Cardiology.cv.hemolymph Flashcards
Right atrium is made up of what two parts?
Sinus venarum cavarum: veins emptyAuricle: conical out pouching
What are the structures that drain into the right atrium?
Cranial vena cava: draining structures of head and neckCoronary sinus: draining coronary circulationCaudal vena cava: drianing abdominal structures into the azygous vein
What is the ova fossa?
Diverticulum at the point of entrance of the caudal vena cava** remnant of the foramen ovale— the communicaiton between the 2 stria of the
Leaflets of the tricuspid valve
- Septal2. Parietal: lies on the right margin3. Angular: between the AV opening & right outflow tract
What the the pulmonary valve leaflets?
RightLeft Intermediate
What are the mitral valve leaflets?
- Septal2. Parietal
The interventricular septum is made up of what tissues?
Muscular tissue (primarily)Fibrous tissue: at its most dorsal extennt (membranous/nonmuscular)
Where is the location of the sinus of Valsalva?
At the base of the Aorta **boulbous in shape—- is hte sinus of valsalva
Where do the 2 coronary arteries originate?
The sinus of valsalva
The ductus arteriosus connects what?
Joints the pulmonary artery to the descending aorta in the fetus
The degree of AV conduction delay is influenced by autonomic tone. With what causing increase/decrease in rate of conduction
Vagal tone: reducingSympathetic tone: increasing
Systole is made up of:
Isovolumetric contraction phase & ventricular ejection
Diastole is made of:
Isovolumic relaxation phaseRapid filling phaseDiastasisAtrial contraction
What marks the beginning and ending of systole?
Beginning: onset of the QRS complexEnding: closure of the aortic valve
What makes up the phase of isovolumetric diastole?
Start when AV closes Ventricular pressure continues to rapidly decline **all cardiac valves are closed
The rate of intraventricular pressure decline during the isovolumic relaxation of diastole?
Determined by the rate of active relaxation of the myofibers
When do mitral valve leaflets open?
When when left ventricular pressure drops below left atrial pressure** onset of rapid filling phase of diastole
Describe/define diastesis (of diastole)
The atriovetnricular pressure difference approaches zeroVentricular volume reaches a plateua**minimal changes in intraventricular pressure and volume
The duration of diastesis is determined by?
Inversely related to heart rate**resting heart rate— diastesis is longest phase of diastole
S1 heart sounds
Closure of the AV valvesmechanical onset of systole
S2 heart sound
Closure of the semilunar valves**end of systole
S3 heart sound
Early ventricular filling **rapid filling phase of diastole
S4 heart sound
Atrial contraction
Systolic function refers to
Ability of the ventricles to contract and eject blood
Diastolic function refers to
The ability of the ventricles to adequately relax and fill
What are the major factors that affect ventricular systolic function
Preload (ventricular end-diastolic volume)Inotropic/contractiel state of myocardiumAfterload: impedence to ventricular outflowHeart Rate
Events that cause an increase in pre-load?
ExerciseAnaemiaFeverPregnancy
Factors that affect myocardial contractility
Autonomic outputCirculating substances (hormones, pharmacologic agents, endogenous & exogenous toxins, etc)Locally produced metabolitesPathologic processes (ischemia, acidosis, infarction, etc.)
Ventircular filling is affected primarily by:
Venous returnAtrioventricular valve functionAtrial functionPericardial compliance Heart rateMyocardial relaxationCompliance
Inadequate end-diastolic volume will result in:
Inadequate stroke volume**reduced coronary perfusion
What are the two major factors that affect ventricular diastolic performance
Chamber complianceMycoardial relaxation
If ventricular compliance is reduced what is required to achieve a given diastolic volume?
A greater filling pressure
Examples of conditions that cause a decrease in ventricular compliance
**chronic conditionsReduction in LV lumen sizePathological hypertrophyFibrosisInfiltrative diseasesPericardial tamponade or constrictionDz or dilatation fo the opposite ventricle
Myocardial relaxation may change acutely in response to
HypoxiaIschaemiaAltered afterloadTachycardiaCatecholaminesVarious pharmacological agents
What are disease processes that produce diastolic dysfunction
Pressure overload states— myocardial hypertrophy or fibrosis (aortic and pulmonic stenosis,, systemic or pulmonary hypertension)
What are examples of dysrhythmias that produce a loss of effective atrial systole resulting in poor exercise tolerance, wekaness or syncope
Atrial fibrillationVentricular tachycardiaHigh degree AV conduction block
What are factors that affect systolic & diastolic function of the atria?
Atrial preloadImpedance to atrial emptyingInotropic state of atrial myocytesAtrial compliance
What are the 3 methods commonly used to determine cardiac output
- Fick method2. Thermodilutioon method (overestimates cardiacoutput)3. Lithium dilution method
What are the parameters measured on echocardiogram to determine LV systolic function?
Fractional shortening: percent decrease of LV minor axisEjection fraction: percent decrease in end-diastolic volumeMean VCF: veloicty of circumferential fiber shortening
Used pulsed doppler on echocardiogram, what measurements can estimate LV systolic function/indexes
Peak and mean velocityAccelerationEjection time**aortic root or pulmonary artery
Indexes of diastolic function on M-mode echocardiography?
-peak and mean velocites of early (passive) ventricular filling (peak and mean E-wave velociteies)Peak and mean velocities of late (atrial systolic) ventricular filling (peak and Mean A wave velocites)-E/a ratio
What is starlings law of the heart?
The more blood which returns to the heart (venous return) and stretches the heart in diastole, the large the stroke volume ejected per beat
Parasympathetic nervous system controls what (in regards to the heart)
Heart rate (chronotropic effects)
Sympathetic nervous system controls what (in regards to the heart)?
Heart rateContractility (inotropic effects)
The sympathetic and parasympathetic control of the heart is controlled by what part of the brain?
Integrated by the brain stem
Baroreceptors sense
Stretch — detect high pressure within the vascular system
Where are baroreceptors located? that detect high pressure
Within the aortic arch and carotid sinus
Baroreceptors that detect low pressure are located (central volume receptors) where?
Atrial tissue (primarily at junction with the great veins)Pulmonary arteries & ventricles
Affarent input to the CNS from the heart are transmitted via the
Glossopharyngeal and vagal nerves
Glossopharyngeal and vagal nerves terminate where
Nucleus tractus solitarius (NTS)
Alpha 2 adrenoreceptor agonists effect o nheart
Increase vagal tone to heartReduce sympathetic tone to blood vessels**bradycardia, hypotension
Cardiac glycosides (digoxin) cause
Increase in parasympathetic tone to heartIncreased baroreceptor stimulation** reflec reduction in sympathetic vasoconstrictor nerve activity**variable depending on physiological state of animal
Why is the effect of cardiac glycosides (digoxin) dependent on
Degree of activation of the natural hormone: endogenous digitalis-like substance— which binds to these receptors
Vasomotor nerves are controlled by which system and hormone?
Sympathetic nerves— Noradrenaline on alpha 1 adrenoreceptors
Acetylcholine is the neurotransmitter that acts on what receptors of the SA and AV nodes
M2 muscarinic receptors
Renin is produced by what cells?
Modified smooth mm cells o the afferent arterioles in the juxtaglomerular apparatus
Renin then acts on angiotensin 1 which is then converted via (BLANK ) to (BLANK)
Angiotensin converting enzyme (ACE)Angiotensin II
Where is angiotenson converting enzyme located?
Endothelial cells— especiallly in the lung
What is synthesized in response to angiotensin II?
Aldosterone
Aldosterone MOA
Mineralocorticoid receptors — to preserve Na reabsorption from teh distal nephrome**results= INC in circulating volume
Hormone: AdrenalineCV and Renal effects:
INC HR and force of contraction (beta 1)Increase vascular resistance, decrease venous capacitance (alpha 1 on vascular smooth mm, beta 2 on sympathetic nerve terminals)Increase in blood flow to skeletal & cardiac mm (Beta2)
Hormone: Angiotensin IICardiovascular and renal effects
Inc vascular resistance, decrease venous capcitance (receptors on vascular smooth mm and on sympathetic nerve termianl which in rease noradrenaline release)Increase in heart rate and force of contraction and sitmualte cardiac mm cell hyeprtrophyEnhance sodium retention by the kidney 9direct effect in proximal tubule and mediated via aldosterone in distal tubule)Increase thirst and possible salt appetite, enhance ADH secretion (effects on brain)
Hormone: Antidiuretic hormone (vasopressin)Cardiovascular and renal effects
Increase water retention at the kidney (V2 receptors)Vasoconstriction (V1 receptors on vascular smooth mm) seen at higher ADH concentrations
Hormone: Aldosterone Natriuertic peptides (ANP & BNP)
Increase sodium retention and potassium excretion by kidneyIncrease salt and water excretion by kidney (direct effects and inhibition of aldosterone)Inhibit renin and ADH secretionInhibit the peripheral and central actions of angiotensin IIVasodilatation (modest) of resistance of blood vesselsIncrease in capillary permeability— reduction in circulating volume
Define Edema
abnormal accumulation of extracellular fluid in the interstitial spaces of the tissues or in body cavities that can be generalized or localized
What are the forces that govern fluid movements at the capillary level?
- intravascular hydrostatic pressure2. interstitial fluid hydrostatic pressure (keep fluid in capillary)3. Intravascular colloid oncotic pressure exerted by plasma proteins4. interstitial fluid colloid osmotic pressure5. vascular surface area capable of fluid transport6. vascular permeability to proteins and water
What are the most common causes of increased capillary permeability?
traumainfectionendotoxemiahypersensitivity (allergic) vasculitis
In horses and ruminants, what is the most common causes of increased hydrostatic pressure?
-CHF-venous thrombosis-liver dz causing obstruction of portal venous thrombosis-lymphadneopathy-cranial mediastinal mass-compression bandage-limb immbolizationtopica administraiton of counterirritants
CHF cause of increased hydrostatic pressure?
pulmonary & vascular systemic congestion–compensatory salt and water retention increases ventricular diastolic, venous and capillary pressure= formation of generalized edema
Causes of hypoproteinemia?
