Pulmonary Hypertension, Heartworm, Pericardial Flashcards
How can you measure pulmonary hypertension
Cannot noninvasively measure pulmonary artery pressure with BP cuff
1) Gold standard: right heart catherization via jugular or femoral vein (RHC)
*requires heavy sedation or anesthesia in SA but anesthesia will throw off results
2) PAWP: Pulmonary Artery Wedge Pressure (PAWP)- surrogate for left atrial pressure
What is a non-invasive , surrogate method to measure left atrial pressure
PAWP: Pulmonary Artery Wedge Pressure (PAWP)- surrogate for left atrial pressure and pulmonary venous pressure
abnormally increased pressure within the pulmonary vasculature/circulation
pulmonary hypertension
normal mean PA pressure is 15mmHg
What is a normal pulmonary vasculature/circulation pressure in a dog
normal mean PA pressure is 15mmHg
systolic mean PA is around 25mmHg
Is pulmonary hypertension a disease
not necessarily -> it is a hemodynamic and pathophysiologic state and you want to determine the cause
What are the broad causes of pulmonary hypertension
1) Increased Pulmonary Vascular Resistance
2) Increased cardiac output/flow (R Vent leads to more blood flow there)
3) Increased pulmonary venous pressure (ex: Mitral disease raises LA pressure and then pulmonary venous pressure)
4) Combination of 1-3
How might you get pulmonary hypertension with MMVD?
Mitral insufficiency leads to increased LA pressure and then backflow to raise the pulmonary venous pressure
What might increase blood flow/CO to the lungs
1) Exercise
2) Left to right shunts
How does pulmonary vascular resistance change to accommodate increased blood flow to the lung (seen in exercise and left to right shunts)
PVR decreases to accommodate the increased flow
-capillary recruitment
-capillary distension
*Both passive processes
Two ways the lungs decrease resistance in increased blood flow to lungs
1) Capillary recruitment
2) Capillary distension
T/F: most shunts do not significantly increase pulmonary arterial pressure
True- unless the patient develops pulmonary vascular disease (and increased PVR)
How do we classify pulmonary hypertension
1) Precapillary PH (pulmonary arterial hypertension)
2) Post capillary PH (pulmonary venous hypertension)
Why might there be pulmonary arterial hypertension (precapillary PH)
due to increases in PVR due to vasoconstricted or fibrotic pulmonary artery
-RV hypertrophies and then might dilate to accommodate for increased in afterload
-La size is normal/small
What do you see as a result of precapillary PH due to constricted or diseased pulmonary arteries
-RV hypertrophies and then might dilate to accommodate for increased in afterload
-La size is normal/small
What causes precapillary PH (fill in later)
nearly all things except for left heart disease
What causes postcapillary PH
1) Isolated postcapillary PH: PVR is normal (most common)
-Chronic severe left heart disease
(Right heart normal, Big LA)
2) Combined postcapillary AND precapillary PH-
Increased PVR (with increased pulmonary venous PH)
-Chronic severe left heart disease with PVD from chronically increase pulmonary venous PH)
(right changes, LA big)
How might you get isolated postcapillary PH
PVR is normal (most common)
-Chronic severe left heart disease
(Right heart normal, Big LA)
How might you get combined postcapillary and precapillary PH
Increased PVR (with increased pulmonary venous PH)
-Chronic severe left heart disease with PVD from chronically increase pulmonary venous PH)
leads to
(right changes, LA big)
What are the causes of pulmonary hypertension
1) Increased pulmonary blood flow: congental L to R shunt or exercise which overwhelms
2) Increased pulmonary vascular resistance: pulmonary vasculopathy, hypoxia-> vasoconstiction, lung disease
3) Increases in Pulmonary venous pressure: Left heart disease (LV systolic dyfunction, LV diastolic dysfunction, inflow obstruction, valvular disease) or compression of a large pulmonary vein
How might you get pulmonary arteriolar vasoconstriction leading to increases in pulmonary vascular resistance and pulmonary hypertension
1) Endothelial cell dysfunction (impaired vasodilation and thrombosis)
2) Hypoxia
How does hypoxia cause pulmonary hypertension
It causes pulmonary arteriolar vasoconstriction (Increased pulmonary vascular resistance)
What are the causes of increased pulmonary vascular resistance that cause pulmonary hypertension
1) Pulmonary arteriolar vasoconstriction: Endothelial cell dysfunction or hypoxia
2) Pulmonary vascular disease: Obstructive lesions -> accumulation of vascilar cells, loss/destruction of precapillary arteries/fibrosis
The RV is meant to pump against
low pressures
-it is a volume pump so increased PH will cause right ventricular strain and dysfunction
How can chronic left heart disease cause pulmonary vascular hypertension
1) decompensated chronic MR
