Patho Heart

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Patho Heart
2012-04-27 18:42:36
Heart lectures

Lectures 9-14
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  1. How does the blood usually flow through the heart?
    • From right atrium to right ventricle via a tricuspid valve
    • From the right ventricle to the pulmonary arteries via the semilunar valve
    • From the pulmonary veins to the left atrium (there are 4)
    • from the left atrium to the left ventricle via the bicuspid valve
    • From the left ventricle to the aorta via the smilunar valve

  2. What are the two components of blood pressure?
    • Diastole
    • Systole
  3. What is diastole pressure?
    • relaxation of the ventricle where the ventricle fills.
    • The aorta is closed
  4. What is systole pressure?
    • The contraction of the ventricle.
    • The ejection of blood out of the ventricle
    • systole pressure reflects stroke volume, rates and force, elasticity of aorta and large arteries.
  5. How to you work out blood pressure?
    BP= CO x PR (peripheral resistance)
  6. The following involves the cardiac cycle and BP
  7. What are congentital heart defects?
    Cardiac anomalies which are structural defects that develop in the first eight weeks of embryonic life
  8. What are some congenital heart diseases?
    • 1. Valvular defects- interfere with normal blood flow
    • 2. Septal defects- allowing mixing of oxygenated blood from pulmonary circulation with unoxygenated blood fom the systemic circulation
    • 3. Shunts- may be cyanotic or acyanotic depending on direction of shunt
    • Or a combination of these
  9. What is cyanotic and acyanotic?
    • Cyanotic not enough oxygen person goes blue
    • Acyanotic- heaps of oxygen they are pinky colour
  10. Examples ofcongenital heart defects
  11. Note fluid always flows from and area of high pressure to low pressure
  12. What is the etiology of congential heart defects?
    • Genetic influences- chromosomal abnormalities eg down syndrome
    • Environmental influences- viral infection such as rubella, maternal alcoholism and diabetes
  13. What are the signs and symptoms of congenital heart defects?
    • Large defects lead to:
    • - pallor and cyanosis
    • - tachycardia
    • - dyspnea on exertion
    • - squatting position in toddlers and older children
    • - clubbed fingers
    • - intolerance for exercise and cold weather
    • - delayed growth and development
  14. How do you diagnosis congential defects?
    • Heart murmurs
    • Severe defects are often diagnosed at birth (untreated = heart failure)
    • Examination techniques:
    • 1. Auscultation- stethoscpoe
    • 2. Diagnostic imaging
    • 3. Echocardiogram (3D)
    • 4. Electrocardiogram (ECG)
    • 5. Cardiac catherisation
  15. How do you treat congenital heart defects?
    • Surgical repair
    • Valve replacement
    • Drug therapy
    • Spontaneous recovery
  16. What is VSD? (Ventricular Septal Defect)
    • THe most common congenital heart defect- 20-30% "hole in the heart.
    • Opening in the interventricular septum- vary in size and location. Atrial septum- foramen ovale fails to close
    • Large openings permit a left to right shunt of blood then may eventually, if untreated, lead to a reveral of the shunt- right to left.
  17. Note in VSD left to right. Blood flows from a high pressue to low pressure. Blood flows from the left ventricle to the right then to the lungs.
  18. What is the result of VSD?
    • Decreased SV and CO
    • increase in oxygenated blood entering pulmonary circuit
    • overloads and irreversibly damages the pulmonary blood vessels = pulmonary hypertension
    • Acyanotic condition results
  19. What hapens if VSD is untreated. RIGHT TO LEFT SHUNT
    • Abnormally high pressure in the right ventricle, from conditions such as pulmonary hypertension, leads to a reversal of the shunt. Right to left.
