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Functional Physiology
- --Systemic Arterial BP
- --Adequate Tissue Perfusion
- --Venous BP
- --Also review:
- Systolic function
- --Preload
- --Afterload
- --Contractility
- Heart Rate
Diastolic Function
- --Factors affecting the above
- --Further Review:
Heart Failure and its Classification(HF)
- --1. Forward versus Backward
- --2. Acute versus Chronic
- --3. Sec. to Myocardial Failure
- --4. Sec. to Left to Right Shunts
- --5. Sec. to Severe Regurgitation
- --6. Sec. to Pressure Overloads
EKG: Technique and Interpretation
Radiography of CVs: Techniques(Survey/Contrast)
Selective Catheterization, Echocardiography,
Phonocardiography, and INTERPRETATION
Minimum Data Base should include:
6.2.1 Signalment
- Primary Complaint
- Clinical History
- Physical Exam
- Clinical Lab. Profile
- EKG
- Thoracic Radiography
- Other Ancillary Tests:
- Phonocardiography
- Echocardiography
- Cardiac Catheterization
- --Selective/Non-selective angiography
- --Pressure Recording & Differentials
- --Cardiac Output measurement
- --Oximetery
6.2.1 SIGNALMENT:
AGE:
Young:
Congenital
Old:
Acquired BREED
Poodle
PDA
E. Bulldog:
Pulmonic Stenosis
Boxer:
Neoplasia
Newfoundland:
Sybaritic Stenosis
Great Dane:
Cardiomyopathy SEX: Less significant
Females:
PDA
Male Cats:
Cardiomyopathy
Male Cocker Spaniels:
Valvular Insuff 6.2.2 HISTORY:
- Should include:
- Current Complaint
- Onset and Duration
- Pertinent Past Disorders
- Environmental details Vaccinations
- Hereditary/Family History
- Medications Currently on and Response
- Attitude and Behavior
- Activity, Excerise tolerance
- Appetite: Food type & water consup.
- Elimination habits
- Seizures or fainting episodes
- Coughing, Vomiting Sneezing
- Ambulation, Dyspnea
- Weight fluctuations
- Edema/Swelling
- Poor growth or Performance
- Try to differentiate between Cardiac and Pulmonary Problems
6.2.3 PHYSICAL EXAMINATION
- Evaluate the entire animal
- Identify all the problems
- Cardiovascular problems need further exploration and delineation from pulmonary problems
6.2.4 OBSERVATION/INSPECTION:
Starts from waiting room
- -Abn. in gait, attitude, appearance, posture.
- -Refusal to lie down, abducted elbows, flared nostrils open mouth breathing.
- -Rate, rhythm and depth of respiration
- -Dyspnea-inspiratory/expiratory?
obstructive/restrictive
- -Coughing-its character, sneezing, or wheezing
- -Ascities, edema-its location
- -CRT & Color of m.m.& comparison
- -Jugular distention
6.2.5 PALPATION:
Evaluate
- -Shifting of Point of maximum intensity(PMI) of the heart beat, cardiac thrill
- -Abd. palpation and contour, fluid waves?
- Abnormalities in femoral pulses-in rate.
- rhythm, intensity. Compare to HR.
6.2.6 PERCUSSION:
- -Cardiomegaly,hyperresonance.fluid waves
6.2.7 AUSCULTATION:
All areas of the heart and lungs are to be evaluated. Evaluated heart over the pulmonic, aortic, mitral and tricuspid area:
Area
Canine Location Feline Location
Pulmonic
L 2-4; ICS just above sternum
L 2-3; ICS; junction. upper & mid. 3rd
Aortic
L4: ICS above Costo-chond.
L 2-3; ICS dorsal Junc. to pulm. area
Mitral L5;ICS at CCJ
L5-6;ICS lower
1/4 of chest
Tricuspid
R3-5;ICS;CCJ
R4-5;ICS;at lower1/4 of chest
SI:
- -Louder, Longer, duller and lower pitched than S2
- - Heard loudest our the mitral area
- - Its intensity may:
Increase in tachycardia, fever, fear & cachexia
Decrease in obesity, pericardial or pleural
effusions, thoracic masses, DH, bradycardia & insuff. ventricular fillings.
