Ch. 66- Shock, SIRS, and MODS
Shock—Syndrome characterized by ↓ tissue perfusion and impaired cellular metabolism resulting in an imbalance b/w the
supply of and demand for O2 and nutrients (exchange is essential for life). When cells experience hypo perfusion, the
demand for O2 and nutrients exceeds the supply at the microcirculatory level.
Cardiogenic Shock
o Occurs when either systolic or diastolic dysfunction
of the heart’s pumping action results in reduced CO.
(Mortality rates ≈60%)
o ↓ Filling of the heart results in ↓ Stroke Volume
(SV)
o Causes & Examples
Systolic dysfunction: inability of the heart
to pump blood forward.
• Primarily affects the left
ventricle, since systolic pressure
is greater on the left side of the
heart.
• When the right side of the heart is
affected, blood flow through the
pulmonary circulation is reduced.
• Cardiogenic shock is the leading
cause of death from acute MI.
• Ex: MI (most common),
cardiomyopathy, blunt cardiac
injury, severe systemic or
pulmonary HTN, myocardial
depression from metabolic
problems
Diastolic dysfunction: inability of the
heart to fill (relax)
, • Ex: Cardiac tamponade, ventricular hypertrophy, cardiomyopathy
Dysrhythmias:
• Ex: Brady dysrhythmias (<60pbm) not enough blood is coming to the heart
• Ex: Tachy dysrhythmias (>100bpm) Heart is overworked and needs more nutrients and O2
Structural factors:
• Ex: Valvular stenosis or regurgitation, ventricular septal rupture, tension pneumothorax
o Clinical Manifestations (S/S)
The early s/s of a pt w/ cardiogenic shock is similar to that of a pt w/ acute decompensated HF.
Cardiac:
• Tachycardia, Hypotension
• Pulse pressure may be narrowed due to the heart’s inability to pump blood forward during systole
and ↑volume during diastole.
• ↑in systemic vascular resistance (SVR) ↑the workload of the heart, thus ↑the myocardial O2
consumption.
• Heart’s inability to pump blood forward also results in a low CO (< 4 L/minute) and cardiac index
(< 2.5 L/min/m2).
• Chest pain may or may not be present
Lungs: ↓oxygenation, tachypnea, crackles (bc of pulmonary congestion), Cyanosis, Rhonchi, ↑in the
pulmonary artery wedge pressure (PAWP), stroke volume variation (SVV), and pulmonary vascular
resistance.
Peripheral hypoperfusion: cyanosis, pallor, diaphoresis, weak peripheral pulses, cool and clammy skin,
delayed capillary refill (>3 sec)
Renal: ↓renal blood flow results in ↑ Na and H20 retention and ↓urine output.
Neuro: Anxiety, confusion, and agitation (cerebral perfusion is impaired)
GI: ↓ Bowel sounds (hypoactive <5 sounds) , n/v
o Diagnostic Findings*
↑ Cardiac markers
↑ b-Type natriuretic peptide (BNP)
↑ Blood glucose (hyperglycemia)break down more glucose to get more energy
↑ BUN
ECG (e.g., dysrhythmias)
Echocardiogram (e.g., left ventricular dysfunction)
Chest x-ray (e.g., pulmonary infiltrates)
o Interprofessional Care:
Overall goal is to restore blood flow to the myocardium by restoring the balance b/w O2 supply and
demand.
Oxygenation:
• Provide supplemental O2 (e.g., nasal cannula, non-rebreather mask)
• Intubation and mechanical ventilation, if necessary
• Monitor ScvO2 or SvO2
Circulation:
• Restore blood flow w/ thrombolytic, angioplasty stenting, emergent coronary revascularization,
valve replacement
• Reduce workload of the heat w/ circulatory assist devices: Intaaortic balloon pump (IABP),
ventricular assist device (VAD)
o The goals of this intervention are to ↓ the SVR and the left ventricular workload so the
heart can heal.
o VAD may be used as a temporary measure for the pt in cardiogenic shock who is
awaiting heart transplantation (option for a small, select group of pts)
Cardiac catheterization is performed ASAP after the initial insult.
Drug Therapies:
• Nitrates (e.g., nitroglycerin)
• Inotropes (e.g., dobutamine)
, • Diuretics (e.g., furosemide)
• β-Adrenergic blockers (contraindicated w/ ↓ ejection
fraction)
• Drug selection is based on the clinical goal and a
thorough understanding of each drug’s mechanism of
action.
o Drugs can be used to ↓ the workload of the
heart by dilating coronary arteries (e.g.,
(e.g., vasodilators), and reducing HR and
contractility (e.g., β-adrenergic blockers).
