BoD Exam I

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interaction of epithelial cells w mesenchymal tissue including blood vessels

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interaction of epithelial cells w mesenchymal tissue including blood vessels

gas exchange fxn of respiratory tract is achieved by:

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  • gas exchange

  • nourishment of pulmonary structures

pulmonary blood serves 2 purposes

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mechanical defense of airways

  • Particles become entrapped in mucus and gases become dissolved in mucus

  • Mucus is moved mechanically by beating cilia, sneezing and coughing, moved to the pharynx, then swallowed

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broncho-alveolar junction

the most vulnerable area in respiratory system

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BALT

makes Abs to inhaled Ags

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IgA

Humoral immunity is based on ___ in upper airways

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IgG

humoral immunity is based on ____ in lower airways

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macrophages

main defense in alveoli

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surfactants

important opsonins in alveoli

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Ruminants, horses, pigs, & cats

spps w PIMs (pulmonary intravascular macrophages)

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sneezing

induced by irritation of the uppermost respiratory tract

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coughing

induced by irritation in the trachea and/or bronchi

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congenital ciliary dyskinesia, environmental, infectious

3 main causes of ciliary dysfunction

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scarring

result if the basement membrane is damaged in URT

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repair

if the basement membrane is intact, the ciliated epithelium will ___

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goblet cell hyperplasia, fibrosis, squamous metaplasia

effects of chronic upper respiratory damage

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Type I

Alveolar cells very vulnerable to damage

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phagocytosis by kupffer cells and splenic macrophages

defense against blood-borne agents in dogs

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phagocytosis by pulmonary intravascular macrophages

defense against blood-borne agents in ruminants, cats, pigs, & horses

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atelectasis

collapse or incomplete expansion of alveoli (typically on margins)

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congenital atelectasis

failure of lungs to expand at birth

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acquired atelectasis

  • Compression - pressure on lungs (air, fluid, viscera)

  • Obstructive - alveoli distal to airway obstruction collapse as gas is gradually resorbed

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emphysema

ruptured alveoli leading to trapping of air, trapped air may extend into the interstitium

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epistaxis

blood may originate from within the nasal cavity or distal to the nasal cavity

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aerogenous

  • most common route

  • leads to cranioventral distribution

  • bacteria, mycoplasma, viruses, toxic gases, foreign particles

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hematogenous

  • common in septicemia and viremia

  • leads to diffuse non-collapsing lung

  • viruses, bacteria, and parasites

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direct extension

penetrating injury, migrating airways, bites, esophageal rupture

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rhinitis

inflammation of the nasal mucosa

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  • acute viral

  • acute allergic

  • acute bacterial

  • foreign bodies

  • chronic

causes of rhinitis

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acute viral rhinitis/sinusitis

sero-mucoid, mild epithelial cell degeneration

  • ex: “red nose”, malignant catarrhal fever, atopic rhinitis

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acute allergic rhinitis/sinusitis

serous discharge (±mucus) - IgE, eosinophils, and mast cells

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acute bacterial rhinitis/sinusitis

purulent to mucopurulent discharge, usually secondary to mucosal damage (viral, trauma, dental, dehorning)

  • ex: murine respiratory mycoplasmosis, “snuffles” in rabbits

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foreign body induced rhinitis

discharge is mucopurulent, often bloody

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chronic rhinits

from progression of untreated acute disease, or fungal agents

  • ex: nasal & nasopharyngeal polyps, chronic granulomatous rhinitis, sinonasal neoplasia

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potential sequelae of sinusitis and rhinitis

  • Bronchopneumonia and pulmonary abscesses

  • Osteomyelitis and turbinate atrophy (atrophic rhinitis, pigs)

  • Meningitis

  • Otitis +/- vestibular syndrome and polyp formation

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Equine Recurrent airway obstruction (COPD or "Heaves")

  • Likely allergic

  • Diffuse bronchiolitis

  • Cough, tachypnea, expiratory dyspnea, exercise intolerance

  • Wt loss & "HEAVE LINE" (bc atrophy of abd mm)

  • Epithelial hyperplasia, mucus

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atopic rhinitis

  • Disease of swine

  • Predisposing factors: infectious (bacteria +/- viral), environmental genetics, nutrition

  • Bordetella bronchiseptica + Pasteurella multocida, type D

  • Toxins from Pasteurella stimulate osteoclasts and inhibit osteoblasts => degeneration and remodeling of nasal turbinates (predisposed to bronchopneumonia)

  • Don’t see scrolls!

