Cardio 1 Flashcards
what is the most common valve affected in endocarditis
+ name order of most to least common valves affected
mitral MC
M > A > T > P
tricuspid in drug users
what is the MC overall cause of endocarditis
strep viridans
MCC acute bacterial endocarditis and what valves are affected
staph aureus - normal valves
MCC subacute bacterial endocarditis and what valves are affected
S viridans - abnormal valves
MCC drug-related endocarditis
S aureus (especially MRSA)
MCC prosthetic valve endocarditis
early (within 60 days) = S aureus (including MRSA) and s. epidermidis
MCC endocarditis if recent GI or GU procedure
enterococcus
HACEK organisms + what type of organisms
haemophilus aphrophilus
actinobacillus
cardiobacterium hominis
eikenella corrodens
kingella kingae
these are gram negative organisms, hard to culture
sx endocarditis (FROM JANE)
fever
rosh spots
osler nodes
murmur
laneway lesions
anemia
spliNter hemorrhages
emboli
what are the 2 most important tests for suspected endocarditis
blood cultures and echo (obtain TTE first –> TEE)
what criteria is used to diagnose endocarditis
duke criteria
major duke criteria
sustained bacteremia - 2 + blood cultures by organism known to cause endocarditis
endocardial involvement documented by either echo (vegetation, abscess, valve perforation, prosthetic dehiscence) or clearly established new valvular regurgitation (aortic or mitral regurgitation)
minor duke criteria
predisposing conditions - abnormal valves, IVDA, indwelling catheters
fever (100.4F)
vascular and embolic phenomena
+ cultures not meeting major criteria
+ echo not meeting major criteria (worsening existing murmur)
how to diagnose endocarditis with duke criteria
2 major or 1 major + 3 minor or 5 minor
treatment for native valve (MSSA) endocarditis
native valve (MRSA) or unknown
prosthetic valve
fungal
native MSSA - nafcillin, oxacillin
native MRSA or unknown - vancomycin + cef or gentamicin
prosthetic valve - vancomycin + gentamicin + rifampin
fungal - parenteral anti fungal (amphotericin, can add flucytosine)
how long is therapy for endocarditis
4-6 weeks
what is the worst risk factor for angina
DM
diagnosing angina
EKG - initial test of choice, ST depression
Stress testing - most important noninvasive
coronary angiography - definitive; defines location and extent
what is used for definitive diagnosis of angina
coronary angiography
treatment for angina
outpatient - aspirin, beta blockers, nitroglycerin, statin
Revascularization with PCI or CABG = definitive
when to do PCI vs CABG for angina
PCI - 1 or 2 vessel disease in non diabetes NOT involving left main coronary artery
CABG - left main coronary artery stenosis, 3 vessel disease, decreased LVEF < 40%, 2 vessel disease in DM
unstable angina is characterized by what 3 things
1) sx suggestive of ACS
2) negative cardiac biomarkers (negative CK and troponin)
3) with or without EKG changes suggestive of ischemia (ST segment depressions or new T waves)
what is the MCC of unstable angina
plaque rupture
when is angina considered “unstable”
rest angina lasting > 20-30 minutes
new-onset angina
change in anginal pattern
not relieved with rest or nitroglycerin
treatment for unstable angina
aspirin, beta blockers, oxygen if hypoxic
aspirin + P2Y12 inhibitor
anticoagulant
what 3 things tend to trigger vasospastic angina
cold weather
alpha antagonists (pseudoephedrine, oxymetazoline, cocaine, amphetamines)
hyperventilation
what 3 things are major risk factors for vasospastic angina
female
smoking
vasospastic disorders (migraine, raynauds)
sx vasospastic angina
chest pain mainly at rest (esp at midnight to early morning)
usually does not pertain to activity
dx vasospastic angina
EKG - transient ST elevation in the pattern of the affected artery == resolve with CCB and/or nitroglycerin and/or symptom resolution
angiography - may show coronary vasospasm with the use of Ergonovine, hyperventilation, or Acetylcholine
what 3 things during angiography may induce a vasospasm if someone has vasospastic angina
acetylcholine
ergonovine
hyperventilation
tx vasospastic angina
smoking cessation
CCB (mainstay of therapy)
nitroglycerin
