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188 Cards in this Set

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What are the two cardiac function components that result in the heart working as a pump?
Muscular (mechanical) & Rhythmic (electrical)
Describe the normal DIASTOLIC phase of the cardiac cycle.
1) Filling of ventricles via active suction

2) short pause

3) Filling of ventricles via atrial contraction
What occurs during SYSTOLE?
Heart contracts to eject blood.
Mitral regurgitation leads to what kind of overload?
VOLUME overload
What are the results of the volume overload produced from Mitral Regurg/Insufficiency?
Activation of compensatory mechanisms via baroreceptors to preserve asymptomatic state.

RAAS --> Vasoconstriction, Na retention

Increase SNS

All leading to Eccentric (Outward) Ventricular hypertrophy.
Subaortic stenosis leads to what kind of overload?
PRESSURE overload
What are the results of the pressure overload produced from subaortic stenosis?
Activation of compensatory mechanism to preserve asymptomatic state....RAAS, increase SNS resulting in CONCENTRIC (inward) ventricular hypertrophy
What are the 6 tools for finding cardiac patients in vet med?
1) Signalment, chief complaint, Hx
2) PE
3) Thoracic rads
4) ECG
5) Echo
6) Blood indicators (biomarkers)
What causes the sound of a heart murmur?
TURBULENCE which can be from:
Valve leakage, narrow outflow, abnormal opening b/w hrt chambers, physiologic murmur (anemia, growing animals)
What is a Gallop sound?
A third heart sound heard with the bell of the stethscope indicating heart failure is imminent or present.
Define Arrythmia.
Irregular heart beat. Maybe be normal or abnormal
What is a pulse deficit?
Missing pulse during an audible heartbeat. Doesn't mean a weak pulse!!
Define the difference b/w Pulmonary Edema and Pleural Effusion.
Pulmonary Edema: effusion of serous fluid into pulmonary interstitial tissue and alveoli, preceeded by pulmonary congestion.

Pleural effusion is the accumulation of fluid in the space b/w the membrane encasing the lung and that lining the thoracic cavity.
What is the best clinical test to evaluate lungs?
Thoracic rads.
What is an echo good at and what is it not so good at?
Good = assessment of cardiac structure and function

Bad = impact of a cardiac lesion on whole body, patient well-being.
Myxomatous mitral valve disease AKA Tricuspid endocardiosis, etc is the most common heart disease of dogs. T/F
True
What is Myxomatous mitral valve disease? What species is it most common in?
MMVD is the sterile degenerative process of the AV valves resulting in valvular regurgitation. 80% occur in the mitral valve.

Most common in dogs and heart a systolic murmur in the left apex (caudally).
Please state the age groups that Myxomatous Mitral Valve Disease commonly affects and some specific breeds.
Middle aged to older; Cavalier King Charles, Min Schnauzer, poodle, etc
What should you do to treat Myxomatous Mitral Valve Disease in the early, compensated stage?
NOTHING! Recheck in 6-12 months, instruct oweners to watch for L CHF, avoid overzealous IV/SQ fluids, etc
What is the evolution of myxomatous mitral valve disease?
Progressive endocardiosis --> compensatory mechanism preserve to keep in asymptomatic state --> progression beyong compensatory capacity --> CHF
How to you treat Myxomatous MV dz and CHF if acute and if chronic?
Acute: Diuretics and O2 supp if needed.

Chronic: Diuretics, ACE Inhibitors +/- pimobendan.
What is Bacterial Endocarditis?
Infection involving the inner lining of the heart either within a heart chamber (very rare) or of a heart valve. Due to Bacti, fungi, etc that can be from various medical & sx procedures (e.g. oropharynx, GIT, IV cath, immunosuppressive drugs, dental manipulations)
What is the sequela of Bacterial Endocarditis?
Vegetative lesions form on the valves (aortic and mitral) causing deformation of the valves resulting in heart murmur (diastolic at L heart base (aortic valve) or systolic at left apex (mitral valve)).

