all 23 terms
TRANSCRIPT
All 23 terms
Print new! Export Combine
Terms Definitions
**What are the common causes of these
valvular lesions:
Mitral Stenosis
Mitral Insufficiency
Aortic Stenosis
Aortic Insufficiency
Mitral stenosis --- rheumatic heart disease (RHD)
Mitral insufficiency --- mitral valve prolapse
Aortic stenosis (AS) --- calcification of valves (normal or
bicuspid)
Aortic insufficiency --- dilation of ascending aorta, most
commonly due to aging or hypertension
What are congenital bicuspid AVs prone to? calcification, IE, CoA (narrowing), and aortic dissection
What is myxomatous degeneration, and
which condition is it most commonly
associated with?
Myxomatous degeneration refers to a pathological
weakening of connective tissue. The term is most often
used in the context of mitral valve prolapse, which is
known more technically as "primary form of myxomatous
degeneration of the mitral valve."
What condition does this describe: one or
both leaflets is (are) enlarged, hooded or
tent-like, and floppy?
mitral valve prolapse
what are common sequelae of Rheumatic
heart disease (RHD)?deforming fibrosis of AV and/or MV
In what disease would you see an Aschoff
body?RHD (acute only)
What is an Anitschkow cell? what disease
do you see them in?
activated macrophage -- RHD (acute only)
(fyi - nuclear chromatin within cell forms a central
irregular ribbon resembling a caterpillar)
*what disease (& where) do you see a
"fishmouth" valve?Chronic RHD causing mitral stenosis (looking from LV)
What is another term for IE? what can cause
it?
bacterial endocarditis, even though can be caused by
fungi, rickettsiae, or Chlamydia
vegetations (offending agent + thrombotic
debris) are common to RHD, IE, NBTE, and
LSE (Libman-Sacks Endocarditis)... which
both sides: LSE (inflmmatory - Lupus linked)
chordae: IE
one has vegetation that affects both sides of
the leaflets? which can affect cordae?
what are verrucae? where do they typically
form?
Small wart-like projections (verrucae) appear along the
lines of closure
** What is carcinoid syndrome?
Carcinoid syndrome is a group of symptoms associated
with carcinoid tumors -- tumors of the small intestine,
colon, appendix, and bronchial tubes in the lungs.
These tumors release too much of the hormone
serotonin, as well as several other chemicals that cause
the blood vessels to open (dilate).
Does carcinoid syndrome usually affect the
L or R heart? why?
Right - first exposure to bioactive substances released by
carcinoid tumors, also serotonin is deactivated when it
passes through the lungs before reaching the left heart.
What is the most common cause of calcific
aortic stenosis?aging
*myxomatous valves are common to MV
prolapse, what substance is more abundant
in these valves? and what color do they stain
(Movat)?
proteoglycans - blue/green
what is the initial infection that leads to
Rheumatic fever?
group A b-hemolytic strep infection, usually pharyngeal
(RHD is an immune mediated disease)
what is the cardiac implication of long term
RHD?
Deforming fibrosis of AV and/or MV which may not
present clinically until years later
* which valve disease are verrucae most
commonly seen in?RHD
Can endocarditis invade the endocardium
and lead to the destruction of the underlying
tissue?
yes, often
FYI* The endocardium is the innermost layer of tissue that
lines the chambers of the heart. Its cells are
embryologically and biologically similar to the endothelial
cells that line blood vessels.
The endocardium underlies the much more voluminous
myocardium, the muscular tissue responsible for the
contraction of the heart. The outer layer of the heart is
termed epicardium and the heart is surrounded by a
small amount of fluid enclosed by a fibrous sac called the
pericardium.
what is another term for nonbacterial
thrombic endocarditis (NBTE)? * what
type of patients does this most commonly
occur in?
