Shock / Ischemia / CPR / Trauma Flashcards
Define shock
Inadequate cellular energy production.
Which conditions is hypovolemic shock commonly associated with?
Internal or external blood loss or excessive loss of other body fluids (e.g., severe vomiting, diarrhea, polyuria, burns).
Why is CO reduced in hypovolemic shock?
Due to decreased venous return
Compensatory mechanisms for hypovolemic shock?
o They are mechanisms that attempt to raise the circulating blood volume.
o An increase in sympathetic activity causes vasoconstriction, increased cardiac contractility, and tachycardia, with a resultant rise in cardiac output.
o Extreme vasoconstriction and microvascular alterations induce mobilization of fluid from the interstitial and extracellular spaces to the intravascular space.
o Additionally, a reduction in renal blood flow activates the renin-angiotensin-aldosterone system, which further up-regulates the sympathetic nervous system and causes sodium and water retention via the production of both aldosterone and antidiuretic hormone, respectively.
Clinical signs of a compensated hypovolemic shock?
Because the net effect of these responses is to increase intravascular volume, clinical signs of shock may be subtle initially:
Mild to moderate mental depression, tachycardia with normal or prolonged CRT, cool extremities, tachypnea, and a normal blood pressure.
Pulse quality is often normal, and this stage is generally referred to as “compensated shock.”
Clinical signs of decompensated hypovolemic shock?
o With ongoing compromise of systemic perfusion, compensatory mechanisms are no longer adequate and often begin to fail.
o Pale mucous membranes, poor peripheral pulse quality, depressed mentation, and a drop in blood pressure become apparent as the animal progresses to decompensated shock.
o If left untreated, reduced organ perfusion results in signs of end organ failure (e.g., oliguria) and ultimately death.
What is a distributive shock? Examples?
A maldistribution of blood flow, result in distributive shock.
Sepsis, anaphylaxis
Phases of sepsis/SIRS?
o Initial hyperdynamic phase of sepsis or SIRS is characterized by tachycardia, fever, bounding peripheral pulse quality, and hyperemic mucous membranes secondary to cytokine (NO) mediated peripheral vasodilation (vasodilatory shock).
o If septic shock or SIRS progresses unchecked, a decreased cardiac output and signs of hypoperfusion often ensue as a result of cytokine effects on the myocardium or myocardial ischemia.
o Clinical changes may then include tachycardia, pale (and possibly icteric) mucous membranes with a prolonged capillary refill time, hypothermia, poor pulse quality, and a dull mentation.
o Hypodynamic septic shock is the decompensatory stage of sepsis and without intervention will result in organ damage and death.
How are cats different than dogs in shock manifestations?
o The hyperdynamic phase of shock is rarely recognized in cats.
o In contrast to dogs, changes in heart rate in cats with shock are unpredictable; they may exhibit tachycardia or bradycardia.
o In general, cats typically present with pale mucous membranes (and possibly icterus), weak pulses, cool extremities, hypothermia, and generalized weakness or collapse.
o In cats the lungs are vulnerable to damage during shock or sepsis, and signs of respiratory dysfunction are common in this species.
Functional classifications and examples of shock
T/F Gradual resolution of tachycardia (and hypotension) often signals successful return of cardiovascular stability, whereas persistent tachycardia indicates ongoing cardiovascular instability.
TRUE
What is the main goal when treating shock?
Optimizing oxygen delivery to the tissues.
How are the following characteristics in a well-perfused patient?
CVP - normal value?
UOP - normal value?
MAP - normal value?
Body temperature, HR, heart rhythm, RR, MM color and CRT (normal/abnormal)
CVP between 0 and 5 cm H2O
UOP at least 1 ml/kg/hr
MAP between 70 and 120 mmHg
Normal body temperature, heart rate, heart rhythm, and respiratory rate; and moist, pink mucous membranes with a CRT of less than 2 seconds
Why would shock patients develop hyperactatemia?
Critically ill patients with inadequate oxygen delivery, oxygen uptake, or tissue perfusion often develop hyperlactatemia and acidemia that are reflective of the severity of cellular hypoxia.
A lactic acidosis in human patients carries a ________ risk for developing multiple organ failure, and these people demonstrate a ________ mortality rate than those without an elevated lactate concentration.
Greater
Higher
T/F Normal neonatal and pediatric patients may have higher lactate concentrations
TRUE
Who much value has one single measurement of lactate?
o Serial lactate measurements taken during the resuscitation period help to gauge response to treatment and evaluate resuscitation end points.
o The changes in lactate concentrations are a better predictor of survival than are single measurements.
What is a pulmonary artery catheter (PAC) and what can we measure with it?
o A right-sided cardiac catheter or pulmonary artery catheter (PAC, also termed Swan-Ganz catheter or balloon-directed thermodilution catheter) is typically used to monitor systemic oxygen transport parameters.
o The PAC enables the measurement of central venous and pulmonary arterial pressure, mixed venous blood gases (PvO2 and SvO2), pulmonary capillary wedge pressure (PCWP), and cardiac output.
o With this information, further parameters of circulatory and respiratory function can be derived (SV, EDV, SVR index, PVR index, arterial oxygen content, mixed-venous oxygen content, DO2 index, VO2 index, and oxygen extraction ratio).
o A PAC allows the clinician to assess the cardiovascular and pulmonary function of shock patients. The response to treatment and titration of fluid therapy, vasopressors, and inotropic agents can also be monitored.
Cardiac output and systemic DO2 should be optimized using intravascular volume loading until the PCWP approaches ___ to ___ mm Hg. A PCWP higher than___ to ____ mm Hg will promote the formation of pulmonary edema, further impairing oxygenation and overall oxygen transport.
10 to 12mmHg
15 to 20mmHg
I we assume a constant VO2, what does affect SvO2?
SvO2 is determined by cardiac output, hemoglobin concentration, and SaO2.
What conditions can alter SvO2
Where should ideally be SvO2 measured?
In the pulmonary artery.
In animals that do not have a PAC, venous oxygen saturation can be measured from the central circulation, using a central venous catheter in the cranial or proximal caudal vena cava. SvO2 is then termed ScvO2 (central venous oxygen saturation).
A maintenance of a continuously measured ScvO2 above ____ (in addition to maintaining central venous pressure above ___ to ____ mmHg, MAP pressure above ____mmHg and urine output above _____ ml/kg/h) resulted in a ____ reduction in mortality compared with the same treatment without ScvO2 monitoring.
70%
8 to 12mmHg
65 mmHg
0.5mL/kg/h
15%
T/F The mainstay of therapy for all forms of shock except cardiogenic shock is based on rapid administration of large volumes of intravenous fluids to restore an effective circulating volume and tissue perfusion.
TRUE
Which type of catheter should we chose for fluid resuscitation
Because speed of fluid administration is proportional to the diameter of the catheter lumen and inversely proportional to its length, short, large- bore catheters should be placed in a central or peripheral vein.
How do isotonic fluids redistribute once given IV?
The administered fluid rapidly distributes into the extracellular fluid compartment so that only approximately 25% of the delivered volume remains in the intravascular space by 30 minutes after infusion.
What is hypotensive resuscitation?
o Resuscitate with fluids the patient until a MAP of 60mmHg / SAP 80-90mmHg
o In patients that are bleeding, it may even be advantageous to perform hypotensive resuscitation until the hemorrhage is controlled, because aggressive fluid therapy in this setting can worsen bleeding and outcome.
