Cardiololgy Flashcards
What is heart failure?
The heart is incapable of deliver oxygenated blood to body tissues to sustain cellular function without elevated right atrium pressure
What affects heart function?
Heart muscle hypertrophy heart valve contractility preload after load
Pathophysiology of heart failure?
Series of compensation ( cardiac and neurohormonal) in response to fall in cardiac output, which lead to irreversible structural, functional, vascular changes of the heart ( increased hypertrophy; poor contractility; increased pre load and after load )
Fall in cardiac output -> activated RAAS -
RAAS- > volume overload ( increased preload )-> vasoconstriction –> elevated BP and increased after load
Starling law reaches its limit despite with increased preload and wall stress compensation
Counter mechanisms that tried to augment RAAS fail
- increased BP
- vaso constriction
- increased preload
- increased after load
- cardiac muscle modeling, hypertrophy, prone of ischaemia and arrhythmia
- cytokines released-> fibrosis
What determines cardiac output?
CO = SV ( stroke volume ) x HR ( heart rate )
stroke volume = preload x contractility ( starling law )
What determines blood pressure
BP = flow x resistance
Flow = CO
Heartworm treatment guidelines
- use of doxy to reduce worm burdens by killing wolbachia- 10mg/kg BID 28 days
- wait 1 month then start adulticide with melarsomine
- 3 dose melarsomine 60 days, 90 days, 91 days IM injection to achieve 99 percent kill
- strict exercise control from the time of diagnosis confirm, and start prednisone when worm preventative start from day 1 with macrocytic lactone ( kill larvae )
pathophysiology of Heartworm disease in dog
- pathological changes in pulmonary artery- worm burden and time dependant- inflammation, thickening
- high worm burden obstruct RV outflow tract –> canal syndrome
- Hypoxia-> vasoconstriction in lung -> Cor pulmonale ( pulmonary hypertension > 25 mmHg -> RV remodelling to increase systolic fx –> tricuspid valve regurgitation –> Right side heart failure ( hepatic congestion, cirrhosis, )
- antigen- antibody complex –> glomerulonephritis
- host immune response to wolbachia ( harbour by D. immitus )
- worms causing pulmonary thromboembolism
- eosinophilic bronchopathy / lung changes
Heartworm test methods
antigen test ( adult female protein of the uterus ): heat test can increase sensitivity
Microfilaria ( larvae produced from adult female, visible on blood smear )
Echo scan
What is ECG?
Shows depolarisation and depolarisation of the heart and how the electrical activity is conducted.
Most common arrhythmia in dogs and cats
Atrial fibrillation and ventricular tachycardia
How does Lidocaine work ?
What class?
In what clinical use in arrhythmia
Na channel blocker class I b Ventricular tachycardia in dog as IV bolus/ infusion
Diltiazem
- mode of action
- class
- clinical application in arrythmia
- Ca channel blocker: negative inotrope, chronotrope: causes vasodilation, slow down conduction through AV node, affect SA node firing.
- IV
- Supraventricular tachyarrythmia, atrial fibrillation,
Digoxin
- mode of action
- class
- clinical application in arrythmia
- cardiac glycoside: affect Na and K channel
- mildly positive inotrope ( compared to pimobendan ) , negative chronotrope by increase vagal tone( via increase baroreceptor sensitivity )
- narrow therapeutic index- any sign of concern toxicity stop the drug rather than lower the dose
- recommended dosage is much lower than once thought
- Use to slow any ventricular tachycardia, and also atrial fibrillation
Drug used in management of stage C MMVD
- diuretic ( frusemide ) : Affect Na pump in ascending loop of Henley causing natriuresis
- ACE inhibitor ( block the production of aldosterone and angiotensin II ) –> reduce pre load and after load , and remodelling of the heart
- Pimobendan : Class III phosphodiesterase inhibitor ( positive inotrope and vasodilator ) -> decrease after load , improve cardiac systolic fx without increase oxygen demand. Preclinical use has advantage of delay CHF onset for 18 months.