    • Leading to cyanosis- venous blood mixes with arterial blood resulting in unoygenated hb back into the systemic system
    • results in a bluish lips and nails etc
  20. What happens to the heart when it is suffering from VSD?
    • increase HR
    • increase force of contraction CO
    • decrease in coronary perfusion
    • increase peripheral resistance
    • increase in respiatory reate
    • Chronically- increase in RBC production as a result of hypoxia
  21. What are some valvular defects?
    • - Stenosis- narrowing of the valve, restricts the forward flow of blood
    • - valvular incompetence- failue of a valve to close completely, flaps back, blood regurgitates or leaks backwards eg mitral valve prolapse, abnormal enlarged, floppy valve leaflets that ballon backwards effect 1-3% pop
  22. Heart valve defects
  23. What are the compensatory effects of VD?
    • decrease in efficiency of the heart pump
    • decrease in stroke volume
    • increase contractility of myocardium
    • hypertrophy of the chamber with the faulty valve
    • with lead to heartfailure and pulmonary congestion
  24. What is the main cause of congestive heart failure (CHF)?
    Valve sternosis
  25. What is the main treatment of valve defects?
    Surgical replacement- mechanical, animal
  26. What is tetalogy of Fallot?
    • Most common cyanotic (R to L shunt) congenital heart condition
    • cyanosis occurs
    • alt pressure within heart and alt blood flow
    • includes four abnormalities:
    • - pulmonary valve stenosis
    • - VSD
    • - Dextropositio of the aorta
    • - right ventricular hypertrophy
  27. Congenital heart defects:
  28. What is the pathophysiological cascade?
    • Pulmonary valve stenosis- restricts flow to lungs
    • increase right ventricle pressure and right ventricle hypertrophies
    • increase pressure R to L
    • Unoxygenated lood R to L ventricular flow
    • Pulmonary circulation decrease of unoxygenated blood
    • systemic circulation receives larger amounts ofmixed blood
    • results in cyanosis
  29. How is the cardiac conduction systems started?
    • Heart is capable of generating its own action potiential.
    • Cells in the heart are able to helpit produce faster impulses, synchronised contrations and normal rhythm
  30. What is the conduction pathway in the heart?
    • Sinoartial node (SA)- pacemaker, sinus rhythm
    • internodal pathways
    • AV node- floor of right atrium
    • AV bundle (bundle of HIS) right and left
    • purkinje fibres- terminal fibres
  31. What is the role of electrolytes with the heart beat?
    • Na, Ca and K are major carriers in cardiac myocytes
    • AP- resting (polaried), depolarized, repolarization
    • Cardiac muscle has 3 types of ion channels
    • AP of cardiac muscle has 5 phases

    • K
    • Na depolarisation
    • K and Cl out- plateu
    • Ca in causes repolarisation
  32. What is an ECG?
    Recording of theelectrical activity of the heart by plaing electrode onthe skin.
  33. What occurs at the P wave?
    Depolarization of the atria (contraction)
  34. What occurs at the QRS wave?
    Depolarization of the ventricles (Contraction)
  35. What occurs at the T wave?
    • Repolarization of the ventricle
    • relaxation
  36. What is an abnoral ECG?
    • Arrhythmias
    • Dysrythmias
  37. Conducting pathway and ECG?
  38. What controls the heart?
    • Cardiac control centre- controls rate and force of contraction (medulla)
    • Brapreceptors- detect changes in the blood pressure, located in the aorta and internal carotid arrteris
    • sympathetic stimulation (cardiac accelerator nerve)
    • Parasymp- decreases hear rate
  39. What factors increase heart rate?
    • increase in thryoid hormones or rpinephrine
    • elevated body temp
    • increase envt temp
    • exercise
    • smoking
    • stress
    • preg
    • pain
  40. What is an arrhythmia?
    Cardiac Dysrhythmias
    Deviations from normal rate- caused by damage to the hearts conduction sstem, electrolyte abnormalities, fever, hypoxia, stress, infection, drug toxicity
  41. What are the two main categories of cardiac dysrhythmias?
    Supraventricular and ventricular
  42. What is the result of caridac dysrhythmias?
    • reduction of the efficiency of the hearts pumping cycle.
    • ECGs detect abnormalities
  43. What are SA node abnormalities?
    • Hear rate altered.
    • Bradycardia- 60 beats/ min, regular but slow HR, results from vagal nerve PNS stimulation. Exception- athletes at rest have conditioned larger stroke volume.
    • Tachycardia- 100-160 beats/ min, regular but rapid HR, normal response to SNS stimulation- exercise etc, compensation for decreased blood volume
    • Sick sinus syndrome- HR irregularity, marked by altering bradycardia and tachycardia, often requires mechanical pacemaker.