Supportive Therapies: Treat dysrhythmias
Hypovolemic Shock
o Occurs after a loss of intravascular fluid volume, when volume is
inadequate to fill the vascular space. Volume loss may be either an
absolute or a relative volume loss.
o Causes & Examples
Absolute hypovolemia Fluid is lost.
• External loss of whole blood.
o Ex: Hemorrhage from trauma, surgery, GI
bleeding
• Loss of other body fluids.
o Ex: Vomiting, diarrhea, excessive diuresis,
diabetes insipidus, DM, dehydration
Relative hypovolemia fluid volume moves out of the
vascular space into the extravascular space (e.g., intracavitary space), called third spacing. (space where
fluid does not normally collect in larger amounts) (Interstitial space)
• Pooling of blood or fluids.
o Ex: Bowel obstruction
• Fluid shifts.
o Ex: Burn injuries, ascites
• Internal bleeding.
o Ex: Fracture of long bones, ruptured spleen, hemothorax, severe pancreatitis
• Massive vasodilation.
o Ex: Sepsis
The size of the vascular compartment remains unchanged while the volume of blood or plasma ↓
Whether the loss of intravascular volume is absolute or relative, the physiologic consequences are similar.
A reduction in intravascular volume results in a ↓ venous return to the heart, ↓ preload, ↓ stroke volume,
and ↓CO.
• A cascade of events results in ↓ tissue perfusion and impaired cellular metabolism
(hallmarks of shock).
o Clinical Manifestations (S/S)
The pt’s response to acute volume loss depends extent of injury, age, and general state of health, etc.
An overall assessment of physiologic reserves may indicate the pt’s ability to compensate.
A pt may compensate for a loss of up to 15% of the total blood volume (approximately 750 mL).
Further loss of volume (15% to 30%) results in a SNS–mediated response, which results in ↑ in HR, CO,
and RR and depth.
• The stroke volume, central venous pressure (CVP), and PAWP are ↓bc of the ↓circulating blood
volume.
• Pt may appear anxious, and urine output begins to ↓.
• If hypovolemia is corrected by crystalloid fluid replacement at this time, tissue dysfunction is
generally reversible.
If volume loss is > 30%, compensatory mechanisms may begin to fail (e.g., tachypnea to bradypnea)
and immediate replacement w/ blood products should be started.
• Loss of autoregulation in the microcirculation and irreversible tissue destruction occur w/ loss of >
40% of the total blood volume.
Shock—Syndrome characterized by ↓ tissue perfusion and impaired cellular metabolism resulting in an imbalance b/w the
supply of and demand for O2 and nutrients (exchange is essential for life). When cells experience hypo perfusion, the
demand for O2 and nutrients exceeds the supply at the microcirculatory level.
Cardiogenic Shock
o Occurs when either systolic or diastolic dysfunction
of the heart’s pumping action results in reduced CO.
(Mortality rates ≈60%)
o ↓ Filling of the heart results in ↓ Stroke Volume
(SV)
o Causes & Examples
Systolic dysfunction: inability of the heart
to pump blood forward.
• Primarily affects the left
ventricle, since systolic pressure
is greater on the left side of the
heart.
• When the right side of the heart is
affected, blood flow through the
pulmonary circulation is reduced.
• Cardiogenic shock is the leading
cause of death from acute MI.
• Ex: MI (most common),
cardiomyopathy, blunt cardiac
injury, severe systemic or
pulmonary HTN, myocardial
depression from metabolic
problems
Diastolic dysfunction: inability of the
heart to fill (relax)
, • Ex: Cardiac tamponade, ventricular hypertrophy, cardiomyopathy
Dysrhythmias:
• Ex: Brady dysrhythmias (<60pbm) not enough blood is coming to the heart
• Ex: Tachy dysrhythmias (>100bpm) Heart is overworked and needs more nutrients and O2
Structural factors:
• Ex: Valvular stenosis or regurgitation, ventricular septal rupture, tension pneumothorax
o Clinical Manifestations (S/S)
The early s/s of a pt w/ cardiogenic shock is similar to that of a pt w/ acute decompensated HF.
Cardiac:
• Tachycardia, Hypotension
• Pulse pressure may be narrowed due to the heart’s inability to pump blood forward during systole
and ↑volume during diastole.
• ↑in systemic vascular resistance (SVR) ↑the workload of the heart, thus ↑the myocardial O2
consumption.
• Heart’s inability to pump blood forward also results in a low CO (< 4 L/minute) and cardiac index
(< 2.5 L/min/m2).
• Chest pain may or may not be present
Lungs: ↓oxygenation, tachypnea, crackles (bc of pulmonary congestion), Cyanosis, Rhonchi, ↑in the
pulmonary artery wedge pressure (PAWP), stroke volume variation (SVV), and pulmonary vascular
resistance.