- marantic endocarditis
- Occurs in debilitated patients (e.g. cancer)
Deposition of small noninfected, loosely attached masses
of fibrin, platelets, and other blood components on valves
Often associated with hypercoagulable state, as in
mucinous adenocarcinoma
what type of patients does Libman-Sacks
Endocarditis most commonly occur in?LSE - lupus (predisposed to clotting)
* what do carcinoid tumors secrete? serotonin
All 84 termsPrint new! Export Combine
Terms Definitions
Standard EKG
small box = 1mm or 40ms, big box = 5mm or 200ms, Pwave = < 100ms
wise and < 3mm high and upright in I/II/aVF and inverted in aVR, 120 < PR
< 200, 60 < QRS < 100?, Q < 3mm, QT < 420?, T wave upright in I/II and
inverted in aVR, T wave </= 5mm in limb leads
prominent U waves in..."hypokalemia, hypercalcemia, digitalis therapy, thyrotoxicosis (U waves
best seen in V3)
hypothermia EKG findings"J wave (osborn wave), conduction delays (PR, QRS, QT prolongation),
dysrhytmias like sinus brady or a-fib with SVR
J wave broad upright deflection at end of upright QRS (EKG sign in hypothermia)
hypokalemia EKG findings U wave, QT prolongation, torsades
hyperkalemia EKG findingshyperacute T waves, prolonged PR interval, widened QRS, sine wave,
Vfib
hypocalcemia EKG findings QT prolongation, torsades
torsades cause QT prolongation (hypokalemia, hypocalcemia, hypomagnesemia,
hypothermia, class IA/IC antidysrhythmics, TCAs)
hypercalcemia EKG
findingsQT shortening
hypomagnesemia EKG
findingsQT prolongation, torsades
digitalis therapy EKG
findingssagging ST, QT shortening (most prominent in lateral leads)
digitalis toxicity EKG
findings
"bigeminal and multiform PVCs are most common, paroxysmal atrial
tachycardia with AV block is pathognomonic
digitalis toxicity symptomsflu-like syndrome (malaise, anorexia, n/v/d), visual changes (yellow/green
halos around objects), MS changes
digitalis toxicity treatmentactivated charcoal, Fab fragments, correct electrolyte disturbances that
may contribute to dig toxicity, lidocaine to control tachydysrhythmias
multifocal atrial tachycardiairregularly irregular, narrow QRS, >/= 3 different P wave morphologies in
one lead
PAC vs PJC vs PVC
"PACs have noncompensatory pause (PJCs/PVCs have compensatory),
PJCs/PVCs have inverted P waves when present (PACs have upright P
waves), PVCs have wide QRS (narrow QRS in PACs/PJCs)
Vtach definition 3 or more consecutive PVCs at rate > 120
Hs and Ts of
PEA/asystole/vfib/vtach
hypovolemia, hypoxia, hypothermia, hypo/hyperkalemia, acidosis, tension
pneumo, tamponade, MI/PE, toxin
incomplete vs complete
BBBcomplete = QRS > 120ms, incomplete = QRS 90-110ms
RBBB QRS > 120, RSR' in V1, wide S waves in I/V5-6
LBBB QRS > 120, Wide R in V5-6, LAD
AV blocks1st degree = PR prolongation, 2nd degree = dropped beats (type 1 vs type
2), 3rd degree (AV dissociation)
1st degree AV block PR prolongation (> 200ms)
2nd degree type 1 AV
blockprogressive PR prolongation to dropped beat
2nd degree type 2 AV random dropped beats (no PR prolongation)
block
3rd degree AV block complete AV dissociation
Wolf-Parkinson-White
syndrom
pre-excitation through bundle of kent (atria to ventricle accessory pathway)
resulting in delta wave, PR shortening, wide QRS
Lown-Ganong-Levine
syndrome
pre-excitation through James fibers (atria to His bundle accessory
pathway) resulting in PR shortening without delta wave/QRS widening
AVNRT treatment"vagal maneuvers then adenosine then synchronized cardioversion if
stable (go directly to cardioversion if unstable)
types of a-fibfirst episode, paroxysmal (recurrent), persistent (recurrent, > 7days),
permanent (recurrent, > 1yr)
CHADS2 score risk of stroke in pt with a-fib - CHF, HTN, Age > 75, DM, prior stroke or TIA
a-fib/a-flutter treatment
if unstable - cardioversion, if stable but symptomatic - control rate first
(BB/CCB unless EF < 40 then use dig/amio) then cardiovert (DC or amio),