- decreased production of plasma proteins: starvation, liver dz, severe heart failure2. augmented loss of plasma proteins resulting form kidney disease, PLE, (johnes disease, chronic inflammatory bowel disease), peritonitis, or pleuritis
lymphedema occurs when lymphatics are absent or obstructed, what are causes of this edema in horses/cattle?
-congenital absence– rare-tumor-local inflammation (lymphangitis or lymphadenitis)-elevated ventral venous pressure (ie: heart failure)
Common causes of peripheral edema, pleural effusion, and ascites in horses
-chronic right sided or biventricular heart failure-pericarditis-pleuritis/pleuropneumonia-peritonitis-pregnancy-neoplasia: lymphosarcoma-cranial mediastinal mass-hypoproteinemia-liver dz-GI malabsorption: infalmmatoyr bowel dz, neoplasia, parasitism-vasculitis-equine infectious anemia-purpura hemorrhagica-Anaplasma phagocytophilum-equine viral arteritis-thrombophlebitis-lymphatic obstruction-ulcerative lymphantiis-lymphadenitis (corynebacterium pseudotuberculosis abscesses)Trauma-Equine viral arteritis-Thrombophlebitis
Uncommon causes of peripheral edema, pleural effusion and ascites in horses
-aortic cardiac fistula-aortopulmonary fistulaheart base tumor other than lymphosarcoma-neoplasia: mesothelioma, melanoma, plasma cell myeloma, squamous cell carcinoma, fibrosarcoma-starvation-kidney dz, glomerulonephritis, amyloidosis-ionophore toxicity-copper deficiency-counterirritant application-hemodilution-ruptured bladder-Cassia occidentalis toxicity
Common causes of peripheral edema, pleural effusion and ascites in ruminants
-chronic right sided heart failure-high altitude disease (brisket disease)-cor pulmonale-pericarditis (traumatic reticulopericarditis)-pleuritis-pregnancy (udder edema in heifers)-cr mediastinal mass: lymphosarcoma-hypoproteinemia-liver disease-kidney disease: amyloidosis, glomerulonephritis-Gi malabsorption, lymphosaromca, Johnne’s dz, parasitism-lymphatic obstruction (corynebacterium pseudotuberculosis, lymphosarcoma)-thrombophlebitis-urolithiasis ruptured urethra or bladder
Uncommon causes of peripheral edema, pleural effusion, and ascites in ruminants
-mycoplasma wenyoni-idiopathic hemorrhagic pericardial effusion-chronic right sides heart failure d/t cardiomyopathy, infectious myocarditis, ionophore toxicity-starvation-hemodilution-copper deficiency-vasculitistrauma-caudal vena caval thrombosis-anaplasmosis-gossypol toxicity-cassia occidentalis-phalaris spp toxicity-oxytropis (locoweed) toxicity
Common causes of cardiac arrythmias in horses
-excitement-autonomic imbalance-fever-sepsis-toxemia-hypoxemia-colic-disorders of acid base or electrolyte homeostasis-congenital defects-myocarditis-valvular disease-idiopathic (presumptive myocardial fibrosis or fibrofatty infiltrate)
Uncommon causes of cardiac arrhythmias in horses
-ionophore toxicity-ziplatrerol toxicty-anesthesia-other drugs-pericarditis-cardiomyopathy-cardiac or heart base tumor-aortic root rupture-aortopulmonary rupture-atypical myopathy-aortic regurgitation-severe hemorrhage-dynamic upper airway obstruction-rattlesnake envenomation-cardiotoxic plants-hyperthyroidism (iatrogenic)
Common causes of cardiac arrythmias in ruminants
-GI disease-Lymphosarcoma-valvular heart disease-myocardial diseases-brisket dz-pericarditis-cor pulmonale-excitement-foot rot-fever-sepsis-toxemia-disorders of acid-base or electrolyte homeostasis-myocarditis
Uncommon causes of cardiac arrythmias in ruminants
-ionophore toxicity-Beta-adrenergic agonist (zilpaterol) toxicity- anesthesia-hypoxemia-cardiomyopathy-autonomic imbalance-cardiotoxic plants (Rhododendron and Taxus spp.)
Automaticity/ the ability to initiate action potentials spontaneously is a property of cells located where?
-sinus note-part of atria-AV junction-His-purkinje system
Primary arrhythmias can be caused by pathologic conditions of the heart, such as:
myocarditisvalvular diseaseconduction system abnormalitiespericarditis
Secondary arrhythmias develop in the absence of heart disease, such as those caused by:
-excitement-fever-sepsis-hypoxemia-acid-base disorders-electrolyte abnormalities-Gi disturbances-anemia-severe hemorrhage-anesthesia-ionophores-other drugs-toxemia
Placement of base-apex lead for ecg
negative lead– 2/3 rigth jugular furrow from the ramus of the mandible to the thoracic inletlead 1 or II: right armlead III: left arm
Common causes of cardiac murmurs in horses:
valvular regurgitationcongenital defectsanemiaexcitementfeverfunctional murmurexercise
Uncommon causes of cardiac murmurs in horses
aortic cardiac fistulaaortopulmonary fistulacardiomyopathypericarditiscranial mediastinal abscess
Common causes of cardiac murmurs in ruminants
-anemia-excitement-fever-functional murmur-valvular regurgitation-congenital defects-lymphosarcoma-pericarditis (usually traumatic reticulopericarditis)
Uncommon causes of cardiac murmurs in ruminants
-cardiomyopathy-myocarditis
What is the graded scale of cardiac murmurs?
Grade 1: softGrade 2: soft murmur heard immediatelyGrade 3: murmur of moderate intensityGrade 4: loud murmur, with faint palpable thrillGrade 5: loud murmur with palpable thrillGrade 6: loud murmur, audible with stethoscope held away form the chest
The presence of a musical murmur indicates:
vibration of a cardiac structure such as rupture of one of the chordae tendinea or torn valve leaflet
Diastolic murmurs occur between which heart sounds?
S2 and S3(ventricular filling murmurs)ORS2 and S1(aortic regurge or rarely, pulmonic)
Which lesion is described as a continuous washing machine murmur?**heard in a foal
patent ductus arteriosus
Which lesion is described as a continuous washing machine murmur?**heard in an adult
aortic cardiac fistula secondary to rupture of the aortic root or of a sinus Valsalva aneurysmaorticopulmonary fistula–Fresian horses
A continuous washing machine murmur in cattle is heard over the left cardiac areas is associated with what lesion?
traumatic pericarditis –d/t accumulation of fluid, gas, fibrin within the pericardium
Reasons for muffled heart sounds:
- pericardial effusion: displacement of the heart from the thoracic wall by fluid2. abscess or tumor: soft tissue mass3. pneumothorax, pneumomediastinum, or emphysema: air
Common causes of muffled heart sounds in horses
obesitylarge or thick chest wallpericarditis or pericardial effusionneoplasia lymphosarcomapleural abscesschronic heart failure
Uncommon causes of muffle heart sounds in horses
pulmonary emphysemapneumothoraxneoplasia: mesothelioma, squamous cell carcinoma, fibrosarcoma
Common causes of muffled heart sounds in ruminants
pneumothoraxidiopathic hemorrhagic pericardial effusion
Common causes of exercise intolerance, weakness and syncope in horses
myocardial diseasecardiac arrhythmiasaortic or pulmonary artery ruptureaortoiliac femoral thrombosiscongenital heart defectschronic heart failurepericardial diseasehyperkalemic periodic paralysis
Common causes of exercise intolerance, weakness or syncope in ruminants:
myocardial diseasecardiac arrhythmiascongenital heart defectschronic heart failure
define syncope
sudden collapse and loss of consciousness (fainting)
The clinical signs of exercise tolerance, weakness or collapse that is caused by cardiovascular disease results from
failure to maintain cardiac output– inability to regulate heart rate or stroke volume
At what heart rates and mechanism do horses maintain cardiac output?
INC cardiac output HR <210 beats/min: tachycardia HR 210-240: INC stroke volume
heart rates greater than 240 bpm limit cardiac output by
decreasing the time for diastolic perfusion of the myocardium or by limit in stroke volume because of the short diastolic intervals leave inadequate time for ventricular filling
What are the most common bradyarrythmias to cause clinical signs?
complete heart blockadvanced second degree heart block
Common causes of jugular venous distention and pulsation in horses
right sided heart failureleft-sided heart failure with pulmonary hypertensioncardiomyopathyatrial fibrillationtricuspid regurgitationcranial mediastinal masslymphosarcomaabscessjugular venous phlebitis and thrombosis
Uncommon causes of jugular venous distention and pulsation in horses
ionophore toxicitypericarditismyocarditisventricular tachycardiasquamous cell carcinomafibrosarcomacor pulmonalechronic obstructive pulmonary diseaseoverhydration
Common causes of jugular venous distention and pulsation in Ruminants
right sided heart failureleft sided heart failure with pulmonary hypertensionVitamin E and selenium defiiciency (white muscle disease)cardiomyopathytricuspid regurgitationpericarditisjugular venous phlebitis and thrombosisheart base abscessheart base tumor lymphosarcomacor pulmonale caused by chronic pneumoniabrisket disease
Uncommon causes of jugular venous distention and pulsation in ruminants
ionophore toxicityidiopathic hemorrhagic pericardial effusionoverhydrationcranial mediastinal mass
Abnormal jugular pulsation are associated with what side of the heart disease?
