Shock Simulation cases Flashcards
Normal CO value
4-8 L/min
Normal Systemic Vascular Resistance (SVR) value
700-1600 Dynes x sec/cm^5
Mild Hypovolemic Shock presentation (
- Cool extremities
- increased capillary refill time
- diaphoresis
- collapsed veins
- anxiety
Moderate Hypovolemic Shock presentation (20-40% blood loss)
same as mild Hypovolemic Shock presentation plus:
- Tachycardia
- tachypnea
- oliguria
- postural changes
Severe Hypovolemic Shock presentation ( > 40% blood loss)
Same as Moderate Hypovolemic Shock presentation plus:
- hemodynamic instability
- marked tachycardia
- hypotension
- mental status deterioration/coma
Receptors which detect effects of hypotension/hypovolemia?
- High-pressure baroreceptors
- Low-pressure baroreceptors
- Renal Juxtaglomerular apparatus
- Central and peripheral chemoreceptors
Autonomic response to hypotension effect on sympathetics/parasympathetics?
↑ sympathetic
↓ parasympathetic
Autonomic response to hypotension effect on effectors?
- ↑ HR (nodal cells)
- ↑ contractility (↑ [Ca2+]i in contractile myocytes)
- ↑ TPR (VSMC contraction; veno- and vasoconstriction) -> Attempt re-establish MAP
- ↑ Circulating epinephrine (Adrenal medulla)
- ↑ Renin (Granular cells in the renal JXG apparatus)
- ↑ Sweat gland activity (Sympathetic cholinergic stimulation; clammy extremities)
What effect will hypotension/hypovolemia have on humoral regulation of vascular tone:
ADH/AVP?
↑ ADH/AVP
↑ vasoconstriction
What effect will hypotension/hypovolemia have on humoral regulation of vascular tone: ANG II?
- ↑ ANG II by activation of RAAS
- ↑ vasoconstriction
- Sympathetic stimulation of juxtaglomerular granular cells –>renin
- Renal vasoconstriction –> ↓ renal pressure –> ↑ renin
How can loss of blood volume be corrected?
- Renal fluid conservation
- Stimulation of thirst –> water intake
- Net capillary reabsorption (Starling’s forces)
“Transcapillary refill”
Which factors promote renal retention of Na+ and H2O?
- ↑ Sympathetic activity
- ↑ ANG II
- ↑ Aldosterone
- ↑ Anti-diuretic hormone/Arginine Vasopressin
How does sympathetic activity promote renal retention of Na+ and H2O?
↑ Sympathetic activity
- Renal vasoconstriction (↓ RBF) –>↓ filtration rate –> ↓ Na+ excretion
- ↑ Renin (Activation of RAAS)
- Direct stimulation of Na+ reabsorption by renal tubule cells
How does ANG II/aldosterone promote renal retention of Na+ and H2O?
↑ ANG II:
↑ Aldosterone
↑ ADH/AVP secretion
↑ Thirst stimulation
↑ Aldosterone:
↑ Na+ reabsorption
How does ADH/Vasopressin promote renal retention of Na+ and H2O?
↑ Anti-diuretic hormone/Arginine Vasopressin:
↑ by ANG II and osmoreceptors
↑ H2O reabsorption
Transcapillary Refill: correction for volume loss
- Net reabsorption of fluid: from interstitial fluid capillaries
- Reabsorption of interstitial fluid helps replace lost blood volume
- Result: initial hemodilution
Effect of normal Pc on capillaries?
- net filtration
Effect of initial hypotension after hemorrhage on capillaries?
