Med Surg Final Study Guide
2022
Week 2; Perfusion (8)
• Shock (5)
• Shock– syndrome characterized by decreased tissue perfusion and impaired cellular metabolism
o Imbalance in supply/demand for O2 and nutrients
o 1st sign perfusion isn’t good – mentation changes/confusion
• Stages of shock
o Initial – Usually not clinically apparent
▪ Metabolism changes from aerobic to anaerobic
• Lactic acid accumulates and must be removed by blood and broken down by liver (increased LA –
no filter)
• Process requires unavailable O2
o Compensatory – body is compensating
▪ Clinically apparent
• Neural
• Hormonal
• Biochemical compensatory mechanisms
▪ Attempts are aimed at overcoming consequences of anaerobic metabolism and maintaining homeostasis
▪ Baroreceptors in carotid and aortic bodies activate SNS in response to ↓ BP
• Vasoconstriction while blood to vital organs maintained
• Hold onto blood – shunting
▪ ↓ Blood to kidneys activates renin–angiotensin system (RAAS)
• ↑ Venous return to heart
• ↑ Na (hyper), increased osmolality and stimulates release of ADH – increases H2O reabsorption
o Increases blood volume = total circulatory volume – increased BP and CO
• Renal failure – may not be able to increase
▪ Impaired GI motility
• Risk for paralytic ileus – absent or hypo bowel sounds
o Decreased perfusion to GI tract
▪ Cool, clammy skin from decreased blood flow
• Except septic patient who is warm and flushed – vasodilation and increased temp
▪ Shunting blood from lungs increases physiologic dead space
• ↓ Arterial O2 levels
• Increase in rate/depth of respirations
• V/Q mismatch
▪ SNS stimulation increases myocardial O2 demands
• Clamp down – increase O2 demand
o Progressive – Begins when compensatory mechanisms fail
▪ Aggressive interventions to prevent multiple organ dysfunction syndrome
• Hard to bring back from
• Increased lactate
• Changes in mental status
▪ Hallmarks of ↓ cellular perfusion and altered capillary permeability
• Leakage of protein into interstitial space – albumin – facilitates exchange
• ↑ Systemic interstitial edema
▪ Anasarca; diffuse profound edema
• Fluid leakage affects solid organs and peripheral tissues
• ↓ Blood flow to pulmonary capillaries
▪ Movement of fluid from pulmonary vasculature to interstitium
• Pulmonary edema
• Bronchoconstriction – buildup of fluid
• ↓ Residual capacity – can’t take in as much O2
▪ Fluid moves into alveoli
Med Surg Final Study Guide 1
, • Edema – pulmonary
• Decreased surfactant
• Worsening V/Q mismatch
• Tachypnea
• Crackles
• Increased work of breathing
▪ CO begins to fall – all fluid is in interstitial – pump not working
• Decreased peripheral perfusion
• Hypotension
• Weak peripheral pulses
o Too absent
• Ischemia of distal extremities
o Lack of O2
▪ Myocardial dysfunction results in
• Dysrhythmias – K buildup
• Ischemia
• Myocardial infarction
• End result; complete deterioration of cardiovascular system
o Get tropes done
▪ Mucosal barrier of GI system becomes ischemic (causes erode)
• Ulcers
• Bleeding
• Risk of translocation of bacteria
• Decreased ability to absorb nutrients
▪ Hypoperfusion leads to renal tubular ischemia
• May result in acute kidney injury
▪ Liver fails to metabolize drugs and waste
• Jaundice – increased BR
• Elevated enzymes – ALT/AST
• Loss of immune function – not happening
• Risk for DIC and significant bleeding
o Irreversible (cycle)
▪ Exacerbation of anaerobic metabolism
▪ Accumulation of lactic acid
▪ ↑ Capillary permeability – fluid and plasma protein leaving vascular space – getting worse
• blood pools in cap beds secondary to constricted venules and dilated arterioles
▪ Profound hypotension and hypoxemia
▪ Tachycardia worsens – trying to save itself
▪ Decreased coronary blood flow worsens myocardial depression and decreases CO further
▪ Failure of one organ system affects others – kidneys usually first, liver, lungs
• Accumulation of waste products – urea, lactate, ammonia, and CO2
▪ Recovery unlikely
▪ Confused – no O2
• Classification of shock
o Cardiogenic – low blood flow; heart can’t contract
• Systolic or diastolic dysfunction of myocardium
o Systolic – inability of heart to pump blood forward
o Diastolic – inability of heart to fill