  44. What is premature atrial contraction or beats (PAC?PAB)
    • extra contraction or ectopic beats
    • irritable artial muscle cells outside conduction pathway
  45. What are heat palpitations?
    • Rapid or irregular heart contractions
    • caffeine, smoking or increase stress
  46. What are some atrial conduction abnormalities?
    • Premature atrial contractions or beats
    • Palpitations
    • Atrial flutter
    • Atrial fibrillation
  47. What is atrial flutter?
    • atrial HR of 160 to 350 beats/ min
    • AV nod delays conduction- ventricular rate is slower
    • decrease in SV which results in pulse deficit could occur
  48. AV node abnormalities
    Heart blocks
  49. What are the different degrees of heart block?
    AV abnormalities
    • first degree- partial block- condcution delay between atrial and ventricular contraction (PR interval)
    • Second degree partial block- every second to third atrial beat is dropped at AV node i. e. missed ventricular contraction
    • Third degree (total block)- no transmission of impulses form atria to ventricles
  50. What is a third degree AV block?
    • Ventrilce contract spontaneously at a slow rate (30-45 beat/min)
    • Independent of atrial contraction
    • decrease cardiac output... light headedness, fainting (syncope)
    • Results: stokes adams attack or cardiac arrest
  51. WHat is stoke adams attack?
    • Temp pause in heart rhythm, pale/ flushing afterwards, light headedness, collapse
  52. What are some ventricular conduction abnormalities?
    • Bundle branch block
    • Ventricular tachycardia
    • Ventricular fibrillation
    • Premature ventricular contractions (PVCs)
  53. What is a bundle branch block?
    Interference with conduction in one of the bundle branches. wide QRS, cardiac output is unchanged
  54. What is ventricular tachycardia?
    • Likely to reduce cardiac output as reduced diastoe occurs
    • decrease filling time and force of contraction
  55. What is ventricular fibrillation?
    • muscle fibres contract independently and rapidly
    • uncoordinated quivering/ ineffective pump
    • hypoxic myocardium
    • cardiac standstill occurs if not treated immediately
  56. What is premature ventricular contractions? (PVCs)
    additional beats from ventricular muscle cells or ectopic pacemaker. May lead to venticular fibrillartion- cardiac arrest
  57. What is the treatment of cardiac dysrhythmias?
    • Cause needs to be determined and treated:
    • defective conductive system
    • electrolyte abnormalities- K and Na
    • drug toxicity
    • Anti dysrythmic drugs are effective in many cases:
    • iebeta blokers- metoprol,atenolo
    • calcium channel blockers- verapamil
    • digoxin
  58. When is a pacemaker necessary?
    • SA node problems or a total heart block
    • defibrillator may be needed to be used/ implanted for conservation of ventricular fibrillation, back to sinus rhythm
  59. What is cardiac arrest? (asystole)
    • Cessation of heart activity- no conduction of impulses- no cardiac output
    • FlatECG (O2 deprivation to brain and heart)- loss of consciousness, no respiration- no pulse
  60. What causes cardiac arrest?
    • Excessive vagal nerve stimulation
    • insufficient oxygen
    • potassium imbalance
    • Cardiogenic shocl
    • Drug toxicity
    • Respiratory arrest
    • blow to heart
  61. what is congestive heart failure?
    heart is unable to pump outsufficient blood to meet metabolic demands of the body.
  62. What are the two main effets of congestive heart failure?
    • Forward effects
    • Backup effects
  63. What are forward effects ofcongestive heart failure?
    • Cardiac output/ stroke volume decreases:
    • - less blood reaches the various organs iekidney
    • - decreased cell function
    • - fatigue and lethargy
    • - mild acidosis develops
  64. WHat are backup effects of congestive heart failure?
    • backup/ congestion develops
    • output from ventricle isless than the inflow of blood
    • congestion in venous circulation draining into the affeced side of the heart.
  65. Notes on congestive heart failure:
    • usually a complication of another cardio-pulmonary condition
    • may present as an acute episode, but is usually chronic
    • Various compesation mechanisms maintain ccardiac output-often some aggravate the condition
  66. What is the etiology of CHF?
    • from a problem in the heart- infarction, congenital heart defect, valve changes
    • may be a result of an increase in demand on the heart- hypertension, pulmonary disease, leading to either left orright sided heart failure
    • coronary artery disease is the leading cause of CHF
  67. Hypertensive heart
    pulmonary disease
    • 1. thichekendleft ventricle wall
    • 2 thickened right ventricle wall
  68. Overview of CHF
    to be broken down
    compenstory mechanisms
  69. what are some of the compensatory mechanisms for those with CHF?