2) Increased in LA pressure
3) Increased Pulmonary venous pressure
4) Increased capillary pressure (pulmonary edema)
5) Overtime -> Increased pulmonary artery pressure
6) RV dilation and contractile dysfunction
What will you see on physical exam of an animal with pulmonary hypertension
1) Increased lung sounds, crackles
2) Right apical systolic murmur
Clinical signs: syncope or right sided heart failure (cardiogenic ascites)
What murmur is typically heard in patients with pulmonary hypertension
right apical systolic murmur
from RV dysfunction and failure
What is the most common clinical sign of severe pulmonary hypertension *
1) Syncope (especially with exertion or inactivity)
2) Right sided heart failure (cardiogenic ascites)
How do you diagnose PH in a dog
rely heavily/solely on echo to diagnose PH
1) Look at tricuspid velocity (systole) and use Bernouli equation (pressure gradient = 4 *V^2)
2) Estimate RVSP need to add RA pressure (0-5mmHg)
3) RVSP is approx. sPAP (unless pulmonic stenosis is present)
4) determine PAP
Normal: 25mmHg
Mild: 30-50mmHg
Moderate: 50-75mmHg
Severe: >75mmHg
clinically significant at 45mmHg
What is the modified Bernouli equation
Pressure gradient = 4*V^2
The Simplified Bernoulli equation states that: Velocity is. ________- proportional to the area of a narrowed region
Inversely proportional to the area of a narrowed region
What can throw off your diagnosis of PH with echo
Pulmonary stenosis
because after determining the pressure gradient at the tricuspid valve on echo you assume the RV systolic pressure is the same as systolic pulmonary artery pressure
If a patient has a tricuspid velocity of 4m/s. Does this patient have pulmonary hypertension
Bernouli Equation: 4 x 4^2 - Pressure gradient of 64mmHg
Add right atrial pressure (0-5mmHg) = 64mmHg
if no pulmonic stenosis:
Systolic PAP= 64mmHg
(Normal is 25mmHg)
What is normal systolic PAP
25mmHg
How do you define the different levels of pulmonary hypertension
Normal PAP: 25mmHg
Mild PH: 30-50mmHg
Moderate PH: 50-75mmHg
Severe: PH >75mmHg
Treat (clinically significant >46mmHg)
What are the 6 causes of pulmonary hypertension in dogs
1) PAH (Idiopathic, Congental Shunts)
2) PH due to left heart disease
3) PH due to respiratory disease, hypoxia, or both
4) PA obstructions (PE, PT, PTE)
5) PH due to parasitic disease
6) Multifactorial and/or unclear mechanisms
pulmonary arterial hypertension that is often a diagnosis of exclusion unless a cardiac shunt is identified
Group 1 PH
pulmonary hypertension that is caused by any cardiac disease (non-shunts) that increase the pulmonary venous (Left atrial pressure) ex: MMVD
-component of postcapillary PH (isolated or combined)
Group 2 PH
What will you see on echo in a patient with Group 2 Pulmonary Hypertension
their pulmonary hypertension is caused by left heart disease so you will see an unequivocal LA enlargement
a diverse spectrum of respiratory diseases (ex: hypoxia, pulmonary parenchymal disease, obstructive) leading to pulmonary hypertension
Group 3 PH
How might respiratory disease and hypoxia cause PH (Group 3 PH)
the lungs must balance ventilation and perfusion
(V/Q mismatch will lead to PH)
Hypoxia: pulmonary arterioles vasoconstrict in hypoxic region of lung leading to pulmonary hypertension
How might you dilate the pulmonary arteries
give oxygen
What effect does altitude impact the pulmonary circulation
altitude and hypoxia causes the pulmonary arterioles to actively vasoconstrict in hypoxic region of the lung
pulmonary hypertension caused by precapillary obstructions (pulmonary thrombi, pulmonary thrombiemboli or pulmonary emboli) and cutting off blood supply
Group 4 PH
Group 4 Pulmonary Hypertension is caused by
pulmonary hypertension caused by precapillary obstructions (pulmonary thrombi, pulmonary thrombiemboli or pulmonary emboli) and cutting off blood supply
Group 5 Pulmonary Hypertension is caused by
Dirofilarial and angiostrongylus causing precapillary pulmonary hypertension
Group 6 Pulmonary Hypertension is caused by
unclear/multifactorial etiologies (1-5 pathologies or masses compressing the pulmonary arteries)
ex: dogs with chronic respiratory disease and MMVD
How should you manage patients with pulmonary hypertension
*Severity-dependent
1) Oxygen supplementation
2) Parasitic prevention, vaccinations
3) Exercise restriction
4) Avoid altitude or air travel
5) Avoid elective anesthesia/ surgery
How might you dilate pulmonary arterioles to treat pulmonary hypertension
1) Give oxygen
2) PDE-5 inhibitors (Sildenafil, tadalafil)
*Prostaglandin analogs and endothelin antagonist are limited
Name PDE-5 inhibitors used to treat pulmonary hypertension
Sildenafil
Tadalafil
Sildenafil is a __________ used to treat __________
PDE-5 inhibitor (Nitric oxide-cGMP pathway) used to treat pulmonary hypertension by causing pulmonary artery vasodilation