This then leads to seeding of the circulations showing fever, thromboemboli, polyarthritis, arrhythmias, immune mediated dz.
What clinical pathology changes do you note with bacterial endocarditis?
CBC: leukocytosis, anemia
Biochem: Organ involvement
Urinalysis: proteinuria
How many samples should you collect for blood culture of bacterial endocarditis?
3 samples - yield is proportional to volume collected. Bacteremia is classically precedes recurrent fever by 1-2 hrs.
What are some of the common pathogens that can result in bacterial endocarditis?
Strep, staph, E coli, Erysipelothrix rhusiopathiae, Bartonella
Define Cardiomyopathy and name the 3 different types.
"Disease of the heart muscle tissue."

Hypertrophic, dilated, restrictive
What is the most common heard disease of cats?
Hypertrophic cardiomyopathy (16% of all cats).

Thickening of the left +/- R ventricle. Stiff.
What is the fundamental problem of HCM?
Ventricle fails to accept incoming blood, ventricular chamber is smaller, leading to crowding caused by hypertrophy.
What is the result of HCM?
Increased pressure in blood vessels that feed into hypertrophied part of the heart = PULM EDEMA & PLEURAL EFFUSION

Poor Blood Supply to Myocardium = ARRHYTHMIAS

Atrial enlargement/distortion, sluggish blood flow = THROMBOEMBOLIC DISEASE
What are the two phases of HCM?
Compensated and Decompensated
What do you usually find with compensated HCM?
Heart murmur, cardiomegaly, anesthetic complications, tachycardia, 3rd hrt sound
What do you usually see with decompensated HCM?
Increased resp effort w/o obvious cause, lethargy, loss of appetite, heart murmur, weak pulse, tachycardia +/- arrhythmia, pale mm, ascites (rare)
What do you see on thoracic rads in an decompensated HCM patient?
Pleural effusion, Pulm edema, pulmonary venous congestion, may see cardiomegaly, etc
How do you confirm if a feline patient has HCM?
Echocardiogram (will provide info on type of cardiomyopathy and severity)
What is the suspect cause of HCM in feline patients?
Mutation of myosin-binding protein C +/- others
How long can a cat go without showing CS of HCM?
Years.
Even though a cat with confirmed HCM is reccommended to be treated with a B-Blocker such as Atenolol, should you ever treat a cat with just a heart murmur with such a drug?
NO! Don't treat a murmur with B-Blockers
What are the requirements of B-Blocker treatment in feline HCM?
Tachycardia, tolerant cat and diligent owner
Why would you not treat a cat with a murmur alone with a B-Blocker?
Because B-Blockers will upset the dynamic RV outflow tract obstruction(DRVOTO) that is a common, non-pathologic cause of murmurs in cats
What drugs should you consider for an asymptomatic HCM cat?
Anticoagulants.
When should you consider using an Anticoagulant in an HCM cat?
When there is an increased risk of thromboembolism (atrial enlargment & past history)
What treatment options should you consider with a cat in the decompensated stage of HCM?
Furosemide, ACE inhibitors, B-Blockers, Low salt diet, supplements. DO NOT USE DIGOXIN or PIMOBENDAN
What is Restrictive/Unclassified Cardiomyopathy?
An inflitration within the ventricular walls (myocardial form) or the thickening of the endocardium (endocardial form) that leads to a loss of pliability of ventricular walls = Stiff!