Synthetic colloids such as the hydroxyethyl starches are _________ to the normal animal and therefore pull fluid into the vascular space after intravenous administration
Hyperoncotic
o Cats 5 to 10 ml/kg compared with 10 to 20 ml/kg in dogs.
What happens after the administration of 7-7.5% hypertonic saline?
o After administration of hypertonic saline, there is a transient (<30 minutes) osmotic shift of water from the extravascular to the intravascular compartment.
o It is administered in small volumes (3 to 5 ml/kg) intravenously over 10 minutes.
o In addition to the fluid shift caused by hypertonic saline, there is evidence that it also reduces endothelial swelling, modulates inflammation, increases cardiac contractility, causes mild peripheral vasodilation, and decreases intracranial pressure.
o The effects of this solution are immediate, with a decrease in heart rate and improvement of pulse quality typically noted within 1 to 2 minutes of administration.
o Should always be used in combination with other resuscitative fluids because of the osmotic diuresis and rapid sodium redistribution that occur after administration.
What happens after the administration of 7-7.5% hypertonic saline?
o After administration of hypertonic saline, there is a transient (<30 minutes) osmotic shift of water from the extravascular to the intravascular compartment.
o It is administered in small volumes (3 to 5 ml/kg) intravenously over 10 minutes.
o In addition to the fluid shift caused by hypertonic saline, there is evidence that it also reduces endothelial swelling, modulates inflammation, increases cardiac contractility, causes mild peripheral vasodilation, and decreases intracranial pressure.
o The effects of this solution are immediate, with a decrease in heart rate and improvement of pulse quality typically noted within 1 to 2 minutes of administration.
o Should always be used in combination with other resuscitative fluids because of the osmotic diuresis and rapid sodium redistribution that occur after administration.
Most fluid-responsive shock patients tolerate acute hemodilution to a hematocrit of less than ____%
20%
Packed red blood cells and fresh frozen plasma are administered at a dose of ________mL/kg and fresh whole blood at a dose of _________ mL/kg
10 to 20 ml/kg
20 to 30 ml/kg
T/F HBOC solutions may increase oxygen delivery to tissues and increase perfusion of capillary beds affected by microvascular thrombosis because of the small size of the free hemoglobin.
TRUE
Despite these theoretical benefits and the long shelf life of this product, HBOC solutions are not widely used because of inconsistent supply, undesirable side effects, expense, and lack of clear benefit over other solutions available.
Cardiogenic shock is characterized by a ______ or ________ dysfunction resulting in hemodynamic abnormalities such as increased HR, decreased SV and therefore, CO, decreased BP; increased SVR; and increases in the RA, PA, and PCWP pressures
Systolic or diastolic cardiac
____________ administered intravenously or intramuscularly is the mainstay of therapy for congestive heart failure.
Furosemide (1 to 8 mg/kg)
T/F Ultimately, the dyspneic patient in cardiogenic shock that fails to respond to therapy should be anesthetized, intubated, and positive pressure ventilated with 100% oxygen to stabilize, remove the anxiety associated with shortness of breath, and allow the clinician to perform a thorough PE and pursue further diagnostics.
TRUE
What is systemic arterial pressure?
It is the force exerted by blood against any unit area of the vessel wall.
Which pressure is more significant in tissue perfusion, systolic, diastolic or mean?
MAP
SV is _________ related to preload and contractility, whereas it is ______ related to afterload.
Directly
Inversely
Heart rate is dictated by the relative balance between input from the ____ and _____
SNS
PNS
Vascular tone, and thereby SVR, is affected by both ________ and ________ mediators, which cause either vasoconstriction or vasodilation.
Systemic
Local
Which mediators are involved with short term control of blood pressure and which ones with long term?
o Catecholamines released by the SNS are primarily responsible for basal systemic vascular tone, as well as minute-to- minute regulation of blood pressure.
o Angiotensin II and vasopressin, also having vasoconstrictive effects, play more of a role in long-term regulation of vascular tone.
Local factors that can affect regulation of SVR?
o Local factors can also serve to affect blood flow in response to changes in metabolic demand, muscle activity, and vascular injury and to circumvent systemic vascular control.
o Vasodilatory substances such as NO, histamine, prostacyclin, and CO2, as well as vasoconstrictive agents such as endothelin, thromboxane, and thrombin.
o Although their effects are to meant to alter local vascular tone, excessive/systemic release can result in significant changes to SVR.
What are the main causes/categories of hypotension?
o Reduction in preload.
o Reduction in cardiac function.
o Reduction in afterload.
Causes of reduction in preload?
o As a reflection of venous return, preload will be affected by any cause of significant fluid loss from the vascular space, including hemorrhage, GI or urinary losses leading to severe dehydration, edema, or cavitary effusions.
o Another important cause of relative hypovolemia and preload reduction is venodilation. Veins have a significant capacity for volume; relaxation results in pooling and diminished venous return.
o Any major obstruction in venous return will result in a preload reduction and the potential for hypotension to develop (obstructive shock).
For patients experiencing acute bleeding, it is typically necessary to have greater than ____% loss of vascular volume before hypotension will develop.
30%
Examples of obstructive shock?
o Gastric dilation/volvulus -> gastric distention results in compression of the vena cava and impedes return of blood from caudal circulation.
o Twisting of the stomach itself results in venous congestion and trapping of vascular volume away from effective circulation.
o Caval or portal venous thrombosis, severe pneumothorax, mesenteric volvulus, massive pulmonary thromboembolism and pericardial tamponade.
Primary vs secondary myocardial dysfunction
o Can occur as a primary disease with dilated cardiomyopathy, characterized by impaired myofibril contraction, decreased contractility, and progressive ventricular dilation.
o Secondary myocardial dysfunction can arise associated with severe acidosis or alkalosis, toxin exposure, drug administration, or systemic inflammatory response syndrome (SIRS)/sepsis.
What is the suspected mechanism behind sepsis induced cardiomyopathy?
o Myocardial ischemia, microcirculatory dysregulation, impact of various cytokines (TNF alpha, IL1,6), impaired calcium transport, catecholamine insensitivity, and mitochondrial dysfunction function, among others.
o No single mechanism has been identified; it is likely a combination of these factors.
Other mechanisms of cardiac hypotension?
o Severe mitral regurgitation is another potential cause of cardiogenic hypotension. As the majority of the left ventricular volume moves backward into the atrium, rather than forward into arterial circulation, there is a significant reduction in effective stroke volume and thereby cardiac output.
o Severe tachyarrhythmias (ventricular or supraventricular) and bradyarrhythmias (third- degree AV block, sick sinus syndrome, hyperkalemia) are also potential causes of decreased cardiac output and hypotension.
T/F Diseases that cause hypotension through a decrease in SVR share a common mechanism of inappropriate vasodilation resulting in mal- distribution of blood flow.
TRUE
T/F Venodilation and associated pooling of blood volume, especially in the splanchnic circulation, causes decreased venous return (preload) and further contributes to cardiovascular collapse.
TRUE
What type of shock is anaphylaxis?
o Distributive
o In susceptible patients, IgE produced in response to allergen exposure binds to mast cells and basophils. This binding triggers release of histamines, leukotrines, and other substances that promote vasodilation and increased vascular permeability.