right sided–R-CHF–constrictive pericarditis-cardiomyopathy-tricuspid regurgitation
Common causes of painful peripheral swellings in horses
thrombophlebitisabscess (Corynebacterium pseudotuberculosis)cellulitishypersensitivity vasculitis (complicated by skin necrosis and secondary infection)Equine viral arteritisEquine granulocytic ehrlichiosis (Anaplasma phagocytophilum)equine infectious anemiapurpura hemorrhagicclostridium spp myositisseptic tenosynovitisbursitismm disruption/hematomafractureinsect biteapplication of topical counter irritants, firing or soring
Uncommon causes of painful peripheral swellings in horses
frostbite piroplasmosisulcerative lymphangitisepizootic lymphangitisglandersmelioidosissporotrichosisimmune vasculitisaortoiliac thrombosissporadic lymphangitiscongenital lymph node and lymphati cdysgenesishemangiosarcomasnakebite
Common causes of painful peripheral swellings in Ruminants
thrombophelbitisabscessclostridial myositismalignant edemablacklegmm disurption/trauma/hematomacarpal hygromafescue footergotismcellulitis (inj site or wound)fracture insect bitefrostbite
Uncommon causes of painful peripheral swellings in ruminants
disseminated hemangiosarcomaheartwater disease (Ehrlichia rumination, exotic)snake biteseptic tenosynovitisbursitis
Common causes of enlarged lymph nodes in horses
strangleslymphosarcomaupper respiratory infectionCorynebacterium pseudotuberculosis lymphadenitis
Uncommon causes of enlarged lymph nodes in horses
ulcerative lymphangitisepizootic lymphangitissporadic lymphangitisglandersmelioidosisgranulomatous lymphadenitisplasma cell myelomatuberculosishemolytic uremic syndrome
Common causes of enlarged lymph nodes in ruminants
caseous lymphadenitis (Corynebacterium pseudotuberculosis)lymphosarcoma (including bovine leukosis virus)abscess or cellulitis of area drained
Uncommon causes of enlarged lymph nodes in ruminants
tuberculosissporadic bovine encephalomyelitismalignant catarrhal fever
Describe when the arterial pressure occurs with heart contraction
-opening of the aortic valve & ventricular ejection-rises rapidly in early systole-pulse pressure reach peak and declines as ventiruclar ejection slows
Common causes of abnormal peripheral pulses in horses
dehydrationshocktoxemiacongestive heart failureelectrolyte imbalancesacid-base disordershypertensionhypotensionexercisefeverlaminitisaortic regurgitationcardiac arrhythmias
Uncommon causes of abnormal peripheral pulse in horses
aortic cardiac fistulaaortopulmonary fistulaperipheral arteriovenous shuntpatent ductus arteriosus
When do hyperkinetic arterial pulses occur in patients with:
-INC cardiac output (fever, exercise, excitement)-INC stroke volume -bradycardia-aortic valave regurgitation-patent ductus arteriosis-aortic cardiac fistulas-aortopulmonary fistulas
In aortic valve regurgitation, the hyperdynamic pulses is caused by:
increased stroke volume (regurgitated blood int he left ventricle)-followed by rapid runoff of pressure later in systole (as a result of regurgitation)
Hypokinetic pulses are present in patients with diminished stroke volume, as seen in what conditions?
hypovolemialeft ventricular failuremitral or aortic valve stenosis (RARE in lg animals)
Common causes of abnormal puerperal pulse in ruminants
dehydrationshocktoxemiacongestive heart failureelectrolyte imbalancesacid-base disordersfevercardiac arrythmias
Uncommon causes of abnormal peripheral pulse in ruminants
patent ductus arteriosusaortic regurgitationperipheral arteriovenous shunt
Cardiac output values in resting horse range from
32 to 40L/min
What are methods to determine cardiac output?
Fick methodDoppler echocardiographydye dilution/ thermodilution/ litium dilution
Where is the most common location of ventricular septal defect in large animals?
perimembranous
VSDs are more common in which equine breeds?
Welsh mountain poniesArabianStandardbredQuarterhorse
Why do ventricular septal defects occur?
failure of fusion of part of the endocardial cushion and the muscular ventricular septum or failure of fusion of the truncal and conal septa
Describe Eisenmenger complex
defect in which right-sided heart resistance to blood flow causes the shunt associated with VSD to become right to left (rare)**cyanosis is a distinguishing feature
What size is a VSD (VSD to aortic root ratio) that is unlike to be hemodynamically significant?
less than 0.3
With moderate to large VSDs, horses are at greater risk for developing congestive heart failure sooner. Why?
-simultaneous heart dz or Left sided heart failure d/t chronic volume overload can increase pulmonary vascular resistance-right ventricle– chronic pressure overload**comb of pressure and volume overload= greater risk for developing CHF
Which horses with VSDs are at risk for development of CHF early in life and have a shortened life expectancy?
Large defects: >3.5 cm or VSD/aortic ratio of 0.64peak shunt velocities: <3.5m/s
define patent ductus arteriosus
persistent patency of the vessel that connects pulmonary arterial system to the aorta(pulmonary artery to aorta)
Why does the ductus arteriosus close?
In response to:-lowered pulmonary vascular resistance-increased systemic vascular resistance-increased blood volume-increased left ventricular pressure when breathing begins-placental circulation removed
Clinical signs of a PDA are dependent on:
-length and diameter of the ductus arteriosusdirection of the shunted bloodpresence of other cardiac defects
Describe PDA murmur
continuous machinery murmurs
Direction of PDA shunt usually occurs?
left to right–produces left ventricular volume overload-pulmonary hypertension & congestion+/- right sided ventricular hypertrophy
When does switch of PDA shunt occur, to right to left?
When pulmonary resistance equal or exceeds the systemic vascular resistance
When is PDA closure expected in foals?
by 96 hours of age
In a foal with PDA, what is risk for future riding?
b/c of marked dilation of the pulmonary artery– rupture of pulmonary artery is possible
Define tetrology of fallot vs pentalogy of fallot
- biventricular origin (overriding) of aorta)2. Ventricular septal defect3. obstruction of pulmonary arterial flow (pulmonary stenosis)4. secondary right ventricular hypertrophy (d/t obstruction of pulmonary arterial flow)5. atrial septal defect or persistent ductus arteriosus
Pathogenesis of tetralogy/pentology of fallot
abnormal development of the conal septum in the embryonic heart– leads to narrowing of the right ventricular infundibulum (pulmonic stenosis), an inability of the conal septum to participate in closure of the interventricular foramen (VSD) and overriding of the aorta
What is the more common congenital cardiac defects that cause cyanosis in large animals?
tetralogy of fallot
C/s of cyanosis is observed when unoxygenated hemoglobin is reduced to:
<5 g/dL (unoxygenated hemoglobin)
Cyanosis resulting from heart failure or respiratory disease improves with what treatment?
oxygen administration
What is the most common atrial septal defect?
ostium secundum defect– patent foramen ovale PFO) is most frequent
Pathogenesis of persistent foramen ovale
failure of septum primum (valve of foramen ovale)- to become adherent to the crista dividens after birth, when changes in left and right atrial pressures produce functional closure of the formen ovale
In calves, what is the most common defect associated with PDA?
persistent foramen ovale
atrial septal defect murmur
holosystolic crescendo-decrescendo murmur at the left heart base
triscupid valve atresia c/s
cyanosiscrescendo-decrescendo or bandshape holosystolic murmur or pansystolic murmur audible over the rigth and left heart basetachycardiatachypneaweak peripheral pulsespolycythemia (common)
Define persistent truncus arteriosus
one arterial vessel leaves the heart above a VSD**coronary and pulmonary arteries and aorta arise from this vessel
Pseudotruncus arteriosus definition
presence of a remnant of an atretic pulmonary trunk**congenital cardiac disease
What are the most common aortic anomalies seen in foals and calves?
dextropositioning or transposition of the aorta**other anomalies: persistence of the right aortic arch and double aortic arch (may cause esophageal compression)
What is Eisenmenger complex?
Switch in blood flow from right to left side of the heart, to the left to right (results in decreased oxygenation of blood)
Ectopia cordis cervicalis is a relatively common defect in which species?
cattle
What defects are associated with ectopia cordis cervicalis?
defects of the heart, great vessels, neck (torticollis), ribs and sternebrae
Chronic active infection such as what, can predispose animals to the development of bacterial endocarditis or nonvegetative valvulitis?
foot abscessesrumenitisreticular abscessother septic process lead to sustained or recurrent bacteria
What are the most common bacterial isolates from equine and bovine endocarditis cases are:
streptococciPasturella or Acitnobacillus sppTruepuerella pyogenes (formerly Arcabobacterium pyognes)
Lesions of aortic and pulmonic valves can produce what kind of murmurs?
systolicdiastolic (most common in lg animals)or Both
Aortic regurgitation in horses is most commonly associated with
degenerative valve disease
pulmonary regurgitation in cattle is most commonly associated with
bacterial endocarditis
Describe aortic valve lesion murmurs
holodiastolicdescrescendomusical murmurs**can be descrescendo, soft & blowingwater hammer or bounding arterial pulse (assoc w/ sig L ventricular overload
Signs of congestive heart failure in cattle/horses
tachycardiacoughingrespiratory distressjugular venous distentionsubcutaneous edemaascitesmammary vein distention (cattle)
describe murmur of ruptured chordae tendinae?
radiating musical murmur– distinctive honking quality*may have band shaped pansystolic murmur
acute onset of respiratory distress with coughing and expectorating foamy pulmonary edema fluid is a relatively consistent feature of what cardiac abnormality?
ruptured chordae tendinae
Describe murmur of mitral valve prolapse
crescendo midsystolic to late systolic or holosystolic murmur with PMI over the mitral valve area(similar with tricuspid valve prolapse)
Triscupid valve lesions in horses vs cattle are most commonly due to:
cattle: bacterial endocarditis, neoplasia of the right atriumhorse: bacterial endocarditis from septic jugular vein thrombosis
Echo evidence of mitral valve regurgitation
-INC left atrial and left ventircular dimensions-rounding of left ventricular apex- pattern of left sided volume overload+/- INC fractional shortening-bulging of interatrial septum toward the right-larger than nomral pulmonary artery (>aortic root)– severe pulmonary hypertension
Tricuspid regurgitation echocardiac evidence
right atrial and right ventricular enlargement with paradoxical septal motion–> visualizing lesions of endocarditis or neoplasia
aortic regurgitation echocardiographic evidence
left ventricular dilationincreased aortic root diameter decreased aortic root diameter during diastole evidence of inc severity of aortic regurgitationINC left ventricular fractional shorteningdiastolic fluttering of the septal mitral valve leaflethigh frequency vibrations of the interventricular septum or aortic valve in diastole–>visualization of valve prolapse, fenestration, healing endocarditis lesions or tears
Besides echocardiographic evidence of bacterial endocarditis, what are other C/s and diagnostics that indicate endocarditis
anemianeutrophilia (a left shift may be present)increases serum globulin concenINC SAAhyperfibrinogenemialiver enzymes INCurinalysis (+/- pyuria or hematuria)positive blood culture w/ febrile episodes other lab abnormalities of sepsis
Most horses with mitral valve regurgitation do not develop fulminant pulmonary edema, instead they develop
chronic pulmonary hypertension leading to subtle respiratory signs associated with interstitial pulmonary edema and subsequent development of right-sided CHF
In regards to valvular heart disease in horses, what is the most common valves involved?
