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SA Cardiology (1) - Coggle Diagram
SA Cardiology (1)
CARDIAC Dz
Small breed, older dog (>5yo)
MMVD
(Myxomatous Mitral Valve Disease)
progresses slowly
Path: affects mitral and tricuspid valve leaflets and chordae tendinae (valve motion, prolapse, thickening, dilation of AV lumen, valve regurgitation)
CS
Heart murmur- apex/left/systolic
Cough- but may not be related
Consequences
CHF (
stage C
) WILL DEVELOP- LCHF first then RCHF
Chordae tendinae may rupture
Arrhythmia- with syncope
Cardia cachexia
Atrium rupture
Myocardial exhaustion
Breed (large, doberman, spaniels, dalmatians, Portuguese water dog),
older, male DOGS
DCM
(Idiopathic Dilated Cardiomyopathy)
Genetics factors- not fully understood
Primary dz of heart m.
Staged in same way to HF
Presentation and CS= breed dependent
PROGRESSES FAST
- usually
presents to you in Stage C
(diff from MMVD)
Dx
Sx
Thoracic radiography ONCE STABLE
(generalised heart enlargement- CHF- large caudal VC)
Echocardiogram
-refer
ECG- if hear arrhythmia on auscultation
Primarily cause LSHF
(reduced CO to systemic circulation, LS congestion- cardiogenic pulmonary oedema, increased pulmonary venous P)
Previous Hx of MMVD/DCM
(not req.)
Absence of HW prophy.
RSHF
why signs of LS forward failure- Dz reduces RS CO- which reduces L sided filling= reduces left sided CO
WHY OCCURS
sig. afterload to RV:
Pulmonary a. affected
Severe lung dz (flow of blood through lung compromised- stenosis, pneumonia/pneumonitis/ LCHF)
Pulmonary a. stenosis (dirofilariasis)
Pulmonic stenosis (PS)
Often see:
Pulmonary Hypertensio
n
what= a sustained increase in pulmonary a. systolic mean/diastolic P AKA afterload of the RV
Causes
Left HD: Chronic MMVD= PV hypertension= high P in pulmonary alveolar capillary bed= PA hypertension
Pulmonary a. dz: thickening E.g. Dirofilariasis OR L to R shunts
Lung Dz and/or hypoxaemia E.g. chronic lung Dz, pulmonary fibrosis
Pulmonary thrombotic or embolic Dz
Dx: Radiography
(CT with contrast, RA and V enlargement and dilation of PA), Echo, ECG-
right chamber enlargemen
t
PE=
Tricuspid murmur
(pulmonic if PS),
Split S2
high systemic venous P= Jugular pulses, hepatomegaly, distended abdomen
- ascites
LS forward failure WITHOUT lung congestion
(
weakness,
pallor, slow capillary refill time,
syncope
)
Large breed dogs
common (Golden retriever, GSD), Idiopathic
Hx: weakness and collapse, shock,
MUFFLED HEART SOUNDS
, signs of reduced CO (low CRT),
signs of RSCHF
Pericardial Effusion
Dx
Thoracic US: definitive, see the effusion and collapse of right side, masses causing effusion
Thoracic Radiographs: large globoid heart
ECG: sinus tachycardia with low voltage QRS complexes, electrical alternans
Right side
more than left: (thinner)
Effect of the P on right ventricle
= diastolic filling problem=
cardiac tamponade
(life threatening)= decreased RS CO= decrease LS CO=
RSHF/collapse
Exercise intolerance, weight loss then lethargy
Coughing- MAIN CS
Dyspnoea, coughing blood, abdominal enlargement-ascites, collapse "caval syndrome."
Heartworm
Feline
CAT EMERGENCY
OFTEN
Incidental murmur/
gallop rhythm
Acute CHF +/- pleural effusion
Resp distress, tachypnoea, anorexia, lethargy,
Recent event
Hing limb paresis
Sudden Cardiac Death
FHCM
(Feline Hypertrophic Cardiomyopathy)
Pathophysiology: NEED TO KNOW
Myocardial wall thickening and inelasticity (stiffness)= diastolic filling problem
Exacerbated by systolic anterior motion (SAM) of mitral valve= left ventricular outflow tract obstruction LVOTO
Severe LA enlargement= may develop thrombi
Preload= cardiogenic pulmonary oedema
Thrombi= embolism (including FATE)
Pleural Effusion
Secondary Hypertrophic Cardiomyopathy
in cats
Assoc. with 2 common syndromes in cats
Feline hyperthyroidism
Systemic hypertension
35-50% cats with HCM
Pain, cardiac dz, hypothermia, cold extremities, absent pulses, cyanosis of feet, no haemorrhage if nails cut short, m. painful/firm, loss of motor function, decreased cutaneous sensation and limb reflexes
ATE
(Aortic Thromboembolism)
Risk Factors
any feline cardiomyopathy
enlargement LA
sluggish BF in LA- "smoke."
Endothelial damage- hard to confirm
thrombus in LA
Typical sites= aortic trifurcation/ iliac a., renal a., brachial (esp right) a.
Clinical Findings
Unremarkable
CS only start when compensatory mechanisms fail.
E.g. Murmurs, Mild arrythmias, Cardiomegaly= no CS
Ambiguous
E.g. Exercise Intolerance: concurrent osteoarthritis
E.g. Coughing: concurrent tracheal Dz
E.g. Dyspnoea: concurrent laryngeal paralysis
HEART FAILURE: HX
Poor growth- congenital
Weight loss- severe (cardiac cachexia)
Poor/ reduced CO/
poor peripheral perfusion
(FORWARD FAILURE)
weakness
syncope
pale mm
prolonged CRT
elevated HR
absence of sinus arrhythmia
weak femoral pulse
cool extremities
Congestion (BACKWARD FAILURE)
LCHF (lungs)= crackles, high RR (>30 for d, >40 for c), coughing, dyspnoea, cyanosis
RCHF (systemic venous): jugular pulse, abdominal distension (ascites, hepatomegaly, Pleural effusion (d)
Tests
Thoracic radiography
Technique= Lateral and DV, DURING INSPIRATION.
Examine: cardiac sillhouette, pulmonary patterns, major vessels, airways, pleural space.
Findings
Left atrial enlargement with
Pulmonary vein distenion/ enlargement with
Pulmonary infiltrates (interstitial/ alveolar) and
Cardiomegaly or tracheal elevation (= remodelling) with increased Vertebral heart Score (VHS)
Findings that DONT SUPPORT
Single lung lobe involvement, bronchial/ modular lung pattern (other dz), no cardiac enlargement/ remodelling
Cardiac biomarkers
To determine if HF definitely present
NT pro-BNP: Idexx (released when ventricles dilate/ hypertrophic/ under tension)
Electrocardiography
Indicated= when arrhythmia is detected
What: ID cardiac rhythm and conduction disturbances
Guides anti-arrhythmic drug medication
Echo
cardiography
MOST USEFUL
What: US examination of the heart
BUT- to get the most out of it need more training
Ddx Resp Dz vs Cardiac Dz
Thoracic Radiography
Cardiac biomarkers