Which system is the main moment-to-moment regulator of blood pressure?
The baroreceptor reflex system.
Through a decrease in stretch of the baroreceptors, it will (not) stimulate the vasomotor center in the medulla and the SNS will lack of inhibition, causing increased HR and SVR.
When SNS is activated due to a decrease in BP, does it affect the arterial system or also the vein system?
o Although most emphasis is placed on arterial vasoconstriction, a significant increase venous tone also occurs.
o This will cause decreased capacitance and promote venous return, thereby supporting preload.
What other receptor reflex is important in regulating BP?
o The chemoreceptor reflex.
o Originating in chemoreceptor organs (such as the carotid and aortic bodies), responds to a decrease in tissue oxygen tension, increase in carbon dioxide, or decrease in pH.
o These changes reflect a decrease in blood flow or oxygen delivery rather than a change in blood pressure per se.
o Unlike the baroreceptors, these changes cause increased signaling from the chemoreceptors and serve to excite the vasomotor center and promote sympathetic outflow.
Will decreases in intravascular volume affect Starling’s forces?
o Yes
o Acute decreases in blood volume or pressure will also promote the movement of fluid from the interstitium into the vascular space.
o Associated decreases in capillary hydrostatic pressure cause a shift in the net balance of Starling’s forces toward the vascular compartment. The resulting internal fluid resuscitation helps to maintain blood volume, preload, and MAP.
What will decreases in BP / renal blood flow activate?
RAAAS
T/F Angiotensin II causes vasoconstriction only by direct (triggering vascular smooth muscle contraction) action.
FALSE - By both direct (triggering vascular smooth muscle contraction) and indirect actions (stimulation of sympathetic activity and release of vasopressin).
Angiotensin II constricts preferentially the _______ arteriole of the glomerulus.
Efferent
What is the non osmotic ADH stimulation?
o When in the face of significant hypovolemia/ hypotension (and with further input from the SNS and RAA system), release of vasopressin increases significantly, independent of osmolarity.
Findings on physical exam related to hypotension?
o Largely related to the systemic reflection of compensatory mechanisms and, for the most part, occur regardless of the underlying cause.
o Tachycardia (sympathetic stimulation of HR), as well as pale mucous membranes, prolonged capillary refill time (CRT), weak peripheral pulses, cool distal extremities, and altered mentation (all reflecting peripheral vasoconstriction or impaired perfusion).
o Cats may also demonstrate bradycardia in shock states (especially cardiogenic and vasodilatory).
o Patients that are in the early (hyperdynamic) stages of vasodilatory shock may have bounding pulses, red mucous membranes, and shortened CRT to reflect the reduction in SVR and increase in peripheral perfusion.
o Many of these signs will develop before a decrease in blood pressure (i.e., during compensation) but should definitely be present once the patient is hypotensive.
Normal arterial BP in dogs and cats
What is considered hypotension in dogs and cats?
o When MAP is below 80mmHg
o Concern for impaired tissue perfusion, especially renal, generally does not occur until MAP gets below 60 to 65mmHg.
o When MAP is not available (doppler), a systolic blood pressure of less than 90 to 100 mmHg could also be considered to reflect hypotension.
What is the gold standard technique to measure BP?
o Direct blood pressure measurement with an arterial catheter and a pressure transducer.
Direct blood pressure monitoring
o More accurate than indirect methods, direct measurement provides continuous reporting of systolic, diastolic, and mean pressures, as well as display of the arterial waveform.
o Used to detect and treat hypotension on a minute-to- minute basis.
o The catheter can be used for arterial blood sampling to monitor acid-base status and blood gas parameters in critically ill patients.
o Direct blood pressure monitoring is less commonly used in cats, except for temporary monitoring (anesthesia) because secondary thrombosis and failure to establish collateral circulation are common in this species.
What are indirects methods of measuring blood pressure?
Doppler
Oscillometry
T/F - Indirect methods is less than direct measurement, with a general tendency to underestimate BP in hypotension and overestimate in hypertension.
FALSE - Tendency to overestimate BP in hypotension and underestimate in hypertension.
T/F Doppler blood pressure only provides a systolic pressure, although there is evidence that may be more reflective of MAP in cats.
TRUE
Which size cuff should we chose to measure a Doppler BP?
40% of the circumference of the limb
If the cuff is too large or too small, measurements may underestimate or overestimate the actual blood pressure, respectively.
Oscillometric sphygmomanometry
o Carry the advantage of being more automated and providing information about systolic pressure, diastolic pressure, and MAP.
o Unlike Doppler ultrasonography, oscillometric readings do not require patient manipulation after cuff placement, and many devices are easily set to cycle for repeated pressure readings.
o Oscillometric measurements are affected by cuff size in a fashion similar to the Doppler technique.
o Other limitations that can affect accuracy include small patient size (especially cats), significant motion, low- perfusion states, and arrhythmias.
T/F Even if hemodynamic parameters are not perfect, we do not need to start any therapy until hypotension has developed.
FALSE - therapy should be initiated at the earliest indication of cardiovascular instability, even if hypotension has not yet developed.
When should we use a positive inotrope?
In cases of documented (through echocardiography) or highly suspected (based on clinical picture) myocardial/systolic dysfunction.
Hypertensive emergency vs hypertensive urgency
o Hypertensive emergency is a patient with an elevated ABP with new or progressive TOD
o Hypertensive urgency is a critically elevated ABP with no evidence of TOD.
How should we decrease the ABP based on hypertensive emergency/urgency?
Patients with a hypertensive emergency require immediate lowering of blood pressure, whereas patients with a hypertensive urgency can have their ABP lowered over hours to days.
T/F The autonomic nervous system serves to prevent chronic changes in blood pressure
FALSE - prevent acute changes in BP
Medium term correction of BP is responsibility of?
o RAAAS, stress relaxation responses of the vasculature, and fluid shifts between the vascular space and the interstitium respond within minutes to hours to correct abnormalities in blood pressure.
T/F - Long-term blood pressure control is largely the responsibility of the kidneys through regulation of extracellular fluid volume.
TRUE
What is hypertension?
High blood pressure, resulting due to inappropriately high systemic vascular resistance with or without concurrent increases in blood volume.
What are the 2 factors that can be causing hypertension ?
MAP = CO x SVR
Therefore, either increases in blood volume or increases in systemic vascular resistance
o CO => Increases in blood volume almost always are due to inadequate volume excretion by the kidneys. This may be due to intrinsic kidney disease or it can occur as a result of active renal reabsorption of salt and water, usually in response to a perceived lack of adequate effec- tive circulating volume or hormonal influence (e.g., aldosterone or glucocorticoid excess).
o SVR => Uncontrolled vasoconstriction is due to local and systemic mediators, including catecholamines, angiotensin II, endothelin I, vasopressin, and thromboxane, in addition to inadequate local production of vasodilators such as nitric oxide and prostacyclin.
Can inflammation cause hypertension?
o Inflammation has been implicated both in the development of hypertension and as a consequence of hypertension.
o Oxidative stress has been demonstrated in animal models of hypertension and human clinical patients.
o Oxidative stress is associated with endothelial dysfunction and has been suggested to cause hypertension through decreased nitric oxide bioavailability (exact role of ROS in hypertension not known).
o The vascular remodeling and endothelial injury that occur as a consequence of hypertension are associated with a proinflammatory response that includes cytokine production, white blood cell activation, and upregulation of endothelial adhesion molecules.
o In human patients with hypertensive emergencies, these inflammatory changes can lead to increased endothelial permeability and activation of coagulation cascades and may also contribute to the TOD seen in patients with chronic hypertension.