Tadalafil is a __________ used to treat __________
PDE-5 inhibitor (Nitric oxide-cGMP pathway) used to treat pulmonary hypertension by causing pulmonary artery vasodilation
T/F: prostaglandin analogs like epoprostenol are used in dogs to treat pulmonary hypertension
False- they are used in humans but need to be constantly injected like insulin pumps so not good for management
*Use PDE-5 inhibitors like sildenafil or tadalafil
T/F: Endothelin antagonist (bosentan) are used in dogs to treat pulmonary hypertension
False- although they cause PA vasodilation they are cost prohibited and mostly only used in humans
*Use PDE-5 inhibitors like sildenafil or tadalafil
In general, you should use PDE-5 inhibitors sildenafil or tadalafil to treat pulmonary hypertension with clinical signs and systolic PAP>46mmHg. When should you not use these?
1) Avoid with LA enlargement (treat left heart disease/lower LA pressure first)
2) Avoid with left to right shunts (close shunt if possible)
When are you likely to treat PH with sildenafil or tadalafil
When there is clinical signs AND echo estimate of systolic PAP >46mmHg
What causes of pulmonary hypertension, should you not treat with sildenafil or tadalafil
1) Avoid with LA enlargement (treat left heart disease/lower LA pressure with pimobendan first) - postcapillary causes
2) Avoid with left to right shunts (close shunt if possible) - drive more shunting with PA vasodilator
Why shouldnt you use sildanafil in patients with LHD and shunts
Pulmonary edema
PA vasodilators can induce pulmonary edema
if you decrease PVR, increase right CO and increase venous return leading to pulmonary edema
*Flood an already flooded Left atrium
How should you treat pulmonary hypertension caused by left-sided CHF
1) Pimobendan/Furosemide to treat left-sided CHF/ LA hypertension (post-capillary causes)
then
2) you can now give sildenafil to treat the pre-capillary hypertension
Where does Dirofilaria immitis reside
in the pulmonary arteries (5-7 years) and produce circulating microfilaria
-hypoxic region
What are the stages of Dirofilaria immitis
1) Mosquito phaseL microfilaria ingested by mosquito goes through 2 molts L1-L3
2) Tissue (SQ) phase: L3 (infective stage) transmitted to neighbor dog- additional molt L3-L4 (susceptible to HW preventatives)
3) Bloodstream phase: L4 migrate to vasculature (resistant to treatment) and undergo final molt to L5
L5 migrate to pulmonary arteries to become adult worms (6-7 months post infection)- completes lifecycle
Are adult male or female Dirofilaria immitis larger
females are larger
What do adult Dirofilaria immitis do in the pulmonary arteries
produce circulating microfilaria into the bloodstream. mosquito will then ingest these to continue the cycle
Microfilaria molt from _____ to ______ in the mosquito
L1 to L3 (2 molts)
What is the infective stage of Dirofilaria immitis
L3: L3 is achieved in the mosquito (2molts; L1 microfilaria to-L3)
When are Dirofilaria immitis susceptible to heartworm preventatives like macrocyclic lactones
In the tissue (SQ) phase
after they have been infected by L3 from mosquito and when they are molting to L4
What occurs once Dirofilaria immitis is an L4 stage
L4 migrate to vasculature (resistance to treatment) to undergo final molt to L5
When are Dirofilaria immitis resistant to treatment (preventative and adulticides)
Once the L4 migrate to the vasculature to undergo final molt to L5
How long post-infection does it take for Dirofilaria immitis to complete its maturation in the dog
6-7 months post infection
How long can mature adult Dirofilaria immitis, producing microfilariae live in the pulmonary arteries
5-7 years
What do larval molts depend on
Wolbachia: an intracellular gram negative symbiotic bacteria
an intracellular gram negative symbiotic bacteria that allow Dirofilaria immitis larval molts to occur
Wolbachia species
What species can be infected by Dirofilaria immitis
Canids (domestic dog, wolves, foxes, coyotes)
but also
Domestic/Nondomestic cats, ferrets, muskrats, sea lions, coatimundi, and humans
What are factors that influence Dirofilaria immitis infection
1) Requires mosquitos and host reservoirs (canids and ferrets)
2) Molts L1-L3 in mosquitoes require temps of >57F
3) Microfilaria greatest numbers in peripheral blood during summer evenings
*Dictates screening, prevention and treatment plans
How does feline heart worm infection differ from dogs
1) Unnatural host, innate resistance
2) Increased aberrant migration in cats
3) Much smaller worm burden
4) Brief microfilaremia
5) Marked pulmonary reaction, especially to dying worms
6) Lack of safe adulticidal therapy
7) Different preventative dosages
Do dogs or cats have a higher Dirofilaria immitis worm burden
cats because they have an innate resistance
*Makes it difficult to serologic diagnosis
Do you test for microfilaria in cats?
