SHOCK
•Als PPT, PDF herunterladen•
4 gefällt mir•1,109 views
A Detail explanation regarding pathophysiology and treatment modalities of different types of shock.
Empfohlen
Empfohlen
Weitere ähnliche Inhalte
Was ist angesagt?
Was ist angesagt? (20)
Ähnlich wie SHOCK
Ähnlich wie SHOCK (20)
Kürzlich hochgeladen
Kürzlich hochgeladen (20)
SHOCK
- 3. 3
- 4. Shock 4
- 5. DIFINITION Shock is a physiologic state characterized by systemic reduction in tissue perfusion, resulting in decreased tissue oxygen delivery. It is a condition in which circulation fails to meet the nutritional needs of the cells & at the same time fails to remove the metabolic waste products. 5
- 6. ETIOLOGIES 6
- 7. Basic Physiology • Unit of life = cell • Cells get energy (ATP) from cellular respiration: O2 + Glucose ATP + water + CO2 No O2 = no energy No energy = no life Remember: Damage to Cell Damage to Tissues Damage to Damage to Organ Damage to 7
- 8. Review of the Cardiovascular System 8
- 9. Cardiovascular System • Transports oxygen (fuel) to cells • Removes carbon dioxide and other waste products • Cardiovascular system must be able to maintain sufficient flow through capillary beds to meet cell’s oxygen and fuel needs Flow = Perfusion Inadequate Flow = Inadequate Perfusion = Hypoperfusion Adequate flow = Adequate Perfusion SHOCK 9
- 11. 11
- 15. Mild shock Clinical features are due to adrenergic constriction of blood vessels . •Pale and cool extremities because of collapse of s.c veins. •May be sweat in forehead,hand and feet. •U.O, B.P, pulse may remain normal at this stage. 15
- 16. Moderate shock Mild shock features + oliguria In the initial stage B.P remains normal and falls in later stage. SO PULSE AND B.P ARE NEVER THE MAIN SIGNS OF SHOCK. SHOCK MAY BE PRESENT EVEN WITH NORMAL PULSE AND B.P 16
- 17. Sever shock •Rapid pulse •Low urinary output •Pallor of extremities •Low B.P 17
- 18. Clinical monitoring • Blood pressure:: It is essential to monitor B.P though it is normal in mild shock. • Respiration:: Increase in rate & depth of respiration is an important indicator of shock. • Urine output:: It is a good indication of severity of shock and good index of adequacy of replacement 18 therapy.
- 19. • Central venous pressure (CVP):: It is important in assessing shock. CVP decreases in hypovoleamic shock Where remain constant in cardiogenic shock.* 19
- 20. SWAN-GANZ CATHETER • It is used to get valuable information about the precise diagnosis and circulatory derangement of shock. • It provides 3 types of information: 1:flow in CVS 2:sampling of blood from pumonary artery to measure the accurate amount of blood gases in venous bllod. 20 3:filling pressure of rt.<. Side of heart
- 22. General Treatment of Shock – – – – – – – – – – – – Remember your ABC’s Administer airway 100% O2 Assist ventilations if necessary Position patient to assist perfusion(in tredelenburg position ) Keep patient warm Perform focused assessment Monitor and adjust O2, gain IV access, cardiac monitor, pulse oximetry Fluid replacement of LR or NS Need 3 liter of fluid to replace 1 liter of blood loss Apply pressure to IV or blood to facilitate faster infusion 22
- 23. MX • • • • Resuscitation. Control of bleeding Extracellular fluid replacement Drugs. 23
- 25. So, • Maintain airway • If require intubate the patient • Maintain adequate ventilation and oxygenation. 25
- 26. Bleeding control • Find out the cause of bleeding and control the bleeding either by raising the foot end of the bed or compression bandage or by surgical intervention if require. 26
- 27. ECF replacement • Most important point in Mx .. • Non sugar,non protein,crystalloid solution with Na concentration that of plasma is best fluid for replacement. • Normal saline NaHCo3 ** • Ringer’s lactate* • Ringer’s acetate* 27
- 28. • 3 litres of fluid given over 45 minutes should resuscitate any pt.with arrested haemrrhage. • Resuscitation should always start with crystalloid solution even if blood is available.* 28
- 29. • Sedatives: Drugs Morphine:use to alleviate pain. :should adminnistrate I.V should not be use in children,in head injury pt.,pt.with acute abdomen Berbiturate are preferred in children. • Vasoconstrictors:help full in hypovolaemic shock. Drug Dopamine Dobutamine Norepinephrine Phenylephrine Indication Renal perfusion hypotension Dose 2-5 mcg/kg/min 5-10 mcg/kg/min MOA Dopaminergic 1& β dopaminergic Hypotension >10 mcg/kg/min 1 α Cardiogenic shock 2.5-25 mcg/kg/min Selective β 1 Hypotension 2-4 mcg/min 1& 1 αβ Hypotension 40-180 mcg/min Selective α 1 Principal actions Renal a. dilation + inotrope vasoconstriction + inotrope Vasoconstriction 29 Vasoconstriction
- 31. 31
- 32. 32
- 33. Etiology ,Chronic congestive heart failure 33
- 34. 34
- 35. Clinical features: • In beginning : skin is pale,cool & U.O is low. • Gradually pulse become rapid & B.P becomes low. • In the case of rt.ventricular dysfunction the neck veins become distended & liver may also be enlarged. • In case of lt.ventricular dysfunction third heart sound is heard. 35