Aortic is most commonly effected with degenerative valve changes**followed by mitral valve, tricuspid valve and pulmonic valve
Jet lesions occur due to
asosciated with high -velocity turbulent regurgitant blood flow**usually found in the receiving chamber
What lesions can cause moderate to severe valvular regurgitation and are more likely to progress rapidly and warrant a guarded to poor prognosis?
ruptured chordae tedinaeflail valve leafletsmarked valvular thickening
Treatment of endocarditis can ultimately result in?
scarring of the valve leaflet, that leads to progression fo regurgitation and death of animal
When treating cattle for bacterial endocarditis, the antibiotic of choise is?
antibiotic with gram positive coverage
Indication of clopidogrel in treatment of bacterial endocarditis? (in horses)
to prevent platelet adhesion and increased size of the valvular mass
Use of what medicatiosn can be used in cattle to prevent platelet adhesion and increased size of the valvular mass?
aspirin (100 mg/kg/day)low-dose sodium heparin (subcu 30 to 40 units/kg twice daily)
Horses benefit (as do other spp) from the use of vasodilators in treatment of heart failure, what drug has been shown to be beneficial in horses with treatment of moderate MR or AR?
angiotensin converting enzyme (ACE inhibitors)**benazepril: 0.5 mg/kg PO once daily
How do effective parasite control measures prevent predisposing causes of valvular heart disease?
trauma to heart valvesmicroembolisminfarction**in horses
Define cor pulmonale
refer to the effect of the lung dysfunction on the heart and therefore a secondary form of heart idsease
Pathogenesis of cor pulmonale
pulmonary hypertension that leads to right ventricular hypertrophy–> dilation or failure
What is the primary cause of the cor pulmonale in cattle?
High mountain disease (brisket disease, high-altitude disease)
Pathogenesis of High mountain disease?
hypoxic vasoconstriction from high-altitude dwelling
What disease or factors contribute to the development of High Mountain disease?
pneumonialungwormingestion of locoweed (Oxytropis and Astragalus spp)chronic pulmonary disease
What are the primary presenting clinical signs of brisket disease?
subcutaneous edema of the brisket, ventral thorax, submandibular area and occasionally limbslethargy weaknessbulging eyesdiarrheacollapsedeath may occurtachycardia (with a gallop rhythm, +/- splitting of S2 heart sound
Why would there be splitting of the S2 heart sound in brisket disease?
because pulmonary hypertension may accentuate the separation of the aortic and pulmonic valve closures, producing an audible splitting of the S2 **most notable on inspiration
Horses with clinical signs of cor pulmonale?
RAO–> leading to cor pulmonalelabored breathingcoughingexercise intolerancewheezes ausculted bilaterally
Differentials for clinical signs of right sided heart failure
bacterial endocarditis or TRcardiomyopathycardiac lymphosarcoma/ other thoracic neoplasmstraumatic reticulopericarditisleft sided heart fialurepleuritis or pleural effusioncongenital pulmonic valve stenosis (rare)
The response to hypoxia in brisket disease is dependent on:
amount of smooth mm in the pulmonary arteries
Brisket disease path:Chronic pulmonary artery hypertension causes
pressure overload in the right ventricle– responds with increased workload with hypertrophy, dilation or failure (dep on speed of which the condition develops)
Chronic right sided heart failure can lead to what?
diastolic dysfunction of the left ventricle
Why does ingestion of locoweed (oxytropis and Astragulus spp) predispose cattle to right sided heart failure?
Swainsonine** causes toxic mycoardial damage
Brisket disease is common in cattle, kept over what altittude?
over 6000 feet
In what seasons is high mountain disease most commonly seen?
fall and winter** due to cold weather exacerbating pulmonary hypertension
Is cor pulmonale reversible in HMD?
Yes–if animal is brought to lower altitudes
When do cattle not have reversible cor pulmonale?
-other lugn disease- mean PAP of 50 to 55 mm HG **rare- once heart failure develops
Selection of breeding stock to prevent HMD?
low or normal PAPs at altitudes above 5000 feet
Define myocarditis
inflammation of the myocardium caused by bacterial, viral or parasitic organism or thromboembolic disease
What are common causes of bacterial myocarditis?
Stpahylococcus aureusStreptococcus equiClostridium chauveoeiMycobacterium spp
What are known viral causes of myocarditis?
foot and mouth diseaseequine infectious anemiaequine viral arteritisequine influenzaAfrican horse sickness
What are known parasitic causes of myocarditis?
strongylosiscysticercosissarcocystic infection in ruminentas
Define cardiomyopathy
subacute or chronic disease of the ventricular myocardium that occurs without anatomic valvular disease, congenital malformations of the heart or vessels or pulmonary disease
Hypertensive cardiomyopathy ahs been detected in horses associated with what diseases?
chronic renal diseasepain assoc with chronic laminitisponies with EMS
Dilated cardiomyopathy is associated with:
-ventricular dilationincreased ventricular massdecreases systolic function
What known genetic predispositions exist for the development of inherited/genetic cardiomyopathy
- red holstein gene in Holstein Friesan cattle2. curly hair coat in polled herefords and in Japanese black calves
What toxic components can cause cardiomyopathy?
monensinlasalocidsalinomycingossypolCassia occidentalisphalris sppvit E and selenium deficiencycopper deficiencyexcessive molybdenum high sulfatestes (secondary copper deficiency)Acer family (plant tox)rattle snake envenomation
It is difficult to distinguish C/s of myocarditis from what diseases?
colicrespiratory diseaselamenesssepticemia–C/s of myalgia, reluctance to move exercise intolerance
Differentials for causes of dilated cardiomyopathy
- nutritional (Vit E, selenium, copper deficiency)2. toxic: monensin, gossypol, salinomycin, lasalocid, hypoglycin A, Cassia spp., or Phalaris)3. Infectious (viral, bacterial, or parasitic)4. Drug induced
Differential diagnosis for dilated cardiomyopathy?
young– congenital heart defects, cor pulmonale, nutritional myodegenerationAdults– bacterial endocarditis, cardiac neoplasia, thoracic abscess, pericarditis, pleuritis, diaphragmatic hernia
In an attempt to compensate for the reduced cardiac output, how is circulating fluid volume increased in cardiomyopathy
activation of renin-angiotensin aldosterone system & iNC arterial resistance
What leads to the development of pulmonary edea in heart failure?
reduced cardiac output–> stim renin-angiotensin-aldosterone system– INC arterial resistance– INC ventricular preload (venous return)– INC afterload (arterial resistance)–> causes pulmonary edema & reduced cardiac contractility
Microscopic abnormalities associated with cardiomyopathy
- INC fibrous tissue in interstitium in absence of inflammation (or foci of inflammation2. variation in cross-section of cardiomyocytes3. degeneration of adjacent myocardial fibers4. myocardial vacuolation and degeneration with necrosis and fibrosis
Prompt administration of what drug can be beneficial to survivors of ionphore toxicosis?
administration of Vit E
Why are corticosteroids controversial in treatment of cardiomyopathy?
Possible viral recruidescence if the cause is viral
What are therapeutic strategies used for treatment of dilated cardiomyopathy?
- positive inotropic agents (digoxin)2. diuretics3. vasodilators4. rest5 +/- removal of pleural or abdominal fluid
When is the use of digoxin contraindicated in the treatment of dilated cardiomyopathy?
monensin toxicosis
Ideally the peak and trough concentration of digoxin should be between:
1 to 2 ng/mL
Before treatment of digoxin therapy what should be addressed int eh patient?
dehydrationacid-base balanceelectrolyte abnormalities
When should the dose of digoxin be reduced in patietns?
with elevated creatinine or blood ure anitrogen levels
What diuretic is most commonly used in large animals?
furosemide: 1 mg/kg
Which ACE inhibitor is most effective in horses?
benazeprilOther ace inhibitors: quinapril, ramipril, enalapril
Define pericarditis
inflammation of the pericardium that results in accumulation of fluid or exudate between the visceral and parietal pericardium
Causes of pericarditis in large animals
-penetration of ingested foreign objects or external wounds -hematogenous spread (septicemia) of infection-extension of infection from the lung or pleura-viral infections (equine viral arteritis or equine influenza)-neoplasia-Mare reproductive loss syndrome (MRLS) (Actinobacillus spp)
What are the most consistent clinical signs on auscultation with pericarditis?
tachycardiamuffling of heart soundsabsence of lung sounds in ventral thoraxdorsally lung ounds are louder thn normal
Contrast auscultation of pericarditis vs pleuritis?
lung sounds are muffled ventrally (heart sounds are not0radiation fo heart sounds over a wider aea than normal
Cattle: When auscultated with splashing sounds sometimes referred to as “washing machine murmur or rub”, what does this mean clinically?