must perform TEE or anticoagulate with heparin x3wks before
cardioversion if a-fib > 48hrs
how to reveal a-flutter give adenosine
VT treatment
"if stable - medical cardioversion (lido, amio, procainamide or Mg), if
unstable - electrical cardioversion then medical maintinance, if pulseless -
defibrillation/epi/lido
Vfib/pulseless VT treatment defibrillation, epi, lido/amio
PEA/asystole treatment epi, search for Hs/Ts
first degree AV block
treatmentnothing
second degree mobitz 1
treatmentnothing if asymptomatic, if symptomatic use atropine or transcu pacing
second degree mobitz 2
treatment
transcu pacing bridge to transvenous pacing (usually happens in acute
anteroseptal MI)
third degree AV block
treatment
treat like mobitz 1 if narrow (usually inferior wall MI), if wide treat like
mobitz 2 (usually anteroseptal MI)
WPW if unstable use cardioversion, if stable depends on ortho vs antidromic - if
narrow complex (orthodromic) treat as SVT
(vagal/adenosine/cardioversion) but if wide complex (antidromic) treat with
procainamide (although will look like VT so will probably use lido first)
pacemaker lettersfirst letter - champer paced, second letter - chamber sensed, third letter -
response to sensing of electrical activity
pts who present with
atypical MIselderly, DM, women, alcoholics, spinal cord disease
serum markers in acute MI
myoglobin - rises first (2-3 hrs) but nonspecific to cardiac muscle, CK -
rises within ~6hrs but nonspecific, CKMB - rises within ~6hrs and fairly
specific, tropinin T/I - rise within ~6hrs and are very specific but remain
elevated for weeks
acute MI treatmentIV/O2/monitor, aspirin/clopidogrel/heparin, morphine(if pain)/NTG(unless
inferior MI or sildenafil), abciximab?, lytics/cath, BB/ACE (within first 24hrs)
MI and AV block
association
anterior MI associated with mobitz 2 (can decompensate to complete heart
block) while inferior MI associated with type 1 or mobitz 1 AV block
ACPE CXR signs cephalization of pulmonary vasculature, vascular congestion, Kerly B lines
normal PAWP ~10mmHg
ACPE treatment
IV/O2/monitor, NTG/furosemide, consider nitroprusside (if need more
preload/afterload reduction), consider dobutamine/norepinephrine (if low
BP or decreased CO), consider CPAP/intubation (if poor ox/vent)
Kussmaul's signincreased JVD on inspiration - sign of poor RV filling (constrictive
pericarditis, restrictive CMP, cardiac tamponade etc)
gallopsS3 (ventricular gallop) = diastolic filling of dilated ventricle; S4 (atrial
gallop) = atrial kick against stiff ventricle
AS vs HOCM murmursAS murmur increases with squatting; HOCM murmur increases with
valsalva (decreased LVEDP)
HOCM ECG findings LVH/LAE, septal Q waves
Wells criteriaassesses PE risk, low risk can be r/o with D-dimer (there is also a Wells
score for DVT)
DVT treatment heparin or lytics (if limb is in danger)
Vichows triad venostasis, hypercoaguability, vessel wall injury
PE triaddyspnea, pleuritic chest pain, hemoptysis (uncommon);
dyspnea/CP/tachypnea (almost always present)
PE treatment heparin or lytics (if hemodynamically unstable)
where does pericarditis
pain radiate to?left trapezius muscle ridge
convex vs concave ST
segments
STEMIs have convex ST segments while pericarditis has concave ST
segments
pulsus paradoxusdecrease in inspiratory (relative to expiratory) blood pressure > 10mmHg;
or the absence of radial pulse during inspiration; sign cardiac tamponade
cardiac tamponade findings
class triad - hypotension, JVD, distant heart sounds (late findings); narrow
pulse pressure, pulsus paradoxus and kussmaul's sign are earlier; low
voltage or electrical alternans on EKG and waterbottle heart on CXR
hypotension and distended
neck veins differential
tension pneumo (look for tracheal deviation), cardiac tamponade (get
echo), massive PE (get echo to look for dilated RV), acute RV MI, SVC
syndrome
myocarditis what do i need to know here? how to diagnose/screen? how to treat?
