Pathophysiology of extremal states


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prepared by M.D., PhD. Marta R. Gerasymchuk, Pathophysiology Department
Ivano-Frankivsk National Medical

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Pathophysiology of extremal states

  1. 1. Actuality • Increasing spectrum of diseases secondary to critical illness • 1/3 of intensive care units (ICU) patients, 55% mortality rate • Increase length of stay and disability • Systematic approach to identify potentially reversible etiologies and prognostic factors • Increased survival among medical and surgical.
  2. 2.  Concept of extreme conditions  Mechanisms of Injury. Brain injury  Level of Consciousness  Coma  Spinal injury  Shock
  3. 3. Concept of extreme conditions ► Intensive-care medicine or critical-care medicine is a branch of medicine concerned with the diagnosis and management of life threatening conditions requiring sophisticated organ support and invasive monitoring. ► A critically ill patient is one at imminent risk of death; the severity of illness must be recognised early and appropriate measures taken promptly to assess, diagnose and manage the illness. ► The approach required in managing the critically ill patient differs from that required in less severely ill patients with immediate resuscitation and stabilisation of the patientis condition taking precedence. ► Priorities are: hypoglycaemia and dysrhythmias analysis of the deranged physiology establishing the complete diagnosis in stages as further history and the results of investigations become available careful monitoring of the patientis condition and response to treatment adhering to advanced life support guidelines and the principles of cardiorespiratory management urgent treatment of life-threatening emergencies such as hypotension hypoxaemia hyperkalaemia prompt resuscitation
  4. 4. Mechanisms of Injury • Injury to brain tissue can result from a number of conditions, including trauma, tumors, stroke, and metabolic derangements. • Brain damage resulting from these disorders involves several common pathways, including the effects of hypoxia and ischemia, cerebral edema, and injury caused by increased intracranial pressure. • In many cases, the mechanisms of injury are interrelated.
  5. 5. BRAIN INJURY • The brain is protected from external forces by the rigid confines of the skull and the cushioning afforded by the cerebrospinal fluid (CSF). • The metabolic stability required by its electricallyactive cells is maintained by a number of regulatory mechanisms, including the blood-brain barrier and autoregulatory mechanisms that ensure its blood supply. • Nonetheless, the brain remains remarkably vulnerable to injury.
  6. 6. • One third of all trauma deaths • 15-45 years of age • 49%-road traffic accidents,28%-falls,23%- gun shot injuries and other causes • Inpatient case fatality rates all head injuries - 2.6%to6.5% severe injuries - 15 to 50% • Good outcome-Glasgow outcome scale of 1or 2 Introduction
  7. 7. Category Description % of pts Good/modera te Severe/vegetati ve Dead No CT data 2.3 5.9 0.0 94.1 Diffuse injury I No visible pathology on CT 7.0 61.6 28.8 9.6 Diffuse injury II Cisterns visible, shift 0 – 5 mm, no high or mixed density lesion > 25 cm3 23.7 34.5 52.0 13.5 Diffuse injury III (swelling) Cisterns compressed or absent, shift 0 – 5 mm, no high or mixed density lesion > 25 cm3 20.5 16.4 49.7 34.0 Diffuse injury IV (shift) Shift > 5 mm, no high or mixed density lesion > 25 cm3 4.3 6.2 37.6 56.2 Evacuated mass lesion Any lesion surgically evacuated 37.0 22.8 38.4 38.8 Nonevacua- ted mass High or mixed density lesion > 25 cm3 not surgically evacuated 4.8 11.1 36.1 52.8 Brainstem injury (no brainstem reflexes by physical exam) 0.4 0.0 33.3 66.7
  8. 8.  Can be minor or serious  Even small lacerations can lead to significant blood loss. › This blood loss may be severe enough to cause hypovolemic shock.  They are often an indicator of deeper, more serious injuries.
