MANAGEMENT

SHOCK MANAGEMENTBY GROUP 7

ContentsDefinitions of ShockStages of ShockTypes of ShockHypovolaemic ShockCardiogenic ShockSeptic ShockNeurogenic ShockAnaphylactic ShockInotropes

Definition of shockShock = a decrease in global tissue perfusion resulting in cellular hypoxia and end-organ damage that lead to multi-organ dysfunction syndrome (MODS) which may result in serious damage or even death.

A state in which there is hypotension resulting in tissue hypoxia.

Organs of vital importance, such as brain, heart and kidneys can suffer irreversible damage, eventually leading to death

3Stages of shockThere are three stages of shock: A)Stage I (also called compensated, or nonprogressive)

when low blood flow (perfusion) is first detected, a number of systems are activated in order to maintain/restore perfusion. heart beats faster, the blood vessels throughout the body become slightly smaller in diameter, and the kidney works to retain fluid in the circulatory system. this serves to maximize blood flow to the most important organs and systems in the body. patient in this stage of shock has very few symptoms, and treatment can completely halt any progression.

4Stage II (also called decompensated or progressive)

In Stage II of shock, these methods of compensation begin to fail. The systems of the body are unable to improve perfusion any longer, and the patient's symptoms reflect that fact. Oxygen deprivation in the brain causes the patient to become confused and disoriented, while oxygen deprivation in the heart may cause chest pain. With quick and appropriate treatment, this stage of shock can be reversed.

5C) Stage III (also called irreversible)

the length of time that poor perfusion has existed begins to take a permanent toll on the body's organs and tissues. heart's function continues to spiral downward, and the kidneys usually shut down completely. cells in organs and tissues throughout the body are injured and dying. the endpoint of Stage III shock is the patient's death

Type of shockHypovolaemicCardiogenicDistributiveIncludes septic, anaphylactic, and neurogenic causes

7HYPOVOLAEMIC SHOCK8DefinitionsHypovolemic shock refers to a medical or surgical condition in which rapid fluid loss results in multiple organ failure due to inadequate circulating volume and subsequent inadequate perfusion.

It results from sudden decrease of intravascular volume9Etiology

Hemorrhagic: Trauma AAA ruptureInternal bleeding such as in GIT

Nonhemorrhagic: BurnDehydrationVomiting

Signs and symptomsHypotensionTachycardiaRapid breathingVasoconstriction Cold skinDiaphoresis clammy skinPale skin colour - PallorMental Status changes confusionUrine Output CVP, PCWP, CO 12 The greater and more rapid the blood loss, the more severe the symptoms of shock.TENNIS STAGINGClass IClass IIClass IIIClass IVBlood Loss (ml)< 750 mls750 - 15001500 - 2000> 2000 mlsLoss (% Blood Volume)< 15%15 30%30-40%> 40%Pulse rate< 100> 100> 120> 140Blood PressureNormalNormalDecreasedDecreasedRespiratory rate14 - 2020 - 3030 - 40> 40CNS Mental StatusSlightly anxiousMildly anxiousAnxious, confusedConfused LethargicFluid replacementCrystalloidsCrystalloidsCrystalloids and BloodCrystalloids and Blood14Management

ABC ( including high flow oxygen)

Raise foot of the bed

IV access X 2 (wide bore)

Identify and treat underlying cause

Infuse crystalloid (NS or Hartman solution) fast to increase the BP

InvestigationsFBC, U&E, glucose, CRPCross match and check clottingBlood culture, urine culture, ECG, CXROthers: lactate, echo, abd CT, USS

Consider arterial line, central venous line and bladder catheter (aim for urine flow >30ml/h)

Further managementTreat underlying cause if possibleFluid replacement as dictated by BP, CVP, urine outputBlood transfusion (>30% blood vol. lost)If persistently hypotensive, consider inotropes CARDIOGENIC SHOCK

CARDIOGENIC SHOCK

A pathophysiologic state in which inadequate tissue perfusion results from cardiac dysfunction.

