Cardiology: Clinical Flashcards
Sodium Nitroprusside
- Main indications
- MoA
- Relevant pharmacology
- Side effects/Contraindications
- Other considerations
Indications: Smooth muscle relaxant, used for treatment of acute severe hypertension and CHF
MoA: provides the smooth muscle cell with nitric oxide. It significantly decreases total peripheral resistance.
Side effects: mainly hypotension. Can also cause irritation at injection sites and extraversion should be avoided
Nitroglycerin
- Main indications
- MoA
- Relevant pharmacology
- Side effects/Contraindications
- Other considerations
Indications: CHF or hypertension
MoA: venodilator therefore reducing preload, myocardial oxygen demand, Essentially it is broken down into nitric oxide
Side effects: rash and headaches, hypotension.
Other: tolerance will develop within 48-72 hours.
What receptors does dobutamine work on?
What is its advantage over dopamine?
Predominantly beta-1
It also has a mild beta 2 and alpha 1 effect - these tend to cancer each other out.
Dopamine leads to a release of endogenous norepinephrine whereas dobutamine does not.
Digoxin
- Main indications
- MoA
- Relevant pharmacology
- Side effects/Contraindications
- Other considerations
Indications: supraventricular arrhythmias (mainly AFib).
MoA:
- Increases myocardial contractility
- Decreases conduction velocity through the AVN
These are thought to result from increased calcium availability to myofibrils and inhibition of Na/KATPase.
Relevant pharmacology: really excreted, careful with MDR1
Side effects:
- Do not extravase
- Arrythmias
- Gastrointestinal upset
Amiodarone
- Main indications
- MoA
- Relevant pharmacology
- Side effects/Contraindications
- Other considerations
Indications: can be used for most arrhythmia but due to the side-effects it is usually a last-line treatment.
- MoA: primarily potassium blockade but also has beta and calcium channel blocking effects.
- Side Effects/Contraindications:
- Don’t use in thyroidal disease patients
- GI, hepatotoxicity, neutropenia, thrombocytopenia, keratopathy
- Skin effects
Pimobendan
- Main indications
- MoA
- Relevant pharmacology
- Side effects/Contraindications
- Other considerations
Indications: heart diesease
MoA:
Positive inotrope, vasodilation, indirect negative chronotrope.
Inhibition of PDEIII and increase in calcium sensitivity of contractile apparatus without changing intracellular calcium concentrations. PDEIII inhibition increases cAMP which increases cardiac contraction but inhibits it in vascular smooth muscle (I think!).
What does PDE III do?
It converts cAMP to AMP.
MoA of aspirin?
COX-1 inhibition through acetylation of the enzyme.
MoA of heparin
Enhances the activity of AT III.
This results in inhibition of thrombin (IIa), Xa, IXa and XIIa.
At higher doses it prevents thrombin from activating V and VIII.
MoA of urokinase/streptokinase
Convert plasminogen to plasmin
MoA Warfarin
Inhibits vitamin K epoxide reductase (so vitamin K epoxide cannot be refreshed into vitamin K to be used in carboxylation of II, IV, VII, IX, X).
It also inhibits the production of protein C and S so can cause an initial hypercoaguable state.
Clopidogrel effects
The membrane ADP(2Y12) receptor on platelets which prevents platelet activation. Altering this receptor prevents membrane complex IIB/IIIA forming fully which prevents release of vasoactive compounds such as ADP and serotonin and also prevents binding to fibrin and vWF. This alteration is permanent throughout the life of the platelet.
What are the main types of heart failure?
Diastolic failure
Volume overload (or reduced ability to pump e.g. DCM, MMVD, shunts)
Increased afterload (e.g. valvular stenosis)
Arrhythmia related
What are the main neurohormonal alterations in heart failure?
Sympathetic stimulation
RAAS activation
ANP and BNP over secretion
Increased adrenomedullin, endothelia and AVP
Increase in pro-inflammatory cytokines such as TNF-a, IL-1 and IL-6.