  9. 9.  Significant force applied to the head may cause a skull fracture.  May be open or closed, depending on whether there is an overlying laceration of the scalp  Injuries from bullets or other penetrating weapons often result in skull fractures. Signs of skull fracture include: •Patient’s head appears deformed •Visible cracks in the skull •Ecchymosis (bruising) that develops under the eyes (raccoon eyes) •Ecchymosis that develops behind one ear over the mastoid process (Battle’s sign)
  10. 10.  Account for about 80% of all skull fractures  Radiographs are often required to diagnose a linear skull fracture because there are often no physical signs.  Linear skull fractures  Result from high- energy direct trauma to the head with a blunt object  Frontal and parietal bones are most susceptible  Bony fragments may be driven into the brain  Compressed skull fractures  Associated with high-energy trauma  Usually occur following diffuse impact to the head  Signs include CSF drainage from the ears, raccoon eyes, and Battle’s sign  Basilar skull fractures  Result when severe forces are applied to the head  Often associated with trauma to multiple body systems  Brain tissue may be exposed to the environment  Open skull fractures
  11. 11. Hypoxia and Ischemia Hypoxia and hypotension are the 2 major causes of secondary CNS injury following head trauma. The brain relies on the ability of the cerebral circulation to deliver sufficient oxygen for its energy needs. Although the brain makes up only 2% of the body weight, it receives one sixth of the resting cardiac output and accounts for 20% of the oxygen consumption. By definition, hypoxia denotes a deprivation of oxygen with maintained blood flow and ischemia, a situation of greatly reduced or interrupted blood flow. The cellular effects of hypoxia and ischemia are quite different, and the brain tends to have different sensitivities to the two conditions. Hypoxia interferes with the delivery of oxygen, and ischemia interferes with the delivery of oxygen and glucose as well as the removal of metabolic wastes.
  12. 12. Hypoxia and Ischemia • Hypoxia usually is seen in conditions such as exposure to reduced atmospheric pressure, carbon monoxide poisoning, severe anemia, and failure to oxygenate the blood. • Contrary to popular belief, hypoxia is fairly well tolerated, particularly in situations of chronic hypoxia. • Neurons are capable of substantial anaerobic metabolism and are fairly tolerant of pure hypoxia; it commonly produces euphoria, listlessness, drowsiness, and impaired problem solving. • Unconsciousness and convulsions may occur when hypoxia is sudden and severe. • However, the effects of severe hypoxia (i.e., anoxia) on brain function seldom are seen because the condition rapidly leads to cardiac arrest and ischemia.
  13. 13. Hypoxia and Ischemia • Unconsciousness occurs within seconds of severe global ischemia, such as that resulting from complete cessation of blood flow, as in cardiac arrest. If circulation is restored immediately, consciousness is regained quickly. However, if blood flow is not promptly restored, severe pathologic changes take place. • Energy sources (i.e., glucose and glycogen) are exhausted in 2 to 4 minutes, and cellular ATP stores are depleted in 4 to 5 minutes. Approximately 50% to 75% of the total energy requirement of neuronal tissue is spent on mechanisms for maintenance of ionic gradients across the cell membrane (e.g., sodium-potassium pump), resulting in fluxes of sodium, potassium, and calcium ions. • Excessive influx of sodium results in neuronal and interstitial edema. • The influx of calcium initiates a cascade of events, including release of intracellular and nuclear enzymes that cause cell destruction. Focal ischemia involves a single area of the brain, as in stroke. Collateral circulation may provide low levels of blood flow during focal ischemia. The residual perfusion may provide sufficient substrates to maintain a low level of metabolic activity, preserving neuronal integrity. Global ischemia occurs when blood flow is inadequate to meet the metabolic needs of the entire brain. In contrast to persons with focal ischemia, those with global ischemia have no collateral circulation during the ischemic event. The result is a spectrum of neurologic disorders.
  14. 14. Hypoxia and Ischemia • Within the brain, certain regions and cell populations are more susceptible than others to hypoxic-ischemic injury. • For example, neurons are more susceptible to injury than are the glial cells. • Among the neurons, the pyramidal cells of the hippocampus, the Purkinje cells of the cerebellum, and the neurons of the globus pallidus of the basal ganglia are particularly sensitive to generalized ischemic-hypoxic injury. • The reason for this selectivity is uncertain but appears to be related at least to some extent on local levels and metabolism of certain excitatory neurotransmitters such as glutamate.
  15. 15. Cerebral Edema  Cerebral edema, or brain swelling, is an increase in tissue volume secondary to abnormal fluid accumulation.  There are basically two types of brain edema: vasogenic or cytotoxic.