- can be attributed to accumulation of gas and fluid in pericardium **indicative of presence of gas forming (anaerobic organisms) **grave prognosis
Electrocardiogram abnormalities that are can be seen with pericarditis?
- decreased amplitude of the QRS complexes (<1.5 mV in the base apex lead)2. electrical alternans (altered congifuration fo the P, WRS or T complexes on a regular basis)3. ST segment elevation or slurring+/- right -axis deviation int eh stanard limb leads
What is the safest site to perofrm a pericardiocentesis?
left fifth (fourth in cattle) intercotal space 2.5 to 10 cm dorsal to teh olecranon, above the level of the lateral thoracic vein
What bacteria is commonly associated with pericarditis and mare reproductive loss syndrome?
Actinobacillus organisms
What are the consequences of pericardial effusion to the heart?
- decreased distensibility (increased ventricular end-diastolic pressure) of the heart– impairs the hearts ability to fill in diastole–INC atrial pressure- reduce venous flow or venous return to the heart and diastolic perfusion of the myocardium–> decreased ventricular contractility, stroke volume and cardiac output
Difference between effusive and constrictive pericarditis
effusive: presence of pericardial fluid causes hemodynamic consequencesremoval of fluid beneficialconstrictive: reduction in ventricular compliance d/t fibrinous or fibrotic involvement of pericardium and epicardiumremoval of fluid not beneficial
Exposure to what was the greatest risk factor for the development of fibrinous pericarditis during the mare reproductive and loss syndrome epidemic?
Eastern tent caterpillars
Traumatic pericarditis is not uncommon in cattle, but occurs in less than what percentage of cattle with traumatic reticuloperitonitis?
less than10%
Treatment of pericarditis in horses
– placement of a large bore indwelling chest tube into the pericardial sac under echocardiographic guidance and drainage and lavage of the pericardial sac –> with local infusion of antibiotics
Why can diuretics results in worsening heart failure with pericarditis?
Reduce venous return and preload in animals with pericarditis= compromise to cardiac output & worsening heart failure
Removal of what trees can be beneficial in prevention of exposure to Eastern tent caterpillar?
black cherry trees
What is the most common cardiac tumor in large animls?
lymphosarcoma
Examples of neoplasias that may involve structures adjacent to the heart and may extend to the heart or heart base in horses,
mesotheliomasmelanomaslipomasfibrosarcomaadenocarcinomasother cacrinomassquamous cell carcinomas
Lymphosarcoma is the most common cause of cardiac tumors in cattle, which has a predilection site for?
right atrial myocardium**RV not uncommon, rare: LA or LV
Although more than 50% of cattle in some parts of the United State are infected with BLV, what percentage develop lymphosarcoma?
1 to 4 %
Thymic lympohosarcoma, which is not associated with BLV infections, also involving the heart can occur in what age of cattle?
cattle younger than 30 months of age
The prognosis for survival for cardiac neoplasia?
poor– death expected within 6 months
Control/prevention of cardiac tumors can only be performed for which tumors?
BLV–> isolation of BLV pos and BLV neg animals–> use of individual or serialized supplies–>feeding colostrum from serologically negative cows only–> frequent testing (at least every 6 months) & isolation of serologically positive animals over 6 months of age)
Define aneurysms
vascular dilations, develop from weakening of the medial elastic coat of blood vessels
Medial weakness of blood vessels seen in aneurysms can be caused by:
progression of intimal atherosclertoic lesions that has enlarged from hemorrhagecalcificationulcerationthrombus formation
Causes of aneurysms in large animsl
**unknowntrauma (internal or external)sepsisparasite migrationdegenerative vascular diseaseatherosclerosisaging changes (dilation, elongation and loss of elasticity of blood vessels)
Congenital aneurysms of what structure of the heart have been reported in horses?
sinus of Valsalva
Define thrombosis
formation of a clot that obstructs blood flow in the circulatory system
causes of thrombosis
traumavenous stasiscatheterization for adminsiterin gmedication or fluidsneedle penetrationindwelling acehtersthrombogenic solutionsbacterial contamination
Secondary thrombosis causes:
perivascular inflammation caused by cellulitis, lymphangitis or other source so fbacterial invasion round the blood vessel
Examples of a hypercoagulable states:
dehydrationendotxemiaanemiahypotensionstress stasis
Define mebolism
foreign material carried in the bloodstream
In large animals, embolis most commonly occur with:
bacterial endocarditisthromboplhebitisomphalophlebitisparasitic arteritis
Calves with aorto or aortoiliac thrombosis clinical signs?
weaknesslamenessknucklingparesisparalysis of the hindlimbsinability to risecold hindlimbslacking a femoral pulse
Aortopulmonary rupture and fistulization occur in what breed?
Fresians
What is the most common outcome of aneurysm of a major vessel?
thoughout to be rupture
Unruptured aneurysms may have other complications such as
thrombosis or emoblization o fthe thrombus
In Friesians, rupture of the aorta occurs into the pulmonary artery at what location?
at the level of th eligamentum arteriosum and into the surrounding perivascular stuctures
Spontaneous thromboembolism is commonly associated with?
parasitism in horses**aorta and cranial mesenteric arteries are the most common sites frequently involved
What are risk factors for catehter associated thrombophlebitis
large intestinal diseasehypoproteinemiaendotoxemiasalmonellosisfeverdiarrhealocalled produced fluids
Arteriosclerosis recognized in cattle is most frequently caused by:
excessive vitamin D3 supplementationingestion of calcinogenic plans: Soamum malaxocylon, estrum dirunum or Trisetum flavescens
In horses arteriosclerotic lesions were caused by lesions induced by what organism?
Strongylus vulgarus
Ingestion of calcinogenic plants in horses, results in lesion in what locations?
aorta
Examples of anticoagulant therapy that may be effective in preventing the thrombus formation
clopidogrel: 2 mg/kg PO twice dailyaspirin; 100 mg/kg PO once daily ruminantssodium heparin: 20 to 40 units/kg SC twice daily
Atrial fibrillation is characterized by
lack of coordinated atrial electrical activity– caused by an abnormality of impulse conduction that results from multiple small rapid and random reentrant activation of the atria or by one or more discrete rotors
What shortens the action potential duration in atrial myocardial cells, making atrial fibrilation more likely to occur in horses?
high resting vagal tone
Causes of atrial fibrillation
atrial enlargement from atrial myocardial diseaseatrioventricular valvular regurgitationventricular failuremyocarditisendocarditisautnomic nervous system imbalanceelectrolyte or acid base distrubancesanesthetic drugs or tranquilzier adminitstration
Define “lone Afib”
no undelrying cardiac disease can befound
Cattle with atrial fibrillation usually have what undelrying disease?
gastrointesitnal disease
Define paroxysmal atrial fribillation
usually lasts no more than 24 to 48 hours abefore spontaneous conversion to sinus thythm occurs
What is a common cause of paroxysmal atrial fibrillation inhorses?
transient potassium depletion associated with administration of furosemide
What supplements are associated with atrial fibrillation in horses?
bicarbonate “milk shakes”- paroxysmal AF-iatrogenic hyperthyroidism– admin of Thyro L-supplements containing kelp or ground up shell fish
Describe atrial fibrillation arrhythmias
irregularly irregular - absent 4th heart sound
Differentiate 2nd degree AV block from atrial fibrillation
Second degree AV block– regularly irregular rhythm, audible fourth heart soundAtrial fibrillation– regularly irregular, absent 4th heart sound
Most cattle with atrial fibrillation of what underlying acid-base distrubance?
metabolic alkalosis**experimentally metabolic alkalosis with hypokalemia have results in devleopmetn of Afib
When is cardiac troponin (cTnI) elevated in horses with afib?
acute AF: w/in 4 to 6 hours after onset of Afib
What if cTnI remains elevated in horses with afib?
Activ emyocardial disease shoul dbe suspected
electrocardiogram abnormalities in Afib
irregular R-R intervalQT interval and appaearnce of T wave may varypwaves absent (replaced by fibrillation waves)
Echocardiographic image that should be performed to indicate left atrial enlargement
2 chamber: measure in peak systole **stbd, thgbd: 13.5cm or lessLA to AO ratio in 2D short axis view (provides mroe info on LA enlargement)
Which breeds have the highest incidence of AF?
standardbredthoroughbreddraft horses
In horses with atrial fibrillation what is the most common valvular lesions?
mitral valve disease
Quinidine in the treatment of atrial fibrillation:
negative inotrope at high dosages-causes systemic hypotension-increases ventricular reponse rate
What are possible negative side effects of quinidine?
nasal edemacutaneous reactions (urticaria or wheals)laminitiscolicmarked diarrheaataxia
Max number of consecutive doses of quinidine to administer?
4 doses
When should therapy with quinidine be discontinued
QRS complex prolongation ( more than 25% of pretreatment value)fast (>80 to 100 bpm) sustained supraventricular arrhythmiaventricular rhythmcolicmarked diarrheaataxianasal edema laminitis
How often administer a dose of quinidine?
1 dose every 2 hours
What medication can be administered in addition to quinidine to assist in cardioversion from afib to normal sinus rythm?
digoxin (11 microg/kgPO twice daily)**can be helpful in cases, if conversion has not occurred in 24 to 48 hours
Caveat to combination therapy of digoxin and quinidine?
concurrent admin of digoxin and quinidine results in an increased plasma digoxin concentration
Digoxin can be indicated prior to pretreatment of atrial fibrillation in what circumstance?
When high heart hearts (want < 60 bpm in horses, <100 bpm in cattle before quinidine treatment)very low FS (<24%) indicative of underlying myocardial disease
If furosemide cannot be removed from therapeutic tx regimen in a horse, what can be added to teh diet to prevent potassium depletion ?
KCL
At exercise, horses with atrial fibrillation heart rate should not exceed?