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nasal & nasopharyngeal polyps

  • From chronic inflammation

  • Composed of a myxomatous matrix, fibroplasia covered w nasal epithelium

  • Control of inflammation will reduce size, but lesion is persistent

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sinonasal neoplasia

  • Most common in dogs

    • Most are malignant & are carcinoma or adenocarcinoma

    • Chondrosarcoma & other tumors sometimes occur

  • Other spp

    • Squamous cell carcinomas - cat/horse

    • Retroviral enzootic nasal carcinoma - sheep

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clinical signs of sinonasal disease

  • Sneezing, foul odor, facial deformity, nasal discharge, noisy breathing, epistaxis, increased resp effort

  • If coughing is a feature, then there is involvement of more proximal respiratory tract structures

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clinical signs of disease of pharynx, larynx, guttural pouch, trachea

  • Stridor, cough, ptyalism, changes in voice/vocalization, nasal discharge, inspiratory dyspnea and cyanosis, dysphagia, head/neck extension

    • Inspiratory stridor => airway obstruction above the glottis

    • Expiratory stridor => tracheal obstruction

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brachycephalic airway syndrome

  • Stenotic nares, elongated soft palate, everted laryngeal saccules & hypoplastic trachea

  • Bulldogs & other brachycephalic breeds

  • Laryngeal edema & saccule eversion is secondary to forceful respiration

  • Stridor (& snoring)

  • Exercise intolerance

  • +/- dyspnea & cyanosis

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diseases of the pharynx & larynx

"calf diphtheria”, “roaring” in horses

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developmental anomalies

  • Palatoschisis/cleft palate

  • Choanal atresia

    • Usually seen in lamb

    • Commonly seen in camelids (obligate nasal breathers)

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Guttural pouch TYMPANY

distention w fluid and gas

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Guttural pouch EMPYEMA

distention w purulent exudate

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Guttural pouch MYCOSIS

fungal necrotizing infxn (Aspergillus sp)

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CAN HAVE ACUTE FATAL BLEEDING DUE TO EROSION OF CAROTID ARTERY

major potential consequence of guttural pouch mycosis

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non-productive, honking cough

primary sign of Canine infectious tracheobronchitis ("Kennel Cough")

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collapsing trachea

  • Dorsal ligament gets loose

  • Small breed dogs

  • Dry, honking cough

  • Dyspnea (worse w stress/exercise)

  • +/- secondary pneumonia

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pneumonia

inflammation of the lung

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fibrin

sign of acute severe injury in alveolar response to pneumonia

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cranioventral distribution

bronchopneumonia, injurious agent arrived via AIRWAYS (aerogenous)

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origination of inflammation at the broncho-alveolar junction

hallmark of bronchopneumonia

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bronchopneumonia

  • Necrosis of type I pneumocytes

  • Type II pneumocytes hyperplasia leading to epithelialization

  • Recruitment of leukocytes & other exudes - type depends on cause and severity

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predisposing factors for bronchopneumonia

  • The site of deposition of small particles

  • No mucociliary blanket - no alveolar macrophages

  • Bottleneck of clearance from alveoli

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Suppurative bronchopneumonia

  • Obstructive - due to exudates

  • Usually bilateral, cranioventral (lobar), lobular

  • ACUTELY the lungs are swollen and consolidated (filled w exudate)

