Pericardial Disease VETM 5291 28 Jan 2025 PDF

PERICARDIAL VETM 5291 - Cardiovascular, Resp, Hemolymph II Mandy Coleman, DVM, DACVIM (Cardiology) DISEASES [email protected] LEARNING OBJECTIVES By the end of this hour, you will be able to… ▪ Understand the anatomy and proposed functions of the pericardium ▪ Understand th...

PERICARDIAL VETM 5291 - Cardiovascular, Resp, Hemolymph II Mandy Coleman, DVM, DACVIM (Cardiology) DISEASES [email protected] LEARNING OBJECTIVES By the end of this hour, you will be able to… ▪ Understand the anatomy and proposed functions of the pericardium ▪ Understand the hemodynamic/clinical consequences of pericardial effusion (PE) ▪ Be able to recognize physical examination findings in a patient with PE ▪ Know the most common causes of PE in dogs, cats, cows and horses ▪ Develop a general approach to the acute and chronic management of PE  Normal pericardial anatomy ▪ Parietal pericardium ▪ Tough, outer fibro-serous membrane ▪ Visceral pericardium (epicardium) ▪ Delicate, inner serous membrane ▪ Single layer of mesothelial cells adhered to myocardium ▪ Pericardial cavity (potential space), contains small amount of fluid: ▪ ¼ mL/kg body weight ▪ Protein – 1.7-3.5 g/dL ▪ Low cellularity www.micc.com Functions of the Pericardium ▪ Anatomical fixation of the heart ▪ Prevents excessive movement with changes in body position ▪ Helps to maintain optimal functional shape of the heart ▪ Prevents chamber overdistension (pericardial restraint) ▪ Supports ventricular coupling (interdependence) ▪ Reduces friction ▪ Provides physical barrier to infection and malignancy Non-essential? ^ Functions of the Pericardium ▪ Anatomical fixation of the heart ▪ Prevents excessive movement with changes in body position ▪ Helps to maintain optimal functional shape of the heart ▪ Prevents chamber overdistension (pericardial restraint) ▪ Supports ventricular coupling (interdependence) ▪ Reduces friction ▪ Provides physical barrier to infection and malignancy Surgical removal of the pericardium does not cause clinically significant hemodynamic alterations in the normal heart Properties of the normal pericardium ▪ Normal pressure in pericardial space ≤ 0 (parallels that Pressure in pericardial space of pleural space) ▪ Minimal effect on cardiac filling ▪ The pericardium has a small reserve volume ▪ When volume of pericardial contents > reserve volume, compliance decreases dramatically, causing intra-pericardial pressure to rise Volume in pericardial space Pericardial effusion (PE) ▪ Excessive, abnormal fluid accumulation in the pericardial space ▪ Most common pericardial disorder affecting veterinary patients ▪ Condition most likely to lead to tamponade and CHF Pericardial effusion (PE) ▪ Effusion > pericardial reserve volume can increase Right atrium Left atrium intrapericardial pressure, compress heart, and impair its function 5-7 ▪ Most susceptible = right atrium/right ventricle in DIASTOLE 0-5 120 5-10 25 ▪ Cardiac tamponade: 0-5 ▪ Occurs when intrapericardial pressure is high enough to impair venous return to the right heart Normal intracardiac pressures (S/D, mmHg) Pericardial effusion (PE) ▪ Consequences of cardiac tamponade: ▪ Right-sided CHF ▪ Increased diastolic filling pressures ▪ Ascites, pleural effusion ▪ Cardiogenic shock ▪ Decreased preload, stroke volume, cardiac output ▪ Death if untreated Pericardial effusion (PE) ▪ With respect to hemodynamic effects, intrapericardial pressure matters more than volume! ▪ Once PE > 2-7 mL/kg (reserve volume), pressure rise depends on rate of fluid build-up ▪ The pericardium can hypertrophy/stretch to accommodate a large volume of fluid without significant elevations in pressure if accumulation is slow Influence of RATE of PE accumulation Pressure in pericardial space Volume in pericardial space How is this clinically relevant? Clinical consequences of PE CHRONIC PE/TAMPONADE ACUTE PE/TAMPONADE ▪ Ex: slowly-developing neoplastic effusion ▪ Ex: acute hemorrhage ▪ Compensatory responses possible ▪ No time for long-term compensatory responses ▪ Pericardial dilation (hypertrophy) ▪ Activation of renin-angiotensin-aldosterone system ▪ Gradual onset of clinical signs ▪ Acute onset, rapidly progressive ▪ Right-sided CHF predominates ▪ Decreased cardiac output, cardiogenic shock predominate