Vary with arrhythmias e.g A-fib., V-Tech.,
APC, VPC and marked sinus arrhythmias
- -May split in large breeds, RBBB or VPC
- -Occurs at the down stroke of QRS
S2:
- -Short high pitched & sharp
- -Heard loudest over base of the heart at aortic area
- -Splitting caused by
Delayed closure of pulm. valve over aortic valve. Seen in pulm. hypertension as in heart worm disease. RBBB, VPC originating from left ventricle, ASD and Pulm. stenosis
Delayed (paradoxical) aortic valve closure though uncommon) e.g LBBB, VPC from Rt.
vent, sybaritic stenosis, severe systemic hypertension and LV failure
- -Occurs near the end of T wave
S3:
- -Occurs during diastole, between S2 & S1 before the P wave
- -Best heard over mitral area. of lower pitch than S2
- -Presence indicates HF, dilated vent., congestive cardiomyopathy or decomp. mitral insuff.
S4:
- -Heard best at the L-base, often at L-apex too
- -Occurs due to ventricular diasystolic dysfunction e.g. HCM or vent hypertrophy
- -Is generated by atrial contract in the P-R interval Gallop Rhythm:
- -Is the presence of S3 or S4 or both in the diastole
- -Is of low frequency, use the bell of the stethoscope
- -Is an early sign of HF & may precede clinical signs
Systolic Click:
- -Sounds like additional heart sounds
- -Occurs in systol between S1-S2
- -Unknown etiology a benign finding
- -Deteriorates in to mital insuff./murmur in 6-12M
- -Can be confused with gallop t=rhythm
e.g. AV valvular insuff., Semilunar stenosis
(less common) e.g aortic & pulm. regurg.
e.g. PDA, AV fistula
occupy entire systole, but S1 & S2 can be heard
Crescendo:-
starts soft and becomes loud
Decrescendo:-
starts loud and becomes soft
Crescendo-Decrescendo:-
starts soft, gets loud and ends soft
6.2.10.1 ELECTROCARDIOGRAPHY.:
- commonly employed to Dx:
- Chamber enlargement
- Arrhythmias & conduction disturbances
- Myocardial status
- Indications fpr EKG:
- -Auscultation of arrhythmias, murmurs, dyspnea, tachypnea, radiographic evidence of cHF or cardiomegaly, cyanosis, drug (digt.) evaluation
- -Non cardiac reasons like fainting, seizures, uremia, pancreatitis, neoplasia, hypoadrenocorticism, FUS, ethylene glycol toxicosis, annual exam of a geriatric patient
- -Hexaxial lead system, 3 biploar 9I, II, II) & 3 augmented unipolar (AVR, AVL, AVF), with animal in Rt. lateral recumbency, limbs perpendicular to the body and clips attached at olecranon and stifle, is the widely used system to determine MEA in frontal plane.
- -Ketamine & Valium in lower dosages could be used for restraint in excitable animals.
- -Avoid over interpretation of EKG and artifacts.
- -Check alteration in rhythm, sequence, duration, amplitude, slurring or covering, deviation in isoelectric line and MEA
6.2.10.2 RADIOGRAPHY:
Survey Views:
- -Two views at 90 degrees to each other (Lat & VD) are the absolute minimum.
- -The images are evaluated for deviations in terms of size, shape, density, location & vascular confirmation.
Cardiac catheterization:
- a) Non selective I/V angiocardiography:
- -Jothalamate meglumine @ 1 ml/kg is injected through Rt. juglar with animal in left lateral recumbency.
- -Can be used to detect chamber size, thromboembolic disease, vascular/valvular stenosis, post stenotic dilatation, septal defects and shunts.
- b) Selective angiography:
- Indicated to:
- -confirm a suspected lesion
- -define its anatomic & physiologic severity
- -detect presence/absence of assoc. abnormalities
- -measure pressure, cardiac output, oxygen tensions
6.2.10.3PHONOCARDIOGRAPHY:
- -Provides graphic display of heart sounds
- -Permits definitive identification of S3, S4, split S2 and systolic ejection sounds & clicks.