  16. 16. Vasogenic Edema  Vasogenic edema results from an increase in the extracellular fluid that surrounds brain cells.  It occurs with conditions such as: Vasogenic edema occurs primarily in the white matter of the brain, possibly because the white matter is more compliant than the gray matter and offers less resistance to fluid accumulation. Vasogenic edema can be localized, as in the case of abscesses or neoplasms, or it may be more generalized. The functional manifestations of vasogenic edema include: tumors prolonged ischemiahemorrhage infectious processes (e.g., meningitis) that impair the function of the blood-brain barrier and allow water and plasma proteins to leave the capillary and move into the interstitium. brain injury focal neurologic deficits disturbances in consciousness severe intracranial hypertensio
  17. 17. Cytotoxic Edema  Cytotoxic edema involves the swelling of brain cells. It involves an increase in fluid in the intracellular space, chiefly the gray matter, although the white matter may be involved.  Cytotoxic edema can result from hypoosmotic states, such as water intoxication or severe ischemia, that impair the function of the sodium-potassium membrane pump. This causes rapid accumulation of sodium in the cell, followed by movement of water along the osmotic gradient. Depending on the nature of the insult, cellular edema can occur in the vascular endothelium or smooth muscle cells, astrocytes, the myelin- forming processes of oligodendrocytes, or neurons.  Major changes in cerebral function, such as stupor and coma, occur with cytotoxic edema.  The edema associated with ischemia may be severe enough to produce cerebral infarction with necrosis of brain tissue.
  18. 18. Cerebral Edema
  19. 19. Definition of Terms  Confusion : – impaired attention and concentration, manifest disorientation in time, place and person, impersistent thinking, speech and performance, reduced comprehension and capacity to reason – Fluctuate in severity, typically worse at night ‘sundowning’ – Perceptual disturbances and misinterpret voices, common objects and actions of other persons  Confusion is also found in dementia (progressive failure of language, memory, and other intellectual functions)
  20. 20. Level of Consciousness  Alert: normal awake and responsive state  Drowsiness: state of apparent sleep, briefly arousal with oral command  Lethargic: resembles sleepiness, but not becoming fully alert, slow verbal response and inattentive. Unable to adequately perform simple concentration task (such as counting 20 to 1)
  21. 21. Level of Consciousness  Somnolent: easily aroused by voice or touch; awakens and follows commands; required stimulation to maintain arousal  Obtunded/Stuporous: arousable only with repeated and painful stimulation; verbal output is unintelligible or nil; some purposeful movement to noxious stimulation  Comatose: no arousal despite vigorous stimulation, no purposeful movement - only posturing, brainstem reflexes often absent
  22. 22. Dementia Confusional state Memory problem Clouding of consciousness Fluctuate Acute Varies little from time to time Longstanding nature Dementia Confusional state
  23. 23. Causes of confusional state Medical or surgical disease • Metabolic disorders • Hepatic • Uremic • Hypo- and hypernatremia • Hypercalcemia • Hypo- and hyperglycemia • Hypoxia • Hypercapnia  Infectious illness •Pneumonia •Endocarditis •Urinary tract infection •Peritonitis  Congestive heart failure  Postoperative and posttraumatic states  Drug intoxication Opiates Barbiturates Other sedatives Diseases of nervous system • Cerebrovascular disease, tumor, abscess • Subdural hematoma • Meningitis • Encephalitis • Cerebral vasculitis • Hypertensive encephalopathy
  24. 24. Definition of Terms COMA - reduced alertness and responsiveness represents a continuum that in severest form, a deep sleeplike state from which the patient cannot be aroused. STUPOR - lesser degrees of unarousability in which the Patient can be awakened only by vigorous stimuli, accompanied by motor behavior that leads to avoidance of uncomfortable or aggravating stimuli. Drowsiness - which is familiar to all persons, simulates light sleep and is characterized by easy arousal and the persistence of alertness for brief periods. Drowsiness and stupor are usually attended by some degree of confusion.