- Spinolactone : aldosterone blocker ( reduce cardiac remodelling, Na/ water retention .
MMVD stages explain
A: asymptomatic , at risk dog
B. 1 : murmur symptoms only
B. 2: Murmurr symptom with cardiac enlargement ( left side )
C: Congestive heart failure needed treatment
D: Advanced congestive heart failure refractory to treatment
ECG
- measures electrical conductivity pattern, rate of the heart
- P : atria depolarisation
- QRS complex: Ventricular depolarisation
- T: dépolarisation of ventricular
- assess rate, any AV block, any ectopic beat ( premature vs escape/ late )
type of AV block
sinus arrythmia : variable PR interval with wandering pace maker
Secondary AV block
type 1 - PR interval increasing then AV block
type 2- there could be some AV block regardless of the PR interval
Third degree AV block
- complete dissociation of P and QRS, complete AV block. Escape beat from either junctional( 40-60bpm) or ventricular ( 20-40bpm )
Explain the RAAS
- Renin produced in the juxtoglomerular( next to glomerulus) apparatus , in response to stimuli
- angiotensinogen ( inactive form ) in liver becomes angiotensin I , in the presence of renin
- ACE found in many endothelium of tissues
- convert angiotensin 1 to II
- angiotensin II stimulates
a ) production of aldosterone
b) ADH release
c) vasoconstriction
d) increase sympathetic activity of heart
DCM definition
a condition where there is systolic dysfunction due to cardiac enlargement .
What is the best way to screen for occult DCM and predict DCM manifestation.
How has biomarker such as proBNP or troponin helped?
Holter 24 hour for ECG evaluation of any AF, VPC, and the heart rate.
Biomarker is less useful compared to holter.
Why is vasodilator use in caution in DCM or dogs with low cardiac reserve
Vasodilation can potentiate hypotension, which lead to reflex tachycardia, more detrimental effect.
Genetic predisposition of DCM , what do we know of.
Among different breeds, some dominant, some recessive, some is sex-linked.
Treatment for DCM
- manage congestive heart failure signs ( diuretics, ACE inhibitor, pimobendan +/- digoxin or diltiazem )
True or false. All dogs with DCM will have arrhythmia as clinical feature.
false.
True or false. Can DCM dog have sudden death before onset of CHF.
True.
has ACE inhibitor help in pre-clinical DCM survival ?
Not on clinical trial so far.
What is the prognosis of DCM
Guarded to poor. Once in stage C, survival time is rarely > 6 months. Most die within 3 months.
Most common myocardial dz in dog
Dilated cardiomyopathy. - Primary ( no underlying cause other than possible genetic mutation )
Nutritional deficiency that may lead to cardiomyopathy
- taurine
- L carnitine
What is heart preferred fuel source for ATP
Fatty acids , e.g acetone rather than glucose
drug of choice for ventricular tachyarrythmia with normal echo
abnormal echo
Sotolol ( negative inotrope )- class III antiarrythmia.
Amiodorone
Most common cause of hemorrhagic pericardial effusion in dog
- HSA
Most common cause of heart tumour in dog
HSA, chemodectoma, mesothelioma, malignant histiocytosis
pathophysiology of pericardial effusion
Intraperitoneal pp > diastolic PP –> impede filling –> poor CO
Decreased filling–> backward congestion
Chronic inflammation –> fibrosis –> constrictive pericardial disease
Technique pericardiocentesis
19-21 gauge needed
from right side, CC jx 4th - 6 th rib, cranial border, towards left shower. Left Recumbancy
Most common congenital heart condition in dog
and cat
PDA & sub aortic stenosis.
Pulmonic stenosis also is common.
cat: AV valve dysplasia; atria/ ventricle septal defect
PDA features
Aorta blood shunts into pulmonary aorta. This ductus is usually closed at birth.
Murmur: continuous machine murmur
loudest at left heart base area
sub aortic stenosis
Murmur heard during systolic- click- crescendo decrescendo. Loudest at left heart base.
mitral valve regurgitation
murmur loudest left apex. Holosystolic systolic murmur.