The demonstratable restriction to ventricular inflow (Doppler echo). Unclassified is not able to be demonstrated but is inferred. Consequences of the 2 are the same.
What occurs to the atria and ventricles with Restricted Cardiomyopathy?
Marked Atrial enlargement (increasing the risk for blood clot formation and thromboembolism)

Ventricles accept incoming blood with difficulty (Diastolic dysfunction...risk of CHF)
What are the typical findings of Restricted Cardiomyopathy?
Signs of aortic thromboembolism, pulm edema and pleural effusion, dyspnea, arrhythmias, heart murmur (rare)
What findings on a echo confirm Restricted Cardiomyopathy?
marked bilateral enlargement, myocardium and endocardium may be abnormal, ventricular dimensions WNL
What is the prognosis for Restricted cardiomyopathy?
Fair at best, recurrence is common and dz often detected at advanced stage
What is the other name for Boxer Cardiomyopathy?
Arrhythmogenic right ventricular cardiomyopathy
What makes Boxer cardiomyopathy so special?
Only cardiomyopathy that produces arrhythmias but no gross structural changes. Echo is normal and effect is only at a microscopic level that occurs as life threatening before visible changes.
What are the first manifestations of Boxer cardiomyopathy?
Syncope, sudden cardiac death, incidental discovery of premature ventricular contraction.
What does the diagnositc evalution of Boxer cardiomyopathy reveal?
Not much - maybe arrhythmia/PVC
What is the underlying mechanism of Boxer cardiomyopathy?
Degeneration of myocytes with replacement by fibrofatty tissue that is highly arrhythmogenic.
Treatment options for Boxer cardiomyopathy?
Sotalol and omeg-3 FA
What are the typical findings of Restricted Cardiomyopathy?
Signs of aortic thromboembolism, pulm edema and pleural effusion, dyspnea, arrhythmias, heart murmur (rare)
Outcome of Boxer cardiomyopathy?
recurrent sycope despite trt, sudden death.
What findings on a echo confirm Restricted Cardiomyopathy?
marked bilateral enlargement, myocardium and endocardium may be abnormal, ventricular dimensions WNL
What is the prognosis for Restricted cardiomyopathy?
Fair at best, recurrence is common and dz often detected at advanced stage
What is the other name for Boxer Cardiomyopathy?
Arrhythmogenic right ventricular cardiomyopathy
What makes Boxer cardiomyopathy so special?
Only cardiomyopathy that produces arrhythmias but no gross structural changes. Echo is normal and effect is only at a microscopic level that occurs as life threatening before visible changes.
What are the first manifestations of Boxer cardiomyopathy?
Syncope, sudden cardiac death, incidental discovery of premature ventricular contraction.
What does the diagnositc evalution of Boxer cardiomyopathy reveal?
Not much - maybe arrhythmia/PVC
What is the underlying mechanism of Boxer cardiomyopathy?
Degeneration of myocytes with replacement by fibrofatty tissue that is highly arrhythmogenic.
Treatment options for Boxer cardiomyopathy?
Sotalol (Class III Antiarrythmic and K+ Channel Blocker) and omega-3 FA
Outcome of Boxer cardiomyopathy?
recurrent sycope despite trt, sudden death.
Please describe Dilated Cardiomyopathy. What species is it more common in?
Enlarged but thin ventricles, poor contractility. Fundamental problem is that the ventrilces weaken and become thin and then poor contractility results and there is then a poor forward flow of blood, poor acceptance of incoming blood. Still see marked enlargement of the ventricles. Common in dogs
What do the thin walled ventricles and subsequent poor contractility of DCM result in?
Increase pressure in the BV that feed into the hypertrophied part of the heat = PULM EDEMA & PLEURAL EFFUSION.

Poor blood supply to myocardium = ARRYTHMIAS

Atrial enlargement, distortion and sluggish blood flow = THROMBOEMBOLIC DZ
What do you see as client chief complaints with DCM?
- Increased resp effort
- Cough
- Lethargy
- Loss of appetite
What are the PE findings of DCM?
- increased resp effort
- heart murmur
- tachycardia
- weak pulse
- pale mm
- ascites
What is confirmatory evidence of DCM on thoracic rads?
- pulmonary edema
- pleural effusion
- cardiomegaly

