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145 Cards in this Set

  • Front
  • Back
What is the most common cause of infective endocarditis?
Strep viridans

IVDU - Staph aureus
NB: Strep bovis associated with colorectal cancer
Which bacteria is commonly involved in IE associated with prosthetic valves
staph epidermidis
Which rises first following a MI
Troponin or CK-MB?
CK-MB rises after 2-6 hours
Troponin rises after 4-6 hours
NB: myoglobin rises first 1-2 hours
Which takes the longest to go down troponin or CK-MB
troponin takes 7-10 days
CK-MB takes 2-3 days
Which disease causes
shortened PR interval, wide QRS with a slurred upstroke seen in lead II?
Wolf Parkinson White syndrome
Management of Wolf Parkinson White syndrome
radiofrequency ablation of accessory pathway
Which coronary artery supplies the inferior area of the heart? Which leads will it be in?
right, leads II, III, aVF
Which coronary artery supplies the anteroseptal area of the heart? Which leads will the problem be in?
left anterior descending, V1-4
Which coronary artery supplies the lateral side of the heart? Which leads will the problem be in?
I, aVL +/- V5-6
Left circumflex
Which coronary artery supplies the posterior side of the heart? Which leads will the problem be in?
all R waves V1-2
Usually left circumflex, also right coronary
Which coronary artery supplies the anteriolateral side of the heart? Which leads will the problem be in?
V4-6, I, aVL
Left anterior descending or left circumflex
First line therapy for uncomplicated hypertension
ACEi
Pharmacological treatment of hypertension in diabetics
ACEi
thiazides may increase glucose intolerance
What does a long QT interval predispose someone to?
ventricular tachycardia specifically vulnerable to torsades de points
Pathophysiology of long QT
Prolonged ventricular repolarisation
Different parts of myocardium repolarising at different times
Set up circuit tachycardia
What typically triggers torsades de points in someone with congenital long QT syndrome?
stress, physical exertion, fright
How do you manage congenital long QT syndrome
Beta blockers - abolish symptoms in 80% of cases but will produce significant bradycardia which does increase the long QT interval - give pacing then
ICD
Pacing
Mexiletine
What are the most common causes of acquired long QT syndrome?
hypocalcaemia
Hypomagnesemia
Hypokalaemia
Drugs - sotalol, amiodarone, procainamide, lithium, TCAs, Quinines
What is brugada syndrome?
Rare syndrome characterised by sudden death due to VF in anb otherwise structurally normal heart
Associated with mutations in the sodium channel gene
How long is a normal QT interval?
2 large squares
460ms
What ECG changes do you see with hyperkalaemia?
peaked T waves
P waves eventually flatten
short QT interval
What ECG changes do you see with hypokalaemia
Prolonged QT interval
Low T waves
Prominent U waves
In what condition do you see osborne J waves on the ECG?
= hump like waves at the junction of the j point and the ST segment
Seen in hypothermia
What ECG changes do you see in pericarditis?
Diffuse ST segment elevation +/- PR depression
upright T waves
What is the definition of low voltage ECG?
Total QRS height in precordial leads < 10mm and limb leads < 5mm
NB: each large square = 5mm
What can give you a low voltage ECG?
Myocardial disease
Pericardial effusion
Thick chest wall/barrel chest
Generalised oedema
What ECG changes do you see with digitalis?
ST downsloping or scooping "reversed tick"
T wave depression or inversion
QT shortening +/- U waves
What is the characteristic sign of PE on ECG?
Often will only show tachycardia BUT:
S wave in lead I
Q wave and inverted T wave in lead III
Can also show RVH
How do you define pathological ST elevation
At least 1mm in 2 adjacent limb leads
OR
at least 1-2mm in adjacent precordial leads
When is a q wave pathological?
if QRS > 1 small square
OR
> 25% height of R
What happens in Type I and Type II second degree heart block?
Type I = wenckebach's
Gradual prolongation of the PR interval precedes the failure of conduction of a p wave
Type II
PR interval is constant, then there is an abrupt failure of conduction of a p wave
What are the causes of wide QRS?
SVT with aberrancy/BBB
VT
What is wolff parkinson white syndrome?
Congenital defect resulting in an acessory conduction tract (bundle of kent) that allows electrical communication between the atria and the ventricles
What ECG findings do you see in WPW?
Shortened PR interval < 120 msec (AV node is bypassed)
Delta wave (slurred upstroke of the QRS)
Widening of the QRS complex
What arrhythmias are associated with WPW?
AF
AV re-entrant tachycardia
What is AVRT
AV re-entrant tachycardia
Seen in WPW
Re-entrant loop via accessory pathway and normal conduction system usually iniaited by a premature atrial or ventricular complex
