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SHOCK
Dilki Punchihewa
Acute circulatory failure with inadequate or
inappropriately distributed tissue perfusion
resulting in generalized cellula...
CIRCULATORY
SHOCK
CIRCULATORY SHOCK
DUE TO DIMISHED
CARDIAC OUTPUT
CIRCULATORY SHOCK
CAUSED WITHOUT
DIMISHED CARDIAC
OUTPU...
The end result of any type of shock would be-
• INADEQUATE O2
• INADEQUATE NUTRIENTS
• INADEQUATE REMOVAL OF WASTE PRODUCTS
STAGES OF SHOCK
I. NON PROGRESSIVE
Reversible stage where the compensatory mechanism get activated.
Person will fully reco...
PATHOPHYSIOLOGY OF SHOCK- COMPENSATORY STAGE
Osmoreceptors in hypothalamus stimulated
ADH (vasopressin) released by posterior pituitary
gland
Constrict peripheral vess...
Anterior pituitary release ACTH
(adrenocorticotropic hormone)
Stimulate the adrenal cortex to release
glucocorticoids
Bloo...
• Other mechanism that return the blood
volume back towards normal
 Absorption of large quantities of fluid
from the inte...
PATHOPHYSIOLOGY OF SHOCK-PROGRESSIVE STAGE
Decrease cardiac output
Tissue hypo-perfusion
Cells switch from aerobic to anae...
• If low perfusion persists then shock will progress to
irreversible state where death is imminent.
• Even in irreversible...
Clinical features of shock
Generalized shock
• mental status-
LOC
restless
Irritable
unresponsive
• Decreased urine output...
• Loss of circulating volume “EMPTY TANK”
‒ Loss of blood- trauma (blunt and penetrating)
BLOOD YOU SEE
BLOOD YOU DON’T SE...
Decreased intravascular volume
Decreased venous return
Decreased ventricular filling
Decreased stroke volume
Decreased car...
1. Hx of trauma, bleeding, burns, diarrhea and vomiting?
2. inadequate tissue perfusion
a) Skin- cold, pale, slate-grey, s...
S/S vary depending on severity of fluid loss:
• 15%[750ml]- compensatory mechanism maintains CO
• 15-30% [750-1500ml- Hypo...
• Put the patient on the bed.
• Have the person lie flat with the feet lifted about 12
inches to increase circulation. How...
• Put two wide bore cannulas.
Blood for grouping, Rh and cross match blood
depending on loss.
Take blood for FBC, urea and...
• Burns- parkland formula
V (volume in ml) = 4 x body mass in kg (%surface area x 100)
Surface area by wallace rule of nin...
• Resuscitate using crystalloids such as Normal saline,
hartmann solution.
• Insert a CVP line.
• If in pain iv anaglegics...
• the impaired ability of the heart to pump
blood.
Causes
CARDIOGENIC SHOCK
Systolic
dysfunction
Diastolic
dysfunction
Inc...
Impaired pumping ability of left ventricle leads to
↓Stroke volume
↓Cardiac output
↓BP
↓Tissue perfusion
Inadequate systol...
Symptoms may vary according to the cause.
• Signs of myocardial failure
a) Elevated JVP
b) gallop rhythm
c) basal coarse c...
• Put the patient on to the bed.
• Best if the patient was in a coronary care unit.
• Give high flow oxygen via a face mas...
• Insert a urinary catheter to measure the UOP.
• Do a arterial blood gas analysis to identify metabolic
acidosis
• Ideally following parameter should be measure
a) Central venous pressure via a CVP Line
b) Mean arterial pressure via an...
a) central venous pressure via a CVP line
adequacy of patients circulating volume and
contractile state of the myocardium....
b) mean arterial pressure through an arterial
pressure line
permits the rapid recognition of BP changes
Arterial cannulati...
c)pulmonary capillary wedge pressure through a
pulmonary artery catheter
pressure measured by wedging a pulmonary catheter...
• Start an infusion of inotropic agents
Dobutamine infusion- if the patient is peripherally
vasoconstricted this is the dr...
• Dopamine infusion- if the patient is not
peripherally vasoconstricted
Start at 2.5 micrograms/kg/min
Main at 2.5-10 micr...
• Determine the cause of cardiogenic shock
Eg- MI, cardiac arrythmias, acute valvular dysfunction,
aortic aneurysms, cardi...