  70. What are some compensatory mechanisms for CHF?
    • Sympathetic nervous system activity:
    • mainttains perfusion of various body organs, increases in HR and contractility and regulation of vascular tone, increase in peripheral resistance and vasoconstriciton.
    • But the increase in HR- decreases the efficiency causing increases in workload. Ventricle wall stress- dilation= hypertrophy can = ischemia
    • Renin-angiotensin-aldosteron secretions:
    • decrease CO = reduced renal blod which increases renin- angio which increases aldosteron secretion that increases vasoconstricition and sodium and water retention therefore increases blood volume.
    • But vasoconstricition increases afterload and increases blood volume increases preload = hard work for heart.
  71. What are the effects of CHF on the left ventricle?
    • Hypertension/ aortic valve stenosis and LV infarction
    • Back upof blood into pulmonary vein, high pressure of blood in lungs, decreased CO, left V weak can cant empty, decrease in renal blood flow.
  72. What are the effects of CHF on right ventricle?
    • Pulmonary disease/ valve stenosis RV infarction:
    • right ventricle weak and cant empty
    • decrease CO
    • dereased renal flow
    • increase in venous pressure can cause eema in legs etc
    • backup of blood into systemic circulation
    • very high venous pressure causes distended neck vein and cerebral edema.
  73. What are the signs and symptoms of CHF forward effects?
    • similar with failure on either side:
    • decrease blood supply to tissues, general hypoxia
    • Fatigue and weakness
    • Dyspnes and shortness of breath
  74. What are the compenstion mechanisms for those with CHF forward effects?
    • tachycarida
    • cutaneous and visceral vasoconstriction
    • Daytime oliguria (low output of urine)
  75. What are the signs and symptons of CHF, backup effects of left side?
    • Are related to pulmonary congestion
    • dyspnea and orthopnea- develops as fluid accumulates in the lungs
    • cough-fluid irriating the respiratory
    • Paroxysmal nocturnal dyspnea- indicates the presence of acute pulmonary edema, usually develops during sleep, hemoptysis and rales
    • excessive fluid in lungs lead to infection
  76. What are the signs and symptons of CHF back up effects of right sided failure?
    • are related to systemic congestions
    • dependent edema in feet, leg or but, increase pressure in jugular veins
    • Hepatomegaly and splenomegaly0 digestive disturbances
    • Ascites- complcation when fluid accumulates in the peritoneal cavity- abdominal distention
    • Acute rightsided failure- flushed face, distended neck veins, headache, visual distrubances
  77. Manifestations of right and left sided CHF
  78. How do you treat CHF?
    • reduce workload on the heart
    • Maintian a healthy diet- low sodium and cholesterol
    • Drugs
  79. Young children with CHF
    • often secondary to congenital heart disease
    • feeding difficulties first sign
    • short sleep periods
    • tripod position to play
    • cough, grunting respirtaion, wheezing
    • radiographsshow cardionegaly
    • arterial blood gases used to measure hypoxia
  80. What is arteriosclerosis?
    • General term for all types of arterial changes
    • degenerative changes in small arteries and arterioles
    • loss of elasticity
    • Lumen gradually narrows and may become obstructed
    • cause of increase blood pressure
  81. What is Atherosclerosis?
    • denoted by the presence of an atheroma in walls of large arteries
    • plaques consisting of lipids, calcium, cell debris
    • thrombi often attach
    • throught to result from epithelial cell injury
    • many risk factors
  82. How are lipids transported?
    attached to proteins- apolipoprotens proteins that bind lipids to form lipoproteins
  83. What is an LDL?
    • low density lipoprotein
    • involved in transpot of cholesterol from liver to cells
    • major factor contributing to atheroma formation
  84. What is a HDL?
    • high density lipoprotein
    • involved in transport of cholesterol away from the peripheral cells to liver
    • Once in the liver the lipoprotein is catabolised and excreted
  85. Transport of lipoproteins
  86. How is atheroma formed?
    • initiates from artery endothelial tissue injury:
    • - migration of inflammatory cells
    • - increase c- reactive protein
    • - white blood cells
    • lipids accumulate in intima (iner lining) and media (muscle layer)
    • smooth muscle cells proliferate/ multiply leading to plaque formation
    • platelets adhere to the inner surface of arterial wall leading to further inflammation