Hypertension definitions (ACVIM)
o Situational hypertension - increases in BP that occur as a consequence of the in-clinic measure- ment process in an otherwise normotensive animal are termed situational hypertension.
o Secondary hypertension - persistent, pathologically increased BP concurrent with a disease or condition known to cause hypertension, or hypertension associated with the administration of a therapeutic agent or ingestion of a toxic substance known to cause an increase in BP.
o Idiopathic hypertension (aka primary or essential) - persistent pathological hypertension in the absence of any identifiable underlying cause and represents a complex multifactorial disorder involving genetic, lifestyle, and environmental factors. Suspected when reliable BP measurements demonstrate a sustained increase in BP concurrent with normal CBC, serum biochemistry, and urinalysis results. Increased BP may induce polyuria (pressure diuresis), and thus the presence of low urine-specific gravity (<1.030) in a patient with high BP does not establish that kidney disease is present.
Diseases associated with secondary hypertension in dogs and cats (ACVIM)
o Dogs: CKD, AKI, Cushing’s, DM, obesity, primary hyperaldosteronism, pheochromocytoma, hypothyroidism, brachycephalic.
o Cats: CKD, Cushing’s, DM, obesity, primary hyperaldosteronism, pheochromocytoma, hyperthyroidism
Therapeutic agents involved with secondary hypertension
Glucocorticoids
Mineralocorticoids
EPO-stimulating agents
Phenylpropanolamine (PPA)
Phenylephrine
Ephedrine / pseudoephedrine
Chronic high dose NaCl
Intoxicants associated with hypertension
Cocaine
Amphetamine / metamphetamine
5-hydroxytryptophan
What are the main organs affected by hypertension?
o Eyes
o Brain
o Kidneys
o Heart & vessels
TOD hypertension - ocular lesions
o Reported prevalence rates of ocular lesions with hypertension are as high as 100%.
o Most often termed hypertensive retinopathy.
o Sudden onset of blindness, intra- ocular hemorrhage, and retinal detachment are the most common indications for emergency lowering of ABP.
o Other ocular lesions associated include retinal vessel tortuosity, edema, and retinal degeneration.
o Effective antihypertensive treatment can lead to retinal reattachment, although restoration of vision is not common and subsequent retinal degeneration leading to blindness may occur.
Hypertensive ocular injury has been reported at systolic ABP as low as _____mmHg, and there is a substantially elevated risk of occurrence with a systolic ABP that exceeds ______mmHg (particularly when this increase occurs suddenly).
168mmHg
180mmHg
In a retrospective study of 42 hypertensive dogs, ____% were found to have major ocular lesions.
62%
TOD hypertension - Neurologic signs
o Altered mentation, disorientation, lethargy, seizures, balance disturbances, head tilt, nystagmus, behavioral abnormalities, and focal neurologic defects.
o Hypertensive encephalopathy is more likely to occur with a sudden rise in ABP or a systolic ABP that exceeds 180mmHg.
o This syndrome, in its early phases, is rapidly responsive to lowering of ABP.
o Hemorrhagic and ischemic strokes are observed in dogs and cats, and these conditions may generally be distinguished from hypertensive encephalopathy by virtue of their slow and incomplete response to lowering ABP.
o Before treating hypertension in the patient with evidence of intracranial disease, Cushing’s reflex (causing hypertension and bradycardia) in response to increased intracranial pressure must be distinguished from neurologic injury secondary to hypertension.
TOD hypertension - kidneys
o Hypertensive injury generally manifests as an enhanced rate of decline of renal function, early renal death, and proteinuria.
o Proteinuria is a marker of hypertensive nephropathy in humans, and severity was directly related to degree of elevation of ABP in an experimental study of chronic kidney disease in cats.
o Treatment of hypertension in cats has been associated with a significant decrease in urine protein/creatinine ratio.
o Malignant hypertension is a syndrome of severe, progressive elevations of ABP causing end-organ damage that is often associated with kidney disease and is a recognized cause of rapidly progressive renal injury in rats and people, necessitating quick reductions in ABP.
o Hypertensive damage to the canine and feline kidneys is almost always a slow and insidious process, requiring weeks to years to fully manifest, and is rarely a rationale for emergency therapy in dogs and cats.
TOD hypertension - cardiovascular
o Cardiac changes in hypertensive animals may include systolic murmurs, cardiac gallops, and left ventricular hypertrophy.
o Although cats with previously undiagnosed hypertension may unexpectedly develop signs of congestive heart failure after receiving fluid therapy, heart failure and other serious complications are infrequent and slow to develop.
o While vascular injury within the eye or central nervous system is a rationale for emergent therapy, cardiac changes rarely mandate rapid reductions in ABP.
T/F - Secondary hypertension is less common than primary in veterinary medicine
FALSE - secondary is more common
Epistaxis can occur as a result of hypertension. Is that considered a hypertensive emergency or urgency?
Hypertensive urgency.
How much should we reduce BP when treating a hypertensive emergency?
o The current human recommendation is to reduce mean arterial blood pressure by no more than 25% within 1 hour
o Then to further reduce the blood pressure to 160/100 to 110 mmHg within the next 2 to 6 hours.
o The goal of antihypertensive therapy is to reduce systolic ABP to 110 to 150mmHg.
o Excessive drops in blood pressure can precipitate organ ischemia and should be avoided.
o Severely hypertensive animals (SBP > 250mmHg), and those with secondary vascular changes, can exhibit signs of hypotension (syncope, weakness, exercise intolerance, and prerenal azotemia) when ABP is lowered rapidly.
o This is uncommon if the systolic ABP is maintained above 120 mm Hg.
How should we follow-up the BP / antihypertensive treatment?
o Measurement of ABP and assessment for changes related to TOD should be performed at least every 8 to 12 hours initially.
o Patients receiving parenteral antihypertensive agents should be assessed more frequently, generally at 1-3h intervals.
o Choice of agents, drug dosage, and dosage interval should be adjusted according to ABP, with a goal of maintaining a stable systolic ABP between 110 and 150mmHg without evidence of effects of low ABP.
o It is important to carefully reevaluate any patient treated with emergency antihypertensive therapy before instituting further therapy.
o Follow-up evaluations should include measurement of ABP, funduscopic examination, and other assessments specific to the individual’s TOD and concurrent diseases. Once TOD and ABP are stabilized, generally within 3 to 5 days, the transition to an oral antihypertensive regimen should be made gradually.
Classification of hypertension in dogs and cats based on risk of TOD (ACVIM)
o Normotensive (minimal TOD risk) SBP <140 mm Hg
o Prehypertensive (low TOD risk) SBP 140-159 mm Hg
o Hypertensive (moderate TOD risk) SBP 160-179 mm Hg
o Severely hypertensive (high TOD risk) SBP ≥180 mm Hg
Diagram on stepwise approach to manage hypertension (ACVIM)
Oral anti-hypertensive agents for dogs and cats (ACVIM)
Rates of CPR survival to discharge
Survival to discharge only 6% to 7%
T/F Early recognition of and response to CPA are critical if survival rates are to be improved.