NO- they have a brief microfilaremia
do not test for microfilaria in cats
What clinical sign do you see with feline heartworm infection
marked pulmonary reaction, especially in dying worms
despite the small worm burden
T/F: there is safe adulticidal therapy for Dirofilaria immitis in cats
False
The severity of Dirofilaria immitis infecton in dogs depend on
worm number and the infection duration
Vascular +/- lung pathology in Dirofilaria immitis infection occurs prior to L5 maturity meaning that
we wont be able to diagnose HWI in these cases because the test is for adults
T/F: physical obstruction of PAs by living worms cause clinical significance disease
False- unless there is an extreme number of worms but generally it is the dead/dying worms that lead to the severe pathology with cytokine and inflammatory reaction
What are the effects of adult Dirofilaria immitis on pulmonary hypertension
Adults cause pulmonary arteritis, vascular reaction, and thrombosis- especially in caudal pulmonary arteries
Narrowed arteries cause increase PVR and lead to precapillary pulmonary hypertension
PH hypertension then leads to PA dilation and increased RV systolic pressure and RV hypertrophy +/- right heart failure
Heartworms cause increased (Precapillary/ Postcapillary) pulmonary hypertension
Precapillary Hypertension
they cause pulmonary arteritis, vascular reaction, and thrombosis
The broad effects of adult Dirofilaria immitis
1) Pulmonary hypertension leading RV hypertrophy +/- right heart failure
2) Pulmonary infarction
3) Hypersensitivity/ allergic (eosinophilic) pneumonitis
4) Inflammatory (permeability) pulmonary edema (NOT due to left heart failure)
5) Pulmonary fibrosis- tissue injury
6) HARD (Heartworm associated respiratory disease) in cats- early in infection
How might you get pulmonary edema with Dirofilaria immitis?
It is not due to left heart failure but rather the inflammatory (permeability) edema caused by the adult worms
Pulmonary larval dirofilariasis
HARD (Heartworm Associated Respiratory Disease) seen in cats
-Immature worms (larva) contribute to respiratory “asthma-like” signs despite resisting mature infection
Immature worms (larva) contribute to respiratory “asthma-like” signs despite resisting mature infection in cats
Pulmonary larval dirofilariasis or HARD (Heartworm Associated Respiratory Disease)
What do you see in pulmonary larval dirofilariasis in cats
Immature worms (larva) contribute to respiratory “asthma-like” signs despite resisting mature infection in cats
*Proliferative and inflammatory pulmonary arterial lesions + disease of bronchioles and pulmonary parenchyma
Clinical signs of heartworm disease
-Respiratory clinical signs predominate (tiring, cough, breathing difficulty)
-CV signs from PH/CHF: weight loss, syncope, exercise intolerance, JVD/P, hepatomegaly, ascites, abnormal cardiac auscultation (TR murmur, split or loud/tympanic S2)
Cats: vomiting, cough, dyspnea, neuro sings
What kind of murmur do you see with heartworm disease
TR murmur, split or loud/tympanic S2
Cats do not typically cough from heart disease but they can if they have
heartworm disease
-proliferative and inflammatory pulmonary arterial lesions+ disease of bronchioles and pulmonary parenchyma seen when immature worms cause respiratory disease (HARD)
What does the Dirofilaria immitis antigen test detect
Adult females only
*ideal for dogs -> higher worm burden
if positive= Heartworm infection
What does a positive Dirofilaria immitis antigen test mean
they are positive for heartworm infection
What Dirofilaria immitis test is ideal for cats
Antibody (Ab) test because they have a low worm number
+: tells you exposure sometime in the life
-: rule out HWI in cat
What does a positive Dirofilaria immitis antibody test mean
they’ve had an exposure (doesnt say they have a current HWI)
You did a routine antigen test for heartworm in a dog and it is positive and asymptomatic. What should you do next?