• Compromised cardiac output (CO)
▪ Precipitating causes
• Myocardial infarction - # 1 cause of cardiogenic shock
• Cardiomyopathy
• Blunt cardiac injury
• Severe systemic or pulmonary hypertension
• Cardiac tamponade
• Myocardial depression from metabolic problems
Med Surg Final Study Guide 2
,▪ Early manifestations
• Tachycardia - compensation
• Hypotension
• Narrowed pulse pressure – hearts inability to pump blood forward during systole and increases
volume during diastole (S/D closer)
• ↑ Myocardial O2 consumption – burning more
o Increased SVR – increases workload of the heart
▪ Physical assessment
• Tachypnea
• Pulmonary congestion
• Pallor and cool, clammy skin
• Decreased capillary refill time
• Anxiety, confusion, agitation – cerebral perfusion impaired
• ↑ In pulmonary artery wedge pressure (PAWP)
o pressures generated by LV, used to assess LV fxn
o Normal – 8-12
• Decreased renal perfusion and UO
o Na and H20 retention
• Peripheral hypoperfusion
o Cyanosis
o Pallor
o Diaphoresis
o Weak peripheral pulses
o Cool, clammy skin
o Delayed cap refill
▪ Dx/labs
• LA; 0.5 – 1
• ABG’s
• Cardiac markers
o Trops; T < 0.5; I <0.1
o BNP < 100
o CK-MB < 4% - 6%
• Lytes
• Serum blood glucose
• CBC
• VS
• CXR
• EKG
• Echo
• UO
▪ Collaborative Care
• 1st – place on O2 NC and call Dr.; get labs and EKG
• Restore blood flow to the myocardium by restoring the balance between O2 supply and demand – until
done heart must be supported to optimize SV and CO
o Cardiac cath ASAP
o Thrombolytic therapy
o Angioplasty with stenting
o Emergency revascularization
o Valve replacement
• Hemodynamic monitoring – decrease workload of the heart
• Drug therapy (e.g., diuretics to reduce preload) – selected based on clinical goal and
thorough understanding of each drugs MOA and decrease workload of the heart
o Nitrates – dilating coronary artery
o Diuretics – decrease preload
o Vasodilator – decrease afterload
o Beta blocker – decrease HR and contractility
• Circulatory assist devices (e.g., intraaortic balloon pump, ventricular assist device) – decrease
Med Surg Final Study Guide 3
, SVR and LV workload so that heart can heal
o Hypovolemic – low blood flow
▪ Hallmark; decreased tissue perfusion and impaired cellular metabolism
▪ Absolute hypovolemia; loss of intravascular fluid volume
• Hemorrhage
• GI loss (e.g., vomiting, diarrhea)
• Fistula drainage
• Diabetes insipidus – increased UO
• Hyperglycemia – sucks up fluid
• Diuresis – trying to
▪ Relative hypovolemia
• Results when fluid volume moves out of the vascular space into extravascular space (e.g., intracavitary
space)
• Termed third spacing – leakage of fluid from the vascular space to the interstitial space from increased
cap perm (burns)
▪ Response to acute volume loss depends on;
• Extent of injury
• Age
• General state of health
• Compensate for 15% (75mL0
o 15-30% - SNS mediated response (increased HR, CO, RR and depth; decreased SV,
CVP, PAWP)
▪ Clinical manifestations
• Anxiety
• Tachypnea
• Increase in CO, heart rate
• Decrease in stroke volume, PAWP, urinary output
• If loss is >30%, blood volume is replaced – CBC
o Compensatory mech begin to fail and immediate replacement
o Corrected by crystalloid fluid replacement at this time – tissue dysfxn generally reversible
o 40% loss of total blood volume – loss of autoregulation in microcirculation and
irreversible tissue destruction
▪ Dx/labs
• LA- 0.5-1
• CBC; Hgb, HCT
• Type and cross match
• Lytes
• ABG’s
• Central venous O2
• US at bedside
▪ Collaborative care (call surgeon – going back to OR)
• Management focuses on stopping the loss of fluid and restoring the circulating volume
• Fluid replacement is calculated using a 3;1 rule (3 mL of isotonic crystalloid for every 1 mL
of estimated blood loss) – LR or 0.9 NS
o FFP; transfusion; albumin
• Vasopressors
•
o Distributive shocks
▪ Neurogenic
• Hemodynamic phenomenon
• Can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above
• Can last up to 6 weeks
• Can occur in response to spinal anesthesia
o Block transmission of impulses from the SNS
• Results in massive vasodilation, leading to pooling of blood in vessels
o Tissue hypoperfusion; impaired cellular metabolism
Med Surg Final Study Guide 4
2022