most common
pericarditis/myocarditis
viruses
cocksakie A/B, echovirus
myocarditis treatmnet supportive (apparently no NSAIDs?), IVIG has some promise
endocarditis signsOsler nodes, Janeway lesions, Roth spots, splinter hemorrhages,
conjunctival hemorrhages
thoracic aortic aneurysm
risk factors
hypertension (THE BIG ONE!), conective tissue disorders (ehlers-danlos,
marfans, lupus, giant cell arteritis, cystic medial necrosis), trauma, syphilis,
and many more...
pathophysiology of aortic
dissection
intimal tear --> blood into media --> seperation of media from adventitia (or
splitting the media depending on source)
hallmark of aortic
dissectionunequal or abscent pulses between extremeties
aortic dissection CXR
findings
mediastinal widening (> 8cm), calcium sign (extension of aortic shadow >
5mm beyond calcified intima), double density, tracheal deviate (to right),
elevated right main stem bronchus and depressed left main stem
bronchus, apical capping
aortic dissection treatmentcontrol BP, HR, dP/dT (metoprolol/nitroprusside), surgery if involve
ascending aortica (type A)
where is a AAA mass felt epigastric puslitile (potentially tender) mass
hypertensive emergency
treatment
nitroprusside is default (reduce MAP by 30% in first hour), nicardipine if
SAH (decreases vasospasms), nitroglycerine if AMI (decreases coronary
steal)
calcium channel blockersdihydropyridines vasodilate (amlodipine, nicardipine), nondihydropyridines
are negative chronotropes (diltiazem > verapamil
hypertensive urgency vs
emergencyurgency = DBP > 115 while emergency = end organ damage
mitral valve prolapse
murmur
late apical systolic with midsystolic click; decreasing LVEDP (valsavla,etc)
moves click closer to S1 and increases length of murmur
mitral valve prolapse
pathophysiology
commonly secondary to myxomatous degerneration of mitral valve leaflets
and cordae tendoneae (usually seen in women)
mitral stenosis etiology usually rheumatic heart disease
mitral stenosis murmur diastolic with early diastolic opening snap
mitral regurgitation etiologyif chronic - RHD, if acute - MI with cordae tendoneae rupture, if MVP -
myxomatous degeneration
mitral regurgitation murmur apical systolic radiating to axilla (after midsystolic click if MVP)
aortic stenosis etiologyif young - congenital bicuspid valve, if old - calcific stenosis, if also MV
disease - RHD
aortic stenosis murmur basal systolic radiating to carotids with opening click
All 96 termsPrint new! Export Combine
Terms Definitions
Tyrosine to dopa enzyme tyrosine hydroxylase
tyrosine hydroxylase inhibitor metyrosine
Dopamine transporter VMAT (transports into synaptic vesicle
blocks dopamine uptake by VMAT reserpine
Allows NE reuptake NE transporter
blocks NE transporter Cocaine, tricyclic antidepressants
Inhibits SNAPs and VAMPs Guanethadine, Bretylium
alpha 1 receptor activates which G protein Gq (IP3 and DAG)
Beta and alpha 2 receptors activate which G protein
beta receptors activate Gs proteins and
increase adenylyl cyclase and cAMP
alpha 2 receptors activate Gi proteins and
decrease adenylyl cyclase and cAMP
Heart has which receptor and effectBeta 1: increases heart rate, increases heart
contractility, speeds AV node conduction
hypotension treated w/ which autonomic drug class adrenergic agonist
Shock treated w/ which autonomic drug class adrenergic agonist
hemistasis treated w/ which autonomic drug class adrenergic agonist
acute heart failure treated w/ which autonomic drug
classadrenergic agonist
chronic hypertension or hypertensive emergencies
treated w/ which autonomic drug classadrenergic beta antagonist
angina treated w/ which autonomic drug class adrenergic antagonist
cardiac arrhythmias treated w/ which autonomic drug
classadrenergic beta antagonist