How do you manage AVRT?
Avoid AV nodal blockers e.g., digitalis and verapamil
For recurrent - ablation of bypass tract is recommended
What is the pathophysiology behind an AV nodal re-entrant tachycardia?
Fast and slow pathways to AV node
Usually AV node is primarily depolarised by fast pathway making it refractory to impulse from slow pathway BUT a critically timed ectopic can reach AV node when fast pathway is refractory and so jump to slow pathway but by time impulse has travelled along slow pathway fast pathway is not available again and so conducts this beat back to the atrium. If this reaches atrial insertion of slow pathway can lead to re-entrant circuit between slow and fast pathways - an AV nodal re-entrant tachycardia
Features of AVNRT on ECG?
Tachycardia
Narrow QRS complex
What is the first choice of pharmacological management of AVNRT?
adenosine
What is the most common bacterial cause of infective endocarditis?
Strep viridans
NB: staph epidermidis for prosthetic valves < 2months after surgery
What is the MOA of clopidegrel?
Blocks platelet ADP receptors
NB: platelets release ADP and thromboxane A2 which stimulate aggregation
What is the MOA of enoxaparin?
Activated antithrombin III
Inhibition of coagulation facotrs Xa
What is the MOA of tirofiban, abciximab?
Blocks fibrinogen to Gp IIb/IIIa
Therefore prevents aggregation
Monoclonal antibody
Features of stable angina
pain lasts 5-15 minutes
exacerbated by stress/exercise
ECG MAY show ST change and flat or inverted T waves OR can be normal
Features of unstable angina
ECG has ST changes and inverted or flat T waves
pain at rest
accelerating
new onset angina
angina post MI or post procedure
Diagnostic triad of pericarditis
chest pain, friction rub, diffuse elevated ST ECG changes
ST change is concave upwards
Commonest cause of acute pericarditis
idiopathic, usually presumed to be viral
Coxsackie virus B is most common
Signs and symptoms of pericarditis
triad of chest pain, friction rub, ECG changes
pleuritic chest pain - alleviated by sitting up and leaning forward
+/- fever and malaise
What has been shown to improve prognosis in heart failure?
ACEi and spironolactone
Which drugs have been shown to improve mortality in patients with chronic heart failure?
* ACE inhibitors
* spironolactone
* beta-blockers
* hydralazine with nitrates
What are the ECG changes in hypokalemia?
flattened T waves
U waves
prolonged PR interval
ST depression
long QT
In Hypokalaemia...
U have no Pot and no T, but a long PR and a long QT!
What waves are seen in hypothermia?
J waves
What is the classical triad in cardiac tamponade?
muffled heart sounds
increased JVP
hypotension
Management of pericarditis
1. treat underlying cause
2. pain relief - NSAIDs
What is the MOA of adenosine?
works via adenosine A1 receptor
causes transient heart block in AV node
When is adenosine CI?
asthma, use verapamil
How do you treat SVT?
1. vagal manoeuvres, Valsalva
2. IV adenosine
3. electrical cardioversion
How do you control rate in AF?
beta blockers preferable to digoxin
Does sotalol control rate or rhythm?
both!
it's a beta blocker AND class III anti arrhythmic (K channel inhibitor)
in the same class as amiodarone
When is digoxin indicated in AF?
AF with coexistent heart failure
What is a normal ejection fraction?
55 - 70%
What is MOA of aspirin?
inhibit production of thromboxane A2
What is mechanism of action of clopidogrel?
inhibits ADP binding to its platelet receptors
MOA of GP IIb/IIIa inhibitors
blocks GP IIb/IIIa receptors --> fibrinogen and vWF binding --> decreased platelet aggregation
What is Marfan's syndrome?
AD mutation of fibrolin 1 gene
aortic root dilatation
long limbs
dislocation of lenses
high arched palate
When is verapamil CI?
in VT
may ppt VF in pts with VTW
What is BNP?
hormone produced mainly by the left ventricular myocardium in response to strain
high levels are associated with a poor prognosis in HF
What anti-anginal drug do patients develop tolerance to?
nitrates
Nitrates are used to control anginal attacks. What is first line as prevention/treatment?
Beta blocker or CCB
Which drugs should not be described with beta blockers?
Verapamail
Risk of 3rd degree heart block
Which statin is stronger simvastatin or atorvastatin?
simvastatin
When do you go on a statin when you have diabetes?
>40 with type 2 diabetes, should be started on a statin if they have risk factors or CV disease
Is diltiazem a positive or negative inotrope?
negative inotrope
What ECG finding is consistent with 3rd degree heartblock?
p waves not related to QRS comlpex
regular bradycardia (30-60)
What ECG finding is consistent with 1st degree heartblock?
prolonged PR interval (>5 small boxes)
What ECG finding is consistent with 2nd degree heartblock?
Type 1 (Weckenbach): progressive prolonged PR, then absent QRS and PR interval resets

