Shock and Stabilization Flashcards
Describe the compensatory mechanism of hypovolemic shock
Baroreceptors in the carotid sinus and aortic arch detect drop in blood pressure because of reduced stretch. This enables sympathetic activation and inhibits parasympathetic activations.
Sympathetic activation activates alpha 1 and beta 1 adrenergic receptors
Increase vasoconstriction
increase heart rate
increase cardiac contractility
increase systemic vascular resistance
increase cardiac output
What does the Medulla Oblongata regulate?
The medulla oblongata is comprised of the cardiovascular and respiratory regulation system.
Descending motor tracts, ascending sensory tracts and origin of cranial nerves IX, X, XI, XII
Describe compensatory mechanism in response to changes in CO2, Hydrogen ions or partial pressure of O2
peripheral chemoreceptors in aortic and carotid bodies respond to changes in CO2, pH, and Partial pressure of O2.
Stimulation of chemoreceptors result in vasoconstriction and increase in minute ventilation.
Central chemoreceptors in respiratory center of medulla oblongata sense increase in CO2 or decrease in pH in CSF causing increase in respiratory rate and tidal volume
What is one complication of Oxygen therapy?
Hypercapnia is primary stimulus for respirations.
Patients with chronic hypercapnia may be dependent on hypoxia as respiratory stimulant because their hypercapnic drive can be diminished.
Definition of Shock:
Severe imbalance between oxygen supply and demand, leading to inadequate cellular energy production, cellular death and multiorgan failure.
When oxygen consumption (VO2) exceeds oxygen delivery (DO2)
VO2>DO2
What are 4 consequences of inadequate cellular energy production at the cellular level?
- Cell membrane pump dysfunction (Na+/K+ ATPase)
- Intracellular edema
- Leakage of intracellular contents extracellularly
- inability to regulate intracellular pH
Tree of Life
Define Cardiac Output and what factors influence cardiac output? Define the relationship as an equation.
Cardiac Output is the blood volume ejected with each cardiac contraction multiplied by number of contractions per minute.
CO=Stroke Volume x Heart Rate
What are the determinants of Stroke Volume
Preload: end diastolic volume, volume entering ventricles during diastole
Afterload: resistance ventricles must overcome to circulate blood.
Contractility: How hard the myocardium contracts for a given preload.
What factors influence preload?
- venous return
- fluid volume
- Atrial Contraction
- Intrathoracic Pressure
- Pericardial Pressure
- Venous tone
Causes for reduction in preload.
Hypovolemia: eg. hemorrhage, severe dehydration, edema, cavitary effusion
Obstructive: eg. GDV, severe pleural space disease, mesenteric volvulus, PTE, caval/portal venous occlusion, pericardial effusion
What factors influence Afterload?
- Pulmonic and systemic vascular resistance
- function and integrity of cardiac values
- ventricular chamber size.
Causes for increase in afterload
Peripheral vasoconstriction
systemic hypertension
aortic stenosis
aortic regurgitation
Causes for reduction in cardiac function (contractility)
Primary:
Cardiomyopathy
Valvular disease
tachy or bradyarrhythmia
Secondary:
Systemic inflammatory response syndrome
sepsis
electrolyte abnormalities
severehypoxia
severe acidosis or alkalosis
Correlation between:
mean arterial pressure
central venous pressure
cardiac output
systemic vascular resistance
SVR=(MAP-CVP)/CO
Decrease in SVR with Increase in CO is suggestive that vasopressors are indicated.
Expected changes in cardiac output, contractility, and systemic vascular resistance with different causes of shock: Hypovolemic
decrease cardiac output, increase contractility, increase systemic vascular resistance
Therapy: fluid resuscitation
Expected changes in cardiac output, contractility and systemic vascular resistance with different causes of shock: Obstructive
Decrease cardiac output, normal to increased contractility, increased systemic vascular resistance
Therapy: Relieve obstruction and fluid resuscitation
Expected changes in cardiac output, contractility and systemic vascular resistance with different causes of shock: Cardiogenic
Decreased cardiac output, decreased contractility, increased systemic vascular resistance
Therapy: Positive inotrope
Expected changes in cardiac output, contractility and systemic vascular resistance with different causes of shock: Maldistributive
increased or decreased cardiac output
increased or decreased contractility
decreased systemic vascular resistance
Therapy: vasopressors
Methods of measuring cardiac output
- Fick’s oxygen consumption
- Fick-based carbon dioxide rebreathing method
- indicator dilution method: Thermodilution vs transpulmonary dilution vs lithium dilution
- Pulse contour/pulse pressure analysis
- Echocardiography
- Transthoracic ultrasound
- Pulse wave transit time
Define Hypoxia
Give 4 causes of hypoxia
Inadequate oxygen delivery (DO2) to meet tissue metabolic demand (VO2)
Caused by:
1. inadequate tissue perfusion
2. metabolic disturbances
3. lack of oxygen supply
4. inability of cells to extract O2
What two factors impact oxygen delivery? Define the relationship.