- -An EKG is recorded simultaneously.
6.2.10.4 ECHOCARDIOGRAPHY:
- -Uses the imaging capabilities of ultrasound to identify and evaluate various cardiac structure & abnormalities e.g pericardial effusions, valvular vegetations, atrial & ventricular dilatation/hypertrophy, and abnormal cardiac motion.
- -M (motion) mode can help measure the thickness, size and excursions of the cardiac chambers and valves.
- -M mode cant image AV insuff., septal defects and regional ventricular dysfunctions. However recognition of assoc. cardiac changes combined with I/V administration of contrast agent can help circumvent above limitations.
MISCELLANEOUS DIAGNOSTICS:
- -CBC, Chemistry, Blood gases, Acid-Base, Anion Gap
- -CVP, Arterial pressure
- -Pericardiocentesis, contrast GI studies.
6.3.1 PATENT DUCTUS ARTERIOSUS:
The most common congenital heart disease. Has a polygenic mode of inheritance.
6.3.1.1 ETIOPATHOGENESIS:
- -Failure of the 6th aortic arch to achieve a functional closure in the immediateprenatal period, resulting in a L-R shunt.
- -Continuous shunting of blood from aorta to main pulm. artery, results in
- a) volume overload
- b) subsequent dilation of the left side of the heart,
- c) resultant mitral insuff. thereby contributing to pulm. venous congestion. pulm. edema and pronounced dyspnea, tachypnea, coughing and other resp. signs
- -Increased shunting through pulm. vasculature may cause initial fibrosis and muscular hypertrophy resulting into increased pulm. resistance and hypertension thereby causing reversed or bidirectional shunting of blood through the ductus
- -In reversed PDA unoxygenated blood is mixed with oxygenated aortic blood and shunted to the caudal areas of the body resulting in differential cyanosis, chronic renal bypoxemia, increased erythropoietin levels and polycythemia.
6.3.1.2 CLINICAL PRESENTATION AND SYMPTOMS:
BP:
Poodles, Spaniels, G. Shep., Yorkies, Pomeranians, Collies, Shelties.
SIGNS:
- -Variable. None in the beginning
- -Exercise intolerance, tachypnea, cough and other progressive resp. problems due to L-sided backward H. failure.
- -Continuous machinery murmur in the lower L-3. I/C space which may radiate to R base. Presence of pericardial thrill, holosystolic S2 murmur, hyperkinetic pulse and pink m.m. are evident unless reverse shunting supervenes where differential cyanosis predominates.
- -Death occurs at an early age in untreated animals.
DIAGNOSIS:
- -BP, history & PE, CBC, Blood gases
- -EKG: LVH with wide P. Very tall R & deep Q waves and S-T segment deviation.
- -Echocardiography. LH enlargement. Dilation of pulm. trunk and ductus image is sometimes visible.
- -Radiography: LHF with L atrial and L auri, enlargement, pulm. over circulation and edema. Aortic bulge
- -Contrast angiocardiography: L-R shunting of opacified blood through the ductus. Mitral or pulm. Valvular insuff.
Cardiact catheterization: Higher blood oxygen levels in pulm. artery Vs. R vent. and increased pressure reading in various cardiac chambers.
TREATMENT:
- -Surgical ligation of L-R shunt as early as possible (2-4 M)
- -Uncomplicated cases, on surgical correction, are expected to have a normal life span.
- -Complicated cases of L-R PDA with L sided HF need additional medical management.
PROGNOSIS:
- -Excellent to good in young and uncomplicated cases.
- -Without surgery 60% die in first year post-diagnosis.
SURGICAL TECHNIQUE:
- -L-4 I/C thoracotomy
- -Reflect the lungs and identify the ductus coarsing/communicating between the aorta and pulm. art.,
- -Incise mediastinal pleura over aorta just dorsal to vagus.
Dissect it dorsally over aorta and ventrally over the pulm. art., The ventral mediastinal flap along with vagus may be tagged with a 3/0 stay suture and retracted
- -Dissect aorta loose from the surrounding areolar tissue along its dorsal and R-medial borders.