- 36. Mx • Airway must be clear with adequate oxygenation. • In a case of rt.sided failure caused by pulmonary embolism should be treated by large dose of heparine I.V. • Diuretics can be help full in cardiogenic shock by reducing volume and decrease filling pressure. 36
- 38. Spinal cord trauma causes a loss of blood vessel tone and results in widespread vasodilation. •is one type of distributive shock. •injury may damage the sympathetic nerve fibers that control vessel tone.* 38
- 39. Clinical features: • Skin remains WARM, PINK, WELL PERFUSED.* • U.O normal. • Heart rate is rapid • B.P is LOW. 39
- 40. Mx • • • • Protect and stabilize c-spine.* Maintain airway. Keep pt.in trendelenburg position. Administrate fluid but it is not much important as in hypovolaemic shock. • Vasoconstrictor drugs by which this shock can be treated safely. 40
- 42. Most frquent organisms are, Gm +ve ,Gm-ve bacteria, And any agent capable of producing infection like viruses,parasites,fungi 42
- 43. Clinical features: • Recognized Initially by chills and temp.>100 0F.* • 2 types: early warm shock & late cold shock. • Early warm shock:Toxins from infected tissue increase body temperature.to bring this down vasodilatation occurs which decrease systemic vascular resistance. • LV has minimal resistance + adrenergic discharge again increase CO. • So skin will become WARM-PINK-WELL PERFUSED. 43
- 44. • LATE COLD SHOCK: due to vasodilatation hypovolaemia takes place which reduces cardiac output . Clinically it is difficult to differentiate it from hypovolaemic or traumatic shock. Only guide remains is the knowledge of existence of a septic focus. 44
- 45. Mx 45
- 46. • Use of steroids is questionable because it impaires the immunity responce of body. It also improves the cardiac,pumonary,renal functions which is life saving. • If steroids given SHORT TERM –HIGH DOSE is recommended. • 15-30 mg /kg- methyl prednisolone or equivalent dexamethasone.(I.V in 5-10 min) • Same dose repeat at 4 hours if benificial effect have been not achieved. 46
- 47. Systemic Inflammatory Response Syndrome (SIRS) • Defined as when generalized inflammation occurs and threatens vital organs • Causes: multiply transfusions, massive tissue injury, burns, and pancreatitis, severe infections or sepsis • Effects: endothelium is damaged and allows fluid to leak into the body tissues, results in poor perfusion of blood to organs • Body is in a hypermetabolic state
- 48. • Diagnosis made when 2 or more of the following are seen: – Temperature less than 97 or greater than 100.4 – Heart rate more than 90 – Respiratory rate more than 20 or PaCO2 less than 32mm Hg – WBC count less than 4000 cells or more than 12,000 – Sepsis is used if patient has SIRS with and infection
- 49. Treatment for SIRS/MODS • Critical care nursing • Goals – – – – Prevent and treat infections Maintain tissue oxygenation Provide nutritional and metabolic response Support failing organs
- 51. Vasodilation moves blood from the central core to the periphery, causing distributive shock. • Mass release of histamine and slow release substance of anaphylaxis due to allergic hypersensitivity reaction (foods, insect bites, blood transfusion, drugs). • Causes bronchospasm,laryngeal edema,and respiratory distress which leads to hypoxia. • Increased capillary permeability with vasodilation reduces venous return and BP. 51
- 53. 53
- 54. 54
- 55. • Now that we have an understanding of what shock is and the different types, lets look at the physiology behind shock. • To understand the physiology of shock we need to understand the following formula: Blood Cardiac Systemic Pressure = Output x Vascular Resistance 55
- 56. • By applying a mathematical aspect to the formula we can start to identify how blood pressure can be maintained. BP = CO x SVR • We need to keep both sides balanced. • If one side of the formula changes, the other side needs to change in the opposite direction to balance this out. • i.e. If BP increases, we need to decrease CO, SVR or both to bring it back down again If BP decreases, we need to increase CO, SVR or both to bring it back up again 56
- 57. What happens if you get a drop in BP? BP = CO x SVR • We need to maintain homeostasis so need to increase BP. • We can increase BP by increasing: - CO - SVR - CO & SVR to increase BP back up again. 57
- 58. What happens if you get a rise in BP? BP = CO x SVR • We need to maintain homeostasis so need to decrease BP. • We can decrease BP by decreasing: - CO - SVR - CO & SVR to bring BP back down again. 58
- 59. Key Issues In Shock • Recognise and treat early (during compensatory phase) Increased resp. rate, Restlessness, Anxiety, Argumentative Early signs of shock • Falling BP = Late sign of shock • Pallor, tachycardia and slow capillary refill = Shock until proven otherwise Hallmark symptoms are: Decreased BP 59 Increased HR
- 60. 60
- 61. Inadequate cellular Oxygen Delivery Inadequate Energy Production Anaerobic Metabolism Lactic Acid Production Metabolic Acidosis Metabolic Failure CELL DEATH 61