TRUE
How often is recommended the refresher CPR training
Every 6 months
What are the main parts of preparedness and prevention of CPR?
o Early recognition
o Training - refresher q6m
o Crash cart w/ algorithms and dosing charts
o Post event-debriefing
Early recognition of CPA
o A standardized assessment leading to early recognition of CPA is crucial and should be applied immediately to any acutely unresponsive patient.
o In non-anesthetized patients, a diagnosis of CPA should be highly suspected in any unconscious patient that is not breathing.
o A brief assessment lasting no more than 10 to 15 seconds based on evaluation of airway, breathing, and circulation (ABCs) will efficiently identify CPA.
o If CPA cannot be definitively ruled out, CPR should be initiated immediately rather than pursuing further diagnostic assessment.
o The rationale for this aggressive approach includes the following: (a) Pulse palpation is an insensitive test for CPA in people, and this may also be the case in dogs and cats; (b) even short delays in starting CPR in pulseless patients reduce survival rates; and (c) starting CPR on a patient not in CPA carries minimal risks.
o Therefore, there should be no delay in starting CPR in any patient with a suspicion of CPA.
What does BLS includes?
o Chest compressions to restore blood flow to the tissues
o Ventilation to provide oxygenation of the arterial blood and removal of CO2 from venous blood.
BLS should be initiated as quickly as possible once a diagnosis of CPA has been made using the treatment mnemonic CAB which means?
Circulation
Airway
Breathing
Which part of CPR has the most significant impact in outcome?
High-quality BLS focused first on chest compressions followed by ventilation.
What is more common in vetmed, respiratory or cardiac arrest? And in humans?
Respiratory
Cardiac
What are the main 2 goals of chest compressions?
o eRstoration of pulmonary CO2 elimination and oxygen uptake by providing pulmonary blood flow
o Delivery of oxygen to tissues to restore organ function and metabolism by providing systemic arterial blood flow.
What percentage of CO can we achieve with well-executed chest compressions?
30%
T/F Any delay in starting high-quality chest compressions or excessive pauses in compressions reduce the likelihood of ROSC and survival to discharge
TRUE
What is retrograde coronary blood flow and why does it happens?
o During ventricular systole in the spontaneously beating heart, coronary blood flow is negligible and at times may be retrograde;
o Several mechanisms have been proposed to explain this finding, including backward pressure waves, the intramyocardial pump theory, coronary systolic flow impediment, and cardiac compression.
What happens during CPR with coronary blood flow?
o Retrograde coronary blood flow has been described during CPR using external chest compressions.
o That the majority of myocardial perfusion during CPR occurs during the decompression phase of chest compressions and is determined predominantly by myocardial perfusion pressure.
Myocardial perfusion pressure (MPP)
o Also known as coronary perfusion pressure (CPP)
o CPP = ADP - RADP
DAP = aortic diastolic pressure
RADP = right atrial diastolic pressure
o There is strong evidence that higher MPP during CPR is associated with better success in both humans and dogs, leading to the use of MPP as a primary marker of CPR quality.
What compression depth and rate should we use when performing CPR?
o 1/3 to 1/2 the width of the chest
o Rate of 100 to 120 compressions per minute regardless of animal size or species.
What happens with coronary blood flow if we do chest compressions too fast?
Higher compression rates lead to higher MPP and coronary blood flow velocity, but because anterograde flow occurred only during chest decompression, net myocardial blood flow decreases at compression rates above 120 per minute, so faster rates should be avoided.
Why should we avoid leaning on the chest while performing chest compressions
Because it will reduce filling of the heart by preventing full elastic recoil of the chest and must be avoided.
Why should we avoid leaning on the chest while performing chest compressions
Because it will reduce filling of the heart by preventing full elastic recoil of the chest and must be avoided.
How long does it takes to get myocardial perfusion pressure to its maximum during chest compressions?
60 seconds
T/F Compressions should be delivered without interruption in cycles of 2 minutes to optimize development of adequate MPP
TRUE
How long should the pauses to do a rhythm check in between BSL cycles be?
2- 5 seconds
To minimize compressor fatigue, a new team member should take over chest compressions during this planned pause.
What are the 2 mechanisms proposed to explain forward flow of blood during chest compressions?
o Cardiac pump
o Thoracic pump
Explain the cardiac pump theory
o Direct compression of the left and right ventricles increases ventricular pressure, opening the pulmonic and aortic valves and allowing blood flow to the lungs and the tissues, respectively.
o Thoracic elastic properties allow the chest to recoil between compressions, creating a subatmospheric intrathoracic pressure that draws venous blood into the ventricles before the subsequent compression.
o Hands placed between 3rd - 5th intercostal space, where we suspect the heart is.
Explain the thoracic pump theory
o An increase in overall intrathoracic pressure during a chest compression forcing blood from the thorax into the systemic circulation is proposed in the thoracic pump theory.
o Rather than as a pump, the heart acts simply as a conduit for blood flow.
o Hands placed in the widest part of the thorax.
Chest compression approaches
Based on what should we apply the thoracic or cardiac pump?
Chest size and conformation
How should we do compressions in a patient that has a wide, flat chest, similar to humans?
o Place them in dorsal recumbency
o Cardiac pump with hands over sternum
Describe compressors position and movements during CPR
o The compressor should lock the elbows with one hand on top of the other and position the shoulders directly above the hands.
o Engaging the core muscles rather than the biceps and triceps by using this posture will allow the compressor to maintain optimal compression force and reduce fatigue.
o The use of a stepstool is recommended if the patient is on a table and the elbows cannot be locked.
o Alternatively, the compressor can kneel over the patient by climbing onto the table or placing the patient on the floor.
T/F Cat’s thoracic cavities are less compliant than dogs
FALSE - cats and small dogs have chests that are more compliant than medium to large dogs.
What other technique other than two-handed chest compressions can we use?
o A single-handed technique with the hand wrapped around the sternum and compressions achieved by squeezing the chest.
o Circumferential compressions of the chest using both hands may also be considered.
T/F Ventilation should start asap, does not matter if it is before or after starting chest compressions
FALSE - ventilate after chest compressions have started
T/F In intubated patients, chest compressions and ventilation are done alternating
FALSE - simultaneously
Do we need to inflate the ET cuff during CPR?
The inflated endotracheal tube cuff prevents gastric insufflation with air, allows pulmonary inflation during chest compressions, and minimizes interruptions in chest compressions.
Ventilation targets during CPR?
Ventilation rate of 10 breaths/min, a short inspiratory time of approximately 1 second, and a tidal volume of approximately 10 ml/kg.
Why do we have such a low RR during CPR?
o Because pulmonary blood flow is reduced.
o Because low arterial CO2 tension causes cerebral vasoconstriction, leading to decreased cerebral blood flow and oxygen delivery, hyperventilation must be avoided.
o In addition, increased intrathoracic pressure caused by positive pressure ventilation will impede venous return to the chest, reducing effectiveness of chest compressions and reducing MPP.
o Therefore limiting the ventilation rate to reduce the mean intrathoracic pressure will improve cardiac output.
