NSG 430 Exam 4 Questions and answers
Low blood flow cardiogenic shock - ✅✅-comprimised cardiac output. systolic and diastolic
dysfunction
CAUSES
-MI, cardiomyopathy, blunt cardiac injury, severe systemic or pulmonary HTN, cardiac tamponade,
myocardial depression from metabolic problems
EARLY MANIFESTATIONS
-tachycardia
-hypotension
-narrowed pulse pressure
-increased myocardial o2 consumption
-tachypnea, pulmonary congestion, decreased cap refill time
-anxiety, confusion, agitation, increased pulmonary artery wedge pressure, decreased UO
INTERPROFESSIONAL CARE
-goal: decrease heart workload
-angioplasty w stenting, vavle replacement
-hemodynamic monitoring
-drugs: nitrates, diuretics, vasodilators, b adrenergic blockers
Low blood flow hypovolemic shock - ✅✅-absolute hypovolemia: loss of intravascular fluid volume
-when fluid moves out of the vascular space into the extravascular space
-*burns?
TYPES?
-hemorrhage, vomiting, diarrhea
-fistula drainage, diabetes insipidus
-hyperglycemia, diuresis
MANIFESTATIONS
-anxiety, tachypnea, increased CO, heart rate
-decrease in stroke volume, PAWP, urinary output
,-*if loss >30%, blood volume needs replacing
INTERPROFESSIONAL CARE
-*3:1 rule- 3ml of isotonic crystalloid for every 1ml of EBL
Distributive shock: neurogenic shock - ✅✅-can occur within 30 minutes of a spinal cord injury at the
fifth thoracic vertebra or above. can last up to 6 weeks.
-can be induced by spinal anesthesia
-DEFINED: massive vasodilation, leading to pooling of blood in vessels, tissue hypoperfusion, impaired
cellular metabolism
MANIFESTATIONS
-hypotension, bradycardia
-inability to regulate body temperature (heat loss)-> poikilothermia (taking on temp of environment)
-dry skin
INTERPROFESSIONAL CARE
-*stability for spinal cord injury
-*atropine for hypotension and bradycardia
-monitor for hypothermia
Distributive shock: anaphylactic shock - ✅✅-acute life threatening allergic reaction
-massive vasodilation, release of vasoactive mediators, increased capillary permeability
MANIFESTATIONS
-anxiety, confusion, dizzy
-sense of impending doom, chest pain
-incontinence
-swelling of lips and tongue, flushing, allergic rxn sx
-*resp distress and circulatory failure
INTERPROFESSIONAL CARE
-epi, diphenhydramine, famotidine
-*maintain patent airway (bronchodilators, aerosolized epi, ET tube may be necessary
,-*fluid replacement
Distributive shock: septic shock - ✅✅-sepsis: systemic inflammatory response to suspected or
documented infection
SEPTIC SHOCK
-sepsis w hypotension despite fluid resuscitation
-inadequate tissue perfusion resulting in hypoxia
MANIFESTATIONS
-increased coagulation and inflammation, decreased fibrinolysis: formation of microthrombi,
obstruction of microvasculature
-hyperdynamic state- increased CO and decreased SVR
-tachypnea, hyperventilation -> *respiratory alkalosis and resp failure
-urine output decreased
-altered neuro status
-GI dysfunction, GI bleed, paralytic ileus
PATHOPHYSIOLOGICAL EFFECTS
-vasodilation
-maldistribution of blood flow
-myocardial dysfunction (decreased EF and ventricular dilation)
INTERPROSFESSIONAL CARE
-antibiotics within 1st hour!!!
-keep glucose <180
-give PPIs for stress ulcer prophylaxis (pantoprazole)
-DVT: heparin, enoxaparin
-exogenous vasopressin
-*IV corticosteroids: for pts who cannot maintain an adequate BP with vasopressor therapy despite fluid
resuscitation
Obstructive shock - ✅✅CAUSES
, -SVC syndrome, abdominal compartment syndrome, cardiac tamponade, tension pneumo, pulmonary
embolism
MANIFESTATIONS
-decreased CO, increased afterload
-*need rapid assessments and immediate tx
CARE
-*early recognition and tx
-mechanical decompression
-thrombolytic therapy
-radiation, debulking, removal of mass
-decompressive laparotomy
Stages of shock - ✅✅1) INITIAL
-not usually clinically apparent
-lactic acid build up and must be removed by liver
2) COMPENSATORY
1. decreased blood to kidneys activates RAAS
-vasocontriction, increase venous return to the heart, release of aldosterone, increased sodium
reabsorption stimulates ADH
-impaired GI motility: *risk for paralytic ileus
-cool, clammy skin
-except septic patient who is warm and flushed
3) PROGRESSIVE
-when compensatory fails
-*pt moved to ICU
-mental status changes
-sustained hypo-perfusion
1. cardiac
-dysrhythmias
Low blood flow cardiogenic shock - ✅✅-comprimised cardiac output. systolic and diastolic
dysfunction
CAUSES
-MI, cardiomyopathy, blunt cardiac injury, severe systemic or pulmonary HTN, cardiac tamponade,
myocardial depression from metabolic problems
EARLY MANIFESTATIONS
-tachycardia
-hypotension
-narrowed pulse pressure
-increased myocardial o2 consumption
-tachypnea, pulmonary congestion, decreased cap refill time
-anxiety, confusion, agitation, increased pulmonary artery wedge pressure, decreased UO
INTERPROFESSIONAL CARE
-goal: decrease heart workload
-angioplasty w stenting, vavle replacement
-hemodynamic monitoring
-drugs: nitrates, diuretics, vasodilators, b adrenergic blockers
Low blood flow hypovolemic shock - ✅✅-absolute hypovolemia: loss of intravascular fluid volume
-when fluid moves out of the vascular space into the extravascular space
-*burns?