chronic heart failure treated w/ which autonomic drug
classadrenergic beta antagonist
ID epinephrine
beta 1 agonist
beta 2 agonist
alpha 1 agonist
ID NEbeta 1 agonist
alpha 1 agonist
ID isoproterenol beta 1 agonist
beta 2 agonist
ID Dopamine
beta 1 agonist
D1 agonist
alpha 1agonist
ID dobutamine
beta 1 agonist
beta 2 agonist
alpha 1 agonist
id Ephedrine beta 1 agonist (treats bronchospasm)
ID pheynlephrine alpha 1 agonist
ID midodrinealpha 1 agonist (treats orthostatic
hypotension)
epinephrine general effect
potent vasodilator and cardiac stimulant
Leads to increased stroke volume, heart rate,
and cardiac output
Epi beta 1 effect
β1-receptors induce positive inotropic and
chronotropic actions (increase in pulse rate,
increase in the rate and force of cardiac
contraction through B-1 receptors)
epi alpha effectα-receptors cause vasoconstriction in
vascular beds (including kidney)
epi beta 2 effectActivates β2-receptors in skeletal muscle
blood vessels and liver which leads to dilation
Isoproterenol general effect potent vasodilator, increase cardiac output
isoproterenol receptor and effect
beta receptor agonist
fall in DIASTOLIC blood pressure; systolic
remains same
Lowers peripheral mean arterial pressure
dopamine activates which receptors, whereActivates D1-receptors in vascular beds
Activates β1-receptors in heart
Low dose dopamine activate D1 in renal and vascular beds = local
vasodilatation, renal blood flow and glomerular
filtration = diuresis
(< 2 µg/kg/min)
mid dose dopamine
activate cardiac beta1-receptors (direct and
indirect) = increased heart rate, cardiac
contractility and stroke volume = increased
cardiac output
(2-10 µg/kg/min)
high dose dopamine
activates systemic α-receptors =
vasoconstriction = increased systemic
resistance (may mimic epinephrine)
primary hypertension treated by blocking and
mechanism
alpha 1
lower peripheral vascular resistance
α1 receptors determine arteriolar and venous
tone of vascular smooth muscle
chronic hypertension, ischemic heart disease and
arrhythmias treated by blocking and mechanism
beta
Lowers BP causing negative inotropic and
chronotropic effects
action of alpha 1 receptor
vasoconstriction of vascular smooth muscle
(arterioles and veins) [responsible for BOTH
arteriolar and venous tone]
increases production of IP3 and DAG =
increase in intracellular Ca ions
action of alpha 2 receptor
Inhibition of NE release and vasoconstriction
of coronary and renal arterioles [responsible
for BOTH arteriolar and venous tone]
decreases production of cAMP = inhibits
further release of NE
action of beta 2 receptor
Vasodilation of vascular smooth muscle
(arterioles except in skin and cerebral)
bronchodilation
glycogenolysis (liver)
action of beta 1 receptor inc heart rate, contractility
speeds up AV node conduction
Increases renin release
increases NE release
stimulates lipolysis
alpha agonist actionlower sympathetic outflow from the brain =
decrease in BP and HR
alpha antagonist actionlower peripheral resistance and blood
pressure
Epinephrine reversal
the fall in blood pressure produced by
epinephrine when given following blockage of
α-adrenergic receptors (alpha antagonist)
you will see a lower peripheral resistance and
a drop in blood pressure
clonidine
alpha 2 agonist
Decreases HR and reduces peripheral
vascular resistance = decreases cardiac
output
Reduces arterial pressure, decreases RENAL
vascular resistance and maintains renal blood
flow
very lipid soluble (enters CNS)
Prazosin, Terazosin, Doxazosin (-azosins)
highly selective alpha 1 antagonist
Relaxes arteriole and venous vascular smooth
muscle; produces less reflex tachycardia
management of hypertension (more effective
when used w/ diuretic or beta blocker)
adverse effects of -azosinsorthostatic hypotension, syncope, dizziness,