What should we do if we are not able to intubate our patient? How can we provide ventilation regardless?
o Mouth-to-snout ventilation is an alternative breathing strategy and will provide sufficient oxygenation and CO2 removal but should only be used if endotracheal intubation is not possible.
o Firmly close the animal’s mouth with one hand while extending the neck to align the snout with the spine.
o The rescuer should then make a seal over the patient’s nares with his or her mouth and inflate the lungs by blowing firmly into the nares while visually inspecting the chest during the procedure, continuing the breath until a normal chest excursion is accomplished.
o An inspiratory time of approximately 1 second should be targeted.
If our patient is not intubated, do we maintain the same rate / rhythm of chest compressions and breathings than when they are?
o No
o Ventilation cannot be accomplished simultaneously with chest compressions in nonintubated patients.
o Rounds of 30 chest compressions should be delivered, immediately followed by two short breaths.
o Compressions and mouth-to-snout breaths at a ratio of 30:2 should be continued for 2 minute cycles and the rescuers rotated every cycle to prevent fatigue.
o This technique necessitates pauses in chest compressions and should only be employed when endotracheal intubation is impossible because of lack of equipment or trained personnel.
What are the 2 most important monitoring devices during CPR?
ECG and ETCO2
When should ECG evaluated?
o ECG is highly susceptible to motion artifact and cannot be interpreted during ongoing chest compressions.
o To minimize pauses in chest compressions, the only time the ECG should be evaluated is between 2-minute cycles of BLS while compressors are being rotated
What should the CPR team do during the ECG rhythm assessment?
o The team leader should clearly announce the rhythm diagnosis and invite other team members to express agreement or dissent to minimize misdiagnosis.
o In the event of differing opinions on the rhythm diagnosis, chest compressions should be resumed immediately and discussion should proceed into the next cycle.
What are the 3 most common arrest rhythms in SA?
The three most common arrest rhythms leading to CPA in dogs and cats are asystole, pulseless electrical activity (PEA), and ventricular fibrillation (VF)
T/F Capnography is resistant to motion artifact
TRUE
Why can we use ETCO2 monitoring?
o To assess endotracheal tube placement
o To monitor quality of chest compressions
ETCO2 suggests (but is not definitive for) correct endotracheal tube placement; however, this may not be a reliable test of correct endotracheal tube placement in the CPA patient because of?
poor pulmonary blood flow
Why ETCO2 can be used to monitor chest compressions efficacy?
o Because when minute ventilation is held constant, ETCO2 is proportional to pulmonary blood flow.
o A very low ETCO2 value during CPR (<10 to 15 mm Hg) has been associated with a reduced likelihood of ROSC in dogs and humans.
o ETCO2 substantially increases upon ROSC and therefore is a valuable early indicator of ROSC during CPR.
When should we implement ALS?
When high quality BSL is established
What does ALS include?
o Monitoring
o Drugs
o Defibrillation
Why are vasopressors useful during CPR?
Because cardiac output during CPR is generally 30% of normal or less, increasing peripheral vascular resistance to redirect blood flow from the periphery to the core can be useful regardless of the arrest rhythm.
Epinephrine effects during CPR
o Epinephrine is a catecholamine that causes peripheral vasoconstriction via stimulation of α1 receptors but also acts on β1 and β2 receptors.
o The α1 effects have been shown to be the most beneficial during CPR, and these vasoconstrictive effects predominate in the periphery while sparing the myocardial and cerebral vasculature and preserving blood flow to these core organs.
o A meta-analysis showed that low-dose epinephrine (0.01 mg/kg intravenously [IV]/ intraosseously [IO] every other cycle of CPR) was associated with higher rates of survival to discharge in people, compared with high-dose epinephrine (0.1 mg/ kg IV/IO every other cycle of CPR).
o Therefore early in CPR low- dose epinephrine is recommended.
o However, after prolonged CPR, a higher dose (0.1 mg/kg IV/IO every other cycle of CPR) may be considered because of evidence that this dose is associated with a higher rate of ROSC.
If we do not have an IV access, how else can we administer drugs during CPR?
Endotracheal administration of epinephrine is possible (0.02 mg/kg low dose; 0.2 mg/kg high dose) and should be accomplished by feeding a long catheter through the tube and diluting the epinephrine 1 : 1 with isotonic saline or sterile water.
When and how should we use vasopressin during CPR?
o An alternative to epinephrine is vasopressin (0.8 U/kg IV/IO every other cycle of CPR), a vasopressor that will activate peripheral V1 receptors.
o It may be used interchangeably or in combination with epinephrine during CPR.
o Unlike epinephrine, it is efficacious in acidic environments in which α1 receptors may become unresponsive to epinephrine.
o It also lacks the inotropic and chronotropic β1 effects that may worsen myocardial ischemia in patients that achieve ROSC.
o Like epinephrine, vasopressin may be administered endotracheally as described earlier.
Administration of parasympatholytics during CPR
o Its administration may be considered during CPR in all dogs and cats (0.04 mg/kg IV/IO every other cycle of CPR) and may be especially useful in patients with asystole or PEA associated with increased vagal tone, such as occurs with chronic and severe or acute gastrointestinal, respiratory, or ocular disease.
o Endotracheal administration is also possible (0.08 mg/kg).
What antiarrhythmics options do we have when a patient is in VF and not responsive to electrical defibrillation?
o Patients with VF refractory to electrical defibrillation may benefit from treatment with the antiarrhythmic drug amiodarone at a dose of 2.5 to 5 mg/kg IV/IO.
o There are reports of anaphylactic reactions in dogs, so close monitoring for signs of anaphylaxis is warranted once ROSC is achieved; if noted, they should be treated appropriately.
o Lidocaine (2 mg/kg slow IV/IO push) is a less effective alternative to amiodarone for patients with refractory VF.
o Although lidocaine has been shown to increase the energy required for successful electrical defibrillation in dogs in one study, others have shown that this drug is beneficial.
What is one of the first drugs we need to think off when a patient goes into CPA?
o Reversal agents!
o Naloxone (0.04 mg/kg IV/IO) for opioids, flumazenil (0.01 mg/kg IV/IO) for benzodiazepines, and atipamezole (0.05 mg/kg IV/IO) or yohimbine (0.11 mg/kg IV/IO) for α2 agonists.
What is one of the first drugs we need to think off when a patient goes into CPA?
o Reversal agents!
o Naloxone (0.04 mg/kg IV/IO) for opioids, flumazenil (0.01 mg/kg IV/IO) for benzodiazepines, and atipamezole (0.05 mg/kg IV/IO) or yohimbine (0.11 mg/kg IV/IO) for α2 agonists.
Are IV fluids always needed during CPR?
o No
o Administration of intravenous fluid boluses during CPR may be harmful to euvolemic or hypervolemic patients because they tend to increase central venous (and hence right atrial) pressure rather than arterial blood pressure in patients in CPA.
o This elevation in right atrial pressure can compromise perfusion of the brain and heart by decreasing MPP and cerebral perfusion pressure.
o Conversely, patients with documented or suspected hypovolemia will likely benefit from intravenous fluids, which will help to restore adequate preload and may increase the efficacy of chest compressions and improve arterial systolic and diastolic pressures, leading to increased cerebral perfusion pressure and MPP.