TYPES?
-hemorrhage, vomiting, diarrhea
-fistula drainage, diabetes insipidus
-hyperglycemia, diuresis
MANIFESTATIONS
-anxiety, tachypnea, increased CO, heart rate
-decrease in stroke volume, PAWP, urinary output
,-*if loss >30%, blood volume needs replacing
INTERPROFESSIONAL CARE
-*3:1 rule- 3ml of isotonic crystalloid for every 1ml of EBL
Distributive shock: neurogenic shock - ✅✅-can occur within 30 minutes of a spinal cord injury at the
fifth thoracic vertebra or above. can last up to 6 weeks.
-can be induced by spinal anesthesia
-DEFINED: massive vasodilation, leading to pooling of blood in vessels, tissue hypoperfusion, impaired
cellular metabolism
MANIFESTATIONS
-hypotension, bradycardia
-inability to regulate body temperature (heat loss)-> poikilothermia (taking on temp of environment)
-dry skin
INTERPROFESSIONAL CARE
-*stability for spinal cord injury
-*atropine for hypotension and bradycardia
-monitor for hypothermia
Distributive shock: anaphylactic shock - ✅✅-acute life threatening allergic reaction
-massive vasodilation, release of vasoactive mediators, increased capillary permeability
MANIFESTATIONS
-anxiety, confusion, dizzy
-sense of impending doom, chest pain
-incontinence
-swelling of lips and tongue, flushing, allergic rxn sx
-*resp distress and circulatory failure
INTERPROFESSIONAL CARE
-epi, diphenhydramine, famotidine
-*maintain patent airway (bronchodilators, aerosolized epi, ET tube may be necessary
,-*fluid replacement
Distributive shock: septic shock - ✅✅-sepsis: systemic inflammatory response to suspected or
documented infection
SEPTIC SHOCK
-sepsis w hypotension despite fluid resuscitation
-inadequate tissue perfusion resulting in hypoxia
MANIFESTATIONS
-increased coagulation and inflammation, decreased fibrinolysis: formation of microthrombi,
obstruction of microvasculature
-hyperdynamic state- increased CO and decreased SVR
-tachypnea, hyperventilation -> *respiratory alkalosis and resp failure
-urine output decreased
-altered neuro status
-GI dysfunction, GI bleed, paralytic ileus
PATHOPHYSIOLOGICAL EFFECTS
-vasodilation
-maldistribution of blood flow
-myocardial dysfunction (decreased EF and ventricular dilation)
INTERPROSFESSIONAL CARE
-antibiotics within 1st hour!!!
-keep glucose <180
-give PPIs for stress ulcer prophylaxis (pantoprazole)
-DVT: heparin, enoxaparin
-exogenous vasopressin
-*IV corticosteroids: for pts who cannot maintain an adequate BP with vasopressor therapy despite fluid
resuscitation
Obstructive shock - ✅✅CAUSES
, -SVC syndrome, abdominal compartment syndrome, cardiac tamponade, tension pneumo, pulmonary
embolism
MANIFESTATIONS
-decreased CO, increased afterload
-*need rapid assessments and immediate tx
CARE
-*early recognition and tx
-mechanical decompression
-thrombolytic therapy
-radiation, debulking, removal of mass
-decompressive laparotomy
Stages of shock - ✅✅1) INITIAL
-not usually clinically apparent
-lactic acid build up and must be removed by liver
2) COMPENSATORY
1. decreased blood to kidneys activates RAAS
-vasocontriction, increase venous return to the heart, release of aldosterone, increased sodium
reabsorption stimulates ADH
-impaired GI motility: *risk for paralytic ileus
-cool, clammy skin
-except septic patient who is warm and flushed
3) PROGRESSIVE
-when compensatory fails
-*pt moved to ICU
-mental status changes
-sustained hypo-perfusion
1. cardiac
-dysrhythmias
