SHOCK

1. SHOCK WHAT IS IT?

2. OBJECTIVES • Upon completion of this section, the student should be able to: • Describe the epidemiology, including the morbidity/mortality and prevention strategies, for shock and hemorrhage. • Discuss the anatomy, physiology, and pathophysiology of the cardiovascular system. • Define shock based on aerobic and anaerobic metabolism.

3. OBJECTIVES • Describe the body’s physiological response to changes in blood volume, blood pressure, and perfusion. • Describe the effects of decreased perfusion at the capillary level. • Discuss the cellular ischemic, capillary stagnation, and capillary washout phases related to hemorrhagic shock. • Discuss the various types and degrees of shock and hemorrhage

4. OBJECTIVES • Predict shock and hemorrhage based on mechanism of injury. • Identify the need for intervention and transport of the patient with hemorrhage or shock. • Discuss the assessment findings and management of internal and external hemorrhage and shock. • Differentiate between the administration rate and volume of IV fluid in patients with controlled versus uncontrolled hemorrhage. • Relate pulse pressure and orthostatic vital sign changes to perfusion status.

5. OBJECTIVES • Define and differentiate between compensated and decompensated hemorrhagic shock • Discuss the pathophysiological changes, assessment findings, and management associated with compensated and decompensated shock. • Identify the need for intervention and transport of patients with compensated and decompensated shock. • Differentiate among normotensive, hypotensive, or profoundly hypotensive patients.

6. OBJECTIVES • Describe differences in administration of intravenous fluid in the normotensive, hypotensive, or profoundly hypotensive patients. • Discuss the physiologic changes associated with application and inflation of the pneumatic anti-shock garment. • Discuss the indications and contraindications for the application and inflation of the PASG

7. OBJECTIVES 20. Give several scenarios, provide the appropriate scene size-up, initial assessment, rapid trauma or focused physical exam and history, detailed exam, and ongoing assessment and provide appropriate patient care and transportation

8. DEFINITIONS • “Manifestation of the rude unhinging of the machinery of life.” (Gross, 1872) • “Shock is a peripheral circulating failure, resulting from a discrepancy in the size of the vascular bed and the volume of the intravascular fluid.” (Blalock, 1940)

9. DEFINITIONS • “Shock is a syndrome resulting from a depression of many functions, but in which impairment of the circulation steadily progresses until it eventuates in a state of irreversible circulatory failure.” (Wiggers, 1942)

10. SHOCK • Modern Definition “Shock may be defined as a clinical condition characterized by signs and symptoms which arise when the cardiac output is insufficient to fill the arterial tree with blood under sufficient pressure to provide organs and tissues with adequate blood flow.” (Simeone, 1964) • Simply Translated: Shock is a condition of “inadequate tissue perfusion.”

11. CLASSIFICATIONS • Shock results from failures in: • The pump (heart) • The amount of fluid that is pumped (blood volume) • Arteriolar resistance in vessels • Capacity of the venous bed (capacitance vessels)

12. CLASSIFICATIONS • Three Categories of Shock • Hematogenic/hemorrhagic • Neurogenic/Vasogenic • Cardiogenic

13. HEMATOGENIC OR HEMORRHAGIC • Anything that causes a reduction in the fluid that may be pumped.

14. NEUROGENIC/VASOGENIC • Neurogenic changes result in: • Change in peripheral arterial resistance • Change in venous capacitance (decreased vascular resistance)

15. CARDIOGENIC • Failure of the heart to operate as an effective pump.

16. ANATOMY & PHYSIOLOGY • To understand what SHOCK is you must understand the physiological norms and the changes that are taking place. • There are a number of systems that attempt to compensate for the SHOCK STATE no matter which category of shock the patient is in. • Ultimately SHOCK will affect all systems if left unchecked.

17. CARDIOVASCULAR & CIRCULATORY SYSTEM • Heart is the center of this system. • Receives blood from the venous system, pumps it to the lungs, where oxygenation takes place and then pumps the oxygenated blood to the rest of the body. • Amount of blood effected in one contraction is referred to as Stroke Volume.