220 bpm
Define ventricular tachycardia
cardiac arrhythmia characterized by a rapid rhythm originating in teh ventricle**originates below hte bundle of HIS in specilized conduction system surround the ventircular myocardium or both
Clinical signs associated with ventricular tahycardia
exerciseintolerancesyncope episodesdepressionweaknesscolicresp distresscoughingventral edemapulmonary edema
In cattle ventricular tachycardia occurs most frequently secondary to
sepsis and toxemia
Large pulse waves seen in teh jugular vein are called cannon “a” waves that occur when?
atrium and ventricle contract simultaenously
When are signs of right sided CHF (ventral edema, venous distention) with ventricular tachycardia?
sustained uniform VT and increase in servity the longer duration and mroe rapid the rate of arrhthmias
When are signs of left sided CHF (coughing, expectoration of foamy fluid, respiratory distress) seen in ventricular tachycardia
multiform VT
What clinical signs help distinguish VT from sinus or supraventricular tachycardia?
presence of jugular pulsesbruit de cannon in an animal with rapid rhythm
Diagnosis of VT is made how?
ECG: series of 4 or mor ventricular premature complexes**VPC may be widened and bizarre or WRS duration and apparent normal
Vtach: morphology of QRS complexes can be described as:
uniform (similar)vary in morphology (multiform)
What is commonly seen with ventricular tachycardia in association with the atrium?
atrioventricular dissociation– atrial rate slower than the ventricular rate– may see fusion and/or capture beats– VT can be sustained or paroxysmal
What should be considered in horses with acute onset of uniform VT and colic?
rupture of the aortic root at the right sinus of valsalva
What is a mechanism described in exercise induced VT in horses?
sympathetic stimulation (increasing the amplitude of early afterdepolarizations)
What is an important cause of sustained VT?
reetnry in the ventricle
What is though tot be one of the leading causes of sudden cardiac death in horses when other causes of death cannot be found on postmortem examination?
Ventricular tachycardia leading to ventricular fibrillation
Which gender is at increased risk for aortic root and sinus of Valsalva rupture?
males– usu. middle-aged at time of rupture
VT is more likely seen in large animals of any age with what diseases?
GI diseasehorses– following severe hemorrhage
Does slow, uniform VT require treatment?
often resolves or improves significantly with correction of underlying electrolyte or metabolic imbalances w/o requiring antiarrhythmic therapy
Horses with sustained heart rate >120 bpm, uniform VT treatment
antiarrythmic therapy
ECG findings associated with life threatening VT
multiform origin for the ventricula rpremature depolarizations-torsades de pointes (wdie VT)-presence of an R wave superimposedon preceding T wave (R on T)
large animal with following C/S treatment recommendation?-C/S of CHF & hemodynamic collapse-Heart rate <120 bpm-Multiform VT (+/- R on T)
treat as cardiovascular emergecy– death from ventricular fibrillation is likely w/o antiarrythmic therapy
What drugs can be used to tx life-threatning VT:
lidocainequinidine gluconatemagnesium sulfateIV procainamide, IV and oral propafenone (refractory VT), IV flecainidesotalol
acute massive blood loss induces hypovolemic shock characterized by:
tachycardiatachypneacold extremitiespale mucous membranesmuscle weaknesseventual death (resulting from CV collapse)
When do you see changes in PCV or total protein with acute blood loss?
within 12 to 24 hours
Hypovolemic shock should be treated with administration of:
40 to 80 ml/kg of sodium containing crystalloid fluids
Hypertonic saline can be administered at what dose, to temporarily reverse the pathophysiologic sequelae of severe hemorrhagic shock?
2 to 4 ml/kg 7.2% sodium chloride
Why is the total volume of crystalloid solution required is much greater than the volume of blood lost because
crystalloid solutions distribute throughout the extracellular space
Why is blood transfusion viewed as a temporary therapeutic procuedure?
because crossmatch- compatible allogeneic RBCs are removed from circulation by mononuclear phagocyte system (MPS) w/in 2 to 4 days of transfusion
Describe routine blood typing crossmatch:
incubating wash RBCs from donor (major) and recipient (minor) with serum from the other
Why is the first blood transfusion of whole blood to a horse or ruminant, not previously transfused or senstized by immunization or pregnancy usually well tolerated
b/c natural alloantibodies are o flow concentration adn weak activity
Severe anaphylactic reactions to blood transfusion should be treated with
epinphreine (0.01 to 0.02 mg/kg
When does normal bone marrow start to replace cells, in cases of acute hemorrhage?
w/in 5 days
Define hemoperitoneum
accumulation of blood in the abdominal cavity**can be life threatening
Causes of hemoperitoneum in the horse
traumapostoperative abdomina lhemorrahgeneoplasiacomplications from pregnancy an dfoaling (utero-ovarian, middl euterine, external ilaic artery rupture)organ rupturemesenteric injurycoagulopathiesovarian hemoatomasystemic mayloidosisidiopathic hemoperitoneum
The underlying cause of hemoperitoneum is identified in what percentage of cases?
76%
What are the most common causes of hemoperitoneum in horses?
trauma (spleen and in mares, repro tract & assoc vessels)neoplasia
Hemorrhagic abdominal effusion is characterized by high red cell count of:
RBC> 2, 400, 0000 RBC/microLPCV >18%total protein >3.2 g/dL*normal t high luek count
What are early indicators of hypovolemia d/t acute blood loss?
central venous pressureblood lactate concentration
Primary goals of therapy in hemoperitoneum
- tx hypovolemic shock2. restore perfusion & O2 delivery to tissues3. correcting fluid deficits4. stopping further blood loss5. preventing complications
Which carries the worse prognosis pre or post partum hemorrhage?
prepartum: 100% vspostpartum: 20% mortality
Causes of hemothorax in neonatal foals
lacerated lung or vessels from fractured ribs
Is exercise induced pulmonary hemorrhage a recognized caused of major blood loss in horses?
no
Causes for chronic blood loss
bleeding GI lesionscertain renal diseaseshemostati cdysfunctionblood sucking external parasiteshaemonchosis (esp goat sand sheep)
Causes of GI hemorrhage
- Neoplasia Horses: gastric SCC cattle: abomasal lymphoma2. parasitism3. mucosal ulceration NSAID tox in horses abomasal ulcers: cattle
Renal sources of chronic blood loss
renal neoplasia (Rare)congenital renal vascular anomalies (RARE)idiopathic hematuriaidiopathic recurrent hematuria of Arabian horses
How does iron deficiency anemia develop?
With loss of erythrocyte iron secondary to chronic severe blood loss** hypoferremia or reduce serum ferritin develops with INC total Fe binding capacity and reduction in marrow iron
What is a good source of iron for patients?
good quality forages
NSAID pathogenesis in right dorsal colitis
inhibit cycolooxygenase – (COX1 than inducible CO2 expressing during state of inflammation–> causes inhibition of prostaglandin E production–> hypoxic or ischemic GI mucosal damage and delayed mucosal healing
What 2 components are involved in hemostasis?
- coagulation2. fibrinolysisfunction: arrest bleeding from damaged blood vessel and maintain nutrient blood flow
After a blood vessel is damaged, what occurs
vasoconstriction occursrapid adherence of plts to subednothelial collage
after rapid adherence of platelets to a damaged blood vessel, then
triggeres aggregation, contraction and granule secretion (basic plaetlet reaction)
What platelet phospholipoprotein provides the necessary surface to catalyze interactions among activate coagulation proteins that result in thrombin formation?
platelet factor 3
What are zymogens?
precursor forms of procoagulant proteins that circulate in the blood **must be altered during coagulation to become active
When is the extrinsic coagulation system activated?
When lipoprotein tissue factor (TF) gains access tohte bloo stream
Where is tissue factor located?
widely dsitirbuted in most tissues (endothelial cells * monocytes
When is intrinsic coagulation system activated?
When blood is exposed to a negatively charged surface (e.g. activated platelets)
When factor XII and prekallikrein in the intrinsic coagulation pathway have reciprocal activation, then
the intinstric pathway stimulats formation of numerous inflammatory mediators such as kinins and complement
What is thrombin generated from?
formation of activated factor X (Xa)
Function of thrombin
catalyzed the conversion of fibrinogen to fibrinpromotes plt aggregationenhances cofactor activities of factor V and VIIIactivates factor XIII & protein C
Examples of plasma anticoagulant proteins include:
- serpins: inhibit activate coagulation factors 2. protein C system: directed against cofactors V and VIII3. Antithrombin III (AT III): main inhibitor of thrombin and Xa
heparin accelerates which anti-coagulant protien by 2000 fold?
AT III
Function of activated protein C
destroys factors V and VII** limiting its own activation** depn on thrombin and entohelial cofactor, thrombomodulin
What is plasmin?
primarily responible for degradation of fibrin
Plasmin exists in plasma as the zymogen
plasminogen
What zymogen has a high affinity for fibrin?
plasminogen**as well as tissue plaminogen activator (tPA)
What ist he main physiologic inhibitor of plasmin
alpha 2 antiplasmin (alpha 2-AP)**competes with the binding of plasminogen to fibrin and clot contains equal amounts of both glycoproteins
Why does a blodo clot not lyse spontaneously?
b/c of molar balance betwen alpha 2- antiplasmin and plaminogen
What is a potent stimulus for release of endothelial tpA
stasis of blood upstream fro teh occluded vessel
What is the most important factor that determines the rate of fibrinolysis?
the rate of fibrin formation
Breeds that have prekallikrein deficiency?
miniature hroses in USbelgian horses in Canada
Abnormal blood parameters from horses with prekallkrein deficiency?
prolonged aPTTsnormal PTs
What is the mode of inheritance of prekallikrein deficiency in horses?
likely autosomal recessive**underlying genetic mutation has not been determined
Measurable deficiencies in factor XI activity have been reported in what breeds?