  25. 25. By definition, coma (decreased arousal) is produced by: Bilateral hemispheric damage Suppression by hypoxia, hypoglycemia, drugs or toxins Brain stem lesion or metabolic derangement that suppresses Reticular Activating System (RAS)
  26. 26. Level of consciousness Pattern of breathing (Cheyne-Stokes) Pupillary changes Oculomotor responses (ie. Doll’s eyes) Motor responses
  27. 27. Posturing  Decorticate  Flexion of arms, wrists, fingers  Adduction of upper extremities  Extension of lower extremities  Decerebrate  Extremities in extension  Pronation of forearms and plantar extension of feet
  29. 29. Mortality Morbidity  Brain death – brain stem death – no potential for recovery – no control of homeostasis  Cerebral death – death of cerebral hemispheres not including the brain stem – vegetative state  Recovery of consciousness  Residual cognitive dysfunction  Psychosocial domain  Vocational domain
  30. 30. Prognosis of coma ► Recovery from coma depends primarily on the causes, rather than on the depth of coma ► Intoxication and metabolic causes carry the best prognosis ► Coma from traumatic head injury far better than those with coma from other structural causes ► Coma from global hypoxic-ischemic carries least favorable prognosis ► At 3rd day, no papillary light reflex or GCS < 5 is associated with poor prognosis
  31. 31. Conditions mimic coma • Brain death • Locked-in syndrome • Vegetative state • Frontal lobe disease • Non-convulsive status epilepticus • Psychiatric disorder (catatonia, depression)
  32. 32. Vegetative State Signifies an awake but unresponsive state. Most of these patients were earlier comatose and after a period of days or weeks emerge to an unresponsive state in which their eyelids are open, giving the appearance of wakefulness. Yawning, grunting, swallowing, limb and head movements persist, but there are few, if any, meaningful responses to the external and internal environment-in essence, an "awake coma.“ Respiratory and autonomic functions are retained. Cardiac arrest and head injury are the most common causes.
  33. 33. Locked-in state Describes a pseudocoma in which an awake patient has no means of producing speech or volitional limb, face, and pharyngeal movements in order to indicate that he or she is awake, but vertical eye movements and lid elevation remain unimpaired, thus allowing the patient to signal. Vertical eye movement and lid elevation remain unimpaired. Etiology: infarction or hemorrhage of the ventral pons, which transects all descending corticospinal and corticobulbar pathways. Such patients have written entire treatises using Morse code.
  34. 34. Akinetic mutism • Partially or fully awake patient who is able to form impressions and think but remains immobile and mute, particularly when unstimulated. • Causes: damage in the regions of the medial thalamic nuclei, the frontal lobes (particularly situated deeply or on the orbitofrontal surfaces), or from hydrocephalus.
  35. 35. Abulia • Aboulia or abulia (from the Greek "αβουλία", meaning "un-will"), in neurology, refers to a lack of will or initiative and can be seen as a disorder of diminished motivation (DDM). • Aboulia falls in the middle of the spectrum of diminished motivation, with apathy being less extreme and akinetic mutism being more extreme than aboulia. A patient with aboulia is unable to act or make decisions independently. It may range in severity from subtle to overwhelming. It is also known as Blocq's disease (which also refers to abasia and astasia- abasia). • Mental and physical slowness and lack of impulse to activity that is in essence a mild form of akinetic mutism with the same anatomic origins.
  36. 36. Catatonia  Catatonia is a state of neurogenic motor immobility, and behavioral abnormality manifested by stupor. It was first described, in 1874, by Karl Ludwig Kahlbaum in Die Katatonie oder das Spannungsirresein (Catatonia or Tension Insanity).  Hypomobile and mute syndrome associated with a major psychosis.  Patients appear awake with eyes open but make no voluntary or responsive movements, although they blink spontaneously, swallow, and may not appear distressed.  Eyes are half-open as if the patient is in a fog or light sleep.  NO clinical evidence of brain damage.
  37. 37. Brainstem Reflexes pupillary responses to light,spontaneous and elicited eye movements, corneal responses PUPILLARY LIGHT RESPONSES: Simmetrically reactive round pupils: Exclude midbrain damage (2 to 5 mm ) Enlarged pupil (>5 mm), unreactive or poorly reactive: Intrinsic midbrain lesion (ipsilateral) by mass effect (contralateral). Unilateral pupillary enlargement: Ipsilaterall mass. Oval and slightly eccentric pupils: Early midbrain third nerve compression. Bilaterally dilated and unreactive Severe midbrain damage by transtentorial pupils: herniation or anticholinergic drugs toxicity. Reactive bilaterally small but not pinpoint (1 to 2.5 mm): Metabolic encephalopathy, deep bilateral hemispheral lesions as hydrocephalus or thalamic hemorrhage Very small but reactive pupil (Less than 1 mm): Narcotic or barbiturate overdose or bilateral pontin damage.