18. FACTORS THAT AFFECT STROKE VOLUME • Preload: • The amount of blood returned to the heart (venous system). Increased preload leads to increased stroke volume.

19. FACTORS THAT AFFECT STROKE VOLUME • Contractile Force: • This is directly related to preload. The more blood returned, the greater the ventricles are stretched. This increased stretch results in an increased contractile force, which results in increased stroke volume. This process is referred to as the Frank-starling Mechanism, (rubber band theory).

20. FACTORS THAT AFFECT STROKE VOLUME • Afterload: • This is the resistance the ventricle must push against to circulate blood through the pulmonary and systemic system. This pressure of resistance is based on the degree of peripheral vascular resistance.

21. PERIPHERAL VASCULAR RESISTANCE • Increased PVR  Increased afterload  Decreased stroke volume • Decreased PVR  Decreased afterload  Increases stroke volume

22. OTHER FACTORS THAT AFFECT PERFUSION • Cardiac Output (CO): • Amount of blood pumped by the heart in one minute. It is a function of the heart rate and stroke volume. • Stroke Volume x Heart Rate = Cardiac Output

23. CARDIAC OUTPUT • If you increase stroke volume and increase heart rate then cardiac output is increased. • If you decrease stroke volume or decrease heart rate then you decrease cardiac output.

24. OTHER FACTORS THAT AFFECT PERFUSION • Blood Pressure: • Cardiac Output x PVR = Blood Pressure • If you increase CO and increase PVR then you increase blood pressure. • If you decrease CO or decrease PVR then you decrease blood pressure.

25. PERIPHERAL VASCULAR RESISTANCE • How does this affect perfusion? • In normal conditions the body keeps BP relatively constant through feedback mechanisms. • These feedback mechanisms are referred to as baroreceptors. • These are sensory fibers located in the carotid bodies and the arch of the aorta.

26. PERIPHERAL VASCULAR RESISTANCE • These fibers contain nerve tissue that monitor changes in BP. • If BP increases, these receptors would send signals to the brain to cause the BP to be returned to normal. Accomplished by: • Decreasing heart rate (cardiac inhibitors) • Decreasing preload (venous dilation) • Decreasing PVR (arterial dilation)

27. PERIPHERAL VASCULAR RESISTANCE • If BP decreases, the receptors are stimulated. This stimulation activates the sympathetic nervous system which causes: • Increased heart rate (cardiac accelerators) • Increased force of contraction (vasoconstriction, increasing preload) • Increased PVR (arterial constriction)

28. PERIPHERAL VASCULAR RESISTANCE • Stimulating the sympathetic nervous system alone does not produce these effects. • The adrenal medulla is also stimulated which causes the release of epinephrine & norepinephrine (catecholamines). • These help to enhance and prolong the sympathetic response.

29. PERIPHERAL VASCULAR RESISTANCE • Other hormonal changes take place to maintain BP, decrease fluid loss and increase hemoglobin capabilities: • Erythropoietin • Angiotensin • Antidiuretic Hormone • Aldosterone • The nervous system and endocrine system play a vital role in the body’s response to shock.

30. PERIPHERAL VASCULAR RESISTANCE • Two other portions of the Cardiovascular/ Circulatory System that are important to understand are the: • Blood Vessels (container) • Blood (fluid)

31. PERIPHERAL VASCULAR RESISTANCE • The fluid of the system is called blood. • Specialized form of connective tissue. • Consistency that is more viscous and adhesive than water. • Flows more slowly than water. • Blood flow is constant through the arterial and venous systems.

32. PERIPHERAL VASCULAR RESISTANCE • When blood is pumped from the left ventricle it enters the aorta (arterial or delivery system). • It then moves into smaller arteries, then to arterioles (BP control) and finally into capillaries (always decreasing in size). • Blood then enters the venules (venous or return system), then to veins, then to the great veins (inferior and superior vena cava). • Finally to the right atrium (always increasing in size).

