Heart & Circulation

SHOCKPHYSIOLOGY OF BLOOD PRESSURESummary of factors that increase blood pressure:

Mechanism of increase cardiac outputThere are 2 mechanism to increase cardiac output:

Instrinsic cardiac regulationExtrinsic cardiac regulation

Extrinsic Regulation of Heart PumpingAutonomic Nervous SystemHormoneChemical SubstanceTemperature1. Autonomic Nervous SystemSympathetic (Cardiac Accelerator)Increases Heart Rate (HR)Increases the force of heart contractionIncreases the conduction of impulses from the atria to the ventricles* Inhibition : decrease cardiac pumpingParasympathetic (Vagus) (Cardiac Inhibitor)Decreases HRSlight decrease in heart contractionDecreases the conduction of impulses from the atria to the ventricles

Serabut parasimpatis dominan berada di atrium, tidak banyak di ventrikel, sehingga tidak berpengaruh banyak pada kontraksi jantung.7

2. HormonesThyroidIncreases metabolism vasodilation increases blood flow increases Stroke Volume(Increases CO)Increases HREpinephrine and NorepinephrineSympathomimetic

ADH / Vasopressin

3. Chemical SubstancesKalium [K+] : decreases HR, block conduction, weaker contraction : increases HRCalcium [Ca2+] : stronger contraction : weaker contractionNatrium [Na+] : weaker contractionCO2 / pHLow pH : increasing sympathetic signal (venous return )O2Low O2 : vasoconstriction

4. TemperatureIncreased body temperatureIncreases HRDecreased body temperatureDecreases HRThese effects presumably result from the fact that heat increases the permeability of the cardiac muscle membrane to ions that control heart rate, resulting in acceleration of the self-excitation process.13

SHOCKDEFINITIONShock is a condition in which the cardiovascular system fails to perfuse tissues adequatelyAn impaired cardiac pump, circulatory system, and/or volume can lead to compromised blood flow to tissuesInadequate tissue perfusion can result in:generalized cellular hypoxia (starvation)widespread impairment of cellular metabolismtissue damage organ failuredeath17Classification of Shock

1. Hypovolemic shock the most common type loss of circulating blood volume. loss of whole blood, plasma, interstitial fluid , or a combination.

2. Cardiogenic shock failure of the heart as a pump, as in arrhythmias or acute myocardial infarction (MI).

3. Vasogenic shock decreased resistance within capacitance vessels, usually seen in sepsis.

3.a. Neurogenic shock is a form of vasogenic shock in which spinal cord injury or spinal anesthesia causes vasodilation due to acute loss of sympathetic vascular tone.

5. Obstructive shock (cardiogenic shock)results from mechanical impediment to circulation leading to depressed cardiac output. such as pulmonary embolism or tension pneumothorax.

6. Traumatic shocksoft tissue and bony injury lead to the activation of inflammatory cells and the release of circulating factors, such as cytokines and intracellular molecules that modulate the immune response.PATHOPHYSIOLOGY OF SHOCK

Stages of ShockInitial stage tissues are under perfuseddecreased COincreased anaerobic metabolismlactic acid is building

Hypoperfusion causes hypoxia. Due to the lack of oxygen, the cells perform lactic acid fermentation. Accumulating pyruvate is converted to lactate by lactate dehydrogenase causing lactic acidosis.

25Compensatory stage ReversibleSNS activated by low CO attempting to compensate for the decrease tissue perfusion.

Progressive stage

Positive Feedback Shock becomes more progressiveCardiac Depression : coronary blood flow decreases below that required for adequate nutrition of the myocardiumVasomotor failure : diminished blood flow to the brains vasomotor center depresses the center so much and become less active Sludged blood : blockage in small vessels because tissues metabolism product Increased Capillary Permeability : Capillary hypoxia lead to increases capillary permeability. Large quantity of fluid transudesRelease of toxins by ischemic tissue : serotonin, histamine, tissue enzymes

Irreversible or refractory stage

The vital organs have failed and the shock can no longer be reversed. Brain damage and cell death are occurring, and death will occur imminently.

One of the reasons that shock is irreversible at this point is that much cellular ATP has been degraded into adenosine in the absence of oxygen as an electron receptor in the mitochondrial matrix. Adenosine easil perfuses out of cellular membranes into extracellular fluid, furthering capillary vasodilation, and then is transformed into uric acid.

Clinical PresentationVital signsHypotensive: < 90 mmHgMAP < 60 mmHgTachycardia: Weak and Thready pulseTachypneic30Clinical PresentationMental status restless, irritable, apprehensive unresponsive, painful stimuli only

Decreased Urine output

31Hypovolemic ShockLoss of circulating volume Empty tank decrease tissue perfusion general shock response

ETIOLOGY: Internal or External fluid lossIntracellular and extracellular compartments

Most common causes:HemmorhageDehydration32Hypovolemic Shock: External loss of fluidFluid loss: Dehydration Nausea & vomiting, diarrhea, massive diuresis, extensive burns

Blood loss: trauma: blunt and penetrating

33Hypovolemic Shock: Internal fluid lossLoss of Intravascular integrity

Increased capillary membrane permeability

Decreased Colloidal Osmotic Pressure34Management Hypovolemic ShockEnsure adequate oxygenation (ABC)Treat Underlying Cause (Ex : Provide control of hemorrhage)Give Fluid Resuscitation Isotonic Crystalloid solution (10-20 mL/kg)Administer PRC if patients have heavy bleeding or unresponsive to fluid resuscitation.

Blood TransfusionHb < 8gr%Ht < 30%In adult with lung or heart abnormality Hb20% blood volume1 unit packed red cell Hb >1 gr% & hematocrit > 2 - 3%.PRC 10 ml/kgbb Hb 3 gr%36Cardiogenic ShockThe impaired ability of the heart to pump bloodCommon cause : Acute myocardial infarctionSevere myocarditisCardiomyopathyMost common cause is LV MI (Anterior)

SVR increase as a compensation to maintain organ perfusion37Highest mortality rate Characteristic:Low cardiac outputCardiac filling pressure Systemic Vascular Resistance

Focus on improve myocardial contractility and pump functionEstablish or maintain airways if needed give mechanical ventilation decrease work of breathingGive Vasopressor or Inotropic drugs, if Hypovolemia present correct with crystalloid or blood product before administeringNorepinephrine (0,5 mcg/min)Dobutamine (5 mcg/kg/min)Treat underlying disease Myocardial Infarction : Acetylsalicylic Acid / Fibrinolytic agents. Arrthymia : give antiarrthymic drug

ManagementSBP 10 mcg/kg per min)ephedrine (12.5-25 mg IV every 3-4 hour)Treat bradycardia with atropine 0.5-1 mg doses to maximum 3 mgSeptic ShockSepsis : Systemic Inflammatory Response (SIRS) to infection manifested by 2 or > of following:Temp > 38 or < 36 HR > 90RR > 20 or PaCO2 < 32WBC > 12,000/cu mm or > 10% Bands (immature wbc) Septic shock :Sepsis with:Hypotension (SBP < 90) Tissue perfusion abnormalities invasion of the body by microorganisms & failure of bodys defense mechanism.

ManagementIdentify site of infection and drainAntimicrobial agentsMonitoring and support with fluids, vasopressors, and inotropic agents

In summary, Treatment of ShockIdentify the patient at high risk for shockControl or eliminate the causeImplement measures to enhance tissue perfusionCorrect acid base imbalanceTreat cardiac dysrhythmias

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