  38. 38. Ocular Movements Eye movements are the second sign of importance in determining if the brainstem has been damaged. EYE MOVEMENTS Adducted eye at rest: Lateral rectus paresis due to VI nerve lesion. If is bilateral is due to intracraneal hypertension. Abducted eye at rest, plus ipsilateral pupilary enlargement : Medial rectus due to III nerve dysfunction. Vertical separation of the ocular Pontin or cerebellar lesion Globes. (Skew deviation) : Coma and spontanous conjugate horizontal roving movements : Midbrain and pons intact “Ocular bobbing”. Brisk downward and slow upward movement of the globes with loss of horizontal eye movements : Bilateral pontine damage “Ocular dipping”. Slower, arrhytmic downward followed by a faster upward movement with normal reflex horizontal gaze : Anoxic damage to the cerebral cortex. Thalamic and upper midbrain lesions: Eyes turned down and inward.
  39. 39. Brainstem Reflexes Respiratory pattern Shallow, slow, well-timed regular Suggest metabolic or drug depression. Breathing: Rapid, deep (Kussmaul) breathing: Metabolic acidosis or ponto- mesencephalic lesions. Cheyne-Stokes breathing, with light Mild bihemispherical damage or metabolic supression. Coma: Agonal gasps: Bilateral lower brainstem damage. Terminal respiratory pattern.
  40. 40. Anatomy and Physiology- General Structure and Function Spinal Column: • Made up of 26 vertebrae stacked on top of one another • Divided into 5 areas; cervical, thoracic, lumbar, sacral, and coccyx • “Joint” at the superior end of the spinal “Long Bone” VERY FLEXIBLE: • Allows flexion, extension, and rotation of the head • The head acts as a weighted lever during acceleration/ deceleration • Common site of spinal injuries
  41. 41.  Bony spinal injuries may or may not be associated with spinal cord injury  These bony injuries include:  Compression fractures of the vertebrae  Comminuted fractures of the vertebrae  Subluxation (partial dislocation) of the vertebrae  Other injuries may include:  Sprains- over-stretching or tearing of ligaments  Strains- over-stretching or tearing of the muscles  Cutting, compression, or stretching of the spinal cord  Causing loss of distal function, sensation, or motion  Caused by:  Unstable or sharp bony fragments pushing on the cord, or  Pressure from bone fragments or swelling that interrupts the blood supply to the cord causing ischemia
  42. 42. Immediate and irreversible loss of sensation and motion Cutting, compression, or stretching of the spinal cord Occurs at the time of impact/injury  Injury Delayed  Occurs later due to swelling, ischemia, or movement of sharp or unstable bone fragments  May be avoided if spine immobilized during extrication, packaging, treatment, and transport Incomplete Spinal Cord Injury Complete injury to specific spinal tracts with reduced function distally Other tracts continue to function normally with distal function intact
  43. 43. Mechanism of Injury  Physical manner and forces involved in producing injuries or potential injuries  Valuable tool in determining if the a particular set of circumstances could have caused a spinal injury  Mechanisms likely to produce spinal injuries occur in MVAs, falls, violence, and sports (including diving accidents)
  44. 44. Hyperextension - Excessive/abnormal bending back of the head beyond its normal range of motion Hyperflexion - Excessive/abnormal bending forward of the chin toward the chest. This is one mechanism seen when patients are ejected from moving vehicles
  45. 45. Flexion injuries The most common fracture mechanism in cervical injuries is hyperflexion. Anterior subluxation occurs when the posterior ligaments rupture. Since the anterior and middle columns remain intact, this fracture is stable. Simple wedge fracture is the result of a pure flexion injury. The posterior ligaments remain intact. Anterior wedging of 3mm or more suggests fracture. Increased concavity along with increased density due to bony impaction. Usually involves the upper endplate. Unstable wedge fracture is an unstable flexion injury due to damage to both the anterior column (anterior wedge fracture) as the posterior column (interspinous ligament). Unilateral interfacet dislocation is due to both flexion and rotation. Bilateral interfacet dislocation is the result of extreme flexion. BID is unstable and is associated with a high incidence of cord damage. Flexion teardrop fracture is the result of extreme flexion with axial loading. It is unstable and is associated with a high incidence of cord damage. Anterior atlantoaxial dislocation
  46. 46. Hyperotation - Excessive/abnormal rotation. This may produce injuries in any area of the spine.