Clinical definition: decreased cardiac output and evidence of tissue hypoxia in the presence of adequate intravascular volume.

Hemodynamic definition: sustained systolic BP < 90mmHg not improved with fluid administration, cardiac index 15mmHg

DEFINITIONSNormal cardiac index: 2.6-4.2 L/min/m2Normal PCWP: 8-12 mmHg19Myocardial infarctionArrhythmiasPulmonary embolusTension pneumothoraxCardiac tamponadeMyocarditisValve destructionAortic dissectionMyocardial depression (drugs, hypoxia, acidosis, sepsis)

ETIOLOGIES PATHOPHYSIOLOGY

Clinical features:Hypotension (low blood pressure)Cold, pale extremitiesShortness of breathCardiomegaly & pulmonary venous congestion seen on CXRA rapid, weak pulserateOliguria ( aiming for oxygen saturation > 95% to maximize tissue perfusion.

Establishing venous access via central venous cannulation. (Subclavian or internal jugular)

Establish the aetiology. => ECG, Cardiac enzymes, Echocardiography

Continuous monitoring and correct abnormalities.

MANAGEMENTBlood pressureArterial blood gasCentral venous pressure reflex amount of blood returning to heart and ability of heart to pump blood into arterial systemUrinary outputBUSEECG every hour until the diagnosis is made

MONITORING24TREATMENT

25 TREATMENT

PHOSPHODIESTERASE INHIBITOR26TREATMENTSYMPATHOMIMETICS DRUGS

eg: Dobutamine, Dopamine and Noradrenaline.

Main effects are: + increase force of contraction (positive inotropic effect)+ increase heart rate (positive chronotropic effect)+ increased automaticity+ repolarisation and restoration of function

These effects are resulted from activation of B1- receptors on the heart.

27SEPTIC SHOCK

SEPTIC SHOCK

29SEPTIC SHOCKMost common type of distributive shockIs associated with severe infection (most frequently gram-negative bacteria) and the systemic response to infection.Commonly associated with complications such as acute respiratory distress syndrome, disseminated intravascular coagulation and multiple organ dysfunction syndrome.

DefinitionsBacteremia Presence of bacteria in blood, as evidence by positive blood cultureSepticemia presence of microbes or their toxins in bloodSystemic inflammatory response syndrome (SIRS) 2 or more of the following: Fever of more than 38C (100.4F) or less than 36C (96.8F)Heart rate of more than 90 beats per minuteRespiratory rate of more than 20 breaths per minute or arterial carbon dioxide tension (PaCO2) of less than 32mm HgAbnormal white blood cell count (>12,000/L or < 4,000/L or >10% immature [band] forms)314. Septic shock Sepsis with hypotension (arterial blood pressure 1 hour and does not respond to fluid or vasopressor administration32Stages of Septic ShockStage 1: extensive peripheral vasodilation include venodilatation in which NO (nitric oxide) is implicated, causing relative hypovolemia

Stage 2: there is widespread endothelial damage causing greatly increased capillary permeability and massive fluid leakage into interstitial space

Stage 3: depression of myocardial contractility 33Inflammatory CascadeEndotoxin/ exotoxinRelease of IL-1 and TNF-Cleavage of NF-kB (nuclear factor)NF-kB able to initiate production of mRNAIncrease in proinflammatory IL : IL-6 and IL-8Release of acute phase reactants , eg. CRP and procalcitonin High grade feverRelease of NO, PAF, prostaglandin and leukotrieneCauses hypotension, and incite endothelial damageMulti-organ damageActivation of complement cascade C3a, C5aVasodilation and increase vascular permeabilityDirectly affect endothelial surfaceExpression of Tissue factorInitiate production of thrombin and cause coagulationComplication of microvascular thrombosis34