• Systemic inflammatory response (SIRS) to infection
manifested by two or more of following.
• Temp > 38 or < 36 centigrad...
• Initiated by gram negative (most commonly), gram
positive bacteria, fungi or viruses.
• Cell wall of organisms contain e...
• Clinical features
a) Fever and rigors
b) Nausea, vomiting
c) Vasodilation so warm peripheries
d) Bounding pulse
e) Rapid...
• Put the patient on the bed.
• Hx and examination will be suggestive of septic shock
• Clear the airway and give high flo...
• Chest xray, uss abdomen, KUB
• 2D echo- if suspect endocarditis
• Maintain fluid balance with Normal saline or colloids
...
• Use a combination of broad spectrum antibiotic. Select
appropriately according to the source of infection
• Get advice f...
ANAPHYLACTIC SHOCK
• Results from widespread systemic allergic
reaction to an antigen
• LIFE THREATENING (Sometimes dead w...
Expoure to an antigen
Body stimulated produe IgE antibodies specific to the antigen
Rexposure to the antigen
IgE binds to ...
• Also activated basophils and mast cells release mixture of
leukotrienes called slow reacting substance of anaphylaxis.
T...
Present with chocking, coughing, stridor, wheezing,
breathless, LOC, itchy rash.
Hx of previous allergic reaction or anaph...
Management
• Put the patient on the bed
• Establish airway patency and breathing
• If necessary endotracheal intubation, i...
• Immediately give 0.5mg im adrenaline 1 : 1000 to vastus
lateralis
Repeat every 5 mins if shock persists
• Meanwhile put ...
Neurogenic shock
• Results from loss or suppression of sympathetic tone
which causes massive vasodilatation in the venous
...
Disruption of sympathetic nervous system
Loss of sympathetic tone
Venous and arterial vasodilatation
Decreased venous retu...
Present with paralysis below the level of lesion
On patient assessment
• Hypotension
• Bradycardia,
• Hypothermia
• Warm, ...
• Put the patient on the bed
• Give high flow oxygen
• Examine the patient and find the level of lesion
• Connect to a pul...
• Alpha agonist to augment tone if perfusion still inadequate
dopamine (> 10 mcg/kg per min)
ephedrine (12.5-25 mg IV ever...
Case scenario
1. A 58 yr patient presented with central chest pain
of tightening nature radiating to the neck and left
arm...
It could be hypotension due to streptokinase allergy so
anaphylaxis shock or due to anterior MI causing
cargdiogenic shock...
If the patient is having a cardiogenic shock due to the MI.
The MI involves the left ventricle hence reducing the
ability ...
Shock
Shock
Shock
Shock
Shock
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Shock

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Shock
what is shock
stages of shock
types of shock, their presentation and management

presentation is made for medical students using kumar and clark and guyton.

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Shock

  1. 1. SHOCK Dilki Punchihewa
  2. 2. Acute circulatory failure with inadequate or inappropriately distributed tissue perfusion resulting in generalized cellular hypoxia and/or an inability of the cells to utilize the oxygen.
  3. 3. CIRCULATORY SHOCK CIRCULATORY SHOCK DUE TO DIMISHED CARDIAC OUTPUT CIRCULATORY SHOCK CAUSED WITHOUT DIMISHED CARDIAC OUTPUT (DISTRIBUTIVE SHOCK) CARDIAC ABNORMALITIES THAT DIMISHED THE ABILITY TO PUMP FACTORS THAT DECREASE THE VENOUS RETURN WHICH DECREASE THE CARDIAC OUTPUT RESTRICTED CARDIAC FILLING AND OBSTRUCTION IN THE OUTFLOW TRACT CARDIOGENIC SHOCK HYPOVOLEMIC SHOCK OBSTRUCTIVE SHOCK SEPTIC SHOCK ANAPHYLACTIC SHOCK NEUROGENIC SHOCK
  4. 4. The end result of any type of shock would be- • INADEQUATE O2 • INADEQUATE NUTRIENTS • INADEQUATE REMOVAL OF WASTE PRODUCTS
  5. 5. STAGES OF SHOCK I. NON PROGRESSIVE Reversible stage where the compensatory mechanism get activated. Person will fully recover without any external help. II. PROGRESSIVE STAGE Failing of compensatory mechanisms. Intervention is necessary to prevent shock from further progression or progressing to irreversible stage. III. IRREVERSIBLE OR REFRACTORY STAGE DEATH IS IMMINENT!!!!