* Can use an echo to confirm and r/o other disorders that look similar (pericardial effusion, chronic mitral valve endocardiosis, congenital heart dz)
T/F DCM produces overt Clinical Signs.
True
What are the more common causes of DCM?
- genetic
- nutrition (taurine deficiency in non-doberman dogs)
What medical treatments can be used for acute DCM?
- Furosemide
- Nitroglycerin, nitroprusside
- O2
- Centesis
What medical treatments can be used for chronic DCM?
- Lasix
- Digoxin
- Enalapril
- B blockers, Ca channel blockers
- Pimobendan
- Low Na Diet
- Taurine, carnitine, Vit E, coenzyme Q10
What are the signs and symptoms of CHF caused by?
When does CHF occur?
Hampered circulation
When compensatory mechanism are overwhelmed by progressive cardiac lesion, heart is not doing enough.
What is myocardial failure?
Muscular tissue of the hrt is exhausted, usually end stage.
Why does CHF cause fluid retention?
Circulation is compromised.
What are the 4 different manifestation of CHF?
L-sided hrt failure
R-sided hrt failure
"Backward" failure
"Forward" failure
What are the manifestations of L-sided CHF?
- pulmonary edema, pleural effusion in cats
- Dyspnea, exercise intolerance, cough
What are the manifestations of R-sided hrt failure?
jugulare and hepatic vein congestion, effusion, ascites, dyspnea due to pleural effusion
What do you see with "backward" failure? (CHF)
- congestion and fluid retention --> edema, ascites, effusion
What do you see with forward failure? (CHF)
- inadequate organ perfusion --> syncope, cool extremities, azotemia
If a patient presents with heart murmur, arrythmia, anxiousness, restless and dyspnea, exercise intolerance, cough, what cardiac condition might you suspect?
CHF
What are the two chief presenting complaints with CHF and what causes them?
Dyspnea & cough: from pulmonary edema (high pressure blood returning to LA, LV)

Plerual effusion, abdominal distention: from high pressure of blood returning to R side of hrt.
When evaluating the CHF patient, what might you see on PE? Thoracic rads?
PE: hrt murmur/gallop sound, increased lung sounds and respiratory effort, anxious expression and restlessnes, cyanosis

Rads: pulm edema and pleural effusion. Ideal for assessment of L-sided hrt failure.
Are ECG and Echos useful in dx of CHF?
Not really.
For CHF trt, what is the first thing you want to do?
Trt fluid retention

Acute trt: goal is to save and maintain vital functions "at any cost"

Chronic: goal is to prevent recurrence of CS using least amount of meds
T/F Patients with acute L-sided CHF are likely to die quickly if untreated?

If True, what is the trt?
True

Furosemide, supplemental O2, thoracocentesis if needed and nitroglycerin ointment
What are the components of chronic CHF trt?
Furosemide, ACE inhibitors (Enalapril, benzapril), sodium restriction, others (including Spironolactone (diueretic, K+ sparing), and Pimobendan (iondilator - increase contractility and vasodilation))
What is the life expectancy of a CHF patient?
Acute: minutes to years
Chronic: Mitral regurg - mo to years; DCM - wks to mo.
T/F Occurence of CHF means high likelihood that animal will die of hrt dz in the future rather than anything else.
True
T/F occurence of CHF means mngmt/trt is absolutely necessary
True
T/F Good management and response to trt for CHF = good QoL
True
How do you suspect congenital heart dz?
- Incidentally found murmur - most common
- Overt CS - less common (CHF, failure to thrive/poor growth, syncope)
What is the biggest pitfall in trying to dx congenital hrt dz?
The normal hrt murmur of youth.
What is the difference in the physiologic hrt murmur of youth and the pathologicl hrt murmur of congenital hrt dz?
Physiologic: decreased intensity of murmur if HR increases

Pathologic: louder murmur w/ increased HR
Pulmonic stenosis, the 3rd most common congenital hrt defect, causes a pressure overload on what side of the hrt?
Right side. Valvular stenosis most common.
Pulmonic stenosis can be asymptomatic or symptomatic. Describe the difference in findings between the 2.
Asymptomatic: incidental finding of a murmur. CS will progress to symptomatic if not treated