Type 2: intermittent absence of QRS
Which cardiac drug should be given to pts with left ventricular impairment?
ACEi
What are the clinical features of patent ductus arteriosus?
acyanotic heart defect, connection btwn pulmonary trunk and descending aorta

collapsing pulse
machinery murmur
left subclavicular thrill
wide pulse pressure
How many blood cultures should you take from a patient suspected of endocarditis?
3, not from the same site
Most common pathogen for infective endocarditis
strep viridans
IVDU: Staph aureus
prosthetic valve: staph coagulase-neg
Duke criteria for endocarditis
2 major, 1 major + 3 minor, 5 minor
major:
2 separate + blood cultures
evidence on echo

minor:
fever >38.3
vascular phenomena: septic emboli and infarcts, mycotic aneurysm, janeway lesions
immunologic phenomena: GN, osler's nodes, roth's spots
1 + blood culture
Empirical treatment of endocarditis
benzylpenicillin PLUS flucoxacillin PLUS gentamicin
Which other cardiac drug is contraindicated when taking bisoprolol?
verapamil
causes heart block
What electrolyte imbalances cause ventricular tachycardia?
hypocalcemia
hypokalemia
hypomagnesia
What drug is firstline for stable angina?
beta blocker
is they have asthma or PVD, diltiazam
If a TOE is performed w someone in AF, and it shows a clot (or it isn't done at all), what should you do?
1. anticoagulate with heparin followed by warfarin for 4 weeks

INR should be 2-3
Pharm and later Mx of cardioversion in AF
1. flecainide OR amiodarone
sotalol used, but no evidence

2. if no cardioversion, 100 joules of DC shock
MOA and Side effects of amiodarone
K+ channel blocker - class III anti-arrhythmic

pulmonary fibrosis
hypo/hyperthyroidism
hepatotoxicity
long QT
What is a bad side effect of a beta blocker (in diabetics)?
may mask hypoglycemia
Characteristic ECG finding in Wolf-Parkinson White Syndrome
delta wave
Mx of STEMI
1. aspirin
2. clopidogrel
3. either PCI or fibrinolytic therapy

**given if symptoms >20 minutes, symptoms have been happening w/in 12 hours, ST elevation on ECG, no CI to reperfusion
MOA of alteplase
alteplase = tPA

catalyzes rxn btwn plasminogen and plasmin --> breaks down fibrin
Absolute contraindications to fibrinolytic therapy
Risk of bleeding:
- active bleeding or bleeding diathesis (excluding menses)
- significant closed head or facial trauma within 3 months
- suspected aortic dissection (including new neurological symptoms)

Risk of intracranial haemorrhage:
- any prior intracranial haemorrhage
ischaemic stroke within 3 months
known structural cerebral vascular lesion (eg arteriovenous malformation)
- known malignant intracranial neoplasm (primary or metastatic)
What is hyperhomocystinemia caused by and why is it important in cardio?
genetic defect, diet low in folate, B6, B12

ppl are more prone to endothelial injury --> more likely to clot
Rx of acute limb ischemia
1. unfractionated heparin
2. if thrombolysis is appropriate, tPA
3. long term therapy = warfarin, at least 3-6 months
Management of critical limb ischemia aka ischemic ulcers, ischemic pain
1. vascular reconstruction
2. regular analgesia,
3. cage and heel pad
4. elevation of head in bed
5. maintain high to normal BP
Side effects of GTN
hypotension
tachycardia
headaches
side effects of ACEi
cough - 15% and may occur 1 year after
angioedema - may occur 1 year after
hyperkalemia
1st dose hypotension- common if taking diuretics
Pts CI and cautioned for ACEi
1. pregnancy and breastfeeding
2. renovascular disease - bilateral renal artery stenosis
3. aortic stenosis
4. high dose diuretics
5, hereditary idiopathic angioedema
MOA of atropine
competitive antagonist of muscarinic ACh receptors
increases firing of SA node and conduction thru AV node
lowers parasympathetic activity
First line hypertensive medication
CCB
What is a gallop rhythm and why is it important?
S3
early and specific sign of LV failure

caused by diastolic filling of ventricle and increased filling pressure
normal if <30 yrs old
also heard in constrictive pericarditis
MOA of digoxin
cardiac glycoside: positive ionotrope and stimulates vagus nerve

inhibits Na/K/ATPase --> inhibits Na/Ca exchange --> increases Ca

blocks AV node conduction and depresses SA node

ionotrope AND rate control
SEs and CIs for digoxin
SEs: increases PR, scooping ST, T wave inversion, blurred vision, N&V