  6. 6. PATHOPHYSIOLOGY OF SHOCK- COMPENSATORY STAGE
  7. 7. Osmoreceptors in hypothalamus stimulated ADH (vasopressin) released by posterior pituitary gland Constrict peripheral vessels and increase water retention
  8. 8. Anterior pituitary release ACTH (adrenocorticotropic hormone) Stimulate the adrenal cortex to release glucocorticoids Blood sugar levels increases to meet increase metabolic needs
  9. 9. • Other mechanism that return the blood volume back towards normal  Absorption of large quantities of fluid from the intestinal tract  Absorption of fluid into blood capillaries from interstitial space of the body  Increase thirst and appetite for salt.
  10. 10. PATHOPHYSIOLOGY OF SHOCK-PROGRESSIVE STAGE Decrease cardiac output Tissue hypo-perfusion Cells switch from aerobic to anaerobic metabolism lactic acid production Cell function ceases & swells membrane becomes more permeable electrolytes & fluids seep in & out of cell Na+/K+ pump impaired mitochondria damage Cell death
  11. 11. • If low perfusion persists then shock will progress to irreversible state where death is imminent. • Even in irreversible shock, therapy can, on rare occasions bring the arterial pressure and cardiac output to near normal but circulatory system nevertheless continues to deteriorate followed by death within mins or hours PATHOPHYSIOLOGY OF SHOCK-IRREVESIBLE STAGE
  12. 12. Clinical features of shock Generalized shock • mental status- LOC restless Irritable unresponsive • Decreased urine output Feature specific for each type of shock?
  13. 13. • Loss of circulating volume “EMPTY TANK” ‒ Loss of blood- trauma (blunt and penetrating) BLOOD YOU SEE BLOOD YOU DON’T SEE ‒ Loss of plasma- severe burns ‒ Loss of body sodium and consequent intravascular water from diarrhea and vomiting HYPOVOLEMIC SHOCK
  14. 14. Decreased intravascular volume Decreased venous return Decreased ventricular filling Decreased stroke volume Decreased cardiac output Inadequate tissue perfusion Compensatory mechanism activation
  15. 15. 1. Hx of trauma, bleeding, burns, diarrhea and vomiting? 2. inadequate tissue perfusion a) Skin- cold, pale, slate-grey, slow capillary filling time, clammy b) Kidney- oliguria, anuria c) Brain-drowiness, confusion, irritability 2. Increased sympathetic tone- a) Tachycardia, narrowed pulse pressure, weak or thready pulse b) Sweating c) Blood pressure initially may be maintained later causes hypotension 3. Metabolic acidosis- compensatory tachypnoea
  16. 16. S/S vary depending on severity of fluid loss: • 15%[750ml]- compensatory mechanism maintains CO • 15-30% [750-1500ml- Hypoxemia, hypotension, generalized vasoconstriction and reduction in urine output to 20-30 ml/hour. • 30-40% [1500-2000ml] -Impaired compensation & profound shock along with severe acidosis hypotension, tachycardia over 120, tachypnoea, urine output under 20 ml/hour and the patient is confused. • 40-50% - refractory stage: marked hypotension, tachycardia and tachypnoea. No urine output and the patient is comatose loss of volume= death
  17. 17. • Put the patient on the bed. • Have the person lie flat with the feet lifted about 12 inches to increase circulation. However, if the person has a head, neck, back, or leg injury • Nil by mouth • Aim of Mx Restoring circulatory volume Tissue perfusion Correct the cause • Early recognition- don’t rely on BP (decreases only when 30% of fluid is lost ) • Connect to a pulse oximeter – PR, RR, BP • Give high flow oxygen
  18. 18. • Put two wide bore cannulas. Blood for grouping, Rh and cross match blood depending on loss. Take blood for FBC, urea and electrolytes Blood sugar • ABG- acidosis • Catheterize and UOP > 30ml/hr • Trauma- no signs of external bleeding, look for internal bleeding. CT SCAN- Head injuries USS- abdomen (blunt force trauma to abdomen) • Transfuse blood if hemorrhage • Electrolyte imbalance- correct it
  19. 19. • Burns- parkland formula V (volume in ml) = 4 x body mass in kg (%surface area x 100) Surface area by wallace rule of nine • fluid replacement within 24 hours. The first half of this amount is delivered within 8 hours from the burn incident, and the remaining fluid is delivered in the next 16 hours.