Always test for microfilaria (except cats)
*Test needed prior to starting preventatie therapy
*Do Knott’s test (recommended) or blood smear
If a dog has a positive antigen test, why do you need another test for microfilaria prior to starting preventative therapy
the rapid death of microfilariae may cause adverse hypersensitivty reactions
*use caution with mibemycin products (Sentinel, Interceptor) in microfilaremic dogs
Why should you use mibemycin products (Sentinel, Interceptor) with caution
if the dog is microfilaremic, the rapid death of microfilariae may cause adverse hypersensitivity reaction
Why are microfilariae test not ideal for screening of heartworm
it only picks up microfilaria and not the adult worms
not ideal for cats because they have very brief microfilariae periods
*only use if you have a dog with previous antigen positive (adult female worm positive)
What does the Knott test detect
microfilariae
What tests detect microfilariae in a dog
1) Knott test (most sensitive)
2) Blood smear methods
Why might a dog be HW negative but be positive for microfilariae
they have Acanthocheilonema reconditum infection (nonpathogenic nematode) - usually smaller and fewer with progressive motion
What do HW microfilariae look like on peripheral blood smear
usually many in blood
stationary motion
straight body and tail, tapered head
300-322 um
Mf positive means
there is a patent infection (there are adults producing offspring)
How else, aside from mosquitos can Dirofilaria immitis be transmitted
microfilariae can be passed transplacentally to offspring
T/F: microfilariae can be passed transplacentally to offspring
true
What should you do in regards to heart worm when a patient is:
Ag positive
MF negative
Do a 2nd antigen test with a different sample and a different lab test
to confirm HWI
Additional diagnostics: *thoracic radiographs, echocardiograph, CBC, Chem, UA
What would you see on thoracic radiography of a patient with HWI
*Signs of pulmonary hypertension and lung injury
-Enlarged tortuous pulmonary arteries
-Dilated main pulmonary artery
-Right sided/generalized cardiomegaly
-Interstitial opacities, patchy alveolar infiltrates
-occasionally bronchial patterns in cats
*essential in determining severity
What is a fairly reliable early radiographic finding in cats with heartworm disease
dilated caudal lobar pulmonary arteries
Why might you not see heartworms on echo, depsite having a HWI
you only visualize the more proximal portion of the pulmonary arteries and they reside in the more distal portion
but if we see them- very sensitive
echo is helpful to diagnose with PA pressures, screening PH
What would you see on CBC in a patient with heartworm
Eosinophilia, Basophilia, monocytosis (classive
anemia: mild nonregenerative or fragmentation
+/- thrombocytopenia
What would you see on biochem in a patient with heartworm
hyperglobulinemia
hypoalbuminemia (PLN)
Increased liver enzymes (congestion vs reactive)
What would you see on UA in HWI
Proteinuria
Hemoglobinuria (caval syndrome)
How do you treat HWI
1) Microfilariacide (HW preventative)- prevents disease spread, slow kill
2) Wolbachia-cide (Doxycycline)- weakens immune response to dying worms, shortens life cycle, adults more suscpetible to melarsomine, and may decrease risk of melarsomine associated PTE
3) Adulticide (Melarsomine- Immiticide) -safest drug to kill adult worms in dogs, not cats
4) Rest- use sedatives as needed
What antibiotics is used in improving the treatment of heartworm
Doxycycline to kill Wolbachia
1) weakens immune response to dying worms, shorting life cycle
2) Adults more susceptible to melarsomine
3) Decrease risk of melarsomine associated PTE
What are the effects of using Doxycycline with HWI
Doxycycline to kill Wolbachia
1) weakens immune response to dying worms, shorting life cycle
2) Adults more susceptible to melarsomine
3) Decrease risk of melarsomine associated PTE
What is the safest drug to kill adult worms in dogs
Melarsomine (Immiticide)
T/F: Melarsomine is used to kill adult worms in cats
False- not for use in cats; only the dogs
Melarsomine (Immiticide) is used to
kill adult heartworms, only in dogs
-Doxycycline makes adults more susceptible and may decrease risk of melarsomine- associated pulmonary thromboembolism
How do you confirm HWI in dog
Antigen test for adult females
+: verify with microfilaria test
-: no adult females present, no HWI
Microfilaria
+: confirm HWI
-: get a new sample and different lab to confirm
What should you do after you test HW antigen and microfilariae postive in a dog
1) Immediately get started on heart-worm preventative (for microfilariae) and then doxycycline for 1 month
2) Day 60: 1st melarsomine (adulticide) is finally given
3) Day 90: 2nd melarsomine
4) Day 91: Third melarsomine injection
*Need to restrict exercise to prevent life-threatening PTE
Why do you need to wait 2 months for the 1st melarsomine injection for HWI in a dog
