Cardiology Flashcards
What is the most common group of organisms implicated in acute infective endocarditis?
GRAM POSITIVE COCCI:
Single most common organism in developed countries = Staph aureus
Staph epidermidis = the most common organism in the initial 2 month period following prosthetic valve replacement (and commonly colonises indwelling lines)
Strep viridans = colonise the mouth, often implicated in those with poor oral hygiene or after a dental procedure - more common causative organism in developing countries.
Strep bovus = associated with colorectal cancer
What is the 1st line Abx regimen for native valve endocarditis?
Amoxicillin + Gentamicin until blood cultures available - for 4-6 wks
If MRSA suspected, patient is severely septic or they have a penicillin allergy = Vancomycin + Gentamicin
Prosthetic valve endocarditis = Vancomycin + Gentamicin + Rifampicin
Which valve is most commonly affected valve in bacterial endocarditis in those without any prosthetic valves?
Mitral Valve
What are the most important risk factors for bacterial endocarditis?
Single most important risk factor = history of previous bacterial endocarditis
Others: rheumatic valve disease, prosthetic valves, congenital cardiac defect, IVDU, recent piercing
What are the typical ECG changes in hyperkalaemia?
Earliest manifestation = peaked T waves
Then = Flattening and widening of the P waves, prolonged PR interval, widening of the QRS with abnormal morphology, bradyarrythmias with conduction blocks.
What are the doses of atorvastatin used for primary v secondary prevention?
Primary prevention = 20mg
Secondary prevention = 80mg
What is HOCM
Hypertrophic Obstructive Cardiomyopathy
= an autosomal dominant disorder of the muscle tissue of the heart.
May present with exertional dyspnoea.
Echo findings = mitral regurg, LV outflow obstruction, assymetrical hypertrophy
Mx = Amiodarone
+/- beta blocker / verapamil for symptom control
May need dual chamber pacemaker.
AVOID ACEi and NITRATES IN HOCM AS REDUCES AFTERLOAD SO REDUCED LV GRADIENT.
Which two beta blockers are shown to reduce mortality in stable heart failure?
Bisoprolol and carvedilol
What is the classical presentation of digoxin toxicity?
Vague: fatigue, GI upset, yellow/green vision (xanthopsia), gynaecomastia, AV block/bradycardia
What is the mechanism of action of digoxin?
Na/K+/ATPase inhibitor.
= decreased AV node conduction (slow ventricular response in AF) + increased cardiac contractility (improves symptoms but not mortality in HF)
What are common precipitating factors for digoxin toxicity?
HYPOKALAEMIA (because digoxin competes with potassium at the Na/K/ATPase pump) -> thus thiazide and loop diuretics can trigger.
HYPERNATRAEMIA
HYPERCALCAEMIA
LOW ALBUMIN
LOW MAGNESIUM
RENAL FAILURE
HYPOTHERMIA
HYPOTHYROIDISM
DRUGS -> thiazide/loop diuretics (through hypokaelamia), spironolactone (because competes for excretion in the kidneys thus leads to higher levels of dig building up!), amiodarone, calcium channel blockers (verapamil and diltiazem), quinidine, ciclosporins
How would you monitor for digoxin toxicity?
Dig -> routine serum levels not check.
Toxicity can occur even with THERAPEUTIC LEVELS
If suspect toxicity, take dig levels 8-12 hrs after the last dose
Therapeutic level is <1. Toxicity is increasingly likely once >1.5
What is the typical presentation of crescendo, variant and decubitus angina?
Crescendo / unstable angina = comes on at rest or with minimal exertion / increasing severity + frequency of episodes.
Variant angina = comes on at rest
Decubitus angina = comes on when lying flat
What are the 1st line agents for SYMPTOM RELIEF in stable angina.
Sublingual GTN + a beta blocker or calcium channel blocker
If beta blocker + calcium channel blocker both contraindicated, isosorbide mononitrate is an alternative option
Which diagnoses are consistent with an ejection systolic murmur?
Aortic stenosis
Aortic sclerosis
Pulmonary stenosis
Hypertrophic cardiomyopathy
Flow murmurs (occur during high flow states eg pregnancy, do not warrant further investigation)
What diameter of AAA should be offered elective repair?
5.5cm or greater
What makes up the CHADVAS score when assessing re need for anticoagulation in AF?
Age (<65 = 0 65-74 = +1, 75 or older = +2)
Female gender +1
Diabetes = +1
Hypertension = +1
Congestive Heart Failure = +1
Prev TIA/STROKE/VTE = +2
Prev arterial event ie MI, aortic plaque or PAD) = +1
What is the typical presentation of an atrial myoxoma?
Benign overgrowth, most commonly in the LEFT ATRIUM
More common in females
= mitral valve obstruction = diastolic murmur, symptoms of heart failure, syncope and dizziness
Causes of LBBB?
- Ischaemic heart disease (new LBBB fits the criteria for STEMI in the presence of symptoms of ACS)
- Idiopathic fibrosis
- Cardiomyopathy
- Hypertension
Causes of RBBB?
- Cor pulmonale
- Cardiomyopathy
ECG changes in hyperkalaemia?
- Tall tented T waves
- Flattened P waves
- Increased PR interval
- Widened QRS complexes
_> progression to VT or VF
ECG changes in hypokalaemia?
everything gets low!!
- Flattened T waves
- ST depression
- prominent U waves (the wave after the T wave)