33. Large veins and reservoirs  34% Small veins and venules  25% Pulmonary vessels  12% Heart  9% Large arteries  8% Small arteries  5% Capillaries  5% Arterioles  2% BLOOD VOLUME IN CIRCULATORY SYSTEM

34. PERIPHERAL VASCULAR RESISTANCE • Changes in circulating blood volume will have a direct effect on the blood vessels and how they respond to these changes. • You can see effects within the blood vessels without changing circulating blood volume, these effects are based on changing blood viscosity.

35. PERIPHERAL VASCULAR RESISTANCE • Increased viscosity (hypothermia) yields decrease perfusion. • Decreased viscosity (blood thinners) yields adequate perfusion and decreased risk of emboli.

36. PERIPHERAL VASCULAR RESISTANCE • Viscosity is one factor that can effect perfusion. • Another factor is the blood vessels (container). • Blood moves through the heart by changes in volume pressures, the same is true with blood vessels. • The greater the push pressure and the lower the resistance  increased perfusion. • The lower the push pressure and the higher the resistance  decreased perfusion.

37. PERIPHERAL VASCULAR RESISTANCE • Remember that blood vessels are under continuous pressure to maintain blood flow: • Arteries  high pressure vessels • Veins  low pressure vessels

38. PERIPHERAL VASCULAR RESISTANCE • Blood vessels are under the control of the autonomic nervous system which gives them the ability to change their size in response to the body’s needs. • Responses primarily take place in the microcirculation (capillaries) where they respond primarily to local tissue needs.

39. PERIPHERAL VASCULAR RESISTANCE • This capability allows the capillaries to selectively supply undernourished tissue while temporarily bypassing tissue with no immediate need. • How is this accomplished?

40. PERIPHERAL VASCULAR RESISTANCE • Capillaries have a sphincter at the origin of the capillary, (pre-capillary sphincter), and another at the end of the capillary, (post-capillary sphincter). • The pre-capillary sphincter responds to local tissue demands, such as acidosis, and opens as more arterial blood (oxygenated) is needed. • The post-capillary sphincter opens when blood is to be emptied into the venous system.

41. PERIPHERAL VASCULAR RESISTANCE • Remember that blood flow through capillaries occurs more in a pulsating fashion than a free flow movement.

42. PERIPHERAL VASCULAR RESISTANCE • Blood flow through vessels occurs because of two characteristics: • Peripheral resistance • System pressure

43. PERIPHERAL VASCULAR RESISTANCE • Peripheral resistance has already been defined as the resistance to blood flow. • Large diameter vessels  create less resistance. • Small diameter vessels  create greater resistance.

44. PERIPHERAL VASCULAR RESISTANCE • Peripheral resistance is dependent on three factors: • Length of the vessel • Diameter of the vessel • Blood viscosity

45. ARTERIAL CIRCULATION • Resistance to flow is very little in the aorta and arteries, but can undergo significant changes at the arteriole level because of its small diameter. • The arterial system increases systemic vascular resistance (afterload) and blood pressure.

46. VENOUS CIRCULATION • The venous system is a low pressure system in comparison to the arterial system and can be effected to contract or dilate quite easily. • Contraction of the venous side of the vascular system results in decreased capacitance and increased cardiac preload.

47. VENOUS CIRCULATION • Dilation will cause the exact opposite (decreased preload). • It is important to understand which effect is occurring, and whether or not that is the desired effect for the situation.

48. OXYGENATION • We defined shock as inadequate tissue perfusion. • We have discussed the perfusion of blood (volume) but there is another aspect of perfusion that is of major importance and that is the ability to perfuse oxygen.

49. OXYGENATION • When a patient develops hypovolemia or any injury or illness associated with blood loss, we can replace the volume but we do not have the capability to adequately oxygenate these patients because our IV fluids will not carry oxygen.

50. OXYGENATION • The body initially attempts to compensate for this oxygen problem through the increased production of RBC’s, thereby making more hemoglobin available to bind with oxygen.