    • Exudate flood & fill bronchoalveolar ducts and adjacent alveoli

  • May progress to healing w early & effective tx, potential for scarring

  • May proceed to fibrosis or abscessation if no tx

  • Necrosis & hemorrhage is common

    • If necrotic tissue is walled off by fibrous tissue, an abscess or necrotic sequestrum will result

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FIBRINOUS bronchopneumonia

  • Usually MORE severe (and more serious)

  • Usually ACUTE to PERACUTE - hemorrhage, fibrin, necrosis

  • Multiple coalescent lobules affected - LOBAR pattern

  • "MARBLED" appearance of lung

  • Prototypical example is SHIPPING FEVER IN CATTLE

  • Can be caused by aspiration

  • Secondary pleuritis common

  • Necrosis and pulmonary sequestra also common

  • COMPLETE RESOLUTION IS UNCOMMON

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pleuropneumonia

common name for fibrinous bronchopneumonia

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bronchiolitis fibrosa obliterans

adverse outcome of fibrinous bronchopneumonia

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diffuse distribution

Interstitial pneumonia, injurious agent arrived HEMATOGENOUSLY, also pulmonary edema is diffuse

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interstitial pneumonia

  • TYPICALLY DIFFUSE, BUT CAN BE DORSOCAUDAL

  • Aerogenous: primary EPITHELIAL damage

  • Hematogenous: primary ENDOTHELIAL damage

  • If you cut the lung and it looks like tuna

  • Lung fails to collapse, rubbery to meaty texture

  • In ACUTE disease there is edema and emphysema

  • Chronic disease is characterized by fibrosis

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dorsocaudal distribution

interstitial pneumonia, VERMINOUS (parasitic) pneumonia

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multifocal distribution

most often EMBOLIC via the blood stream, can be via AIRWAYS, also common w granulomatous pneumonia

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embolic pneumonia

  • HALLMARK IS RANDOM MULTIFOCAL DISTRIBUTION

  • Septic emboli lodge in pulmonary vessels, infxn spread into interstitium

  • Most common sources

    • Hepatic abscesses

    • Infected jugular thrombus

    • Valvular endocarditis

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Granulomatous Pneumonia

  • CHARACTERIZED BY THE TYPE OF INFLAMMATORY RESPONSE (NOT PORTAL OF ENTRY OR SITE OF LESION)

  • Well circumscribed, variable sized, firm nodules

  • May be mineralized (caseous necrosis)

  • Random distribution

  • May be aerogenous or hematogenous

  • THE MAIN DIFFERENTIAL IS NEOPLASIA

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Causes of granulomatous pneumonia

  • Fungi: Cryptococcus, Coccidioides, Histoplasma, Blastomyces

  • Higher bacteria: Mycobacterium, Rhodococcus

  • Foreign material: grass, ET tube, contrast media

  • Migrating parasites

  • FIP - granulomatous inflammation secondary to Ag-Ab complexes

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Actinobacillus pleuropneumonia, aspiration pneumonia, hypostatic congestion (prolonged recumbency)

causes of irregular distributions on lungs

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pulmonary hypertension

  • Increased pulmonary vascular resistance

    • Vasoconstriction of pulmonary arteries

    • Vascular obstruction

    • Volume overload

  • lead to congestion & edema

  • If long standing, fibrosis can occur

  • Almost all euths and natural deaths have this bc agonal breathing

  • Increasingly common in fed cattle and chickens

  • Cardiac disease: L heart failure, L to R shunts

  • Lung disease: hypoxia from high altitude, pulmonary fibrosis

  • Thromboembolism

  • Hypervolemia: IV fluids, etc

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Pulmonary edema

  • May be inflammatory or cardiogenic

  • Fluid accumulates in interstitium 1st

    • RESTICTS LUNG INFLATION

  • Fluid in alveoli later - occurs abruptly

    • OBSTRUCTS VENTILATION

  • Increased rate and depth of respiration

  • Loud lung sounds initially - crackles

  • W severe effects lung sounds may be diminished

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Restrictive respiratory failure