Symptomatic: R sided CHF, stunted growth, exercise intolerance, syncope
What are the signs of R CHF often seen with pulmonic stenosis? What about on radiographs?
Hepatomegaly, ascites, dyspnea (pleural effusion), jugular vein distention, SQ edema

Rads: prominece of cranial aspect of the hrt due to R ventricular enlargement
Why do you use an echo when investigating pulmonic stenosis?
Because you need an echo to differentiate from subaortic stenosis (murmur will sound the same on auscultation)
What information can the use of a Doppler tell you about pulmonic stenosis?
Doppler pressure gradient = severity. Increased pressure, increased stenosis (narrower)
Does compensated mild-moderate pulmonic stenosis req trt?

Severe compensated or decompensated?
1) mild-mod compensated = no trt

2) severe compensated, decompensated = Trt (Surgery - catheter-based ballon valvuloplasty, open chest instrument dilation)
Describe PDA.
PDA is a congenital, hereditary malformation more common in females that is the abnormal persistence of the L 6th aortic arch/ ductus arteriosis that runs between the aorta and pulmonary artery in the fetus so that blood is allowed to bypass the lungs. This presents a problem when the ductus arteriosus remains patent after birth, so blood then shunts from the high pressure of the aorta in the pulmonary trunk therefore overwhelming the L side of the heart and wasting time because the blood is already oxygenated. This also leads to poor oxygenation of the rest of the body. Considered a L-->R shunt that has a mortality rate of 65% w/ in 1 year of dx in dogs
What do you see on PE in a PDA patient? Radiographys?
CRANIAL continuous murmur (dorsal around the 3rd rib), bounding pulse, Signs of CHF (Dyspnea, exercise intolerance, stunted growth)

Rads: Marked cardiomegaly (eccentric hypertrophy) because the baroreceptors try to compensate when they sense there is not adequate perfusion to the body.
What are the two treatment options for PDA? What is the prognosis?
1) Thoracotomy - "Old fashioned way"

2) Amplatzer occlusion - uses fluroscopy and a catheter through the femoral artery

2% intraoperative mortality, normal or near-normal long term prognosis with Sx correction.
Name 3 important forms of tachycardic arrhythmias.
- Atrial premature complex (APC)
- Atrial Fibrillation
- Ventricular Premature complex
- Ventricular Tachycardia
Name 2 forms of bradycardic arrhythmias.
- Atrial Standstill
- A-V block
Describe the origin and pathway of the normal heart beat.
Hrt beat orginates in the SA node and travels through and depolarizes the atria. Normal delay through the AV node and then impulse travels through and depolarizes the ventricles.
Describe the normal heartbeat in terms of ECG.
Atrial depolarization: P wave
AV node: interval b/w P wave and QRS
Ventricular depolarization: QRS
Ventricular repolarization: T-wave
What are the 3 key features of the ECG?
Rate, rhythm, mean electrical axis
What does having a QRS complex for every P-wave indicate?
Shows appropriate connection b/w atria and ventricles.
Is Respiratory Sinus Arrhythmia normal?
Yes. Due to high vagal tone from intrathoracic pressure when animal breathes in causing pressure on the vagus nerve.
When an animal presents with a large volume of mitral regurg on echo you dx myxomatous mitral valve dz. What else will you be worried about as sequela to this dz?
Pulmonary edema and CHF
What is an atrial premature complex? What do you see on Echo?
When the heart beat starts prematurely in the atria.

QRS complexes occur prematurely and P waves ride into the previous T-wave.
T/F Atrial premature complexes are a marker for atrial dz.
True
T/F APCs require trt.
False. Trt can make it worse.
Describe atrial fibrillation and what it is associated with.
Rapid chaotic series of atrial impulses directed toward the ventricles and converge on AV node (confined to the atria b/c of endocardial cushion). Associated with dz of enlarged atria.
T/F The AV node is considered the gate keeper to the ventricles.
True.
Describe the ECG of a patient with Atrial fibrillation.
QRS complexes look the same shape because ventricles being told to act the same. The inconsistency is the pattern between the R-R intervals: R-R intervals are irregular (short, long, in-b/w)
What does Atrial fibrillation sound like on auscultation?
"Sneaker in a clothes dryer"
What is a DDx for Atrial fib?
Multifocal ventricular tachycardia.
What are the 2 treatment options for atrial fibrillation?
Want to slow conduction through the AV node.
- Digitalis (digoxin)
- Beta-blocker (atenolol)
What is the difference between Ventricular Premature Complexes and Ventricular Tachycardia?
Both are spontaneous and premature depolarization of the ventricles.