Holstein cattle (US, Canada & UK)Japanese Black cattle
Activation of factor XI occurs in what step of coagulation pathway?
intrinsic pathway ** second step
Factor XI deficient Holsteins show what clotting time abnormalities?
normal PTsprolonged aPTTs
How is Factor XI deficiency inherited?
autosomal recessive trate
What gene encodes factor XI?
F11
What spp & breeds have Factor VIII deficiency?
- horses: thoroughbreds, standardbreds, quarter horses, tennessee walking horses2. cattle: hereferods & japanese brown cattlesheep: alpine white sheep
Coagulation panel results in a patient with Factor VIII deficiency:
normal PTprolonged aPTT
Clinical signs of factor VIII deficiency (hemophilia A)
inappropriate bleeding incidents: epsitaxispetechial hemorrhageformation of IM hematomashemoarthorsishemopericardiumhemoperitoneiumprolonged, life-threaning bleeding at sites of invasiv procedures, umbilical cords and castration
Animals with true Factor VIII deficiency should also have normal levels of what other factor?
vWF
Factor VIII deficiency (Hemophilia A) inheritance
X linked and recessive** clinical dz reportedin male horses and cattle
Treatment of factor VIII deficiency in humans
factor replacement therapy
Prognosis for animals with factor VIII deficiency (hemophilia A)
poor**most owners choose euthanasia
Von willebrand factor function
stablizes factor VIII in circulationpromotes plt endothelial adhesion at site sof vascular injury
Von willebrand factor deficiency reported in
-a QH filly-simental cattle- 10 mo Heifer
What are the vitamin K dependent coagulation factors?
factor II, VII, IX and X
Deficiency of vitamin K dependent factors have been reported in?
5 lambs from a flock of rambouillet sheep
coagulation profile of vit K deficient coagulation factors:
prolonged aPPT and pT
Suggested genetic mutation results in vit K deficient coagulation factors in sheep?
autosomal recessivesingle nucleotide polymorphism exon 4 of the gene encoding y-glutamyl carboxylase (GGCX)mutation creates a STOP codon leading to premature termination of the protein
Fibrinogen deficiency has been reported in what spp?
Saanen kid (goat)border leicester lamb
Clinical coagulation tests for vitamin K dependent coagulation factors cannot be differentiated from what other deficiency in the coagulation cascade?
fibrinogen deficiency
Define Thrombasthenias
rareinherited defectsin platelet functionresult in spontaenous or excessive bleeding
Thrombastenias coagulation panel
normal aPTT, PT and plt count**INC plt or buccal mucosal bleeding times
Glanzmann Thrombasthenia
quantitative or qualitative deficiencies of the plt membrane integrin alphaIIbBEta3 (glycoprotein IIb-IIIa)-alpha11b and Beta3 proteins: expressed by separate genes & form heterodimers that bind fibrinogen and mediate plt aggregation
Glanzmann Thrombasthenia: platelet dysfunction
unable to aggregate in response to collagen or ADP ** blood forms loose clots with limited serum separation & decreased tensile strength
Glanzmann Thombasthenia has been reported in what breeds?
-thoroughbred cross gelding– homozygous mutation in exon2-Quarter horse filly- heterozygous or exon 2 missense mutation & 10 base pair deletion in second ITGA2B allele-Peruvian Paso horse-Oldenburg filly: homozygous for distinct missense mutation in exon 2
Recommendations for owners of Glanzmann thrombasthenia horses?
-alert for signs of bleeding requiring supportive care-regularly monitor for anemia
Atypical equine thrombasthenia is a case report in
1 thoroughbred filly
What is atypical equine thrombasthenia?
AET plts have significantly reduced fibrinogen binding & limited prothrombinase activity & reduced factor V released from AET plt alpha grnaules
Simmental Hereditary Thrombopathy: blood has what:
diminished clot retractionreduced aggregation in response to ADP or collagen**SHT platelets fail to aggregate in response to the calcium ionophore A23187
Bovine Chediak Higashi Syndrome is characterized by
abnormal secretory granules in plts, leuks, & melanocytes
Bovine Chediak Higashi syndrome has been identified in what breeds?
HolsteinBrangusJapanese Black cattle
Pathogenesis of Bovine Chediak Higashi syndrome that leads to bleeding
Dense granules have markedly reduced the ADP content & release disproportionately less ADP– plts aggregate normally in reponse to ADP**CHS plts have slow & transient aggregation in response to collagen
Bovine Chediak Higashi syndrome gene mutation
Missense mutation in gene encoding protein lysosomal trafficking regulator LYST**autosomal recessive- 8.8% Japanese Black cattle were carriers
Clinical signs of Bovine Chediak Higashi Syndrome
-hypopigmentation of skin, hair & eyes-photophobia-increased susceptibility to infection**present with infections or inapprorpiate bleeding
Define vasculitis
inflammation and necrosis of blood vessel walls, regardless of size, location or cause
Cause of vasculitis in large animals:
secondary to manifestation of a primary infectious, toxic or neoplastic disorder**has characteristics of the hypersensitivity vasculitis in humans
Clinical manifestations of vasculitis
-demarcated areas of dermal or subcutaneous edema- infarction, necrosis and exudation-hyperemia, petechial and ecchymotic hemorrhages-ulceration of mucous membranes–>besides skin can occur in any organ system: lameness, colic, dyspnea, and/or ataxia
Name examples of vasculitis syndromes with predominant cutaneous involvement
equine purpura hemorrhagica (EPH)equine viral arteritis (EVA)equine infectious anemia (EIA)equine granulocytic anaplasmosis (EGA)
Definitive diagnosis of vasculitis involves:
histopathology of involved vessels**full thickness punch biopsies
Define purpura hemorrahgic
noncontagious disease of horses characterized by vasculitis leading to extensive edema and hemorrhage of the mucosa and subcutaneous tissues
What bacterial organisms have been known to cause/lead to purpura hemorrhagica?
Streptococcus equi (**Vaccination against S. equi)Streptococcus zooepidemicusRhodococcus equiCorynebacterium pseudotuberculosis
Clinical signs of equine purpura hemorrhagic usually occur within what time frame of development of respiratory infection?
2 to 4 weeks
What age range are commonly affected by equine purpura hemorrhagica?
young to middle aged horses (mean 8.4 years, range 6m to 19 yrs)
Predominant clinical signs of purpura hemorrhagica
subcutaneous edema of all four limbslethargyanorexiafever hemorrhages on mucous membranestachycardia(other C/S: tachypnea, reluctance to move, serum exudation from the skin, colic, epistaxis).
The predominant laboratory abnormalities seen with Equine purpura hemorrhagica?
anemianeutrophiliahyperproteinemiahyperfibrinogenemiahyperglobulinemiaelevated mm enzymesthrombocytopenia–Rarely seen
Skin biopsy of equine purpura hemorrhagica
acute luekocytoclastic or nonluekocytoclastic vasculitis with necrosis of blood vessels-marked dermal and subcu hemorrhage, protein rich edema, multifocal areas of dermal infarction
What immune complex deposition on blood vessel walls have been identified in Equine purpura hemorrhagica?
IgM or IgA ,strep M protein (type III hypersensitivity rxn)
Horses with infarctive purpura hemorrhagica present with clinical signs of:
colic lamenessmuscle swellingstiffness
Horses with infarctive purpura hemorrhagica may have what changes on bloodwork?
high CK values
What is the recommended treatment for purpura hemorrhagica?
Antibiotics (penicillin)hydrotherapy/limb bandages/light exercise (handwalks)IV fluidsProlonged treatment with corticosteroids (2-4 weeks)
Corticosteroid treatment regimen recommended for treatment of Purpura hemorrhagica?
minimum of 2 to 4 weeks dexamethasone: 0.04 to 0.2 mg/kg IV q24 (morning)prednisolone: 0.5 to 1 mg/kg PO q24 (morning)
Possible complications of purpura hemorrhagica
skin sloughinglaminitiscellulitispneumoniadiarrhea
What is the prognosis for purpura hemorrhagica?
fair with early aggressive therapy & supportive care-retrospective: 53 horses: mortality rate of 7.5%
Equine viral arteritis (EVA) is an infectious disease characterized by:
pan vasculitisedemahemorrhageabortion in pregnant mares
Equine viral arteritis describe the infectious organism:
enveloped, spherical, postive stranded RNA virus (diamter 50 to 70 nm)-nonarthropod borne virus
Equine viral arteritis virus epidemiology
order: nidoviralesfamily: ARterivridae
Equine viral arteritis clinical signs:
pyrexialethargyanorexialimb edemastiffnessrhinorrheaepiphoraconjunctivitisrhinitisabortionedema (periorbital, supraorbital, ventrum, mammary gland, scrotum or limbs)Other: urticarial rash, abortion, resp signs, ataxia, mucosal eruptions, submaxillary lymphadenopathy and intermandibular and shoulder edema
With natural exposure to Equine viral arteritis (EAV) , what is theepidemic abortions rate?
abortion rate: <10% to >60%
Abortion due to Equine viral arteritis occurs in what months of gestation?
3 to 10 months
Do mares infected with Equine viral arteritis become chronic shedders and have fertility problems?
No
What is the pathogenesis of EAV in blood vessels?
localized in endothelium, medial myocytes and pericytes– virus causes vasculitis with necrosis of the tunica media, abundant vascular and perivascular lymphocyte & lesser granulocytic infiltration with karyorrhexis, loss of endothelium and formation of large fibrinocellular stratified thrombi
How is EAV transmitted?
aerosols from respiratory, urinary, or reproductive tract secretions of acutely affected animsl**semen from persistent infected stallions
Does EAV remain viable in frozen semen?
Yes (fresh, chilled and frozen semen
Is transmission of EAV through fomites possible?
yes
With natural exposure to EAV does it cause short or long term immunity?
Long-term immunity
How long does it take for mares/geldings to eliminate the infection?
w/in 60 days
What percentage of acutely infected stallions become persistently infected?