  • Anything that takes up space in chest cavity

  • Lesions in pleural cavity, mediastinum, thoracic wall

    • Pleural effusion

      • Hydrothorax, Hemothorax, Pyothorax, Chylothorax

    • Pneumothorax

    • Masses

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Obstructive respiratory failure

  • Pathology that results in REDUCED VENTILATION of the lungs

  • Can be caused by

    • Obstruction of movement of air in airways or alveoli

    • Reduced elasticity of the lung parenchyma

  • RAPID, DEEP RESPIRATIONS => HYPOXIA, HYPERCAPNIA

  • Obstruction of movement of air in airways or alveoli

    • EXUDATIVE PNEUMONIA - exudates fill alveoli (common w bronchopneumonia)

    • Pulmonary edema - when edema is in alveoli

    • Bronchitis or bronchiolitis - exudates, mucous, and hyperplastic epithelium obstruct airways

  • Ex: Feline asthma

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ARDS (acute respiratory distress syndrome)

  • SYNDROME OCCURRING SECONDARY TO MANY OTHER DISEASE CONDITIONS

  • Diffuse alveolar damage following

    • Sepsis, Burns, Pancreatitis, Major trauma/sx, Aspiration, Drugs, Inhaled toxins

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diffuse damage to alveolar wall

basic lesion of ARDS

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move sufficient volume of blood to all organs in the body

role of cardiovascular system

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epicardium

outermost layer of cardiac wall

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myocardium

thick muscular middle layer of cardiac wall

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endocardium

innermost layer which is continuous w the tunica intima of the great vessels entering and leaving the heart

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epicardium, myocardium, endocardium

3 layers of the the cardiac wall

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SA node

node that has the most frequent rate of depolarization and is therefore dominant

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mural & valvular endocardium, myocardium, pericardium

3 broad anatomic divisions of the heart

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valvular insufficiency

failure to seal or close completely

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valvular stenosis

narrowing, failure to open

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Increased VOLUME loading during DIASTOLE (PRELOAD)

valvular insufficiency results in:

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Increased SYSTOLIC workload characterized by increased PRESSURE load during contraction (AFTERLOAD)

valvular stenosis results in:

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Vegetative ENDOCARDITIS

  • More common lesion of myocardium

    • Bacteria seeded out on endothelium (cause ulcer=> clot)

      • Fibrin forms, leukocytes

        • Thickens valves, cause incompetency

  • May result in embolism

  • Scarring can distort valve leading to insufficiency or stenosis

  • Gross lesion: ROUGH, YELLOW/TAN/GREY/RED, FRIABLE LESIONS ON VALVE, SOMETIMES ALSO MURAL ON VENTRICULAR WALL

  • Histo lesion: fibrin, leucocytes, bacteria

  • Pathogenesis: BACTEREMIA => endothelial injury/turbulence/hypercoagulability => bacterial adherence to valve, clot material forms => proliferative inflammatory lesions

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ENDOCARDIOSIS

  • common in dogs

    • Small or medium breed dogs

    • Males > females

  • Degenerative thickening of the valve typically produces incompetency w regurg and leads to CHF

  • Leads to incompetence

  • Left AV valve is most commonly affected

  • NOT febrile

  • Gross lesion: THICK, SMOOTH, WHITE, OPAQUE NODULES

  • Histopath lesion: myxomatous degeneration

  • Regurgitation => L atrial dilation & ventricular dilation => ECCENTRIC hypertrophy

  • LV dilation worsens due to decrease CO => increase RAS => increase blood volume which increases preload

  • Can have tendon chordae rupture

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responses of the myocardium to injury

myocardial infarction, change in mm mass or dimension, replacement fibrosis, dysrhythmia, dilated ventricular lumen accompanied by a nx to thin ventricular wall, increase in ventricular wall thickness or mass

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Dilated ventricular lumen accompanied by a nx to thin ventricular wall