- Cardiac output
- arterial oxygen content
DaO2=CO x CaO2
Arterial oxygen content (CaO2)
Depends on what two factors?
What is the equation?
- Depends on hemoglobin concentration
- Binding affinity or degree of oxygen saturation (SaO2) of the hemoglobin present:
most of arterial O2 is delivered by hemoglobin
small fraction of O2 is dissolved in plasma
CaO2(ml/L)=[1.34(mO2/g) x SaO2% x hemoglobin (g/dL)] + [PaO2(mmHg) x 0.003(ml O2/dl/mmHg]
Define: Sepsis
Life-threatening organ dysfunction caused by a dysregulated host response to infection
Define: Septic Shock
subset of sepsis when underlying circulatory and cellular metabolism abnormalities are profound enough to substantially increase mortality
What are three definitions of massive transfusion
- Entire blood volume in 24 hours
- 50% of blood volume in 3-4 hours
- Administration of blood at 1.5ml/kg/min for 20 minutes
What are the consequences of hypocalcemia? What can cause hypocalcemia?
Clinical signs:
* Hypocalcemia can impair coagulation and decrease myocardial contractility and vascular tone.
* muscle tremors
* fasciculations
* seizures
* muscle cramping
* facial rubbing
* panting
* pyrexia
* PU/PD
* rare: hypotension and death
Causes:
- Massive transfusion can cause hypocalcemia.
- AKI/CKD
- eclampsia
- hypoparathyroism
- ethylene glycol toxicity
- GI disease from PLE
- acute tumor lysis syndrome
What are two complications of massive transfusion?
- Ionized hypocalcemia
- hypomagnesemia due to chelation by citrate anticoagulant
What are the endpoints for hypotensive resuscitation?
MAP: 60 mmHg
Systolic: 90 mmHg
What is delayed resuscitation? When is it indicated?
Withholding all fluid therapy until definitive control of hemorrhage
When can post-surgical patients begin to hemorrhage from surgical site? Why?
1-3 hours post-op because hypotension and hypothermia is resolving upon recovery and vasoconstrictive drugs are wearing off.
What is neurogenic shock?
Usually from trauma to the brain or spinal cord resulting in abnormally low sympathetic tone and unopposed parasympathetic stimulation of vascular smooth muscle.
Define: Hypoxemia
arterial partial pressure of oxygen is below 80 mmHg at sea level
5 causes of hypoxemia
- hypoventilation
- ventilation/perfusion mismatch
- Diffusion impairment
- Decrease [O2] in inspired air
- intrapulmonary shunting
What are PAMPs?
Pathogen-associated molecular patterns
The immune system uses PAMPs to identify pathogens.
PAMPs recognized by Pattern Recognition Receptors (PRR)
DAMPs
Damage associated molecular patterns
What do DAMPs activate?
DAMPs interact with pattern recognition receptors (PRR), activating innate immune system and triggering pathologic response
What are PRRs?
Pattern Recognition Receptors
Function: Trigger innate immune response by recognizing PAMPs and DAMPs
Activates cytokines, leukocytes, coagulation system and complements
What is Cryptic Shock?
The disconnect between microcirculatory perfusion and systemic hemodynamics
Microcirculatory disturbances can occur prior to changes in macrohemodynamic variables (e.g. blood pressure)
What are pathogen factors that can affect the extent and direction of the inflammatory response?
- Pathogen load
- pathogen virulence
- PAMPs
What are host factors that can affect the extent and direction of the inflammatory process?
genetic characteristics
age
coexisting illnesses
medications
What are septic shock risk factors?
S uppressed Immune system
E xtreme Age (infant/elderly)
P eople who have received organ transplant
S urgical procedure (anything invasive)
I ndwelling devices
S ickness
Why is cytopathic hypoxia? What does it contribute to?
Dysfunctional mitochondria
Diminishes ability to produce ATP despite adequate PO2
What is Nitric Oxide and its role in sepsis or septic shock?
Nitric Oxide is produced from the endothelium
NO is a powerful vascular smooth muscle relaxant that contributes to the vasodilatory state of patients with septic shock.
clinical signs (in dogs and people): hyperemic mucous membranes
short capillary refill times
tachycardia
Define: Anaphylaxis
Type 1 hypersensitivity reaction that may occur secondary to a variety of antigens.