When should we consider steroids in a patient that is in CPA?
o Most studies have shown no definitive evidence of benefit or harm from corticosteroid administration during CPR, although most were confounded by coadministration of other drugs.
o One prospective observational study in dogs and cats showed an increased rate of ROSC in dogs and cats, but the type and dose of steroids administered were highly variable and a causative effect could not be inferred because of the study design.
o It is well known that significant gastrointestinal ulceration can develop from a single high dose of corticosteroids.
o In addition, immunosuppression and reduced renal perfusion because of decreased renal prostaglandin production are known side effects.
o Because of this nonadvantageous risk/benefit ratio, the routine use of corticosteroids is NOT recommended during CPR.
When should we consider bicarbonate therapy during CPR?
o Severe metabolic acidosis can develop with prolonged CPA (>10 to 15 minutes), leading to inhibition of normal enzymatic and metabolic activity as well as severe vasodilation.
o Administration of sodium bicarbonate (1 mEq/kg, once, diluted IV) may be considered in these patients.
o It should be remembered that these metabolic disturbances may resolve rapidly after ROSC; therefore bicarbonate therapy in patients with prolonged CPA should be reserved for those with severe acidemia (pH < 7) of metabolic origin.
What is the main therapy for pulseless VT and VF?
o Electrical defibrillation
Describe the 3 phase model of ischemia during VF in the absence of CPR
o The initial electrical phase during the first 4 minutes is characterized by minimal ischemia and continued availability of cellular energy stores to maintain metabolic processes.
o The subsequent 6 minutes, constituting the circulatory phase, are characterized by reversible ischemic injury caused by depletion of cellular adenosine triphosphate (ATP) stores.
o After 10 minutes, the metabolic phase and potentially irreversible ischemic damage begin.
If the duration of VF is known or suspected to be 4 minutes or less, what should we do?
Chest compressions should be continued only until the defibrillator is charged, and the patient should then be defibrillated immediately.
If our patient has been on VF for more than 4min, what should we do? And why?
o One full cycle of CPR should be done before defibrillating.
o This allows blood flow and oxygen delivery to the myocardial cells, which can then generate ATP and restore normal membrane potentials, making the cells more likely to respond favorably to electrical defibrillation.
Difference between monophasic and biphasic defibrillators
o Monophasic defibrillators deliver current in one direction between the paddles and across the patient’s chest.
o Biphasic defibrillators deliver current in one direction before reversing polarity and delivering a current in the opposing direction.
o Biphasic defibrillators have been shown to successfully defibrillate patients at a lower energy output, leading to less myocardial damage, and are therefore recommended over monophasic devices.
Doses for defibrillation
o Monophasic defibrillators 4 to 6 J/kg
o Biphasic defibrillation dosing starts at 2 to 4 J/kg.
o The dose may be increased by 50% with each defibrillation attempt up to a maximum dose of 10 J/kg.
What should we do after we have defibrillated our patient once?
o ALS algorithms no longer recommend three stacked shocks.
o Instead, chest compressions should be resumed immediately after a single defibrillation attempt without a pause for rhythm analysis.
o A full 2-minute cycle of BLS should then be administered before reassessing the ECG.
o If the patient is still in VF, defibrillation should be repeated at the end of this cycle of BLS.
What is the difference outcome wise between open chest CPR and close chest CPR?
o A number of experimental studies in dogs and clinical studies in people indicate improvements in hemodynamic variables, MPP and cerebral perfusion pressure, and outcome when comparing OCCPR and closed-chest CPR.
o There is also evidence that delays in starting OCCPR lead to poorer outcomes and that after 20 minutes of closed-chest CPR in dogs OCCPR is unlikely to be effective.
o Current evidence suggests that improved outcomes from CPA are likely with OCCPR compared with closed- chest CPR, and in cases in which owner consent has been obtained and no underlying diseases that would be contraindications to OCCPR are present (such as thrombocytopenia or coagulopathy), the procedure should be employed as soon as possible after diagnosis of CPA.
Describe the technique for open chest CPR
o A left lateral thoracotomy in the fourth to fifth intercostal space is performed with the animal in right lateral recumbency, and Finochietto retractors are used to open the chest for access to the heart.
o The pericardium may be removed in all cases to facilitate compressions but should always be removed in patients with pericardial effusion or other pericardial disease.
o The ventricles can then be directly compressed using either a two-hand technique with the right ventricle cupped in the left hand and the fingers of the right hand placed over the left ventricle or a one-hand technique with the fingers of the right hand placed over the left ventricle and the heart compressed against the sternum.
o Care should be taken to compress the ventricles from apex to base to maximize forward blood flow. If ROSC is achieved, intensive post–cardiac arrest care will be required after the thoracotomy is closed and a chest tube placed to reduce the risk of pneumothorax.
In which conditions is open chest CPR recommended over close chest?
o Conditions making external chest compressions futile include pleural space disease, pericardial effusion, and penetrating thoracic injuries.
o In addition, it is likely that closed-chest CPR will be ineffective in giant-breed dogs with round or barrel-chested conformation and OCCPR is preferable.
o Patients already in surgery that experience CPA should likely have OCCPR rather than closed-chest CPR. In patients undergoing abdominal surgery, the heart is easily accessible via an incision in the diaphragm, so thoracotomy is not required.
Prognosis of perianesthetic CPA?
47% survival to discharge for dogs
42% survival to discharge for cats
ROSC % and survival to discharge in human in hospital CPA? And in vetmed?
o 45% ROSC, only 17% survival to discharge
o 35-45% ROSC, 6-7% survival to discharge
Chain of survival graph
Steps to follow when we have an unresponsive patient
o On guidelines -> circulation no longer recommended, is not very reliable
o It is ok to do it as long as the assessment does not take longer than 10-15 sec
Unresponsive patient algorithm
Chest compression posture
Chest compressions technique and bp (graph)
Chest compressions technique when cycle <2min
Ventilation humans vs SA
Useful monitoring during CPR (pic)
ETCO2 guidelines
Vascular access during CPR
Intratracheal -> not clear, from 2 to 10 times more than the IV dose
What kind of rhythms can we have during CPR when we assess our ECG at the end of the 2min cycle?
o Shockable rhythms -> pulseless ventricular tachycardia or ventricular fibrillation
o Non-shockable rhythms -> asystole or pulseless electrical activity (PEA)
o ROSC
CPR ECG algorithm
Vasopressor therapy during CPR
Epinephrine for CPR
Epinephrine low vs high dose during CPR
Epinephrine guidelines for CPR
Atropine therapy during CPR
o Half-life of atropine a bit longer, no need to give it every other cycle, but guidelines say we can give it every other cycle
Shockable rhythms
T/F The more ischemic the myocardial cells get, the more difficult it will be to depolarize them with the defibrillator to drive them into the refractory period
TRUE
Electrical defibrillation
Defibrillation technique
What if we don’t have a defibrillator and our patient has a shockable rhythm?
First part of post CPA care algorithm - respiratory optimization
Should all patients be on 100% oxygen in the PCA period?
o No, if they are hyperoxemic we can make the ischemia reperfusion injury therefore we should decrease the FiO2
o Same, hypoxemia not ideal, we want normoxemia
o If we need >0,6 FiO2, then consider PPV
Hemodynamic optimization in the PCA period (second part of algorithm)
T/F Mild hypertension in the post cardiac arrest period is actually beneficial
TRUE
After our patient is normotensive, what should be our next question to try to answer?