CI: Wolf-Parkinson-White, hypokalemia (increased digoxin because it binds where K+ should be), 2nd or 3rd degree AV block
Uses for digoxin
CHF
not first line for AF
MOA of frusemide
at thick ascending limb, inhibits NK2Cl co transporter --> diuresis
SEs of loop diuretics
hypocalcemia
hypokalemia
meatbolic alkalosis
MOA of thiazide
at distal tubule, inhibits NaCl co tranporter
SEs of thiazide
hypercalcemia
hypokalemia
hypomagnesium
metabolic alkalosis
hyperlipidemia, hyperglycemia - dont give to diabetics
hyperuricemia - dont give in gout
MOA of spironalactone and amiloride
aldosterone antagonist --> less eNAC

amiloride blocks eNAC
SEs of spironolactone
hyperkalemia
anti-androgen - gynecomastia
Allergy you need watch out with thiazide and loop diuretics
sulfa
MOA of clopidogrel
inhibits ADPr --> blocks gIIb/IIIa expression --> inhibits fibrinogen
SE of clopidogrel
TTP
SE of aspirin
gastric bleeding
MOA of warfarin
vitamin K antagonist also takes out protein C and S

increased PT
Caution for warfarin
teratogen
MOA of heparin
catalyzes activation of antithrombin III, decreases thrombin and factor Xa
How do you reverse heparin?
protamine sulfate
What is heparin induced thromboycytopenia?
heparin binds to platelets --> develop Ab to platelets, platelets that are not attacked by Ab become overactive and thrombotic

thrombocytopenic, hypercoaguable state
Cautions in beta blockers
asthma, verapamil, bradycardia, 2nd or 3rd degree heartblock, WPW syndrome

don't give in decompensated CHF
SEs of beta blockers
exacerbate reynauds, claudication
impotence
When do you use adenosine for rhythm control?
SVT: re-entrant SVT, not atrial fib
Which beta blockers are only beta 1 and which ones are beta 1 + 2?
Beta 1 blockers: atenolol, bisoprolol, metoprolol

Beta 1 + 2 blockers: propanolol, labetolol, carvedilol
Difference between non-DHP and DHP CCBs
non-DHP (verapamil and diltiazem): work more on heart mm, not as peripheral

DHP (nifedipine and amlodipine): work peripherally, used more for HTN
SEs of verapamil and diltiazem
verapamil: hypotension, HF, constipation, bradycardia

diltiazem: same + peripheral edema, but not constipation
arrhythmia that verapamil treats
SVT
SEs of DHP CCBs
flushing, ankle swelling, headache
CI to DHP CCBs
severe aortic stenosis, liver failure
CIs of ACEi
pregnancy, renal artery stenosis
SEs of ACEi
cough, hyperkalemia

reduced GFR by preventing constriction of efferent arterioles (aka vasodilating efferents)
MOA of nitrates
NO relaxes smooth mm, reduces preload

dilates veins > arteries
SEs of nitrates
reflex tachycardia, flushing, headache, tolerance
MOA of statin
HMG CoA reductase inhibitor

lowers LDL significantly, not as much effect on HDL or triglycerides
SEs of statins
reversible increase in LFTs
myalgia
rhabdomyolysis
MOA of fibrates
upregulates LPL, activates PPARalpha --> increases Triglyceride clearance

significantly reduces triglycerides
SEs of fibrates
dyspepsia, gallstones, myositis, increased LFTs

use with statin --> risk of rhabdomyolysis
Which drugs causes long QT syndrome?
anti-histamines, anti-psychotics, anti-depressants, quinine, chloroquine
When do you do carotid endarterctomy?
asymptomatic: <70% medical mx, >70% surgery

symptomatic: <80% medical mx, >80% surgery
Treatment of stroke without AF
aspirin, DO NOT give warfarin

if pt has second stroke on aspirin, then put pt on warfarin
Medical mx for carotid stenosis
aspirin or clopidogrel (2nd line)
What do you NOT use in unstable angina?
tPA
Rx of unstable angina
1. heparin
2. send to cath lab