you want to avoid massive worm death and life threatening PTE. this is why rest is also really important
Why is it critical to decrease activity level in dogs getting melarsomine
Melarsomine kills the adult worms which with exercise can cause life-threatening PTE
When are the Melarsomine injections given to dogs with HWI
1) Day 60: after treatment of doxycycline for 1 month and preventatives
2) Day 90
3) Day 91
Why do you have to wait 2-3 months after diagnosis of HWI to administer adulticide
At diagnosis, the animal is on a preventative (macrocyclic lactone) that kills the microfilariae
if there are younger worms, you need to wait the 2 months to allow for the younger worms that the macrocyclic lactone didnt kill to grow up to then be susceptible to the melarsomine injections
How do you treat the cough/respiratory signs associated with HWI
Prednisone and rest
How do you treat HWi in cats
-Preventative
-Doxycycline
-HW extraction surgery ($)
*hope worms die without killing the cat
uncommon but severe pulmonary hypertension and physical obstruction from a heavy worm burden (60+) leading to reduced cardiac output and hepatic congestion, right heart failure, and kidney (glomerular) injury
Caval syndrome
What are the effects of caval syndrome
1) Reduced CO and hepatic congestion
2) Right heart failure
3) Kidney (glomerular) injury
4) Hemoglobinuria with HWD -? pathognomonic from fragmentation of RBCs (schistocytes)
5) +/- DIC, heptocellular injury
What will you see on blood smear with caval syndrome
Hemolysis, Schistocytes
How do you diagnose caval syndrome
you will see hemoglobinuria with hemolysis and schistocytes
confirm with echo for diagnosis
How do you treat cvaal syndrome
heartworm extraction toreduce worm burden
-jugular venous approach and manual removal with snaore or forcepts
*guarded prognosis- 50% survive the procedure, not done very often but its either this or euthanasia
how many layers is the pericardium
2 layers
1) visceral pericardium
2) parietal pericardium
T/F: there is normamly fluid in the pericardium cavity
true but only 0.25ml/kg for lubrication
plasma ultrafiltrate from epicardial and parietal pericardial capillaries (contains prostaglandins)
HOw is the pericardial effusion plasma ultrafiltrate normally drained
lymphatics
The pericardium is not essential for life but what are its functions
1) Fixes position of heart within thoracic cavity (attached to great vessels at heart base)
2) Limits short term cardiac distension
3) Maintains pressure-volume relation of the cardiac chambers and output from them
4) Lubricates, minimizes friction
5) Mechanical barrier to infection
> 50% of normal diastolic pressure is due to
pericardial influence
*Helps with cardiac filling
What effect does inspiration have on venous return to RA/RV
inspiration creates decreases in intrathroacic pressure leading to increased venous return to RA/RV, generating increased RV stroke volume (Frank-Starling)
as lungs expand, there is increased pulmonary blood volume leading to decreases in pulmonary venous retunr and decreased LV stroke volume
Inspiration causes _______ in RV stroke volume and _________ in LV stroke volume
increased RV stroke volume
decreases LV stroke volume (usually <5%)
Expiration causes _______ in RV stroke volume and ________ in LV stroke volume
decreased RV stroke volume
increases LV stroke volume
What is the effect of marked changes in intrathoracic pressure that exceeds the pericardium’s reserve volume (ineleastic parietal pericardium)
impaired LV filling
Is the RV larger in inspiration or expiration
inspiration
Is the LV larger in inspiration or expiration
expiration
With pericardial effusion, cardiac function becomes impaired when the pericardial pressure exceeds the:
cardiac filling (diastolic) pressure
fluid accumulation in the pericardial sac that compresses the cardiac chambers and impairs normal filling (diastole)
typically with acute pericardial effusion
cardiac tamponade
The pericardium is relatively (elastic/inelastic)
inelastic
*cardiac function is impaired when the pericardial pressure exceeds the cardiac filling (diastolic) pressure
*slow effusions permit pericardial growth and further stretch
How does acute pericardial effusion differ from chronic pericardial effusion
with rapid effusion (acute effusion) you reach critical tamponade more easily
with slow effusions, like tumor- permit pericardial growth and further stretch
Pulse quality decreases after (inspiration/expiration)
inspiration
Pulse quality increases after (inspiration/expiration)
expiration
pulsus paradoxus
a normal phenomenon where pulse quality will change with inspiration and expiration
inspiration causes decrease in pulse quality because the RV expands and LV’s filling is impaired
expiration causes increase in pulse quality because the LV expands and RV’s filling is impaired
*Made worse with pericardial effusion
alterations in pulse pressure associated with respiration