Mechanisms of septic shock are related to inflammatory mediatorsManagementSuccessful management requires urgent measures to treat the infection, to provide hemodynamic support, and to eliminate the offending microorganisms.These measures should be initiated within 1 hour of the patients presentation with severe sepsis or septic shock36Addressing the infection-Antibiotic therapyBroad-spectrum intravenous antibiotics: should be initiated within the first hour after obtaining appropriate culturesFor pneumonias, the initial broad-spectrum antibiotic coverage should be narrowed to focus on the causative organisms identified on culture.For intra-abdominal infections, therapies remain broadly directly at the range of intra-abdominal organisms-Source controlDrainage, debridement, or removal of the infectious source, through surgical372. Circulatory support-Early goal-directed therapyAdjustments of cardiac preload, afterload, and contractility to balance oxygen delivery with oxygen demand -In the first 6 hours, the goal of resuscitation are as follows:CVP (central venous pressure) 8 to 12mmHgMAP (mean arterial pressure) at least 65mmHgUrine output at least 0.5mg/kg/hour383. Vasoactive medications To maintain CO (cardiac output), heart rate usually is increased. Septic patient who fail to achieve rapid hemodynamic stability with fluids and small doses of vasoconstrictors often undergo insertion of Pulmonary Artery catheter to optimize cardiac performanceIf PA (pulmonary artery) catheter is placed, a higher filling pressure are needed (pulmonary capillary wedge pressure of 14 to 18 mmHg) to optimize performance

39-Dopamine and Norepinephrine(do not use in pt with vasoconstrictive or low CO states) 0.1-0.2g/kg/min up to 1. If need more, reevaluate do not exceed 5g/kg/minare both commonly used. (Dopamine associated with a significantly higher rate of dysrhythmias)

-Circulatory concentrations of endogenous vasopressin increase initially then decrease, and lower compared to cardiogenic shock. Low dose of vasopressin will increase MAP(mean arterial pressure), SVR (systemic vascular resistance), and urine output in patient who are hyporesponsive to catecholamines

4. Adjunctive treatments-Activated protein C: improves survival in patient with severe sepsis; associated with an increase in serious bleeding 40NEUROGENIC SHOCK

41Neurogenic ShockIs caused by decreased sympathetic control of blood vessel tone

CausesBrain injury CNS depressant: drugs, general anesthesia, hypoxia or lack of glucoseEmotional causes (transient form)Spinal anesthesia or spinal cord injury above mid thoracic region, interrupt the transmission from vasomotor centreNeurogenic shock results from interruption of the spinal cord at or above the thoracolumbar sympathetic nerve roots, which produces loss of sympathetic tone to the vascular system, causing vasodilation.

TPRPatient are typically peripherally vasodilated ( warm extremities) and tachycardic; jugular pressure is usually low.The loss of sympathetic tone may impair the ability to redirect blood flow from the periphery to the core circulation leading to excessive heat loss and hypothermia.44ManagementThe initial evaluation and care of the patient with potential neurogenic shock is the same as for all trauma patients, that is, rapid identification and stabilization of life-threatening injuries.

Airway control should be insured with spinal immobilization and protection. Followed by volume infusion

452. Crystalloid IV fluids should be infused to maintain a mean arterial blood pressure above 70 mmHg. To prevent excessive fluid administration, a pulmonary artery catheter may be placed to monitor hemodynamic response. If fluid resuscitation is inadequate to insure organ perfusion, inotropic agents such as dopamine 2.5 to 20.0 g/kg per min and dobutamine 2.0 to 20.0 g/kg per min may be added to improve cardiac output and perfusion pressure.A peripheral vasoconstrictor, such as phenylephrine or norepinephrine is administered centrally to increase vascular tone if hypotension is refractory to volume infusion 463. If necessary, severe bradycardia may need to be treated with atropine 0.5 to 1.0 mg IV (every 5 min for a total dose of 3.0 mg) or with a pacemaker.

4. In the presence of neurologic deficits, high-dose methylprednisolone therapy should be instituted within 8 h of injury. A 30 mg/kg bolus should be administered over 15 min followed by a continuous infusion of 5.4 mg/kg per h for the next 23 h.