Week 2; Perfusion (8)
• Shock (5)
• Shock– syndrome characterized by decreased tissue perfusion and impaired cellular metabolism
o Imbalance in supply/demand for O2 and nutrients
o 1st sign perfusion isn’t good – mentation changes/confusion
• Stages of shock
o Initial – Usually not clinically apparent
▪ Metabolism changes from aerobic to anaerobic
• Lactic acid accumulates and must be removed by blood and broken down by liver (increased LA –
no filter)
• Process requires unavailable O2
o Compensatory – body is compensating
▪ Clinically apparent
• Neural
• Hormonal
• Biochemical compensatory mechanisms
▪ Attempts are aimed at overcoming consequences of anaerobic metabolism and maintaining homeostasis
▪ Baroreceptors in carotid and aortic bodies activate SNS in response to ↓ BP
• Vasoconstriction while blood to vital organs maintained
• Hold onto blood – shunting
▪ ↓ Blood to kidneys activates renin–angiotensin system (RAAS)
• ↑ Venous return to heart
• ↑ Na (hyper), increased osmolality and stimulates release of ADH – increases H2O reabsorption
o Increases blood volume = total circulatory volume – increased BP and CO
• Renal failure – may not be able to increase
▪ Impaired GI motility
• Risk for paralytic ileus – absent or hypo bowel sounds
o Decreased perfusion to GI tract
▪ Cool, clammy skin from decreased blood flow
• Except septic patient who is warm and flushed – vasodilation and increased temp
▪ Shunting blood from lungs increases physiologic dead space
• ↓ Arterial O2 levels
• Increase in rate/depth of respirations
• V/Q mismatch
▪ SNS stimulation increases myocardial O2 demands
• Clamp down – increase O2 demand
o Progressive – Begins when compensatory mechanisms fail
▪ Aggressive interventions to prevent multiple organ dysfunction syndrome
• Hard to bring back from
• Increased lactate
• Changes in mental status
▪ Hallmarks of ↓ cellular perfusion and altered capillary permeability
• Leakage of protein into interstitial space – albumin – facilitates exchange
• ↑ Systemic interstitial edema
▪ Anasarca; diffuse profound edema
• Fluid leakage affects solid organs and peripheral tissues
• ↓ Blood flow to pulmonary capillaries
▪ Movement of fluid from pulmonary vasculature to interstitium
• Pulmonary edema
• Bronchoconstriction – buildup of fluid
• ↓ Residual capacity – can’t take in as much O2
▪ Fluid moves into alveoli
Med Surg Final Study Guide 1
, • Edema – pulmonary
• Decreased surfactant
• Worsening V/Q mismatch
• Tachypnea
• Crackles
• Increased work of breathing
▪ CO begins to fall – all fluid is in interstitial – pump not working
• Decreased peripheral perfusion
• Hypotension
• Weak peripheral pulses
o Too absent
• Ischemia of distal extremities
o Lack of O2
▪ Myocardial dysfunction results in
• Dysrhythmias – K buildup
• Ischemia
• Myocardial infarction
• End result; complete deterioration of cardiovascular system
o Get tropes done
▪ Mucosal barrier of GI system becomes ischemic (causes erode)
• Ulcers
• Bleeding
• Risk of translocation of bacteria
• Decreased ability to absorb nutrients
▪ Hypoperfusion leads to renal tubular ischemia
• May result in acute kidney injury
▪ Liver fails to metabolize drugs and waste
• Jaundice – increased BR
• Elevated enzymes – ALT/AST
• Loss of immune function – not happening
• Risk for DIC and significant bleeding
o Irreversible (cycle)
▪ Exacerbation of anaerobic metabolism
▪ Accumulation of lactic acid
▪ ↑ Capillary permeability – fluid and plasma protein leaving vascular space – getting worse
• blood pools in cap beds secondary to constricted venules and dilated arterioles
▪ Profound hypotension and hypoxemia
▪ Tachycardia worsens – trying to save itself
▪ Decreased coronary blood flow worsens myocardial depression and decreases CO further
▪ Failure of one organ system affects others – kidneys usually first, liver, lungs
• Accumulation of waste products – urea, lactate, ammonia, and CO2
▪ Recovery unlikely
▪ Confused – no O2
• Classification of shock
o Cardiogenic – low blood flow; heart can’t contract
• Systolic or diastolic dysfunction of myocardium
o Systolic – inability of heart to pump blood forward
o Diastolic – inability of heart to fill
• Compromised cardiac output (CO)