30 to 60%
In stallions where is the virus maintained?
w.in the accessory organs: ampullae, vasa deferentia
Seroprevalence for EAV is common is what breeds?
standardbredwarmblood breeds** has been recently estab. in Quarter horses
How can EAV be diagnosed?
virus isolationviral nucleic acid (PCR)serology
How can a diagnosis of EVA be made on serology?
fourfold or more increase din serum neutralizing antibodies between acute and convalescent samples (3 weeks apart)
Stallions that test with a positive titer of 1:4 should be tested for persistent infection by virus isolation from what sample?
sperm rich ejaculate
Prior to vaccination of stallions for EAV, what should be performed?
Should have serum submitted to a US department of Agriculture (USDA) approved laboratory to confirm seronegative status
After a stallion is vaccinated for EAV, what should then be performed?
Horses should be isolated for 28 days **can potentially shed the virus (MLV vaccine)
Is there evidence that vaccinated stallions become carriers?
No
Anaplasma phagocytophila describe appears within neutrophils/eosinophils
vacuoles/ inclusion bodies (1.5 to 5 miccrom in diameter) in cytoplasm-pleomorphic-contain one or more coccobacillus or large granular aggregates (morulae)
Anaplasma phagoctyophila cases in horses most commonly occur during which season (s)
late fallwinterspring
Is Anaplasma phagocytophila considered zoonotic?
Yes- human infection can occur via tick bite or transmission of infected blood
What are the vectors of Anaplasma phagocytophila ?
Ixodes pacificus- CaliforniaIxodes scapularis- eastern and midwestern USIxodes ricinus- Europe
What are potential/proposed reservoirs for Anaplasma phagocytophila?
white footed micechipmunkswhite tailed deerdusky footed wood ratscervidslizardsbirds
Anaplasma phagocytophila: observed pancytopenia is thought to be caused by:
cytolysisinduction inflammationcell sequestrationconsumptiondesruction
Clinical signs of Anaplasma phagocytophila
early signs: FUO, partial anorexiareluctance to movefever (102.9-106.3F)mild to mod tachycardia (50 to 60 bpm)decreased appetitelimb edemapetechiationicterusweaknessataxiarecumbency
What is the incubation period for Anaplasma phagocytophila?
Believed to be less than 14 days
What is the prepatent period for Anaplasma phagocytophila in experimental exposure to infected ticks or inoculation with infected blood?
experimental exposure to infected ticks: 8 to 12 daysinoculation with infected blood: 3 to 10 days
Anaplasma phagocytophila clin path abnormalities:
anemialeukopenia characterized by granulocytopenia and lymphopeniathrombocytopenia
What is the definitive diagnosis of Anaplasma phagocytophila?
morulae w/in the cytoplasm of neutrophils and eosinphilsORpositive PCR assay in peripheral blood
False positive Anaplasma phagocytophila morulae can occur with
Dohle bodies in toxic neutrophils
What does a four fold increase in IFA titer for Anaplasma phagocytophila mean?
confirms recent exposure
Pathologic findings of Anaplasma phagocytophila
petechiae and ecchymosis of subcu tissueedema of ventral abdomen, limbs and prepuceproliferative and necrotizing vasculitis, thromboses and perivascular cuffing in sucu tissue, fascia, kidneys, heart, brain, lungs, ovaries and testes
What is the treatment of choice for Anaplasma phagocytophila?
oxytetracyline: 7 mg/kg or doxycycline
Anaplasma phagocytophila if left untreated, resolves in what time frame?
in 2 to 3 weeks if left untreated
Prevention for Anaplasma phagocytophila?
tick control
Mechanisms of thrombocytopenia
- decreased production2. abnormal sequestration (spleen)3. inc consumption or destruction
At what level of thromboctyopenia can spontaneous hemorrhage start to occur?
<10,000/uL
When is prolonged bleeding from wounds, injections, or surgical procedures and propensity to form hematomas after minor trauma seen?
<40,000/uL
Persistent life-threatening hemorrhage due to thrombocytopenia can be treated with transfusion of what biologic products?
fresh whole bloodplatelet rich plasma (preferable)
Causes of Immune mediated thrombocytopenia
- primary2. secondary drug administration, neoplasia or other immunologic disorders (EIA lymphoma, autoimmune hemolytic anemia)
Thrombocytopenia in a horse, with obvious primary disease should the prompt a workup to rule out what disease process?
DIC
Alloimmune thrombocytopenia of neonates include clinical signs of
depressionloss of sucklea bleeding tendencyblood lossrapidly developing anemia d/t profound thrombocytopenia
Alloimmune thromboctyopenia in foals results from what?
multiparous dams immunoglobulins form mare, found in her plasma, serum and milk bind to the foal’s platelets
Differentials for alloimmune thrombocytopenia in foals include
neonatal sepsisneonatal maladjustment syndromeneonatal isoerythrolysis
Laboratory abnormalities associated with alloimmune thrombocytopenia
severe thrombocytopenia (<40,000/L)prolonged bleeding timeabnormal clot retractionnormal thrombin time, PT, APTT, plasma fibrinogen+/- INC FDPs (fibrin degradation products)
In IMTP what is seen on bone marrow aspirate or biopsy?
megakaryocytic hyperplasia
Definitive diagnosis of IMTP
demonstration of INC quantities of plt assoc IgG or C3 or anti-plt activity in serum**flow cytometry (detect plt surface assoc IgG (PSAIgG)
Without PSAIgG testing, the diagnosis of IMTP can be made based on:
small vessel hemorrhagic diathesis and severe thrombocytopenia in a horse with normal coagulation times & no other evidence of DIC**response to therapy– supports diagnosis
pathogenesis of IMTP
plt destruction mediated by antibodies coating the plt surface that cause premature plt removal from circulation by MPS
In secondary IMTP pathogenesis is
Ig bound to plt surface is part of an immune complex composed of antibody that directed against a drug, microbe or neplastic ag**nonspecifically attached to plt Fc receptor
Thromboctypenia caused by the chrysotherapy (gold therapy) may persist for how long after discontinuation of therapy?
weeks to years
Why is the spleen the major site of plt phagocytosis?
- much antiplt antibody is secreted locally2. more than 30% of circulating plts are normally stored there3. stagnant splenic blood flow allows sensitized plts to pass slowly through a dense network fo phagocytic cells
Effect of treatment with corticosteroids for IMTP?
improve capillary integrityimpair clearance by the MPSdecrease number and avidity of macro Fc receptorsimpair antiplt ab productionimpede plt ab interactionsinc thrombocytopoeisis
Blood coagulation proceeds with what 3 key reactions:
- formation of activated factor X2. formation of thrombin3. formation of fibrin
The pathologic process of DIC is described as
widespread fibrin deposition in the microcirculation and development ofhemorrhagic diathesis caused by the consumption of procoagulants and hyperactivity of fibrinolysis
DIC in large animals is described in association with what other disease processes:
localized or systemic septic processesneoplasiaGi disordersrenal diseasehemolytic anemia
what renal disease is caused by DIC
ischemic cortical necrosis followed by acute tubular necrosis
Negative effects of DIC can be seen in which organs?
GIT (microvascular thrombosis)Renal (acute tubular necrosis)Pulmonary (micorvascular thombrosis, uncommon in lg animals)CNS (neurologic signs, uncommon in lg naimals)Lamina (digital ischemia)
What diseases must be differentiated from DIC:
IMTPwafarin toxicosis (horses)moldy sweet clover toxicosisinherited coagulation abnormalities
Diseases initiate DIC by what 2 major mechanisms?
- generation of excessive procoagulant activity within the blood 2. contact of blood with abnormal surfaces
Gram negative endotoxins stimulate DIC through
direct factor XII activationcytokine production by mononuclear phagocytes
What is the net result of any triggering mechanism for DIC is
exaggerated generation of systemic thrombin which causes widespread microcirculatory thrombosis
What are the effects of thrombin in DIC:
-activates factor XIII to render fibrin more resistant to fibrinolysis-enhances cofactor actiity of factors V and VIII-induces plt aggregation and exposure of plt phospholipid
In DIC plasmin contributes to factor consumption by destorying factors:
V, VIII, XIIa, IX, XI**in addition to fibin and fibrinogen
Plasmin contributes to factor consumption in DIC by destroying factors
V, VIII, XIIa, IX and XI
The macrophage system in the liver and spleen play a vital role in pathogenesis of DIC, how?
Tissue fixed macro normally remove FDPs & activated clotting factors, until their rate of formation exceeds the ability of ht eMPS to clear them
IV fluid administration in the treatment of DIC
helps prevent organ dysfunction after microvascular thrombosis & correct existing acid-base or electrolyte imbalances
Flunixin meglumine treatment in DIC
mitigates the effects of endotoxin caused by eicosanoids an dused at dose of 0.25 mg/kg IV q8h
Corticosteroids int he tretmetn of DIC
reduce phagocytic action of the MPS and potetniate hte vasoconstrito effects of catechoalmines
What can be administered if DIC is causing life threatening hemorrhage (rare in lg animals)?
fresh plasma (15 to 30 ml/kg) to replace used coagulant and anticoagulant proteins
What can be administered to stall disseminated microvascular thrombosis that precipitates organ failure in DIC?
low molecualr weight heparin
For heparin to work in the treatment of DIC, what must be true?
appropriate ammounts of ATII, which is necessary for heparin to work and is often depleted by DIC
What are clinical signs of warfarin toxicosis in horses?
hematomasecchymosis of mucous membranesepistaxishematuria
How are horses potentially exposed to warfarin?
rodenticides ** used to be a tx for horses with navicular dz
Coagulation panel abnormalities with warfarin toxicosis
prolongation of PT (earliest sign)APTT becomes prolonged eventually+/- blood loss anemia and hypoproteinemia
The diagnosis of warfarin toxicosis is made by:
history of exposureclinical signs of large vessel hemorrhagic dithesisprlonged PT w/ or w/o APTT
Mechanism of Warfarin toxicsosi
-competitive inhibition of vitamin K– necessary for liver production of clotting factors II, VII, IX and X