Mast cell degranulation releasing:
histamine
tryptase
heparin
cytokines
2 types of Anaphylactic Reactions
Immune-mediated
non-immune mediated
What is atopy?
Genetic predisposition to produce IgE following exposure to antigen.
These individuals are at risk for hypersensitivity response
Function of Histamine Receptor H1
Pathophysiology during anaphylaxis?
Activates smooth muscle contraction and endothelial changes resulting in vasodilation and increased vascular permeability.
Anaphylaxis: vasodilatory shock.
Function of Histamine Receptor H2
Pathophysiology during anaphylaxis?
Modulating gastric acid secretions and regulation of cardiac myocytes.
Anaphylaxis: cardiogenic shock, dysrhythmia, evidence of cardiac ischemia
Function of Histamine Receptor H3 and H4
Pathophysiology during anaphylaxis?
H3: peripheral neurotransmitter release
H4: central neurotransmitter release
Release vasoactive substances such as dopamine and epinephrine is compromised
What are the clinical signs of dogs in anaphylaxis?
GI compromise
hepatic congestion -> coagulation, increase ALT
portal hypertension
Can also exhibit cutaneous manifestations:
urticaria
pruritus
angioedema
What are the clinical signs of cats in anaphylaxis?
Acute respiratory distress, airway edema, and bronchial secretions may be more prominent.
Cutaneous manifestations:
urticaria
pruritus
angioedema
Role of prostaglandins in anaphylaxis
constriction of coronary and bronchial smooth muscles
Role of leukotrienes in anaphylaxis?
Slow-acting substance of anaphylaxis. Longer time to onset, longer duration of action.
What is Biphasic Anaphylaxis?
Initial improvement then relapse. Generally not associated with mortality in humans.
Biomarks of Anaphylaxis
- increase ALT 85-98% sensitive
- POCUS for free fluid (excluding pericardial effusion) + Gallbladder wall edema 93%-98% sensitive
- +/- Increase in PT/PTT
Treatment for anaphylaxis
what are the mechanism of action on adrenergic receptors?
Epinephrine
alpha-1 –> vasoconstriction
beta-1 –> positive inotropy/chronotropy and improved cardiac output
beta-2 –> bronchodilation; stabilization of mast cells, preventing further degranulation and relase of anaphylaxis mediators
Dose: 0.01mg/kg IM +/- CRI 0.05 mg/kg/min
Which receptor does diphenhydramine act on?
H1 receptor
Can be used in acute stabilization period of anaphylaxis
Indicators for glucocorticosteroid use in anaphylaxis
- Onset of action is hours after administration
- works to down regulate late phase eosinophilic response and block the arachadonic cascade tempering delayed inflammatory cascade
- if used, administer anti-inflammatory dose (not immunosupressive dose)
- 0.1mg/kg IV of dexamethasone
Normal values: Blood pressure
Dogs: Systolic 150 +/- 20mmHg
Mean 105 +/- 10mmHg
Diastolic 85+/- 10mmHg
Cats: systolic 125 +/- 10mmHg
Mean 105 +/- 10mmHg
Diastolic 90 +/- 10mmHg
Calculating Mean Arterial Pressure
MAP = diastolic + [(systolic + diastolic)/3]
When can arterial blood pressure monitoring produce erroneous readings?
- compliant tubing is used
- catheter lodged against arterial wall
- a clot at the tip of the catheter
- air bubbles present in catheter tubing
- catheter tubing kinked
CENTRAL VENOUS PRESSURE
1. What is it monitoring?
2. How is it monitoring it?
3. When is it indicated?
- measuring hydrostatic pressure in the intrathoracic vena cava.
- used to estimate right ventricular end diastolic volume and the relationship between blood volume and blood volume capacity
- low central venous pressure (<0cm H2O) can indicate hypovolemia, fluid loss or vasodilation secondary to decrease in venous resistence.
CENTRAL VENOUS PRESSURE
What are the normal values?
0-5 cm H2) but that can vary from animal to animal
Indications of high vs low central venous pressure
LOW CVP (<0 cm H2O)
may indicate hypovolemia
- fluid loss
- vasodilation secondary to decrese peripheral venous resistence
HIGH CVP (>10cm H2O)
may indicate volume overload, right-sided heart dysfunction or failure
pericardial effusion or restrictive disease
blood flow obstruction, significant pleural effusion
Conditions taht promote thrombosis
- multiple catheter attempts
- catheter site irritation
- phlebitis
- hypovolemia
- hypotension
- immobilization of patient
- hypercoagulable state
- endothelial injury
- blood sampling
- excessive manipulation of catheter
- inexperienced operators
- infusate type
- antibiotic and long corticosteroid administration
What are 7 terms for catheter complications?