Which enzyme is present in the adrenal medulla that allows the conversion of nEP to EP?
Phenyletholamine N-methyltransferase (PNM)
CNP - what does it do, where is it produced?
It is produced in the vasculature and may relax vessels.
What are the receptors and functions that AVP can act on?
V1A = increases inotropy and causes vasoconstriction V2 = renal reabsorption of H20 V2r = baroreceptors to augment the baroreceptor reflex
Why is AVP thought to be released in heart failure?
Probably due to a reduced cardiac output, as otherwise the state is one of low osmolality.
What is the result of sympathetic stimulation on the vasculature?
There is increased venous return which helps to increase preload but there is also increased after load which will lead to further cardiac remodelling.
Why might endothelin-1 be increased in CHF?
It is unregulated by many of the vasoactive hormones e.g. AVP, ANGII, nEP, and bradykinin. It will contribute to vasocontstriction
What are the three stages of cardiac hypertrophy?
- Initiation of hypertrophy in response to increased wall stress (pressure/volume).
- Compensation
- Exhaustion (cardiomycocyte death etc.)
Why are cats more prone to a pleural effusion with left sided CHF?
Their pleural veins drain into the pulmonary vein so back pressure from the LA will affect them more.
Prevalence of canine infective endocarditis?
0.09-6.6%
What congenital cardiac diseases IS IE likely in?
PDA and aortic stenosis
What are the more common bacteria causing IE?
Staphylococcus, streptococcus and Bartonella.
How does the type of bacterial infection relate to presentation of IE?
Gram positive is often more chronic, Gram negative often more acute.
Which valve is most likely to be affected by IE?
Mitral, then aortic.
Outline the modified Duke’s criteria for diagnosis of IE
3 major criteria
7 minor criteria
definite vs possible criteria
Most common congential cardiac diseases
PDA, subaortic stenosis, pulmonic stenosis
What is Eisenmonger’s syndrome?
Right to left shunting. This results when PHT becomes so severe it reverses the left to right shunt.
Why does the ductus arteriosus normally close?
Sudden decrease in pulmonary vascular resistance following birth means that the flow stops across the vessel and the oxygenated blood inhibitis local prostaglandin release.
What are the defining features of tetralogy of fallot?
RVOTO - pulmonic stenosis
Right ventricular hypertrophy (secondary to above)
VSD
Right transposed (overriding) aorta
What amino acid deficiency was historically responsible for DCM in cats?
Taurine
Is MMVD more common in male or female dogs?
Male (1.5x more likely)
What percentage of small breed dogs may be affected by MMVD when over 13 years of age?
85%
How often should dogs with B1 MMVD be monitored echocardiographically?
Every 6-12 months
Which of the following is not reccomended in dogs with stage B2 MMVD?
Pimobendan
ACE inhibitor
Cough supressant
Spironolactone
Spironolactone
What is the frusemide cutoff that defines a dog as stage D MMVD?
8mg/kg/day, although this must be with appropriate rate control in dogs with AFib.
What is the starting dose reccomendation for in hospital therapy of CHF caused by MMVD?
2mg/kg then repeat hourly.
What degree of SBP elevation is expected in sighthouds compared to mixed-breed dogs?
10mmHg
What is the next step in the diagnostic pathway for diagnosis of hypertension in a dog that has a blood pressure 165mmHg and no evidence of TOD?
repeat the SBP a further 2 times within 4-8 weeks
How often should patients with a risk factor for hypertension (e.g. phaeochromocytoma) be re-evaluated?
Every 6 months
What is the ideal target for management of hypertension?
<140mmHg
What treatment should be instituted for a dog with NIBP >200mmHg and evidence of TOD?
RAAS inhibitor as well as a CCB
What is the correct starting dose of amlodipine for a cat with a SBP >200mmHg in which you have decided to treat?
1.25mg