Physical examination findings ▪ Jugular venous distension/pulsation ▪ Muffled heart sounds ▪ Systemic hypotension ▪ Tachycardia ▪ Abdominal distension “Beck’s Triad” ▪ “Pulsus paradoxus” (more soon) Because findings are variable and inconsistent, index of suspicion is very important! Physical examination findings Jugular venous distension/pulsation in a horse with chronic PE Physical examination findings Severe abdominal distension due to acites in a Jugular venous distension and ventral edema dog with chronic PE (head/brisket) in a cow with PE Physical examination findings: Pulsus paradoxus (dogs) Exhalation: ▪ Phasic variation in arterial pulse quality: ▪ Inspiratory pressure decrease >10 mm Hg IVS ▪ Exaggeration of normal phenomenon! During inhalation (vs. exhalation): ▪ Decreased intra-thoracic pressure = better venous return to right heart = greater right-sided filling RV Inhalation: = leftward shift of interventricular septum (IVS) LV ▪ Blood pools in pulmonary vessels ▪ Result - decreased filling of the left ventricle, weaker pulse on those beats ▪ Pericardial effusion exaggerates this ventricular interdependence, making pulse variation detectable de cre ure ased ess intrapleural pr  Diagnostic testing – Thoracic radiographs Classic findings: “Globoid” cardiac silhouette without specific chamber enlargement pattern(s) Sharply delineated (“crisp”) margins of cardiac silhouette Bilateral contact between the cardiac silhouette and thoracic wall (DV or VD) Small pulmonary vasculature  Diagnostic testing – Thoracic radiographs Classic findings: “Globoid” cardiac silhouette without specific chamber enlargement pattern(s) Sharply delineated (“crisp”) margins of cardiac silhouette Bilateral contact between the cardiac silhouette and thoracic wall (DV or VD) Small pulmonary vasculature Diagnostic testing – Thoracic radiographs Vertebral heart score (R lateral) = 12.0 Diagnostic testing – Echocardiography PE PE Echocardiography Confirm presence of effusion Assess for tamponade is used to: Look for cardiac/pericardial tumors Causes of PE: DOG NEOPLASTIC NON-NEOPLASTIC ▪ Right atrial hemangiosarcoma* ▪ Idiopathic hemorrhagic PE* ▪ Infectious (bacterial/fungal) ▪ Heart base tumors* ▪ Traumatic, penetrating foreign body ▪ Chemodectoma (syn: aortic body tumor) ▪ Coagulopathy (e.g., warfarin toxicity) ▪ Ectopic thyroid carcinoma ▪ Left atrial rupture ▪ Mesothelioma ▪ Small volumes seen with: ▪ Lymphoma ▪ Uremia ▪ Hypoalbuminemia ▪ Other primary and metastatic sarcomas/carcinomas ▪ Congestive heart failure Canine PE are typically hemorrhagic/serosanguinous, non/mildly inflammatory, non-septic * These three causes account for >90% of canine cases Causes of pericardial effusion NEOPLASTIC NON-NEOPLASTIC Notes Left-sided CHF* Lymphoma PE of enough volume to cause FIP (“wet” form)* tamponade is VERY RARE in the cat Primary cardiac tumors (rare) Sepsis, idiopathic pericarditis, toxoplasmosis, uremia (uncommon to rare) Idiopathic pericarditis* Lymphoma (rare) Bacterial/viral pericarditis PE in horses are typically fibrinous, Mesothelioma (rare) inflammatory, and often septic Trauma/vessel rupture, penetrating foreign bodies (rare) Traumatic reticulopericarditis (hardware disease)** Most PE in cattle are fibrinous, Lymphoma Idiopathic hemorrhagic pericarditis inflammatory, and often septic Septicemia, extension of pleural/pulmonary infection Bovine traumatic reticulopericarditis Images from Braun, Vet J 2009 Acute management of PE ▪ Ultrasound useful to confirm presence of PE and guide tap ▪ Pericardiocentesis (pericardial “tap”) ▪ Diagnostic and therapeutic ▪ ASAP! If stable, postpone until after echocardiogram ▪ “Tap” from the right, 4-6 intercostal space ▪ Intravenous fluids if animal is unstable ▪ Hypotension, tachycardia, collapse ▪ Supportive until pericardiocentesis performed ▪ Do not administer diuretics! These patients are highly dependent on preload to maintain CO! “Chronic” management of PE ▪ Submit fluid obtained by pericardiocentesis ▪ Likely to obtain diagnosis in cases of lymphoma or infectious diseases ▪ Recurrent pericardial effusion NOT due to aggressive neoplasia (e.g., hemangiosarcoma): pericardiectomy following 2 recurrences ▪ Septic pericarditis ▪ Appropriate antimicrobial therapy ▪ Continuous/intermittent pericardial drainage