.  Ca breaks down lysosomal membranes > also destroys cell membranes.

• Heart – has high O2 demand – needs BP of 60-70mmHg.  Prolonged shock >> acidosis, hypoglycemia >> decreased contractility

• Kidneys – renin, aldosterone, ADH and angiotension all released >> more vasoconstriction >> decreased tissue perfusion >> MOD (mutiple organ failure / disfunction ) – BP below 60 mmHG >> oliguria and anuria result.  Oliguria – good early indicator of shock.  Acute renal failure (vasomotor nephropathy – from ischemia = can be reversible.

• Liver and intestines – vasculature compromised >> bacterial endotoxins are absorbed and poorly handled by reticuloendothelial system of liver >> sepsis/endotoxemia.  Also get mucosal ulceration and hemorrhage >> more pooling of blood.  Can even get bowel perforation.  ( Shock Gut )

• Lungs – Shock lung or Acute respiratory distress syndrome (ARDS), pul edema, thickening of alveolar walls, ventilation-perfusion mismatching.

• Pancreas – hypoxia >> lysosome fragmentation >> vasoactive and myocardial depressant factor >> inhibits Ca mediated contraction in heart

• Disseminated Intravascular Coagulation (DIC)- helped by bacterial toxins, hypotension, thrompoplastin (from damaged cells), acidosis and capillary stasis.

• Low rectal temp
• Poor pulses
• Pale MM
• Prolonged CRT
• Cool limbs
• Tachycardia
• Depressed mentation (hypoxic encephalopathy)
• Note - in cats, ¯ temp > poor response to catacholamines.

• Severe hypoxia even to brain and heart (from SNS stim) >> depresses respiratory and sympathetic center
• Decreased HR, BP, CO >> cardiac failure
• Clinical signs – heart failure, severe mental depression, abnormal resp paterns >> CPA to soon follow
• Even with aggressive Tx – usually irreversible

• Produces oxygen free radicals, (H2O2, OH and O2)
• Ishemia alone does not result in all the cellular damage, but also the reperfusion and subsequent inflammation.

• Crystalloids- provides volume
  • Dogs 90 mls/kg,  Cats 45 mls/kg
  • Large animals should have 2 catheters
  • 75% leaves intravascular space within 1 hour
• Colloids- Provide oncotic pressure
  • Fresh whole blood, pRBC’s, plasma, Hetastarch, gelatins, stroma free Hb, albumin, Dextran-40 and 70, Pentastarch and Pentafraction
  • Dose – 10-20 mls/kg/day – dose can be bolused and then followed by same dose over 24 hours.  Dose can be doubled in extreme cases.  Colloids should always be used with crystalloids
  • Like to keep albumin > 2 and assist oncotic pressure with colloids.
  • Watch for volume overload. 
  • Colloids without crystalloids, in volume depleted animals, can decrease GFR.
• Hypertonic saline – 7.5%
  • Comes as 23%
  • Dose – 4-10 mls/kg
  • Causes rapid shifts of fluid from extravascular to intravascular space
• HSD – Hypertonic Saline-Dextran solution
  • Used to get benefit of both fluids
  • Dose 5 mls/kg

• Dehydration needs crystalloids ( extravascular )
• Hypoperfusion ( intravascular ) needs intravascular expanders + / -  positive inotropes.
• Can have dehydration without hypoperfusion and vice versa. 
• Need to monitor CVP more, also vitals, BP, - soon - gastric mucosal pH, and serum lactate

• Supranormal end point resuscitation- therapeutic goal is not to return cardiovascular values to normal but rather, supranormal levels.
  • Cardiac index > 50% normal
  • VO2 > 30% normal
  • Blood volume 5-10 ml/kg above normal
• Hypotensive end point resuscitation
  • closed cavity hemorrhage ( ­ BP can dislodge a clot )
  • cerebral or pulmonary edema
  • want better vitals, but not back to normal
• Cats especially - start w/ ¼ shock dose and re-evaluate - Important to warm up cat before too much fluid is given, especially colloids.