- -A R- angled Mixter forceps or a Halstead mosquito forceps are passed medially around the ascending aorta proximal to PDA and a 2/0-0 non-absorbale suture (e.g. silk) of 40-50 cm length is caught in the forceps at its midpoint and withdrawn so as to rest it around the medial aspect of the aorta.
- -The same forceps are passed in a similar manner around the descending aorta caudal to the PDA. The free ends of the suture are caught in and withdrawn by the forceps thereby seating the suture loop on the R-side of PDA.
- -The loop is divided to form two free strands. One strand is tied so as to ligate the PDA as close to the aorta as possible.
Next the 2nd strand is tied to ligate the pDA again close to the pulm..art.,
- -Routine thoracotomy closure. Maintain negative pleural P.
POST-OPERATIVE PATIENT MONITORING:
- -Repeat radiographs & EKG before discharge.
- -Monitor EKG every 6 M.
6.3.2 PERSISTENT RIGHT AORTIC ARCH
6.3.2.1 ETIOPATHOGENESIS:
- -A developmental anomaly where aorta is formed by the R-4 aortic arch instead of the usual L-4.
- -Results into the entrapment of esophagus and trachea in vascular ring comprised of aortic arch on the right, base of the heart ventrally, pulm. art. and ligamentum arteriosum on the left, and dorsal aorta dorsally.
- -Results in regurgitation of food and sec. aspiration pneumonia.
6.3.2.2 CLINICAL PRESENTATION AND SYMPTOMS:
BP:
- Doberman, Great Dane, Irish setter, Weimaraner.
SIGNS:
- -Regurgitation after eating. Starts at weaning on a diet of solid or semi-solid food
- -Thin, emaciated, malnourished animal with ravenous appetite.
DIAGNOSIS:
- -Signalment & History, and survey thoracic radiograms.
- -Barium swallow esophagram confirms distended esophagus cranial to the base of the heart.
- -R/O other causes of mega-esophagus.
TREATMENT:
- Surgical division of ligamentum arteriosum between two ligatures
- Free esophagus from the surrounding mediastinal adhesions
- Follow surgical procedure as (nearly) outlined in PDA
POST-OPERATIVE MANAGEMENT:
Frequent feeding of semisolid or gruel consistency of feed at table-top level with animal standing on its hind legs.
6.3.3 PULMONIC STENOSIS
6.3.3.1 ETIOPATHOGENESIS:
- -One of the most common congenital cardiac disorder with multifactorial etiology.
- -Most cases are moderate to severe(grade 2) with subvalvular or valvular lesions.
- -Resultant outflow (blood) obstruction causes Rt. ventricular concentric hypertrophy, decreased CO, syncope, CHF, and subsequent tricuspid regurgitation. Rt. atrial dilation, and increased potential for atrial arrhythmia.
- -Turbulent blood produces both the murmur and the post stenotic dilatation of pulm. art.,
- -Concentric ventricular hypertrophy may limit coronary blood flow resulting into myocardial infarction, arrhythmia and sudden death.
6.3.3.2 CLINICAL PRESENTATION AND SYMPTOMS:
BP:
- Bengal, Fox terrier, English bulldog, Chihuahua, Samoyed, Schnauzer, Boxer.
SIGNS:
- -Asymptomatic to mild exercise intolerance to syncope to Rt-sided CHF i.e. jugular pulsation, hepatic enlargement, ascites etc.
- -Systolic, crescendo-decrescendo murmur of varied intensity, IV/V to VI/VI, at L 2-3, I/C at heart base. It radiates up toward scapula and to Rt. chest at heart base.
6.3.3.3 EKG:
- -Rt. axis deviation (120+), P-pulmonale, sT segment deviation, A-Fib.
6.3.3.4 RADIOGRAPHY:
- -RV & Rt, atrial enlargement, Normal to hypoperfused lungs .Post stenotic dilatation on DV views
6.3.3.5 CARDIAC CATHETERIZATION:
- -Pressures: Increased RV end diastolic and Rt. atrial
- Pressure drop across pulm. valve area.