- catheter site irritation
- catheter site inflammation/phlebitis
- catheter coloization
- catheter site infection
- catheter related blood stream infection (CRBSI)
- catheter site sepsis
- catheter associated blood stream infections
Catheter site irritation
localized catheter entrance site reaction with visible signs of bruising or erythema only
Culture negative
Catheter site inflammation/phlebitis
localized catheter entrance site reaction with visible signs of erythema and at least one other physical anormality (swelling, induration, discomfort, warmth, purulence)
- sterile inflammation: culture negative
- catheter site contamination: culture positive or cytology positive for organisms
Cather site infection
Visualized catheter site inflammation and confirmed organism identification.
1. microbioloical: exudate at catheter site yields an organism with or without concomitant bloodstream infection.
2. clinical: phlebitis noted within 2cm of catheter entrance site. Maybe associated with fever or mucopurulent exudate emerging from the site with or without concomitant bloodstream infection.
Catheter colonization
Significant growth of microorganisms in a quantitative or semiquantitative culture of the catheter tip, subcutaneous catheter segment, or catheter hub.
Includes false-positive cultures (skin contaminant during catheter removal secondary to inadequate sterile skin preparation)
Catheter-related bloodstream infection (CRBSI)
Catheter site infection or unexplained fever in a patient with identical organisms found on both catheter and blood culture.
Patient exhibiting clinical symptoms of bloodstream infection without any other apparent source of infection.
Catheter-related sepsis
Patient exhibiting signs of systemic inflammatory response syndrome and confirmed CRBSI.
Catheter associated bloodstream infection
An identified blood stream infection, patient exhibiting signs of systemic inflammatory response syndrome or unexplained fever, in light of having an intravenous catheter in place with no confirmed or suspected organism identified from the catheter tip.
- unable to remove catheter, undiagnostic culture
- unable to rule out another cause being the source of bloodstream infection.
____________________ has been associated with increased incidences of CRBSI
Thrombosis
likely secondary to the clinically silent fibrin sheath that forms 24 hours after catheter insertion. The sheath is similar to biofilm matrix, increasing bacterial and fungal adherence and promoting coagulase enzyme to escalate thrombogenesis. The sheath/thrombus promotes repeat circulating organismal innoculation and potential for persistent bacteremia.
Cardiac Index
Cardiac output (ml/min) refereced against body weight (ml/min/kg)
or surface area (ml/min/m^2)
Cardiac index for dogs and cats 120-200mls/min/kg
Methodologies to determine cardiac output (6)
Fick Method
indicator dilution
pulse contour dialysis
echocardiography
transthoracic doppler
pulse wave transit time
Fick’s Oxygen Consumption
- Tissue oxygen consumption is dictated by cardiac output and the difference between arterial and venous content
- cardiac output can be calculated in oxygen consumption and oxygen extraction ratio:
Cardiac Output = VO2/(CaO2 - CvO2)
CaO2 = (1.36 x [Hb] x SO2) + [0.003 x PaO2]
Oxygen consumption is determined by measuring difference in oxygen concentration between inhaled and exhaled air over time. –> requires the patient be intubated
Define: Hypoxemic hypoxia
Inadequate oxygen delivery because of inadequate oxygen carrying capacity
Define: Hypemic hypoxia
AKA: Anemic hypoxia
When anemia causes decreased circulating hemoglobin thus reducing oxygen carrying capacity and oxygen delivery
Deifne: Hemoglobinopathy
Adequate amount of hemoglobin however the avaialble hemoglobin is dysfunctional and unable to transport oxygen.
e.g. Carbon monoxide toxicity
methemoglobinemia
Define: Stagnant hypoxia
AKA Circulatory hypoxia
Caused by low cardiac output and low blood flow
therefore low oxygen delivery to tissue (AKA circulatory shock)
Define: Histiotoxic hypoxia
Adequate delivery of oxygen to tissues but tissues are unable to extract and utilize the oxygen.
e.g. Cyanide poisoning
Carbon monoxide toxicity
mitochondrial dysfunction of sepsis
Define: Metabolic hypoxia
Occurs when there is an increased intracellular consumptionof oxygen.
e.g. sepsis
Oxygen extraction ratio
oxygen extraction (O2ER)
O2ER = oxygen consumption / oxygen delivery
O2ER = VO2/DO2
Normal O2ER
Most tissue: 0.3
Brain: 0.6
VO2 is __________________ of DO2 under normal circumstances
Independent
VO2 is ____.
Body responds by ____ oxygen extraction and ____ cardiac output.
- constant
- increasing
- increasing
Critical oxygen delivery
The point at which oxygen consumption declines because oxygen delivery is unable to keep up with demand.