    • thrombus- partial obstruction- embolus
    • weakened wall and risk of aneurysm
  87. COnsequences of atherosclerosis
  88. What is the cause of atherosclerosis?
    • Multifactorial:
    • - non modifiable- age, gender, family history, genetics
    • - modifiable- obesity, high cholesterol diet, high LDL, smaking, low LDL, promotes platelet adhesion, increase in vascular tone
    • sedentary lifestyle- obesity high BP
    • Hypertension- high BP- endothelial damage
    • Diatets mellitus- increase lipid levels, endothelial degeneration
    • Hyperhomocysteine- folate and B6 deficiency
    • COmbination of the above
  89. How to treat atherosclerosis?
    • Lifestyle changes
    • Mdication- lipid reducing drugs, antihypertensive drugs, anticoagulants
    • Surery- percutaneous transluminal coronary angioplasty, leser angioplasty, stent
  90. What are the consequences of artherosclerosis?
    • Peripheral arteris
    • aorta- aneurysm- occlusion, rupture and hemorrhage
    • Legs- iliac arteris- peripheral vascular disease- gangrene and amputation
  91. What occurs with an aorta aneurysm?
    • Dilation and weaking of a blood vessle
    • Abd and thoracic aorta most common
    • saccular, fusiform and dissecting shapes
    • caused by atheroma, defect in the medial layer, trauma or infection
    • over time the dilaion increases, throbi develop, may rupture causing hemorrhage
  92. Peripheral arteial disease and your legs?
    • COnsequence of atherosclerosis- partial or total occlusion- relative ishemia- impaired mm function/ activity and sensory function
    • increasing fatigue and weakness in the legs
    • pain associated with exercise due to mm ischemia- intermittent claudication- anaerobic build up of lactiv acid activating nociceptors
    • peripheral nerve dsfunction- lack of oxygen supple to nerve tissue- tingle, numbness
    • pulse distal to occlusion becomes weak
    • appearance of the skin of the feet and legs change
    • loos of blood means necrosis, ulcers, gangrene
  93. Peripheral venous disease- DVT?
    • Thrombus formation in the vein
    • standing or sitting for long periods of time
    • restrictive clothes
    • trauma, inflammation
    • increased blod coagulation
    • lack of blood movements- blood clot
    • embolus- pulmonary embolism
  94. Peripheral venous disease varicose veins
    Weakness or defect in vein wall or valve
  95. What is the arterial disease hypertension?
    • Persistent elevated BP
    • there are three categories- primary, secondary and malignant.
  96. What is primary/ essential hypertension?
    • BP constantly over 140/90
    • increase in arteriolar vasoconstricition- results in increase in total peripheral resistance and shuting of blood centrally, increasing diastolic pressure
    • over long period of time- damage to arterial walls: atheroma or aneurysm
    • Blood supply to involved area is reduced- ischemia and necrosis
  97. What is secondary hypertension?
    • Results from renal or endocrine disease, or pheochromocytoma (benign tumor of the adrenal medulla)
    • underlying roblemmust be treat to reduce BP
  98. What is malignant or resistant hypertension?
    • Uncontrollable, severre, rapidly progressive form with many complications
    • Diastolic pressure is extremely high
  99. What are the consequences of hypertension?
    • areas:
    • kidneys
    • heart
    • brain
    • retina
  100. What are the predisposing factors of hypertensions?
    • increase incidence with age
    • men more frequent and severe
    • incidence in women increases after middle age
    • genetics
    • sodium and alcohol leaves
    • obesity
    • smokng
    • prolonged or recurrent stress
  101. What are the coronary arteries?
  102. What are the functions of the cornonary arteries?
    • Supply heart with oxygen- 60-80% the heart extracts- no reserve
    • need to increase their bloodflow to meet demands during increased activity.