Does my patient has a good DO2
Is blood pressure the only hemodynamic parameter indicating the patient hast a good oxygen delivery?
o No
o If they are hypotensive, they are for sure in the supply dependent part of the VO2/DO2 curve, but once they are normotensive we do not know where they stand.
o That is because DO2 depends on CO x CaO2, therefore we have optimized the CO part but we need to check where they are in the CaO2 part of the equation
What is one of the best ways to identify deficits on DO2 in a PCA patient?
o With central venous oxygen saturation - ScvO2
o In a healthy patient at rest, ScvO2 should be more than 70% - if we are pushing the right amount of O2 from the arteries, there should be still a lot of O2 left in the veins.
Can we use lactate to identify DO2 deficits?
What is the final step on the PCA algorithm?
o Neuro protection
o Hypothermia if comatose - can be protective, especially for the brain but also for all tissues as it reduces inflammatory processes and production of ROS - do not raise temp more than 1 degree / hour -> most likely they will need the vent
o Mannitol / hypertonic -> neurons have been ischemic, they have been firing a lot and probably having a lot of Na intracellularly, consider osmotic therapy.
o If they have a seizure in the PCA period we should treat them.
T/F Lidocaine increases the defibrillation threshold for both monophasic and biphasic defibrillators.
FALSE - only in monophasic defibrillators in dogs. In pigs it has been shown that it does not happen with biphasic.
What are the main physiological processes that occur in the post resuscitation phase?
o Ischemia / reperfusion injury
o PCA brain injury
o PCA myocardial dysfunction
o Persistent precipitating pathologic conditions
T/F The majority of dogs and cats that are initially successfully resuscitated die within the first few hours because of rearrest.
TRUE
What is the goal immediately after ROSC?
The goal immediately after ROSC is to sustain spontaneous circulation and perfusion of vital organs, such as the brain and the myocardium, attenuating further injury and preventing rearrest.
What are the common cardiac rhythms after ROSC in people?
o In people, shockable and nonshockable rhythms are equally prevalent, with ventricular fibrillation (VF) and pulseless ventricular tachycardia (VT) identified in 15% and 29%, respectively.
o The incidence of rearrest rhythms has not been systematically reported in veterinary patients.
Once sustained ROSC has been achieved for the first ___ to ___ _______, the clinician’s attention can be directed toward attenuation of the evolution of further organ injury that arises as a consequence of IR and to titrate supportive care to the needs of the patient.
20 to 40 minutes
What does the IR syndrome looks like after CPA? How is it called in humans?
o The syndrome shares many characteristics with sepsis, specifically in regard to inflammation, coagulation, and the endothelium.
o Sepsis-like syndrome
What are the therapeutic considerations in a PCA patient knowing that the PCA period is similar to sepsis/MODS?
1) Early hemodynamic optimization
2) Glycemic control
3) Critical illness–related corticosteroid insufficiency (CIRCI)
What are the end points of hemodynamic stabilization in PCA patients in veterinary medicine?
o Central venous pressure (CVP; 0 mm Hg < CVP < 10 mm Hg)
o Mean arterial blood pressure (MAP 80 to 120 mm Hg)
o Perfusion parameters (central venous oxygen saturation [ScvO2] > 70 %; lactate < 2.5 mmol/L).
o Markers of vasodilation, such as injected mucous membranes or shortened capillary refill time, pulse quality, and echocardiographic determination of LV function should also be included in a comprehensive hemodynamic assessment.
Hyperglycemia commonly occurs after cardiac arrest in humans and has been associated with ______ outcome
Worse
CVP waveform
o Three positive waves are seen, a, c, and v waves, and two negative depressions are seen, x and y descents.
o The a wave represents the increase in the CVP caused by right atrial contraction.
o The c wave is caused by bulging of the tricuspid valve into the right atrium, which increases right atrial pressure and CVP as the right ventricle contracts.
o The x descent is caused by the decrease in atrial pressure during ventricular ejection.
o The v wave is caused by increasing pressure from blood flowing into the right atrium before the tricuspid valve opens.
o The y descent represents rapid emptying of the right atrium as the tricuspid valve opens, allowing blood to flow into the right ventricle.
Stroke volume
Factors that affect afterload
Control of blood flow
Myocardial contractility
Describe phases of capnograhy
o Phase 0 corresponds to inspiration, and no carbon dioxide should be measured during that phase. Phase IV is the early part of inspiration, when CO2–free gas starts entering the airway.
o Some authors include phase IV in phase 0 or in phase III.
o Expiration is divided into the three remaining phases:
* I is early expiration, corresponding to the emptying of the anatomic dead space (no carbon dioxide should be measured);
* II is a rapidly changing mixture of alveolar and dead-space gas, resulting in a steep increase in measured carbon dioxide concentration; * III is the alveolar plateau, during which alveolar concentration of carbon dioxide is measured. The plateau usually has a slight increasing slope
In which circumstances will we have an elevated baseline in our capnography?
o Increased apparatus dead space, rebreathing with a circle system (e.g., faulty unidirectional valve, exhausted carbon dioxide absorbent), and rebreathing with a nonrebreathing system (inadequate fresh gas flow, leak or disconnection of the inner tubing of a Bain circuit) all result in an elevated baseline, increased inspired PCO2 and, if ventilation does not change, increased end-tidal PCO2.
o The end-tidal to PaCO2 gradient will be normal or decreased.
o The slope of phase IV usually is decreased.
What will we see in our capnography when we have inappropriate endotracheal tube sealing?
Usually results in low, nonzero end-tidal readings
What are cardiogenic oscillations and how will we see them in the capnography?
o These are small oscillations in phase IV.
o The slope of this downstroke is also decreased.
o The frequency of these oscillations corresponds to heart rate.
o Cardiogenic oscillations are due to gas movement in the airway caused by the heart beat
How will we see bronchoconstriction in capnogaphy?
Bronchoconstriction (asthma, bronchospasm) is a typical cause of prolonged expiration (phases II and III) and a decreased slope of phase II and increased slope of phase III.
Same as airway obstruction (patient or tube)
What is a curare cleft?
Is a decrease in carbon dioxide concentration during the alveolar plateau. This is due to a spontaneous inspiratory effort in mechanically ventilated patients
ETCO2 and increased alveolar dead space (graph)
Causes of decreased CO2 on capnography (normal tracing, just not as tall)
Causes of increased ETCO2 (normal tracing but taller)
Capnography with airway leak
Common factors leading do secondary brain injury
Monroe-Kellie doctrine
o Vintracranial = Vbrain + VCSF + Vblood + Vmass lesion
o V = volume.
o Sudden increases in any of these volumes as a result of primary and secondary brain injuries can lead to dramatic increases in ICP.
o Initially, increases in ICP will trigger the Cushing’s reflex, or central nervous system (CNS) ischemic response, a characteristic rise in MAP and reflex decrease in heart rate.
o The CNS ischemic response in a patient with head trauma is a sign of a potentially life-threatening increase in ICP and should be treated promptly.
Interpretation of PLR and pupil size in head trauma
Drugs and fluids for TBI
Head/brain trauma vs. head/brain injury vs traumatic brain injury?
Meninges and spaces anatomy (pic)
Secondary brain injury and excitotoxicity mechanisms (algorithm)
Secondary injury TBI (graph)
TBI and hyperglycemia
TBI patient assessment algorithm
TBI patient treatment end points
Estimating total body surface area burned (rule of 9’s)