- Net reabsorption
Effect on capillaries following compensation for volume loss (↑↑↑ arteriolar & ↑ venular resistance):
- Net reabsorption
Hypovolemic Shock:
- Tachycardia
- Hypotension
- Generalized arteriolar vasoconstriction & venoconstriction
- Oliguria
Negative-feedback (compensatory) mechanisms for Hypovolemic Shock:
- Baroreceptor reflexes
- Chemoreceptor reflexes
- Transcapillary reabsorption of interstitial fluid
- Renal conservation of salt and water
Positive-feedback (decompensatory) mechanisms for Hypovolemic Shock:
- Cardiac failure
- Acidosis
- CNS depression
After temporary improvement: hemorrhagic shock may become irreversible (even with transfusion) due to the following multiple failures:
- Vasoconstrictor response
- Capillary refill response
- Heart failure
- CNS response
Failure of the Vasoconstrictor Response:
Prolonged hemorrhagic hypotension:
TPR: initial increase tapers off and return to pre-hemorrhage levels
Failure of the Vasoconstrictor Response:
“Sympathetic escape”
- Desensitization α1-adrenoceptors
- Depletion of neurotransmitters
Failure of the Vasoconstrictor Response:
Metabolites and vasodilators released by ischemic tissues
- Counteract vasoconstrictor stimuli
- Late phases of irreversible shock: May be completely unresponsive to vasoconstrictor drugs
Failure of the Vasoconstrictor Response:
Decline in plasma AVP/ADH from early peak response
- Decline in trigger to release
- Depletion of AVP/ADH posterior pituitary stores
- Restoration of ADH to initial peak can significantly increase BP
Failure of Transcapillary Refill Process: Failure of vessels to sustain resistance
- Precapillary vessels tend to fail before post capillary vessels
- ↓ precapillary constricton»_space; ↓ postcapillary constriction
- ↑ relative ratio R post/R pre–> ↑ Pc –> promotes net filtration
Failure of the Heart:
- Prolonged, severe hypovolemic shock –> cardiogenic shock (inadequate coronary perfusion)
- Negative inotropy:
- Ischemic cardiac tissue
- Acidosis
- Other ischemic organs may release cardiotoxic factors
Failure of the CNS: decreased cerebral perfusion
- detected as ↑ PCO2 and ↑ [H+]:
- ↑ central chemoreceptor activation
- ↑ CV control center stimulation
Failure of the CNS: Prolonged inadequate cerebral perfusion
- leads to ischemia
- ↓ neural activity
- ↓ sympathetic output
- ↓ vascular and cardiac responses to hemorrhage
Physiologic Characteristics of Hypovolemic sock:
- Dec CVP and PCWP
- Dec CO
- Increased SVR
- Dec Venous O2 saturation
Physiologic Characteristics of Cardiogenic shock:
- increased CVP and PCWP
- Dec CO
- Increased SVR
- dec venous saturation
Physiologic Characteristics of Early (hyperdynamic) septic shock:
- no change in CVP and PCWP
- increased CO
- Dec SVR
- Increased Venous O2 saturation
Physiologic Characteristics of Late (hypodynamic) septic shock:
- no change in CVP and PCWP
- dec CO
- increased SVR
- no change in venous O2 saturation
Frank Starling Curve: Systolic Failure
- At a given EDV or Pressure: ↓ SV (↓ CO)
- ↑ EDV remaining after systole in impaired heart results in insignificant increase in SV despite ↑ LVEDP
What change to the curve is expected in a failing heart with cardiogenic shock?
↓ SV ↓ CO ↓ MAP ↓ Tissue perfusion ↓ Inotropy
Cause of Pulmonary Edema
- ↑ pulmonary v.v. pressure–> ↑ pulmonary capillary hydrostatic pressure
- Promotes filtration
Evidence of Pulmonary Edema in a patient
- Distended jugular veins
- Mild pitting edema
- Slight hepatomegaly
Initial DX steps of cardiogenic shock
- Hx and PE
- ECG
- Echo
- Labs
- CXR
- pulmonary artery cath
Initial management of cardiogenic shock
- supplemental O2/mechanical ventilation
- Venous access
- Pain relief
- Hemodynamic support (fluid if no pulmonary edema, vasopressors for hypotension unresponsive to fluids)
sepsis host response is initiated via:
- Pathogen Associated Molecular Patterns (PAMPs)
- Pattern Recognition Receptors
Activation of pattern recognition receptors such as ______ results in _____.
MyD88 / NF-kB Signaling…..Pro-inflammatory Cytokines and Vascular Adhesion Molecules
Acute, Local Inflammation
- Leukocyte extravasation
- Alterations to endothelial cell junctions
- Warmth, erythema, edema
Leukocyte extravasation basic steps
- rolling
- integrin activation by chemokines
- stable adhesion
- migration through endothelium
Pro-Inflammatory Cytokines Involved in sepsis
- Tumor Necrosis Factor (TNF-a)
- IL 1
- IL 6
Role of TNF alpha, IL 1, and IL 6 in inflammation
- Stimulates the recruitment and activation of neutrophils and monocytes –> Leads to the production of IL-1
- Activates vascular endothelial cells to express cellular adhesion molecules
- Can induce extrinsic apoptosis
How does local, acute inflammation transitions to systemic effects?
When the concentration of Pro-Inflammatory Cytokines exceeds local boundaries
Systemic cellular effects of Pro-Inflammatory Cytokines
- Tissue Ischemia
- Cytopathic Injury, Mitochondrial Dysfunction (NO)
- Cell Death
Effects of Pro-Inflammatory Cytokines on Central nervous system
- Hypothalamus
- Febrile Response
Effects of Pro-Inflammatory Cytokines on liver
- Hepatocytes
- Acute Phase Response
Effects of Pro-Inflammatory Cytokines on CV system
- Vasodilation: NO and prostaglandins
- Hypotension
- Decreased CO
- Thrombosis via activation of tissue factor
End organ damage from Pro-Inflammatory Cytokines Microcirculatory damage / disorder:
- CNS
- Lungs
- GI
- Liver
- Kidney