  20. 20. • Resuscitate using crystalloids such as Normal saline, hartmann solution. • Insert a CVP line. • If in pain iv anaglegics • Control bleeding – surgery may be needed
  21. 21. • the impaired ability of the heart to pump blood. Causes CARDIOGENIC SHOCK Systolic dysfunction Diastolic dysfunction Increase after load Valvular structural abnormalities Arrhythmias MI Ventricular hypertrophy Aortic stenosis Papillary muscle rupture Ventricular tachyarrhythmia Myocardial depressants- antiarrythmics, beta blockers, calcium channel blockers. Restrictive cardiomyopathy Cardiac tamponade Malignant hypertension Aortic and mitral regurgitation
  22. 22. Impaired pumping ability of left ventricle leads to ↓Stroke volume ↓Cardiac output ↓BP ↓Tissue perfusion Inadequate systolic emptying ↑Left ventricular filling pressure (preload) ↑Left atrial pressure ↑Pulmonary artery and capillary pressure Pulmonary odeama
  23. 23. Symptoms may vary according to the cause. • Signs of myocardial failure a) Elevated JVP b) gallop rhythm c) basal coarse crackles d) reduced pulse volume with tachycardia e) low BP • Obstructive – cardiac tamponade a) Pulsus paradoxus b) Muffled heart sound • Symptoms and Signs of pulmonary emboli a) Sudden onset dyspnoea b) Tachypnoeic, tachycardia with hypotension c) Localized Plural rub d) Massive emboli- severe central chest pain • Other signs cold clammy peripheries with pallor and peripheral and central cyanosis
  24. 24. • Put the patient on to the bed. • Best if the patient was in a coronary care unit. • Give high flow oxygen via a face mask or if patient is unconscious endotracheal tube. • Connect the patient to a pulse oximeter and look for o2 saturation, BP, PR, RR • Put two wide bore cannulas take blood for cardiac troponin, FBC, blood gluocose, CRP, ESR, Urea and electrolytes, LFT. • Meanwhile do a ECG and look for evidence of MI, arrythmias. • Chest xray- cardiomegally and pulmonary odeama
  25. 25. • Insert a urinary catheter to measure the UOP. • Do a arterial blood gas analysis to identify metabolic acidosis
  26. 26. • Ideally following parameter should be measure a) Central venous pressure via a CVP Line b) Mean arterial pressure via an arterial pressure line c) Pulmonary capillary wedge pressure through a pulmonary artery catheter
  27. 27. a) central venous pressure via a CVP line adequacy of patients circulating volume and contractile state of the myocardium. in cardiac failure venous pressure is usually high; patient will not improve in response to volume replacement which will cause further dramatic rise in CVP.
  28. 28. b) mean arterial pressure through an arterial pressure line permits the rapid recognition of BP changes Arterial cannulation also allows repeated arterial blood gas samples to be drawn without injury to the patient. Arterial lines can be placed in multiple arteries, including the radial, ulnar, brachial, axillary, posterior tibial, femoral, and dorsalis pedis arteries. But the commonest site is radial artery and second commonest is femoral artery
  29. 29. c)pulmonary capillary wedge pressure through a pulmonary artery catheter pressure measured by wedging a pulmonary catheter with an inflated balloon into a small pulmonary arterial branch Indirect measure of left atrial pressure Gold standard in determining cause of acute pulmonary odeama. diagnose severity of left ventricular failure and mitral stenosis pulmonary edema with normal PWP suggested a diagnosis of acute respiratory distress syndrome (ARDS) or non cardiogenic pulmonary edema
  30. 30. • Start an infusion of inotropic agents Dobutamine infusion- if the patient is peripherally vasoconstricted this is the drug of choice. Start with 2.5 microgramas/kg/min Maintain at 2.5-10 micrograms/kg/min enable the SBP to be kept at 90mmhg.