what meds should be avoided in people with vasospastic angina
beta blockers
definition of sinus tachycardia
HR > 100 BPM
tx for persistent sinus tachycardia
beta blockers
definition of sinus bradycardia
HR < 60 BPM
tx sinus bradycardia
symptomatic:
atropine
epinephrine or subq pacing (2nd line)
asymptomatic
observation
sinus node dysfunction is also called
sick sinus syndrome
tx sick sinus syndrome
unstable:
atropine (first line)
dopamine
epinephrine
temporary pacing (transq or trans venous pacing)
stable/asymptomatic:
observation
symptomatic:
pacemaker
definition of first degree AV block
prolonged AV conduction – prolonged PR interval > 0.20 seconds
2 most common causes of first degree AV block
increased vagal tone (highly conditioned endurance athletes)
AV node-blocking meds (beta blockers, non-DHP CCB, digoxin)
what meds can cause first degree AV block
BB
Non-DHP CCB
Digoxin
EKG for first degree AV block
prolonged PR interval > 0.2 seconds + all P waves are followed by QRS complexes
tx first degree AV block
asymptomatic - observation
symptomatic - atropine
definitive - permanent pacemaker
what will EKG show for mobitz 1 second degree AV block (Wenckebach)
progressive lengthening of PR node until an occasional non-conducted atrial impulse (dropped QRS complex)
tx mobitz 1 (Wenckebach)
asymptomatic - no treatment
symptomatic - atropine first line
definitive - permanent pacemaker
what will EKG show for mobitz 2 second degree AV block
constant PR interval before and after the non-conducted atrial beat (dropped QRS complexes)
tx mobitz 2 second degree AV block
symptomatic - transq pacing and/or atropine
unstable - atropine, temporary cardiac pacing
definitive - permanent pacemaker
EKG for third degree AV block
AV dissociation - evidence of P waves and QRS complexes (atrial and ventricular activity) – regular P-P intervals and regular R-R intervals independent of each other
tx third degree AV block
symptomatic and stable - atropine
unstable - atropine and temporary pacing
definitive - permanent pacemaker
what is cardiac tamponade
accumulation of pericardial fluid
what is more important in cardiac tamponade: the rate or the amount of fluid
THE RATE
what is impaired during cardiac tamponade: diastolic filling or systolic pumping
diastolic filling
decreased diastolic filling in cardiac tamponade leads to
decreased stroke volume and decreased cardiac output
cardiac output equation
CO = HR + SV
common causes of cardiac tamponade
penetrating or blunt trauma
iatrogenic - central line placement, pacemaker insertion, etc.
pericarditis
post-MI free wall rupture
aortic dissection
key findings to diagnose cardiac tamponade
is this a clinical diagnosis?
THIS IS A CLINICAL DIAGNOSIS
key findings: beck’s triad and pulsus paradoxus
beck’s triad
hypotension
muffled heart sounds
elevated JVP (distended neck veins)
pulsus paradoxus
exaggerated decrease in arterial pressure during INSPIRATION > 10 mmHg drop
decrease in amplitude of carotid or femoral pulses during INSPIRATION (pulse is strong during expiration and weak during inspiration)
dx cardiac tamponade
echo - most sensitive & specific
CXR - enlargement of cardiac silhouette when > 250 mL has accumulated; clear lung fields
EKG - electrical alternans (altering QRS amplitudes)
cardiac Cath
tx cardiac tamponade
nonhemorrhagic + stable - observe; can do dialysis if renal failure
non hemorrhagic + unstable - pericardiocentesis
hemorrhagic - emergent surgery; pericardiocentesis is only a temporizing measure
what is the difference between pericardial effusion and cardiac tamponade
Pericardial effusion = fluid in the pericardial space. Cardiac tamponade = when pericardial effusion leads to increased pressure, impairing ventricular filling and resulting in decreased cardiac output.
an enlarged heart without pulmonary vascular congestion suggests
pericardial effusion
tx pericardial effusion
pericardiocentesis is not indicated unless there is evidence of tamponade; analysis of pericardial fluid can be useful if the cause of effusion is unknown
if the effusion is small and clinically insignificant, a repeat echo in 1-2 weeks is appropriate