- -Contrast angiography: Selective RV injection confirms the stenosis and post-stenotic dilatation. Nonselective?
6.3.3.6 ECHOCARDIOGRAPHY:
- -Concentric RV hypertrophy, thickened pulm. valves, post-stenotic dilatation.
- -Doppler study demonstrates pressure gradients/ differentials
6.3.3.7 DIAGNOSIS:
- -PE, BP, Signs & symptoms, EKG, Radiography, Pressure gradients, Echocardiography and Catheterizations etc.
- -R/O: Atrial septal defects, dirofilarisis, tetralogy of Fallot, and aortic stenosis.
6.3.3.8 TREATMENT:
- -Supravalvular stenosis repaired by a bypass conduit.
- -Valvular or subvalvular stenosis by:
- Inflow occlusion-pulm. arteriotomy in mature animals.
- Patch graft technique for immature animals.
- Bistoury or modified Brock procedure or Valve dilator
- technique or Balloon valvoplasty.
6.3.3.9 INDICATIONS FOR SURGERY:
- -Severe RV hypertrophy to syncope to CHF
- -RV pressure or gradient of 100+ mm Hg. across the valve in mature animals.
- -RV pressure of less than 70 mm and gradient of less than 50 mm Hg does not require surgery.
6.3.3.10 SURGERY:
Patch technique:
- -Left 4, I/C thoracotomy (6, I/C in cat)
- -Incise an elliptical pericardial graft 1.5 times wider than the diameter of pulm. artery, ventral to the pherenic nerve, and store in physiologic saline until needed
- -A curved atraumatic needle with a 3/0 multifilament steel wire suture is inserted through the RV wall into the RV, up the pulm. (valves) outflow tract and out of the pulm. artery.
- -Absorbable 3/0-4/0 purse-string sutures are (pre?) placed at the points of entrance and emergence of the needle to control hemorrhage.
- -The wire is positioned over the RV and pre- harvested pericardial patch is sutured, with sutures placed 2 m m apart, from the pulmonary art. to the RV tenting it over and covering the outer limb of the wire suture. The wire ends emerge through a 2-3 mm gap at the lower ventricular edge of the graft where a horizontal mattress suture is placed through the patch and left untied.
- -The outflow tract and valve are opened by withdrawing the wire with a sawing motion. The horizontal mattress suture is tied after pulling the wire suture through the gap.
- -Routine closure of thoracotomy incision.
6.3.4 AORTIC STENOSIS
6.3.4.1 ETIOPATHOGENESIS:
- -Subvalvular aortic fibrosis is the most common congenital, autosomal dominant, defect of the large breed dogs.
- -Resultant LV outflow obst. causes pressure overload leading to LV concentric hypertrophy, myocardial ischemia, ventricular arrhythmia and sudden death.
- -Stroke volume drops due to impaired ventricle inflow and outflow accompanied by papillary M. and subendocardial fibrosis and mineralization.
6.3.4.2 CLINICAL PRESENTATION AND SYMPTOMS:
HISTORY:
- -Dyspnea, exercise intolerance, syncope, collapse, sudden death.
BP:
- -Newfoundland, German Shepherd, Boxer, Golden retriever, German short hair pointer, Rottweiler etc.
SIGNS:
- -Crescendo-decrescendo systolic murmur, heard best at left base of the heart, radiating to thoracic inlet and neck along with weak femoral pulses and signs listed in history.
- -Mitral insuff. secondary to LV outflow obstruction
6.3.4.3 EKG:
- -L-axis deviation, LV hypertrophy (tall & wide qrs), ST segment deviation, tall T waves and disarrhythmia.
6.3.4.4 RADIOGRAPHY:
- -LV enlargement, loss of caudal waist, cardiomegaly, post- stenotic dilatation, LH failure.
6.3.4.5 CARDIAC CATHETERIZATION:
Pressures: -LV outflow tract pressure gradient of more than 70 mm (100-220 mm)Hg.
- -Higher the gradient lesser the chances of survival.
- -May be asymptomatic at less than 50 mm.