  31. 31. • Dopamine infusion- if the patient is not peripherally vasoconstricted Start at 2.5 micrograms/kg/min Main at 2.5-10 micrograms/kg/min • If the PCWP is <15mmhg or if not measurable in the background of hypovolemia and clear lung field in CXR- give colloids/ plasma expanders 100ml every 15 mins untill PCWP is 15-20mmhg • Excess fluid can be detrimental in cardiogenic shock!
  32. 32. • Determine the cause of cardiogenic shock Eg- MI, cardiac arrythmias, acute valvular dysfunction, aortic aneurysms, cardiac tamponade • Then treat according MI- thrombolytics or Percutaneous intervention Acute valvular dysfunction- surgery Arrythmias- cardioversion • Correct any metabolic and electrolyte imbalances • SEEK SPECIALIST ADVICE EARLY.
  33. 33. • Systemic inflammatory response (SIRS) to infection manifested by two or more of following. • Temp > 38 or < 36 centigrade • HR > 90 • RR > 20 or PaCO2 < 32 • WBC > 12,000/cu mm or < 4,000 • Septic shock is SIRS with confirmed infectious process associated with hypotension and organ failure. SEPTIC SHOCK
  34. 34. • Initiated by gram negative (most commonly), gram positive bacteria, fungi or viruses. • Cell wall of organisms contain endotoxins or exotoxins (antigenic protien produced by bacteria such as staphylococcus, streptococcus and pseudomonas ) • Endotoxins causes release of inflammatory mediators (systemic inflammatory response) • Which causes vasodilatation and increased capillary permeability • Alters the peripheral circulation and massive dilation leads to shock.
  35. 35. • Clinical features a) Fever and rigors b) Nausea, vomiting c) Vasodilation so warm peripheries d) Bounding pulse e) Rapid capillary refilling f) Hypotension g) evidence of infection at local site- lungs, kidneys, meningies, brain, intra-abdominal. Other signs a) Jaundice b) Come, stupor c) Bleeding due to coagulopathy d) rashes- and meningism e) Hypoglycemia
  36. 36. • Put the patient on the bed. • Hx and examination will be suggestive of septic shock • Clear the airway and give high flow oxygen If hypoxia persists intubation and ventilation may be necessary • Put two wide bore cannulas and take blood for investigations FBC, CRP Blood glucose, urea and electrolytes, CT/BT • Meanwhile catheterize the patient and send urine for UFR. Maintain UOP > 30ml/hr • Culture samples- blood, urine, CSF(meningitis), swabs from open wounds
  37. 37. • Chest xray, uss abdomen, KUB • 2D echo- if suspect endocarditis • Maintain fluid balance with Normal saline or colloids • Give fresh whole blood if Hb <10g/dL • Fever- antipyretics – paracetamol 1 g 6hrly • Hypotension managed by fluid replacement If persistant give vasoconstrictor Norepinephrine 1-12 micrograms/mins And or Epinephrine 1-12 micrograms/mins
  38. 38. • Use a combination of broad spectrum antibiotic. Select appropriately according to the source of infection • Get advice from a microbiologist • Identify and drain any collection of pus/ septic foci. Seek surgical assistance in ressecting dead tissues • Treat the complications accordingly Acute renal failure Acute liver failure DIC Acute respiratory distress syndrome • Once culture and ABST reports available treat accordingly
  39. 39. ANAPHYLACTIC SHOCK • Results from widespread systemic allergic reaction to an antigen • LIFE THREATENING (Sometimes dead within minutes)
  40. 40. Expoure to an antigen Body stimulated produe IgE antibodies specific to the antigen Rexposure to the antigen IgE binds to mast cells and basophils Which release histamine or a histamine like substance Which causes 1. Increase in vascular capacity because of venous dilation causing decrease venous return 2. Dilation of the arterioles, resulting in greatly reduced arterial pressure 3. Greatly increased capillary permeability, with rapid loss of fluid and protein into tissue space
  41. 41. • Also activated basophils and mast cells release mixture of leukotrienes called slow reacting substance of anaphylaxis. These causes spasms of the smooth muscles of bronchioles • Antigens enter specific skin areas and cause localized anaphylactoid reactions (urticaria). Histamine release locally cause ―Vasodilation hence red flares ―Increase local permeability so swelling of skin
  42. 42. Present with chocking, coughing, stridor, wheezing, breathless, LOC, itchy rash. Hx of previous allergic reaction or anaphylactic shocks? 1. Signs of profound vasodilation a) Warm peripheries b) Low BP c) Tachycardia 2. Pale cyanosed 3. Erythema, urticaria,pluritus odeama of the face, pharynx and larynx. 4. Bronchospasms, rhinitis 5. Nausea, vomiting, abdominal pain, diarrhea