- 62. • What happens in compensated shock??? 62
- 63. Compensated shock • Baroreceptors detect fall in BP • Sympathetic nervous system activated (see diagram 1) 1. Cardiac Effects - increased force of contractions - increased rate (tachycardia) - increased cardiac output 2. Peripheral Effects - arteriolar constriction - increased peripheral resistance - shunting of blood to main core organs (causing cold clammy skin) 63
- 64. Control of Blood Pressure via the Baroreceptor Reflex brain cardiovascular centre Baroreceptors on aorta and carotid sinus send information about changes in BP to cardiovascular centre sympathetic innervation of arterioles heart sympathetic innervation of myocardium arterioles sympathetic and parasympathetic innervation of Sino-atrial node key parasympathetic nerves sympathetic nerves afferent sensory nerves © Roger McFadden – University of Central England 2003 64
- 65. 3. Respiratory Effects Tachypnoea is one of the first signs that reflects reduced blood flow and oxygen transport. the cardiovascular and respiratory systems work together- If blood flow around the body is compromised in any way, oxygen delivery to tissues is reduced. To compensate for this, ventilation will increase to attempt to increase oxygen uptake in the lungs. 65
- 66. So how does this happen ?? brain respiratory centres in medulla phrenic nerve to diaphragm chemoreceptors on aorta and carotid artery heart intercostal nerve to external intercostal muscles ribs The Baroreceptors not only stimulate the cardiovascular control centre but also the respiratory centre in the medulla, increasing 66 the respiratory rate.
- 68. Renin – Angiotensin – Aldosterone Pathway JUXTAGLOMERULAR cells in the kidney respond to a REDUCTION IN BLOOD VOLUME from EXCESS VOMITING, SWEATING, & HAEMORRHAGE etc. RENIN released into blood ANGIOTENSIN I ANGIOTENSINOGEN ANGIOTENSIN CONVERTING ENZYME VASOCONSTRICTION ANGIOTENSIN II BLOOD PRESSURE BLOOD VOLUME KIDNEYS increase Na+ reabsorption from filtrate BP THIRST ADRENAL CORTEX ALDOSTERONE 68
- 69. . 5.Hypothalamus Effects - decreased blood flow to hypothalamus - release of ADH from post pituitary (see diag 3) results in retention of salt, water and peripheral vasoconstriction 69
- 70. Role of ADH in dehydration osmoreceptors in hypothalamus detect increase in osmolarity of blood and release ADH into blood stream FILTRATE capillary nephron ADH increases the amount of water reabsorbed from the filtrate to the blood ADH ADH water blood urine urine output is reduced as more water is returned to the blood 70
- 71. 6. Hormonal Effects - Glucagon (contributes to hyperglycaemia) - ACTH (stimulates cortisol release and glucose production) 71
- 72. Progressive Shock 1. 2. Cardiac Effects - decreased RBC oxygenation - decreased coronary blood flow - myocardial ischaemia -decreased ventricular filling - decreased force of contraction Peripheral Effects - peripheral pooling of blood - plasma leakage into interstitial spaces - cold, grey waxy skin - confusion, slow speech - tachycardia, weak thready pulse - decreased BP - decreased body temperature 72
- 73. 3. Respiratory effects If oxygen delivery to tissues continues to be inadequate, cells must do anaerobic respiration to continue ATP production. Anaerobic respiration produces lactic acid as a waste product – this must be removed. Central chemoreceptors will detect a fall in pH and stimulate the respiratory centre to increase ventilation. This allows the excess acid to be ‘blown off’ in the form of CO2. 73
- 74. Response to acidosis Anaerobic respiration Lactic acid PCO2 and H+ in blood expiration of PCO2 rate and depth of ventilation H+ in CSF stimulation of central chemoreceptors frequency of impulses to medullary rhythm generator 74
- 75. Irreversible Shock • Loss of peripheral vascular resistance • Confusion, slurred speech, unconscious • Slow, irregular, thready pulse • Falling BP (diastolic is zero) • Cold, clammy cyanotic skin • Slow, shallow, irregular respirations • Dilated, sluggish pupils 75
- 76. Irreversible Shock leads to: • Renal failure • Hepatic failure • Multiple organ systems failure • Adult respiratory distress syndrome • Death 76
- 77. OU Y NK HA T 77
Hinweis der Redaktion
- Talking Points Shock is simply defined as inadequate tissue perfusion. It is also often referred to as hypoperfusion. During a shock state, inadequate amounts of oxygen and glucose are delivered to cells. In other words, the amount of oxygen delivered to the cells is less than the amount required for normal metabolism. In addition, an impaired elimination of carbon dioxide and other waste products occurs. Organs of vital importance, brain, heart, and kidneys can suffer irreversible damage, eventually leading to death. Tissue ischaemic sensitivity: - heart, brain, lung: 4-6 min.- GI tract, liver, kidney: 45-60 min.- muscle, skin: 2-3 hours
- The three basic etiologies of shock are inadequate volume, inadequate pump function, and inadequate vessel tone.