5. Because patients with spinal shock tend to equilibriate body temperature with their environment, fluids and ambient room temperature must be kept warm

47ANAPHYLATIC SHOCK48Definition

Also called anaphylaxisA sudden, severe allergic reaction characterized by a sharp drop in blood pressure, urticaria, and breathing difficulties that is caused by exposure to a foreign substance, such as a drug or bee venom, after a preliminary or sensitizing exposure.The reaction may be fatal if emergency treatment, including epinephrine injections, is not given immediately.

49Is part of the manifestations of systemic anaphylaxis, caused by immune-mediated reaction in which vasodilatation substances such as histamine are released into the blood.

Is characterized by massive vasodilatation, pooling of blood in the peripheral blood vessels, and increased capillary permeability.

Common causes are reactions to drugs (penicillin), food (nuts, shellfish), insect venoms (bees, wasps, fire ants).

The onset of anaphylaxis depends on the sensitivity of the person, the rate and quantity of antigen exposure.Etiology

1. Immunologic IgE-mediated reactionsFoodDrugInsect stingAspirinNSAIDsACE inhibitors

3. Nonimmunologic reactionsOpioidsDextransProtamineVancomycin2. Immunologic IgE-independent reactionsBlood productsIntravenous immunoglobulinAnimal antiserum

51Pathophysiology1) IgE-mediatedImmunoglobulin E (IgE) binds to the antigenAntigen-bound IgE then activates FcRI receptors on mast cells and basophilsThis leads to the release of inflammatory mediators such as histamineThese mediators subsequently increase the contraction of bronchial smooth muscle, trigger vasodilation, increase the leakage of fluid from blood vessels, and cause heart muscle depression

2) NonIgE-mediated IgG and immune complex complementmediated are involve in the activation of mast cell and basophils

3) Nonimmunologic anaphylaxis events resulting in sudden mast cell and basophil degranulation in the absence of immunoglobulins

52

TPRPresentation Cutaneous/ocular - Flushing, urticaria, angioedema, cutaneous and/or conjunctival pruritus, warmth, and swellingRespiratory - Nasal congestion, rhinorrhea, throat tightness, wheezing, shortness of breath, cough, hoarsenessCardiovascular - Dizziness, weakness, syncope, chest pain, palpitationsGastrointestinal - Dysphagia, nausea, vomiting, diarrhea, bloating, crampsNeurologic - Headache, dizziness, blurred vision, and seizure (very rare and often associated with hypotension)Other - Metallic taste, feeling of impending doom54ManagementEpinephrineAdults 1:1000 (100kg) give 0.75mlChildren 1:10 000 (1 yr /10kg) give 1ml, 3yr/15kg give 1.5ml, 5yr/20kg give 2ml, 8yr/25kg give 2.5ml (10g/kg max 500g(5ml))Given intramuscular, the injection may be repeated every 5 to 15 minutes if there is insufficient responseIntravenously is prefer for severe casePeople on beta-blockers may be resistant to the effects of epinephrine.In this situation if epinephrine is not effective intravenous glucagon can be administered which has a mechanism of action independent of beta-receptor

552) IV fluid3) Oxygen4) Antihistamines5) Inhaled beta adrenergic agents6) Corticosteroids7) Removal of venom sac or other allergens

56INOTROPES57An INOTROPE is an agent which increases or decreases the force or energy of muscular contractions.

Negatively inotropic agents weaken the force of muscular contraction.Positively inotropic agents increase the strength of muscular contraction.