▪ Precipitating causes
• Myocardial infarction - # 1 cause of cardiogenic shock
• Cardiomyopathy
• Blunt cardiac injury
• Severe systemic or pulmonary hypertension
• Cardiac tamponade
• Myocardial depression from metabolic problems
Med Surg Final Study Guide 2
,▪ Early manifestations
• Tachycardia - compensation
• Hypotension
• Narrowed pulse pressure – hearts inability to pump blood forward during systole and increases
volume during diastole (S/D closer)
• ↑ Myocardial O2 consumption – burning more
o Increased SVR – increases workload of the heart
▪ Physical assessment
• Tachypnea
• Pulmonary congestion
• Pallor and cool, clammy skin
• Decreased capillary refill time
• Anxiety, confusion, agitation – cerebral perfusion impaired
• ↑ In pulmonary artery wedge pressure (PAWP)
o pressures generated by LV, used to assess LV fxn
o Normal – 8-12
• Decreased renal perfusion and UO
o Na and H20 retention
• Peripheral hypoperfusion
o Cyanosis
o Pallor
o Diaphoresis
o Weak peripheral pulses
o Cool, clammy skin
o Delayed cap refill
▪ Dx/labs
• LA; 0.5 – 1
• ABG’s
• Cardiac markers
o Trops; T < 0.5; I <0.1
o BNP < 100
o CK-MB < 4% - 6%
• Lytes
• Serum blood glucose
• CBC
• VS
• CXR
• EKG
• Echo
• UO
▪ Collaborative Care
• 1st – place on O2 NC and call Dr.; get labs and EKG
• Restore blood flow to the myocardium by restoring the balance between O2 supply and demand – until
done heart must be supported to optimize SV and CO
o Cardiac cath ASAP
o Thrombolytic therapy
o Angioplasty with stenting
o Emergency revascularization
o Valve replacement
• Hemodynamic monitoring – decrease workload of the heart
• Drug therapy (e.g., diuretics to reduce preload) – selected based on clinical goal and
thorough understanding of each drugs MOA and decrease workload of the heart
o Nitrates – dilating coronary artery
o Diuretics – decrease preload
o Vasodilator – decrease afterload
o Beta blocker – decrease HR and contractility
• Circulatory assist devices (e.g., intraaortic balloon pump, ventricular assist device) – decrease
Med Surg Final Study Guide 3
, SVR and LV workload so that heart can heal
o Hypovolemic – low blood flow
▪ Hallmark; decreased tissue perfusion and impaired cellular metabolism
▪ Absolute hypovolemia; loss of intravascular fluid volume
• Hemorrhage
• GI loss (e.g., vomiting, diarrhea)
• Fistula drainage
• Diabetes insipidus – increased UO
• Hyperglycemia – sucks up fluid
• Diuresis – trying to
▪ Relative hypovolemia
• Results when fluid volume moves out of the vascular space into extravascular space (e.g., intracavitary
space)
• Termed third spacing – leakage of fluid from the vascular space to the interstitial space from increased
cap perm (burns)
▪ Response to acute volume loss depends on;
• Extent of injury
• Age
• General state of health
• Compensate for 15% (75mL0
o 15-30% - SNS mediated response (increased HR, CO, RR and depth; decreased SV,
CVP, PAWP)
▪ Clinical manifestations
• Anxiety
• Tachypnea
• Increase in CO, heart rate
• Decrease in stroke volume, PAWP, urinary output
• If loss is >30%, blood volume is replaced – CBC
o Compensatory mech begin to fail and immediate replacement
o Corrected by crystalloid fluid replacement at this time – tissue dysfxn generally reversible
o 40% loss of total blood volume – loss of autoregulation in microcirculation and
irreversible tissue destruction
▪ Dx/labs
• LA- 0.5-1
• CBC; Hgb, HCT
• Type and cross match
• Lytes
• ABG’s
• Central venous O2
• US at bedside
▪ Collaborative care (call surgeon – going back to OR)
• Management focuses on stopping the loss of fluid and restoring the circulating volume
• Fluid replacement is calculated using a 3;1 rule (3 mL of isotonic crystalloid for every 1 mL
of estimated blood loss) – LR or 0.9 NS
o FFP; transfusion; albumin
• Vasopressors
•
o Distributive shocks
▪ Neurogenic
• Hemodynamic phenomenon
• Can occur within 30 minutes of a spinal cord injury at the fifth thoracic (T5) vertebra or above
• Can last up to 6 weeks
• Can occur in response to spinal anesthesia
o Block transmission of impulses from the SNS
• Results in massive vasodilation, leading to pooling of blood in vessels
o Tissue hypoperfusion; impaired cellular metabolism
Med Surg Final Study Guide 4