1-3: ventricular premature complexes
4+: ventricular tachycardia
What is the hallmark of VPC?
Wide bizarre QRS complex
What is the abnormal spread of electrical activity with VPC?
Impulse travels from myocyte to myocyte with is inefficent.
What is the significant of VPC?
Any problem if severe enough can cause ventricular ectopy can be primary cardia or systemic problem.
Because of the rapid ventricular filling with VPC, what do you see in terms of pulse and CO?
- Pulse deficits
- Risk of decreased CO
When should you treat a patient with VPC?
- Trt if high HR or symptomatic. (if you see pulse strength change)
What is a right bundle branch block?
When the conduction system is blocked and RV doesn't depolarize right away so impulse has to wrap around from the LV. RBBB is an imposter of VPC
What is an escape rhythm?
Slow steady rhythm when normal HR not able to be maintained there is a back up system. i.e <30bpm
What is the major factor controlling the impact of an asymptomatic ventricular arrhythmia?
Heart rate
What kind of clinical sign would present that would cause you to want to treat ventricular premature complexes?
Syncope
What would you use for acute and chronic treatment of ventricular ectopy?
Acute: Lidocaine (slows depolarization by acting on Na channels. But req's K to work therefore if hypovolemic will cause VPC)

Chronic: Sotalol, Mexiletine or Procainamide
With respect to an AV block, what determines in clinical signs are present?
Ventricular rate
What is a 1st Degree AV block?
Longer P-R interval because of delay through the AV node. Usually incidental
What is a 2nd Degree AV block?
- A dropped beat. Nothing happens after the P wave because impulse did not get through.
What is a 3rd Degree AV block?
When several beats are dropped. See syncope and weakness. Needs pacemaker implantation
What are the 4 classes of antiarrhythmic drugs? What do you use each class to treat?
Class I: Na-channel blockers (Ventricular arrhythmias)
Class II: Beta-blockers (Supraventricular arrhythmias)
Class III: Repolarization modifiers (K-Channel blockers) (ventricular arrhythmias)
Class IV: Ca channel blockers (supraventricular arrhythmias)
Give 3 examples of Class I antiarrhythmics (Na Channel Blocker)
Lidocaine (only IV)
Procainamide
Quinidine
When, why and how do we use ACE inhibitors? Examples?
Always a chronic treatment for CHF and may delay recurrence/progression.
Oral admin (not an emergency drug)
Proven benefit in CHF: prolongs dz free interval.

E.g Enalapril and Benzapril
What is Pimobendan?
Inodilator (positive inotrope and vasodilator)
When do you consider using a diruectic?
Life saving trt of cardiogenic pulmonary edema.
T/F Pimobendan works by Ca senstization.
True.
If you have an animal with large volume pleural effusion, what is the one method of treatment that would be best?
Thoracocentesis
What are some differentials to cause a large volume pleural effusion?
Neoplasia
CHF (HCM, RCM, etc)
Chylothorax
How much fluid should you remove in pleural effusion in a cat? In a dog?
Cat <120mL
Dog 3-4L
What would be some treatment options to slow the recurrence of pleural effusion?
Furosemide
ACEI
Beta Blocker (don't give if current CHF)
Why might you need to take fluid from one side of the chest and then the other in cats with pleural effusion?
Because the mediastinum can be complete or incomplete.
What is ascites a sign of and how do you treat it?
RHF. Abdominocentesis
A canine patient presents with mild dyspnea at rest, thin body condition, marked abdominal enlargement, a systolic murmur and shows generalized cardiomegaly, mild pleural effusion and possibly pulmonary edema on thoracic rads. What is a diagnosis you should consider and what sides of the heart are affected. What side of the hear should you treat first?
DCM resulting in RHF and LHF.