58Inotropic Drugs Positive Negative Cardiac contractility Cardiac contractilityAdrenaline Beta blockersNoradrenaline Calcium channelDopamine blockerDobutamineDigoxinIsoprenaline

59Adrenergic ReceptorClass ofmetabotropic G protein-coupled receptorsthat are targets of thecathecholamines.Main group of adrenoreceptor :Alpha receptors Subtypes : 1 and 2 receptorBeta receptors Subtypes : 1, 2 and 3 receptor

60Main group of Adrenoceptor receptors1Located in vascular smooth muscleMediate vasoconstrictionIncrease in peripheral resistance and in blood pressure2Located throughout the CNS, plateletsMediate sedation, analgesia & platelet aggregation

61Main groups of Adrenoceptor receptors1Located in the heartMediate increased contractility & heart rate2Located mainly in the smooth muscle of bronchiMediate smooth muscle relaxation3Located mainly in adipose tissueLinked to theregulation of body weightPromote lipolysis

621) Dopamine Acts on D, 1 and 1 receptors, depending on the dose administered.Low dose stimulates mainly dopaminergic receptors Produces renal and mesenteric vasodilationHigher dose stimulates both 1 and D receptorsProduces cardiac stimulation and also renal vasodilationLarge dose stimulates 1 receptorsProduce vasoconstriction, also renal vasoconstriction

63Half-life : 2 minOnset : 5 minDuration : 10 min

Indications : HypotensionLow cardiac outputPoor perfusion of vital organsSeptic shock patient who remain hypotensive after adequate volume expansion

64Warning : may cause peripheral ischemia in patient with history of occlusive vascular diseaseContraindication :Hypersensitivity to dopamineVentricular fibrillation/tachyarrythmiaCautions :HypovolemiaOcclusive vascular diseaseVentricular arrythmiaPost myocardial infarction652) Dobutamine Strong 1 and weak 2 or 1 receptorincreased rate and force of cardiac contraction resulting in increased cardiac output, blood pressure and heart rate but decrease in peripheral vascular resistance.Half-life : 1-2 minOnset : 10 minPeak time effect : ~15 min

66Indications : Cardiogenic shock When myocardial depression complicates a shock state (e.g. severe septic shock with low cardiac output)Adverse effects :Tachyarrhythmia (10%)Hypertension (7.5%)Premature ventricular beats (5%, dose related)Angina, dyspnea, fever, headache, palpitation (1-3%)Used with caution in atrial fibrillation as it has the effect of increasing the atriovenrticular (AV) conduction

67ReceptorEffectsDrugIV Dose (g/kg/min)D12VDVCINTCHTDopamine

0.5-2 (renal)2-55-1015-20++++++++++++--++++-+++++---------++++++-+++++-++++++Dobutamine2.5-15-+++++++-++++Adrenaline0.01-0.1>0.1--++++++++++++++--++++++++++++Noradrenaline0.5-1 (highly variable titrate SBP 90-100)-++++++--++++++At low dose dopamine act on dopamine receptor, causing vasodilatation to renal vessels therefore improving renal perfusion (conserve kidneys) and increase urine output.At higher dose, more beta 1 effect, giving positive inotropic and chronotropic effects.At much higher dose, more alfa effects giving rise to vasoconstriction.. Which also constrict renal vessels.Dobutamine, although name almost similar to dopamine, does not act on dopamine receptor.

683) AdrenalineAdrenaline acts on a1, b1 and b2 receptors. It is said to prepare the body for a "fight or flight" response.-Adrenergic effects are more pronounced at low doses and 1-adrenergic effects at higher doses.IndicationCVS: Due to its vasoconstrictive effects, adrenaline is the drug of choice for treating anaphylaxisRS: Bronchial smooth muscle is relaxed resulting in bronchodilation (b2).

Adverse effectspalpitations, tachycardia, arrhythmia, anxiety, headache, tremor, hypertension, and acute pulmonary edema.DoseInfusion can be start at dose 0.05-0.1ug/kg/min to a maximum 0.2ug/kg/min

694) NoradrenalineActs mainly on a1 receptors with few effects on b1 receptors.Actions Increases blood pressure by peripheral vasoconstriction. Less likely to cause tachycardia than adrenaline.Indications Septic shock where peripheral vasodilation may be causing hypotension.Cautions Acts by increasing afterload and therefore not appropriate for use in patients in cardiogenic shock. Blood supply to kidneys and peripheries may be reduced.DoseInitiated at an infusion rate of 8-12 ug/min and then maintenance dose 2-4ug/min