pulsus paradoxus
a normal phenomenon where pulse quality will change with inspiration and expiration
inspiration causes decrease in pulse pressure because the RV expands and LV’s filling is impaired
expiration causes increase in pulse pressure because the LV expands and RV’s filling is impaired
*Made worse with pericardial effusion
rapid accumulation of small volume of pericardial effusion leading to decreases in SV, CO, and systemic arterial blood pressure via impaired filling of RV
acute cardiac tamponade
What are the clinical effects of acute cardiac tamponade
Syncope, weakness, hypotension, obstructive (shock)
acute peripheral pulse
slow accumulation of typically large volume pericardial effusion leading to
decreases in SV, cardiac output, and systemic arterial blood pressure
but since its slow there can be compensatory increase venous pressure to maintain cardiac filling (RAAS, SNS, ADH)
chronic cardiac tamponade
What allows chronic cardiac tamponade to develop
since there is only a slow accumulation of pericardial effusion it allows for the compensatory mechanisms to increase venous pressure to maintain cardiac filling to occur (fluid retentive state)
a) Increase RAAS
b) SNS
c) ADH/vasopression
d) Lack of increase in B-type natiuretic peptide (BNP) to retain the blood volume
What are the clinical signs of chronic cardiac tamponade
- Mimics- Clinical manifestations of right sided congestive heart failure (systemic venous congestion)
a) jugular venous distension, pulsation
b) distended caudal vena cava and hepatic veins
c) enlarged/congested liver
d) abdominal effusion (ascites)
e) GI upset (hyporexia, vomitting, diarrhea)
*The RV is unable to fill -> leading to backup of blood into the systemic circulation and there is also compensatory mechanism to increase venous pressure (Increased RAAS, SNS, ADH)
Why are animals with right sided heart failure often presenting with vomiting or diarrhea or hyporexia
because there is systemic venous congestion backing up and leading to GI upset
Clinical signs of pericardial effusion (cardiac tamponade)
abdominal distension, collapse (syncope), weakness, ADR, vague GI signs, hypotension, jugular venous distension/pulsation
What will the heart sound like in a patient with pericardial effusion (cardiac tamponade)
muffled (quiet/diminished) heart sounds
Do you see tachycardia or bradycardia with pericardial effusion
tachycardia- compensatory mechanism (SNS)
Does every patient with pericardial effusion have cardiac tamponade
NO- there can be incidental pericardial effusion but confirm tamponade with clinical signs
What is the best way to diagnose pericardial effusion
Echo is useful to diagnose PE and determine the causes of PE
What will you see on radiograph of a patient with pericardial effusion
enlarged, globoid cardiac silhouette with sharp/well defined cardiac margins
On radiograph you see enlarged, globoid cardiac silhouette with sharp/well defined cardiac margins. What is this?
Pericardial effusion
Why o you see sharp/well defined cardiac margins on radiograph of animal with pericardial effusion
because normally you dont get good margins because the heart is beating. when there is pericardial effusion, you get good sharp/well defined margins because the heart is surrounded by the fluid and pericardium
What is electrical alternans *
alterations in R wave voltage due to the heart moving around from pericardial effusions
(low and high alternating R)
alterations in R wave voltage due to the heart moving around from pericardial effusions
(low and high alternating R)
Electrical alternans
What will you see on ECG of an animal with pericardial effusion
Electrical alternans
alterations in R wave voltage due to the heart moving around from pericardial effusions
(low and high alternating R)
the process of removing effusion of the pericardial to improve filling and cardiac function
pericardiocentesis
Why is a pericardiocentesis indicated for patients with pericardial effusion
removing the fluid improves filling and cardiac function
Why should you have intravenous access when performing a pericardiocentesis
to give lidocaine in case you induce an arrhythmia
What side do you tap from when doing a pericardiocentesis
patient in left lateral recumbency or sternal
-TAP ON RIGHT SIDE
because there are less coronary arteries in LV and larger window through the lungs
Why do you tap from the right side when doing a pericardiocentesis
1) Less coronary arteries in LV
2) Larger window through the lungs
Should pericardial effusion clot?
No- clotting factors should have been consumed
if it does clot then you went into the ventricle
What does it mean when the blood clots upon pericardiocentesis
that you likely went into the ventricle
-pericardial effusion should not clot
What is goal of pericardiocentesis
to remove most of the fluid
but the main goal is to make a hole in the pericardium to drain out the fluid into the cavity on its own.