  • Commonly reflects increased preload on the heart

  • Due to AV or semilunar valvular insufficiency or a vascular shunt

  • In the absence of an inciting cause, dilated cardiomyopathy should be considered

  • Myocardial contractility diminishes

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increase in ventricular wall thickness or mass (hypertrophy)

  • Associated w increased afterload

  • Due to stenotic valve, shunt btwn chambers or great vessels, or increased peripheral resistance

  • Commonly secondary to hyperthyroidism in cats

  • If no obvious cause for hypertrophy then primary myocardial disease, such as hypertrophic cardiomyopathy, should be considered

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DISTURBANCES OF IMPULSE FORMATION OR IMPULSE CONDUCTION

  • Arise from injury to atrial and ventricular MYOCYTES

    • Causes include electrolyte disturbance, coronary arterial thrombosis or embolism, nutritional deficiencies, bacterial and viral infxns, and toxins esp plant toxins

    • ECTOPIC PACEMAKERS often arise from cells in close proximity to necrotic/apoptotic myocytes

      • Irritable myocytes that are adjacent to area of injury, they develop a rhythm of depolarization that is different than the SA node

  • The predominant alteration in HR and rhythm are an increased rate and an erratic rhythm (TACHYARRHYTHMIAS)

  • Resulting from diseases of sinus node, conducting fibers - the intra-atrial conduction pathways, AV node, common bundle, R and L bundle branches, purkinje fibers

    • Can result in a decrease or an absence of impulse conduction

    • Manifest as various forms of bradyarrhythmias (heart block)

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depression in cardiac output

arrythmia due to these disturbances causes erratic filling and contraction , leading to a _______

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depressed myocardial contractile strength

Decrease in ventricular myocardial contractile critical mass

  • Eg massive myocardial necrosis

Ineffective contraction w sufficient ventricular myocardial mass

  • Eg dilated cardiomyopathy, esp in dogs and cats

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impeded blood flow

  • Occurs w stenosis (narrowing) of the AV or semilunar valves

  • Results in either a restriction of blood flow form one chamber to another (atrium to ventricle), or from a ventricle to the major arteries

  • Results in increased systolic workload (afterload) on the affected chamber

  • Stenotic valves can also be mildly regurgitant/insufficient

  • Stenosis can either be congenital or acquired

    • Distorting fibrosis secondary to scarring of valvular endocarditis is a common form

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regurgitant blood flow

  • Due to effaced AV and semilunar valve structure (INSUFFICIENT)

  • There is backflow of blood from ventricle to atrium or from a great vessel back to its ventricle

  • Increased diastolic load (preload)

  • Can be

    • Congenital (eg congenital mitral insufficiency)

    • Acquired (eg healed endocarditis or endocardiosis)

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abnx pattern of blood flow (shunted blood flow)

  • Commonly congenital in origin

    • Patent ductus arteriosus

    • Patent foramen ovale/atrial septal defect

    • Ventricular septal defect

  • Pathophysiology is complicated

    • May result in variable changes in both preload and afterload

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response to reduced cardiac output

  • Compensatory mechanisms work to maintain tissue perfusion

    • Changes in mm mass & HR

    • Peripheral vascular changes mediated by the renin-angiotensin-aldosterone system

      • Maintains tissue perfusion by

        • Increasing blood volume, via renal retention of Na & water

        • Increased peripheral resistance via arterial constriction

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stroke volume and HR

Cardiac output dependent upon:

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myocardial contractility, preload, and afterload

Stroke volume dependent upon

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Activation of neuro-hormonal mechanisms due to decreased cardiac output

  • Increased sympathetic tone

    • Increased HR

    • Stronger contractions

    • Peripheral vasoconstriction

  • Renin-Angiotensin System

    • Peripheral vasoconstriction

    • Increase ADH => water retention

    • Increase aldosterone => Na (and water) retention

  • W excessive or prolonged response, increased workload and CARDIOGENIC EDEMA can result

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