• Routinely used in all shock patients even if not hypoxemic
• Benefit – Ex – SpO2 – 95%, PaO2 – 90, PCV 40, – without O2
  • CaO2 – (1.34 x 13.3 x .95) + (0.003 x 90) = 17.2
  • CaO2 = 16.93   +   0.27  = 17.2
• Give nasal O2 at 50% (FiO2 = .5 ) = SpO2 = 100%, PaO2 = 300
  • CaO2 = (1.34 x 13.3 x 1.0) + (0.003 x 300) = 18.72
  • CaO2 =  17.82   +   0.9  =  18.72
• Improvement of 8.8%

• Help stabilize lysosomal and capillary membranes, block arachidonic acid metabolism and stimulate gluconeogenesis
• Sounds cool but no benefit (based on morbidity or mortality)

• DexSP- 2-8 mg/kg
• Solu-Delta-Cortef – 15-30 mg/kg
• Do not use dexamethasone – has propylene glycol – decreases BP
• Give slow ????????

• Dobutamine – 2-10 mcg/kg/min
• Dopamine – 5-10 mcg/kg/min
• Monitor EKG for arrhythmias

• Nitroprusside – 2 mcg/kg/min
• Want MAP > 80 and systolic BP >100 mmHg
• Severe hypotension can occur very quickly – monitor closely

• Dopamine – 10-20 mcg/kg/min
  • Caution since most organs may have ongoing local vasoconstriction and these vasopressors can actually reduce local blood flow.
  • Monitor urine output, HR, EKG, pulse intensity and MM.
• Epinephrine – 2-20 mcg/kg/min (alpha and beta)
• Phenylephrine – 1-3 mcg/kg/min (alpha)
•  Treating hypotension does not solve the underlying problem. 

•  Naloxone – supposedly counteracts effects of neuropetides – not proven to increase survival rate – and it increases pain.
• Digoxin IV
• Antibiotics – consider gram neg bacteria from GIT

• CVP, BP, EKG, HCT, blood gas, HR, pulse intensity, MM, CRT, rectal temp.
• However – these have been shown in people to tell you where the patient has been, rather than where it is going. 
• Future – DO2, VO2, PCWP

• Due to valvular disease and cardiomyopathy
• Pathophysiology
  • Dilated Cardiomyopathy (DCM) – decreased CO due to poor contractility
  • Mitral disease – mitral regurgitation (MR) decreases stroke volume
  • Both cause increased left atrial pressure and pulmonary edema when heart failure occurs.
  • SNS is stimulated and therenin-angiotension-aldosterone system (RAAS) are activated.  This increases pre-load and afterload. The tachycardia from SNS stim does not allow for adequate diastolic filling, decreasing CO even more.
• Need to differentiate MR from DCM
• Both can benefit from decreasing pre-load

• Diuretic- Furosemide IV 2-4 mg/kg
• Venodilator- Nitroglycerine
• Decrease afterload
  • Nitroprusside
  • Hydralazine
  • Enalopril – reduces pre-load also
• Positive inotropes
  • Dopamine, dobutamine
  • Digoxin – different mechanism of action
• Cats with HCM -  need Diltiazem

• Have decreased intravascular fluid volume due to dehydration, fever, and extravasation, peripheral vasodilation, decreased BP and decreased VO2.
• Initially have increased CO, but not enough to perfuse tissues due to decreased BP.
• However, this hyperdynamic shock state rapidly deteriorates into a hypodynamic state. 
• Hyperdynamic state – have brick red MM, fever, tachycardia and hyperpnea (not always recognized for what it is)
• Hypodynamic – pale MM, tachycardia or bradycardia, prolonged CRT, and cool limbs.
• Similar stages of shock

• Fluids – large volumes, including colloids – HES may be better than plasma due to less loss through leaky capillary membranes
• Glucose +/-
• Potassium  +/-
• Positive inotropes
• Vasopressors
• Antibiotics – KEY
• Drain any abscess
• Culture & Sensitivity testing
• Surgical intervention