Not all dogs with perciardial effusion need a pericardiocentesis. When should you do a pericardiocentesis
largely based on clinical signs of cardiac tamponade
What should you do prior to pericardiocentesis if the patient is “shock” (hypotensive, weak pulses, history of collapse)
administer IV fluid boluses to help stabilize
If a patient has atrial enlargement and a small volume of PE, is a pericardiocentesis necessary
No- the pericardial effusion is likely secondary to right sided CHF (typical in cats)
How do you tell the difference between pericardial effusion leading to RV diastolic dysfunction or right sided CHF leading to pericardial effusion (typically in cats)
if the right atrium is enlarged then its is likely right sided CHF and the cat has pericardial effusion for that reason
What should you not do if the dog is in cardiac tamponade
give furosemide- this will just make the RV diastolic dysfunction worse
giving fluids will help this if the cardiac failure is secondary to pericardial effusion
What are the 3 broad categories of pericardial effusion
1) Cardiac neoplasia (bleeding tumors)
2) Idiopathic (pericarditis)
3) Other less common, weird things
What are the three cardiac neoplasia that lead to pericardial effusion
1) Hemangiosarcoma*
2) Chemodectoma (aortic body tumor/ heart base mass) *
3) Ectopic thyroid carcinoma
*Others: mesothelioma, lyphoma, other sarcomas, metastatic neoplasms
Should you perform echo to identify a cardiac neoplasm prior or after doing pericardiocentesis
Prior to pericardiocentesis because pericardial effusion makes it easier to identify the cardiac mass (sonolucent fluid around the mass)
but patient stability always comes first
T/F: cytological analysis of pericardial effusion is helpful in identifying the type of cardiac neoplasia cause
false- rarely helpful unless atypical in appearance
Where does hemangiosarcoma typically occur
1) tip of the right auricle 2) right atrioventricular groove
*cavitated tumor
hemangiosarcoma typically occurs in
older purebred dogs (german shepherds, golden retrievers)
How should you treat hemangiosarcoma
*aggressive tumor likely already metastasis
1) palliative resection/auriculectomy sometime possible to prolong life
2) palliative intravascular stenting
3) Chemotherapy (likely dont treat)
Where do chemodectomas typically occur
the aortic body (heart base mass)
What is a consequence of chemodectomas?
since it is located near the aorta and pulmonary artery it can obstruct inflow and outflow
What breeds typically get chemodectoma
brachycephalic breeds- chronically hypoxia (neoplasia of the chemoreceptor)
a neoplasm of the chemoreceptor
seen in bracycephalic breeds
located at the aortic body leading to obstruction in inflow and outflow of aorta and PA
tend to be slower growing, slower to metastasize
chemodectoma
How can you treat chemodectomas
1) palliative intravascular stenting to open up PA and allow more blood flow to lungs
2) Palliative chemo
3) Some success with radiation therapy
*Surgical resection is rarely possible
What should you do if idiopathic pericardial effusion recurs 3 times
pericardial window (pericardial window) or pericardiectomy
is pericardial window or pericardiectomy more invasive more invasive
pericardiectomy is more invasive
pericardial window is less invasive because you can do it with thoracoscopic techniques
What are other rare causes of pericardial effusion, non-neoplastic
1) Manifestation of CHF (cats), right sided CHF (dogs)
2) Left atrial rupture (secondary to severe MR/MMVD)
3) Trauma
4) Coagulopathy
5) Infectious (bacterial, fungal, protozoal)- cloudy, atypical appearance
6) Hypoalbuminemia
7) Pericardial foreign body (porcupine)
8) Others: diaphragmatic hernia
How might a dog with MMVD get PE
Left atrial rupture (secondary to severe MR/MMVD)
PE in cats is most likely due to
CHF (tell by giant left atrium )
constrictive pericardial disease
thickened inelastic pericardium leading to right sided CHF
treat with window or ideally pericardiectomy
Patients with acute cardiac tamponade typically present with
obstructive shock (hypotension, syncope, weakness, weakpulses)
Patients with chronic cardiac tamponade typically present with
signs of right sided CHF without right heart enlargement
Patients with acute cardiac tamponade typically present with ____________
While,
Patients with chronic cardiac tamponade typically present with
_____________
Acute: obstructive shock (hypotension, syncope, weakness, weakpulses)
Chronic: signs of right sided CHF without right heart enlargement
Cardiac tamponade requires emergency treatment with
pericardiocentesis often preceded by IV fluid therapy (if no signs of shock)