Trt the left heart failure first - furosemide, ACE Inhibitor, Taurine if the blood levels indicate it, Digoxin and Pimobendan.
Name 4 kinds of Pericardial Dz.
Pericardial Effusion
Constrictive Pericarditis
Effusive constrictive pericarditis
Peritoneopericardial diaphragmatic hernia
What is cardiac tamponade?
Cardiac tamponade is a situation in which excess pericardial pressure causes circulatory problems as the result of any pericardial disorder exerting excessive pressure on the heart.
What is the normal pericardium and is it essential to life?
Thin, tough, non-elastic fibrous sace that restricts expansion of the heart. The serosal inner surface provides lubrication of the epicardial surface. Not essential to life.
Why are acute pericardial effusions life threatening?
Because the pericardium can only stretch very slowly, therefore with acute effusions there is not enough time for it to stretch. The R heart is affected due to increase pressure in the cranial and caudal vena cava and R heart affected because so thin.
What are some clinical signs of Pericardial dz?
Lethargy
Acute collapse
Loss of appetite
Tachypnea, increased respiratory effort
Vomiting, Diarrhea
Asymptomatic abdominal distention.
What 3 signs are very indicative of pericardial effusion?
Tachycardia
Muffled heart sounds
Pulse alterations (weak, rapid pulse, pulsus paradoxus)
What is pulsus paradoxus?
When you breath in with pericardial effusion, more blood returns to the R heart but the effusion is then displaced and the LA pays the price therefore the hrt beat is weaker. When hrt beat stronger on expriation and weaker on inspiration (opposite of normal)
What is the pathophysiology of cardiac tamponade?
Inadequate ventricular filling (restricted by effusion)
Suboptimal filling means poor output (therefore weak pulse and reflex tachycardia)
In what species is pericardial effusion more common?
Dogs
What doe thoracic rads look like with an animal with pericardial effusion?
Diffuse cardiomegaly
Enlarge CVC
Normal to small Pulm a & v
Lungs may be difficult to interpret due to crowding by large cardiac silhouette
How do you establish a diagnosis of pericardial effusion?
Do an echo. RA & RV caved in due to pericardial effusion and can't fill very well. Poor transport to lungs therefore poor filling of the LA and decreased CO and death b/c of poor perfusion.
What are some causes of pericardial effusion?
Idiopathic benign effusion
Malignancy
CHF
Infecitous (bacti, viral, etc)
Frank blood (LA rupture, coagulopathy)
Congenital PPDH
Metabolic (uremia)
Describe Benign Idiopathic Pericardial effusion and Malignant.
Idiopathic: Sterile inflam, Self terminating, recurrent effusion or constrictive pericarditis result

Malignant: Hemangiosarcoma of the RA, rapid reffusion and hemorrhage is common. Can also be chemodectoma(heart base tumor), mesothelioma, metastatic (lymphoma, carcinoma)
T/F It is hard to differentiate b/w Malignant and Idiopathic Pericardial effusion.
True
What are you treatment options for pericardial effusion and what one would you most likely use in an acute setting?
# 1 for acute setting = Pericardiocentesis

Pericardectomy via thoracoscopy or thoracotomy (effusion falls into the pleural space and is reabsorbed)
T/F The outcome of pericardial effusion is highly dependent on the etiology
True
What is another name for Feline Arterial Thromboembolism?
Saddle Thrombus
What is systemic hypertension? What are the normal values for systolic arterial pressure in a minimally stressed, in-clinic patient?
Consistently elevated arterial blood pressure risking or actually causing end-organ damage.