    • - autoregulatory mechanism
    • change in vessle tone
    • vasoactive mediators - vaso con/dia andpot, adenosine, nitric acid and endothelins
  103. What is CAD
    • Coronary artery disease
    • leading cause of death world wide
    • due to imparied coronary blood flow- ischemic heart disease
    • artherosclerosis most common cause
    • Include:
    • - angina pectoris (temporary ischemic heart disease)
    • - myocardail infarction/ Heart attack
  104. What is angina pectoris?
    Chect pain that is due to an imbalancebetween hearts O2 and demand ischemia
  105. What are the types of angina pectoris?
    • Classic/exerctional/ stable
    • Unstable/crescendo
    • - prolonged pain
    • - break in atheroma
  106. What is the etiology of angina?
    • increase demand on heart eg exercise
    • obstruction by atherosclerosis
    • vasospasm in coronary arteries
    • myocarial hypertrophy
    • severe anaemia
    • respiratory disease
    • tachycardia
    • hypertension (increase force of contraction)
  107. What is a myocardail infarction (MI)?
    coronary artery is conpletely obstructed (prolonged ischemia)
  108. What is the most common cause of myocardial infarction?
    atherosclerosis usually with thrombosis attached
  109. How is the serverity of a myocardail infarction determined?
    • Size and location of infarct
    • Most common is theleft ventricle and all three layer of the heart
  110. With MI what happens to the tissue?
    • Becomes necrotic and inflammed, cell destruction resleases enzymes into tissue
    • area of necrosis is replaced by fibrotic (non contractile tissue)- which blocks the electical conduction of the heart! Cardiac dysrhythmias
  111. What are the MI onesand what do they entail?
    • ZOnes of infarction:
    • - irreversible damage to myocardium, eletrically dead
    • Zone of injury:
    • - surrounds area of infarction
    • - blood supply decreases
    • - myocardium never completely polarises
    • Zone of ischemia:
    • - surroundsare of injry
    • - reversible damage
    • impaired repolaristaion
  112. What are the signs and symptoms of MI?
    • sudden pain in chest, left arm, shoulder, jaw, neck- cannot aleviate with rest or vasodilators
    • Pallor, diaphoresis, nausea, dizziness
    • dyspnea
    • anxiety and fear
    • hypotension
    • low CO, shock
  113. What are the complications of MI?
    • Sudden death- due to arrhythmia and fibrillation
    • cardiogenic shock- due to impaired cardiac function, decreases pumping capability of the heart
    • Congestive heart failure- due to reduced contractility of ventricles, left or right sided
  114. What are some less frequent complications of MI?
    • Rupture of necrotic heart tissue/ cardiac tamponade- build up of fluid in the pericardium, compresses heart-decrease CO
    • thromboembolism causing cerebrovascular accident (with left ventricular MI)- due to thrombus dveloping over the infarted surface.
  115. What is shock?
    • a hypotensive event
    • not a specific disease but a syndrome
  116. What does cases of shock involve?
    • low cardiac output
    • decrease in circulating blood volume
    • decreased tissue perfusion
    • general hypoxia and reduced nutirents to cells
    • organ dysfunction and failure
  117. What are some of thecauses of shock?
    • los of circulating blood
    • inability of heart to pump
    • changes in peripheral resistance
  118. How so you determine BP and CO?
    • BP= CO x PR
    • CO= HR x SV
  119. What are the different types of shock?
    • Hypovolemic shock
    • Cardiogenic shock
    • Distributive or Vasogenic shock
    • Subcategories:
    • - Neurogenic
    • - Anaphylactic
    • - Septic
  120. What is hypovolemic shock?
    • - Loss of circulating blod volume (whole blood, plasma)
    • - due to hemorrhage, burns, peritonitis, dehydration
    • - Acute loss of 15-20% of blood
  121. What is cardiogenic shock? (subcategory obstructive)
    • - inability of heart to maintain cardiac output to circulation (failure of left ventricle)
    • - Due to MI, arrhymias, congenital heart defects
    • - Cardiac tamponade, pulmonary embolus
  122. What is distributive or vasogenic shock?
    • - loss of blood vessel tone- vasodilation
    • - normal volume of blood doesn't fill the circulatory system ie the capacity of the vascular compartment expands
  123. What is neurogenic shock?
    • - involvement of the nervous system
    • - sympathectic acitity decreases- decreased peripheral resistance, shunting of blood to the periphery, reduction of cardiac return
    • - metabolic dysfunction- severe acidosis- vasodilation
  124. What is anaphylactic shock?
    • results from an immunologically mediated reaction
    • - release of histamine- vasodilation and increased capillary permeability and other symptoms
  125. What is septic shock?
    • systemic response to severe infection
    • - toxins released by fungi or bacteria (mainly gram negative endotoxins) may cause tissue damage
    • - inflammatory response vasodilation