  47. 47. Axial Loading - Sudden/excessive compression of the spine. Examples include falling and landing on your feet or ejection from a vehicle and landing on your head Axial compression injuries  Jefferson fracture is a burst fracture of the ring of C1 with lateral displacement of both articular masses.  Burst fracture at lower cervical level
  48. 48. Axial Distraction - Sudden/excessive elongation of the spine caused by stretching or tearing anywhere along the spinal column. Example: hanging. This is a hang man’s fracture suffered by a woman that was ejected from her car in a roll-over MVA. She apparently got hung up on the shoulder belt and got hung. Lateral radiograph of type II Hangman's fracture (pars interarticularis fracture of C2 – Levine and Effendi's classification 20,21); it is an unstable spine because of the discontinuity of central axial spinal pillar
  49. 49. Shock is a condition in which the cardiovascular system fails to perfuse tissues adequately  An impaired cardiac pump, circulatory system, and/or volume can lead to compromised blood flow to tissues  These three parts can be called the “perfusion triangle.” – When a patient is in shock, one or more of the three parts is not working properly.
  50. 50. Shock • Inadequate systemic oxygen delivery activates autonomic responses to maintain systemic oxygen delivery • Sympathetic nervous system  NE, epinephrine, dopamine, and cortisol release • Causes vasoconstriction, increase in HR, and increase of cardiac contractility (cardiac output) • Renin-angiotensin axis  Water and sodium conservation and vasoconstriction  Increase in blood volume and blood pressure
  51. 51. Shock • Cellular responses to decreased systemic oxygen delivery • ATP depletion → ion pump dysfunction • Cellular edema • Hydrolysis of cellular membranes and cellular death • Goal is to maintain cerebral and cardiac perfusion • Vasoconstriction of splanchnic, musculoskeletal, and renal blood flow • Leads to systemic metabolic lactic acidosis that overcomes the body’s compensatory mechanisms
  52. 52. Global Tissue Hypoxia • Endothelial inflammation and disruption • Inability of O2 delivery to meet demand • Result: • Lactic acidosis • Cardiovascular insufficiency • Increased metabolic demands
  53. 53. Cell death Inadequate oxygen delivery Catecholamines and other responses Anaerobic metabolism Cellular dysfunction Generalized State of Hypoperfusion What is shock?
  54. 54. Shock. Kinds of shock. Mechanisms of disorders of general hemodynamics and microcirculation at shock.  Shock is a state of organ hypoperfusion with resultant cellular dysfunction and death.  Mechanisms may involve: decreased circulating volume, decreased cardiac output, vasodilation, sometimes with shunting of blood to bypass capillary exchange beds.  Symptoms include altered mental status, tachycardia, hypotension, and oliguria.  Diagnosis is clinical, including BP measurement and sometimes markers of tissue hypoperfusion (eg, blood lactate, base deficit).  Treatment is with fluid resuscitation, including blood products if necessary, correction of the underlying disorder, and sometimes vasopressors.
  55. 55. STAGES OF SHOCK  Non-progressive Stage Reflex compensatory mechanisms are activated. Profusion of vital organ is maintained  Progressive Stage Tissue hypoperfusion. Circulatory & metabolic imbalances leading to Acidosis.  Irreversible Stage Cellular & tissue injury. Even with correction of haemodynamic defects, survival is not possible.
  56. 56. Stages of Shock ❇ Initial stage - tissues are under perfused, decreased CO, increased anaerobic metabolism, lactic acid is building ❇ Compensatory stage - Reversible. SNS activated by low CO, attempting to compensate for the decrease tissue perfusion. ❇ Progressive stage - Failing compensatory mechanisms: profound vasoconstriction from the SNS ISCHEMIA Lactic acid production is high metabolic acidosis ❇ Irreversible or refractory stage - Cellular necrosis and Multiple Organ Dysfunction Syndrome may occur DEATH IS IMMINENT!!!!
