Topic Review: Sepsis Spectrum and effect on Organs

Systemic
Inflammatory
Response
Syndrome
(SIRS)
Sepsis
Severe Sepsis
Septic Shock

2 of the following
Temperature > 38C or <36C
Heart Rate > 90 beats per minute
Respiration Rate > 20 breaths per minute (Tachypnea) or PaCO2 < 32 mmHg
White Blood Cells > 12,000 cells/mm3, or <4,000 cells/mm3, or > 10% band cells
SIRS + suspected infections
Sepsis + organ dysfunction, hypoperfusion, or hypotension
Signs of hypoperfusion may include lactic acidosis, oligouria, change in mental status
Sepsis-induced hypotension despite adequate fluid resuscitation, along with signs of
hypoperfusion
Patients typically have abnormal vital signs (tachycardia and tachypnea) and a narrow pulse
pressure in addition to low blood pressure.

Shock Basic Definition: Generalized hypoperfusion of the body (i.e., not enough blood is being circulated to
supply the organs with the oxygen they require)

Presentation of Shock: Presents with tachycardia, hypotension, and malfunction of under perfused organs.
o Autonomic Response:
Autonomic response vagal response, heart rate (HR), cardiac output (CO), glycogenolysis
and gluconeogenesis
Baroreceptors detect blood pressure (BP) activates Sympathetic nervous system (Cathecolamines
may be secreted (Epi and NE)
- Cardiac Effects Force of contractions, Rate, and CO
- Peripheral Effects
Arteriolar constriction (via Adrenergic stim) Pre-/Post- Capillary sphincter contraction
SVR Maintained CO and BP
Intracapillary hydrostatic pressure transcapillary refill from interstitial fluid
intravascular fluid volume venous return Maintained CO and BP
Peripheral resistance
Shunting of blood to core organs
o

Neurologic/Brain: CNS dysfunction (altered mental status/loss of consciousness)

Continuum of mental status changes frequently encountered in shock begins with agitation,
progresses to confusion or delirium, and ends in coma.

Renal: Anuria/oligouria BUN/Cr ratio

Physiologic response of the kidney to hypoperfusion is to conserve salt and water.
- Renal blood flow (RBF) and afferent arteriolar resistance accounts for glomerular filtration
rate (GFR)
- Blood flow to kidney Kidneys secrete renin Initiating Renin-Angiotensin-Aldosterone
System (RAAS) Angiotensin stimulates aldosterone leads to reabsorption of sodium and
water urine formation.
- BP initiates ADH (vasopressin) release from posterior pituitary gland H2O reabsorption
by kidneys conserves blood volume urine output
- Aldosterone and Vasopressin enhance H2O reabsorption and cause vasoconstriction

Toxic injury causes necrosis of tubular epithelium and tubular obstruction by cellular debris with
back leak of filtrate
Depletion of renal ATP stores that occurs with prolonged renal hypoperfusion contributes to
subsequent impairment of renal function

Page 1 of 8

Blood: Lactic acid production Lactic Acidosis

Sympathetic Nervous System (Hormonal): Anterior pituitary releases adrenocorticotropic hormones
stimulates adrenal cortex to release glucocorticoids blood sugar increase to meet Basal
Metabolic Rate (BMR)
- BMR amount of energy used in the functioning of vital organs.
Anaerobic metabolism energy needed is not being supplied by enough oxygen created through
the breaking down of carbohydrates.
- Breakdown of glucose to pyruvate to ultimately lactate (minimal net energy production)
- Plasma lactate indicates anaerobic metabolism and inadequate tissue perfusion
- Metabolic acidosis develops as shock progresses, reflecting decreased clearance of lactate by the

Liver: Increased AST and ALT

Ischemic hepatitis due to hypoxia and/or low BP inadequate O2 to liver causes centrolobular
hepatocellular necrosis (most sensitive to hypoxic damage) results in increased aspartate
aminotransferase (AST) and alanine aminotransferase (ALT) concentrations (usually > 1000 IU/I)

Pulmonary/Respiratory: Shortness of breath

Tachypnea Hypoxia Respiratory alkalosis atelectasis acute lung injury acute
respiratory distress syndrome (ARDS)
- Shock-induced tachypnea tidal volume, dead space and minute ventilation
- Tachypnea + Hypoxia induce a respiratory alkalosis
- Recumbency and involuntary restriction of ventilation secondary to pain reduce functional
residual capacity may lead to atelectasis
- Shock and, in particular, resuscitation-induced oxidant radical generation, is recognized as a
major cause of acute lung injury and subsequent acute respiratory distress syndrome

Cardiovascular/Heart: Tachycardia, Chest pain

Systemic tissue perfusion is determined by the cardiac output (CO) and systemic vascular
resistance (SVR) Systemic tissue perfusion is a consequence of diminished CO, SVR, or both

SVR is the vascular tone and is a large determinant of diastolic BP.

SVR is governed by the vessel length, blood viscosity, and vessel diameter
CO is the major determinant of tissue perfusion

SV is determined by three parameters (1) ventricular filling (preload), (2) the resistance to
ventricular ejection (afterload), and (3) myocardial contractility

Preload = volume of blood in ventricles at end of diastole (EDV) (ed in Hypervolemia,

Regurgitation of cardiac valves, Heart Failure) Preload (Volume) SV (EDV)
EDV = filled ventricular volume prior to systolic contraction determined by preload
volume SV (via FrankStarling curves) where diastolic filling volumes CO
Filling pressures stimulate release of brain natriuretic peptide (BNP) to secrete

sodium and volume to relieve pressure on the heart.

Levels of BNP correlate with outcome following severe stress.

Page 2 of 8

 Afterload = Resistance LV must overcome to circulate blood ( Afterload = Cardiac

Workload) (ed in HTN and vasoconstriction) Afterload (Contractility) SV
(ESV)
ESV = residual blood left in ventricle after emptying during systole determined by
cardiac contractility and it as heart ejects a greater percentage of its diastolic
volume.

Page 3 of 8