Peripheral hypoperfusion: cyanosis, pallor, diaphoresis, weak peripheral pulses, cool and clammy skin,
delayed capillary refill (>3 sec)
Renal: ↓renal blood flow results in ↑ Na and H20 retention and ↓urine output.
Neuro: Anxiety, confusion, and agitation (cerebral perfusion is impaired)
GI: ↓ Bowel sounds (hypoactive <5 sounds) , n/v
o Diagnostic Findings*
↑ Cardiac markers
↑ b-Type natriuretic peptide (BNP)
↑ Blood glucose (hyperglycemia)break down more glucose to get more energy
↑ BUN
ECG (e.g., dysrhythmias)
Echocardiogram (e.g., left ventricular dysfunction)
Chest x-ray (e.g., pulmonary infiltrates)
o Interprofessional Care:
Overall goal is to restore blood flow to the myocardium by restoring the balance b/w O2 supply and
demand.
Oxygenation:
• Provide supplemental O2 (e.g., nasal cannula, non-rebreather mask)
• Intubation and mechanical ventilation, if necessary
• Monitor ScvO2 or SvO2
Circulation:
• Restore blood flow w/ thrombolytic, angioplasty stenting, emergent coronary revascularization,
valve replacement
• Reduce workload of the heat w/ circulatory assist devices: Intaaortic balloon pump (IABP),
ventricular assist device (VAD)
o The goals of this intervention are to ↓ the SVR and the left ventricular workload so the
heart can heal.
o VAD may be used as a temporary measure for the pt in cardiogenic shock who is
awaiting heart transplantation (option for a small, select group of pts)
Cardiac catheterization is performed ASAP after the initial insult.
Drug Therapies:
• Nitrates (e.g., nitroglycerin)
• Inotropes (e.g., dobutamine)
, • Diuretics (e.g., furosemide)
• β-Adrenergic blockers (contraindicated w/ ↓ ejection
fraction)
• Drug selection is based on the clinical goal and a
thorough understanding of each drug’s mechanism of
action.
o Drugs can be used to ↓ the workload of the
heart by dilating coronary arteries (e.g.,
(e.g., vasodilators), and reducing HR and
contractility (e.g., β-adrenergic blockers).
Supportive Therapies: Treat dysrhythmias
Hypovolemic Shock
o Occurs after a loss of intravascular fluid volume, when volume is
inadequate to fill the vascular space. Volume loss may be either an
absolute or a relative volume loss.
o Causes & Examples
Absolute hypovolemia Fluid is lost.
• External loss of whole blood.
o Ex: Hemorrhage from trauma, surgery, GI
bleeding
• Loss of other body fluids.
o Ex: Vomiting, diarrhea, excessive diuresis,
diabetes insipidus, DM, dehydration
Relative hypovolemia fluid volume moves out of the
vascular space into the extravascular space (e.g., intracavitary space), called third spacing. (space where
fluid does not normally collect in larger amounts) (Interstitial space)
• Pooling of blood or fluids.
o Ex: Bowel obstruction
• Fluid shifts.
o Ex: Burn injuries, ascites
• Internal bleeding.
o Ex: Fracture of long bones, ruptured spleen, hemothorax, severe pancreatitis
• Massive vasodilation.
o Ex: Sepsis
The size of the vascular compartment remains unchanged while the volume of blood or plasma ↓
Whether the loss of intravascular volume is absolute or relative, the physiologic consequences are similar.
A reduction in intravascular volume results in a ↓ venous return to the heart, ↓ preload, ↓ stroke volume,
and ↓CO.
• A cascade of events results in ↓ tissue perfusion and impaired cellular metabolism
(hallmarks of shock).
o Clinical Manifestations (S/S)
The pt’s response to acute volume loss depends extent of injury, age, and general state of health, etc.
An overall assessment of physiologic reserves may indicate the pt’s ability to compensate.
A pt may compensate for a loss of up to 15% of the total blood volume (approximately 750 mL).
Further loss of volume (15% to 30%) results in a SNS–mediated response, which results in ↑ in HR, CO,
and RR and depth.
• The stroke volume, central venous pressure (CVP), and PAWP are ↓bc of the ↓circulating blood
volume.
• Pt may appear anxious, and urine output begins to ↓.
• If hypovolemia is corrected by crystalloid fluid replacement at this time, tissue dysfunction is
generally reversible.
If volume loss is > 30%, compensatory mechanisms may begin to fail (e.g., tachypnea to bradypnea)
and immediate replacement w/ blood products should be started.
• Loss of autoregulation in the microcirculation and irreversible tissue destruction occur w/ loss of >
40% of the total blood volume.