- Hypovolemic shock means shock that is caused from a low blood volume. Hypovolemic shock is the most common form of shock. It can be due to blood loss or loss of some other fluid. The most common cause of hypovolemic shock is hemorrhage. Hemorrhage can be post surgical , can be Due to trauma ,G.I bleeding, Nonhemorrhagic forms are associated with fluid loss from burns and dehydration either due to vommiting, or diarrhoea,or swetting.
- Mild tachycardia: pulse increase up to more than 100 beats / minute. Oliguria is due to adrenergic discharge and circulating aldosterone and vasopressin. To have hypotention with hemorrhage,30% of circulating blood volume has been lost.
- In hypovoleamic shock blood volume decreases so CVP decreases and in cardiogenic shock CVP do not cahange because there is no decrease in volume in cardiogenic shock.
- *ringer lactate and acetate should not give in patient with pre-existing liver disease. ** NaCo3 will reduce the acedosis.
- *because if resuscitation is started with acidotic cold bank blood with a potassium conc.,efficacy of myocardium is tremendously jeopardized.
- The heart is the pump responsible for generating the force necessary to move the blood throughout the body. If the pump fails, regardless of the blood volume, the delivery of oxygen and glucose to cells will be decreased. Ineffective pump function can result either from damage to the heart or from a mechanical obstruction. In either condition, the patient requires improvement of pump function to eliminate the shock state. A patient with pump failure has not lost any blood volume. Administering fluids will not improve the condition and may actually worsen it.
- Cardiogenic shock is caused by ineffective pump function of the heart. The patient has an adequate blood volume and vessel tone; however, hypoperfusion results from the inability of the heart to contract effectively. When the left ventricle fails to generate enough force to eject sufficient blood from the chamber into the systemic circulation, the result is a reduction in stroke volume, cardiac output, and systolic blood pressure, leading to poor tissue perfusion resulting in cardiogenic shock.
- Neurogenic shock, also commonly referred to as vasogenic shock, is another type of distributive shock. Spinal cord injury is a cause of neurogenic shock. * so Blood will begin to pool in the peripheral vessels, causing a decrease in the preload, stroke volume, cardiac output, and systolic blood pressure. This causes a further decrease in perfusion.
- *WHERE IN HYPOVOLAEMIC SHOCK SKIN BECOME COOL,& PALE.
- *Emergency care focuses on spinal immobilization and management of the airway, ventilation and oxygenation.
- *.release of endotoxins results in:-production of TNF,IL-1,6,8. -results in vasodialation and hypotension. -acute respiratory distress syndrome.
- three stages of shock are compensatory, decompensatory, and irreversible: Compensatory shock or compensated shock, is a stage of shock in which the body is able to maintain a near normal blood pressure and perfusion of the vital organs. Decompensatory shock, decompensated shock, or progressive shock, is an advanced stage of shock in which the body’s compensatory mechanisms are no longer able to maintain a blood pressure and perfusion of the vital organs. If the shock state continues unopposed and is not managed effectively, the compensatory mechanisms become exhausted or overwhelmed, leading to a failure to maintain pressure inside the vessels and perfusion of the vital organs. Irreversible shock is the stage where, regardless of the intervention, the patient outcome is death. Cell, tissue, and organ failure and damage is so pervasive and severe that no matter what treatment is provided, organ death is inevitable and unable to be reversed.
- The central portion of the kidneys release the hormones epinephrine and norepinephrine within a few minutes. Epinephrine stimulates alpha and beta receptors while norepinephrine mostly stimulates alpha receptors. The stimulated alpha receptors result in vasoconstriction, which attempts to increase systematic vascular resistance and, in turn, blood pressure. The beta1 effect stimulates the heart and causes an increase in the heart rate and force of contraction. It also speeds the electrical impulse traveling through the conduction system of the heart.