  57. 57.  NEUROHUMORAL MECHANISMS MAINTAIN CARDIAC OUTPUT AND BLOOD PRESSURE:  Baroreceptors reflexes  Release of catecholamine  Activation of renin-angiotensin axis  ADH release  Generalized sympathetic stimulation  DIFFERENT CLINICAL OUTCOME OF THESE COMPENSATORY MECHANISMS:  Tachycardia  Peripheral vasoconstriction (cool & pale skin)  Renal conservation of fluid
  58. 58.  WIDESPREAD HYPOXIA: Anaerobic glycolysis Production of lactic acidosis pH lead to blunting of vasomotor response leading to vasodilatation Peripheral pooling of blood cardiac output  DIFFERENT CLINICAL OUTCOME OF THESE FAILING MECHANISMS: Feeble, failing pulse Mental confusion Urine output PROGRESSIVE STAGE
  59. 59. WIDESPREAD CELLULAR INJURY:  Damage to the organelle of cells  Leakage of lysosomal enzymes  Production of nitric oxide by cells  Worsened myocardial contractility DIFFERENT CLINICAL OUTCOME OF CELLULAR INJURY:  Septic shock (entry of intestinal flora into circulation)  Complete renal shutdown (acute tubular necrosis)  Downward clinical spiral IRREVERSIBLE STAGE
  60. 60. COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)- Adrenal Response  SNS - Neurohormonal response Stimulated by baroreceptors Increased heart rate Increased contractility Vasoconstriction (Afterload) Increased Preload
  61. 61. COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)- Adrenal Response  SNS - Hormonal: Renin-angiotension system Decrease renal perfusion Releases renin angiotension I angiotension II potent vasoconstriction & releases aldosterone adrenal cortex sodium & water retention ( intravascular volume)
  62. 62. COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)-Adrenal Response  SNS - Hormonal: Antidiuretic Hormone Osmoreceptors in hypothalamus stimulated ADH released by Posterior pituitary gland Vasopressor effect to increase BP Acts on renal tubules to retain water
  63. 63. COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)-Adrenal Response  SNS - Hormonal: Adrenal Cortex Anterior pituitary releases adrenocorticotropic hormone (ACTH) Stimulates adrenal Cortex to release glucorticoids Blood sugar increases to meet increased metabolic needs
  64. 64. Types of Shock • Hypovolemic or Haematogenic • Traumatic Shock. • Septic • Cardiogenic • Anaphylactic • Neurogenic • Obstructive
  65. 65. Complications of Shock • Acute Respiratory Distress Syndrome
  66. 66. Literature: 1. General and clinical pathophysiology / Edited by Anatoliy V. Kubyshkin – Vinnytsia: Nova Knuha Publishers – 2011. – P. 642–651. 2. Gozhenko A.I. General and clinical pathophysiology / A.I. Gozhenko, I.P. Gurcalova // Study guide for medical students and practitioners. Edited by prof. Zaporozan, OSMU. – Odessa. – 2005. – P. 314–320. 3. Essentials of Pathophysiology: Concepts of Altered Health States (Lippincott Williams & Wilkins), Trade paperback (2003) / Carol Mattson Porth, Kathryn J. Gaspard. – P. 328 – 336; 725 – 745. 4. Symeonova N.K. Pathophysiology / N.K. Symeonova // Kyiv, AUS medicine Publishing. – 2010. – P. 531–536. 5. Robbins and Cotran Pathologic Basis of Disease 8th edition./ Kumar, Abbas, Fauto. – 2007. – Chapter 20. – P. 758–775. 6. Copstead Lee-Ellen C. Pathophysiology / Lee-Ellen C. Copstead, Jacquelyn L. Banasik // Elsevier Inc, 4th edition. – 2010. – P. 927–930, 936–937. 7. Pathophysiology, Concepts of Altered Health States, Carol Mattson Porth, Glenn Matfin. – New York, Milwaukee. – 2009. – P. 1299–1453.