Dog <160mmHg
Cat <160-180mmHg
What are the manifestations of decompensated systemic hypertension?
Acute internal bleeding (CNS, ocular)
Chronic renal effects (proteinuria --> tubular damage, glomerulosclerosis)
How big should your doppler cuff be? At what level should it be places and why? How many measurements should you take?
<30-40% of the circumference of the limb

At the level of the RA to remove the influence of gravity

Average of 3-5 measurements
What clinical signs might you see on PE of a systemic hypertension patient?
Retinal hemorrhages
Hyphema
CNS deficits/seizures
Small, asymmetrical firm kidneys
What are the causes of systemic hypertension in the cat?
Hyperthyroidism: Increased CO because increased HR b/c increased T4

Chronic Kidney Dz: abnormal Na handling and inappropriate activation of RAAS and nephron loss augments effects on remaining ones. (Aldosterone increases circulating volume and Angiotensin II causes vasoconstriction = hypertension)
What are the causes of systemic hypertension in the dog?
Hyperadrenocorticism (cortisol increase aterial sensitivity to endogenous vasoconstrictors)

CKD

Diabetes Mellitus (loss of glucose damages glomerulus)

Pheochromocytoma
What factors make up Mean Arterial Pressure?
Systemic vascular resistance x CO (HR x SV)
What drugs can you use to trt hypertension?
Amlodipine (Norvasc) - vasodilating Ca channel blocker w/ very high efficacy in cats

ACE-I: Enalapril & Benzapril. less effective but useful in CKD

Atenolol - B-Blocker reduces Co and renin. Good w/ amlodipine.
What drug should you use for urgent care in systemic hypertension?
IV sodium nitroprusside
What drug do you want to avoid in cats w/ CKD causing systemic hypertension?
Furosemide
What is the prognosis of systemic hypertension?
Highly variable
What are the clinical signs of arterial thromboembolism?
Acute paresis.

Typically involved the terminal aorta so loss of function in rear limbs and tail. Less severe if affects a forelimb.

Vascular: cold, pulseless legs, pale limbs and toe pads

Muscular: painful (initially), contracted muscles and increased CK.

LMN: ischemic neuropathy with loss of proprioceptive, motor and sensory function (distal is worse).
What causes arterial thromboembolism?
Heart Dz that causes sluggish blood flow and atrial enlargement. Clot forms and travels aorta and lodges in bifurcation above external iliac a.
What drug do you want to avoid in cats w/ CKD causing systemic hypertension?
Furosemide
What do you have to consider with thromboembolism treatment?
- Trt underlying heart dz
- Reperfusion injury (inflam mediators localize in ill-perfused tissue. Necortic cells release K and restoration of blood flow releases ROS. Systemic release of K)

Prognosis is generally guarded.
What is the prognosis of systemic hypertension?
Highly variable
What are the clinical signs of arterial thromboembolism?
Acute paresis.

Typically involved the terminal aorta so loss of function in rear limbs and tail. Less severe if affects a forelimb.

Vascular: cold, pulseless legs, pale limbs and toe pads

Muscular: painful (initially), contracted muscles and increased CK.

LMN: ischemic neuropathy with loss of proprioceptive, motor and sensory function (distal is worse).
What causes arterial thromboembolism?
Heart Dz that causes sluggish blood flow and atrial enlargement. Clot forms and travels aorta and lodges in bifurcation above external iliac a.
What do you have to consider with thromboembolism treatment?
- Trt underlying heart dz
- Reperfusion injury (inflam mediators localize in ill-perfused tissue. Necortic cells release K and restoration of blood flow releases ROS. Systemic release of K)

Prognosis is generally guarded.
What drugs should you consider with Home treatment or Chronic trt w/ arterial thromboembolism?
Asprin and Clopidogrel
What drugs should you consider with acute hospital care treatment of arterial thromboembolism?
Anticoag: Heparin
Analgesia: Butorphanol
Thrombolytics: urokinase, streptokinase, recombinant tissue plasminogen activator (TPA - very specific to thrombus but lots of risks)