Contrast angiography: -Radiographs taken 6-8 sec post I/V injection will image the post stenotic dilatation.
6.3.4.6 ECHOCARDIOGRAPHY:
- -helps visualize the obstructing band, ventricular and septal hypertrophy.
- -Aortic valve is thickened, diminished in range of motion and may appear to flutter in systole.
- -Doppler study may help detect turbulence and regurg. assoc. with concurrent mitral & aortic insuff.
6.3.4.7 DIAGNOSIS:
- -BP, History, pE, EKG, Radiography, Chamber pressures & gradients, Echocardiography.
- -R/O. Pulmonic stenosis, Septal defects.
6.3.4.8 TREATMENT:
- -Beta adrenergic blocking agents.
- -Limited success with surgery. Techniques advocated are:
- Balloon angioplasty
- -Valvular Dialator
- -Bistoury technique
- -LV-aortic conduit bypass
VALVULAR DILATOR TECHNIQUE:
- -L-5, I/C thoracotomy.
- -Incise pericardium parallel to long axis of the heart starting the incision just below the pherenic nerve towards the apex.
- -Place a purse-string suture (one and a half cm. in diameter) deep into the myocardium at the left ventricular apex using a 2/0 abs. suture.
- -Make a stab incision about 1 cm long in the center of the purse-string suture and insert the valve dilator into the ventricle and carefully advance it till the tip of the dilator is palpated in the aorta.
- -The dilator is progressively opened till it tears the subvalvular fibrous ring, whereupon it is removed and the purse-string suture is tightened.
- -Thoracotomy is routinely closed.
6.3.5 FELINE AORTIC EMBOLISM
6.3.5.1 ETIOPATHOGENESIS:
- -A wide spread but uncommon major arterial disease occurring secondary to underlying feline cardiomyopathy.
- -The embolus may originate from atrial or ventricular chambers and lodges at aortic termination.
- -Clot generates vasoactive substances which block collaterals.
6.3.5.2 CLINICAL PRESENTATION AND SYMPTOMS:
- -Sudden onset of pain, posterior paresis/paralysis.
- -Distress, shock, constant crying, absence of femoral pulse.
- -Affected limb(s): cooler, swollen, ischemic, cyanotic foot-pads and nail-beds, spastic gastrocnemius muscle(s).
- -Cardiac murmur or abn. heart sounds on auscultation.
- -Hematology may show slight hemoconcentration
- -Clinical chemistry is normal or has elevated muscle enzymes
6.3.5.3 EKG:
- May show LV hypertrophy, arrhythmias, incomp. LBBB.
6.3.5.4 RADIOGRAPHY:
- -Hyportrophic or dilated cardiomyopathy.
- -Venous angiography demonstrates the aortic blockage.
6.3.5.5 DIAGNOSIS:
- -History, PE, EKG, Radiography
- -R/O: Traumatic injuries, spinal compression
6.3.5.6 TREATMENT:
- -Surgical removal of the embolus with in the first 4-6 hrs. yields best results.
6.3.5.7 SURGERY:
- -Atropine and thiopental induction, isoflurane maintenance.
- -R/L fluids spiked with soda-bicarb. (1 ml/10ml)
- -Dorsal recumbent position with lumbar elevation
- -Caudal linea-alba incision
- -Pack off intestine cranially and incise the parietal peritoneum to expose aorta and illacs.
- -Apply a bulldog clamp/umbilical tape cranial to the embolus
- -Heparinized the cat (1 mg/lb). Open the aorta over the embolus and remove the obstruction
- -Temporarily slacken the clamps to flush out remaining tiny emboli
- -Suture the aortotomy with 6./0-7/0 monofilament polypropylene in a simple continuous/interrupted fashion
- -Confirm presence of femoral pulses(s) before abdominal closure
6.3.5.8 POSTOPERATIVE MANAGEMENT:
- -Maintain a volume/osmotic diuresis
- -Heparin therapy, @ 10-15 mg tid, to continue for next 48 hrs.
- -Antibiotic Rx for 10-14 days
- -Aspirin 75 mg every 72 hrs for long term RX.
- -Manage primary cause of cardiomyopathy.