  43. 43. Management • Put the patient on the bed • Establish airway patency and breathing • If necessary endotracheal intubation, if it fails emergency cricothyroidotomy • Consult an anesthetist for advice regarding ventilation • Give high flow oxygen • • Connect to a pulse oximeter and measure the BP Oxygen saturation RR and PR. • If Hypotensive- head low position
  44. 44. • Immediately give 0.5mg im adrenaline 1 : 1000 to vastus lateralis Repeat every 5 mins if shock persists • Meanwhile put 2 large bore (14/16) cannulas • Give iv chlorphenamine (antihistamine) 10-20mg or 25mg of promethazine • Give 100mg iv hydrocortisone • If hypotension persists- 1-2L of normal saline • Broncospams- nebulize with salbutamol 5mg • Give oral steroids and antihistamine for 24-48 hrs or longer if urticaria persists
  45. 45. Neurogenic shock • Results from loss or suppression of sympathetic tone which causes massive vasodilatation in the venous vasculature therefore venous return decreases and cardiac output decreases. • Causes  Spinal cord injury above the level of T6  Deep general anesthesia (depress vasomotor centre)  Spinal anasthesia (block the sympathetic nervous outflow)  Brain damage (contusions, concussions, ischemia)
  46. 46. Disruption of sympathetic nervous system Loss of sympathetic tone Venous and arterial vasodilatation Decreased venous return Decreased stroke volume Decreased cardiac output Decreased cellular oxygen supply Impaired tissue perfusion Impaired cellular metabolism
  47. 47. Present with paralysis below the level of lesion On patient assessment • Hypotension • Bradycardia, • Hypothermia • Warm, dry skin Goal of therapy is to treat or remove the cause and prevent cardiovascular instability and promote optimal tissue perfusion
  48. 48. • Put the patient on the bed • Give high flow oxygen • Examine the patient and find the level of lesion • Connect to a pulse oximeter and measure RR, PR, BP • Put two wide bore cannulas. • If hypovolemic- fluid replacement • Observe closely for fluid overload- pulmonary odeama • Hypothermia- warming the patient • CT/MRI of the spinal cord
  49. 49. • Alpha agonist to augment tone if perfusion still inadequate dopamine (> 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 mg • patient with obvious neurological deficit can be given I.V. steroids, such as methylprednisolone in high dose, within 8 hours of commencement of neurogenic shock. • Surgery is needed in case of accident/trauma/ injury/ to the patient.
  50. 50. Case scenario 1. A 58 yr patient presented with central chest pain of tightening nature radiating to the neck and left arm. It was associated with sweating, nausea, vomiting. ECG showed a extensive anterior STEMI. During the streptokinase infusion patients BP dropped to 90/60mmhg. What are the possible causes for hypotension? How would you treat? And why?
  51. 51. It could be hypotension due to streptokinase allergy so anaphylaxis shock or due to anterior MI causing cargdiogenic shock or reperfusion arrythmia causing cardiogenic shock Treatment depends on type of shock If its anaphylaxis due to streptokinase (confirm by looking for other features like urticaria, swelling, warm peripheries) streptokinase infusion should be stopped. Ideally should give IM adrenaline 0.5ml 1:1000 units to vastus lateralis. However since this patient is just after a MI, adrenaline may cause increase contractility of the heart, increase excitation of the heart making it more prone for arrythmias, increase the oxygen demand and vasoconstriction may aggravate the tissue ischemia. Therefore to correct this patient hypotension in anaphylaxis shock would be to give a fluid bolus.
  52. 52. If the patient is having a cardiogenic shock due to the MI. The MI involves the left ventricle hence reducing the ability to contract. So we can administer dobutamine which has a positive inotropic effect and which decreases the afterload therefore improving the cardiac output. However if the case was an inferior STEMI it will involve the right ventricle. So rather than giving dobutamine, giving fluid boluses will increase the venous return to right heart therefore venous return to left heart will increase so LV which is functioning normally can pump the blood to systemic circulation.

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