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Types of ShockInotropes72CASE SCENARIO-HYPOVOLEMIC SHOCK-ID patient:Mr Tg Zachris 43 years old Malay gentleman from Wakaf Bharu was admitted on 21/5/2015 (6 days ago) and we clerked him on 24/5/2015 (3 days ago)

Chief Complaint:Vomiting out blood on the day of admission

HOPIPatient, ex IVDU on syrup methadone and chronic smoker was apparently well until 1 day prior to admission when he developed sudden onset of epigastric pain. The pain was dull and intermittent in nature. There was no radiation, and the pain score is 5/10. He then took paracetamol and painkiller to relieve the pain. The pain resolves spontaneously after that. No change in bowel habit, no jaundice,no tea coloured urine and no abdominal distension.HOPIOn the day of admission, he started to vomit out blood 7 times. For the first episode, the vomitus contain food particle mixed with blood. For subsequent episodes, it contains only blood and there was presence of blood clot. The amount of vomitus for each episode is about 2 cups and patient described the vomitus as bright red in colour.HOPIDue to excessive blood loss, he experienced lethargy and giddiness. His wife noted that he looked pale. There were no SOB, chest pain, palpitation and loss of consciousness.On further questioning, patient claimed of passing out blackish stool on the day of admission twice. No altered in consistency and amount. No similar history noted before.No history of taking traditional medication before.No family history of malignancySystemic review was unremarkable.

Physical ExaminationAlert, conscious ,pale and lethargic lookingVital signs at A&E BP: 98/52mmHg (hypotension) PR:109 bpm (tachycardia) T: 37 degree celcius Spo2: 100 % under room air

Respiratory system: Lungs clearCVS: S1S2 ,no murmurAbdominal: Soft, non tender, no hepatosplenomegalyPer rectal examination: fresh melena noted, no mass felt, normal anal tone felt.SummaryPatient, 43 years old Malay male, ex IVDU, chronic smoker presented with hemetemesis 7 episodes on the day of admission associated with epigastric pain and melenic stool. On examination, patient appeared pale, not jaundice, tachycardic, and hypotensiveInvestigationsFBC : WBC: 5.5 x 10^9/L (normal) Hb: 7.4 gm/dl (anemia) Hematocrit: 20.8 % (low due to anemia) MCV: 90.8 fL (normal) MCHC : 35.5 g/dl (normal) Platelet: 77 x 10^9/L (thrombocytopenia maybe due to repeatedly reactive hepatitis C)ABG: under room air PH : 7.37 ( normal) PCO2: 35 mmHg ( normal) PO2 : 98.9 mmHg (normal)BUSE : Sodium: 139 mmol/l (normal) Potassium : 4.7 mmol/l (normal)BUN: 9.5 mg/dl (normal)

Liver function test : AST : 94 u/l ( high) ALP: 167 u/l ( high) ALT: 59 u/l (high) Total bilirubin: 38 AST, ALP, ALT and total bilirubin high due to hepatitis C

Coagulation profile: INR: 1.7 ( prolonged) APTT: 48.8 s (prolonged) PT: 19.7s (prolonged) Coagulopathy due to thrombocytopeniaOGDS (21/5): oesophageal varices-banded 6 times, forrest III antral ulcer and portal gastropathyForrest 3: lesions without active bleeding, clean basePortal gastropathy : changes in mucosa of the stomach in patients with portal hypertensionManagementPlan at A&E:Resuscitated with 2 pint packed cell (anemia), 4 unit of fresh frozen plasma (stop massive hemorrhage), 4 units of platelet (thrombocytopenia)IV Drip 5 pints ,3 pints of normal saline and 2 pints of dextrose 5%Keep NBMStrict I/O chartIV pantoprazole 80mg stat and infusion 8mg/hIV maxolon 10mg stat (dopamine antagonist, to prevent vomiting)IV tranexamic acid 1g stat then tds (to stop or reduce heavy bleeding)Plan for OGDS

Diagnosis: Upper GI Bleed secondary to esophageal varices THANK YOU