tolerance
Which -azosin is most water solubleterazosin, higher bioavailability and longer
t1/2 life compared to prazosin and doxazosin
which -azosins are used to treat BPH terazosin and doxazosin
key adverse effects of alpha antagonist Postural hypotension - d/t antagonism of
sympathetic nervous system stimulation of α1-
receptors in venous smooth muscle
(after first dose of -azosins)
Reflex tachycardia - result of exposure to
nonselective α-antagonists when BP is lower
than normal (the release of norepinephrine
activates primarily β-receptor as a result of
agents that block α2-presynaptic receptors)
Beta blocker action and types
Competitively block catecholamines and β-
agonists at the receptor
Most are pure antagonists
Some are partial agonists
Few are inverse agonists
NOT always SPECIFIC to Beta 1. (dose
dependent, diminishes at higher
concentrations)
pharmokinetics of beta blockers
low bioavailability EXCEPT: betaxolol,
penbutolol, pindolol, and sotalol
avg half life 3 to 10 hours EXCEPT: esmolol
(10 min)
most are metabolized well EXCEPT: nadolol
which is excreted unchanged
effects of beta blockers
Negative inotropic and chronotropic effects
Slowed atrioventricular conduction with an
incr. PR interval
Opposed β2-mediated vasodilation which May
lead to a rise in peripheral resistance d/t
unopposed α-receptor mediated effects
When to use beta blockers (clinical applications)
Hypertension
Glaucoma
Migraine
Thyrotoxicosis
Arrhythmia prophylaxis after MI
Supraventricular tachycardias
Angina pectoris
Propanolol properties beta blocker
extensive first pass metabolism (low
bioavailability)
very lipid soluble (crosses BBB)
treatment of hypertension, angina and
arrhythmias, myocardial infarction, and
congestive heart failure
propanolol indications
treatment of hypertension, angina and
arrhythmias, myocardial infarction, and
congestive heart failure
propanolol adverse effects
decreased glycogenolysis and decreased
glucagon secretion, fatigue and exercise
intolerance
bronchoconstriction, diabetes, peripheral
vascular disease
metoprolol properties
beta 1 selective blocker (safer for patients
who experience bronchoconstriction with
propanolol)
CYP2D6 metabolism
treatment of hypertension, stable angina,
acute myocardial infarction and chronic heart
failure
metroprolol indicationshypertension, stable angina, acute myocardial
infarction and chronic heart failure
Esmolol IV
Ultra-short acting beta 1-antagonist
Gets metabolized by esterases in RBC
Peak effect occurs within 6-10 min
Block lasts ~20 min post-infusion
Clinical Indications: supraventricular
arrhythmias, arrhythmias associated with
thyrotoxicosis, perioperative hypertension and
myocardial ischemia in acutely ill pts
Adverse Effects: hypotension, diaphoresis
Safe to use in critical ill patients
Esmolol IV indications supraventricular arrhythmias, arrhythmias
associated with thyrotoxicosis, perioperative
hypertension and myocardial ischemia in
acutely ill pts
Pindolol, Acebutolol
Partial β-agonists with intrinsic sympathetic
activity (ISA)
Exhibiting low level agonist activity while
acting as a receptor site antagonist
Pindolol is a non-selective β-blocker
Acebutolol β1-blocker
indicated for hypertension, angina, patients
that show bradycardia
pindolol, acebutolol indicationshypertension, angina, patients that show
bardycardia
Labetalol
Reversible antagonist (also has α1-receptor
antagonist properties)
2 isomers one is a potent β-blocker and one is
a potent α-blocker
Clinical Indications: Hypertension,
hypertensive emergencies and congestive
heart failure
Hypotension is less than with other α-blockers
Does not alter serum lipid or blood glucose
levels
Adverse Effects: hypotension, syncope
labetalol indicationsHypertension, hypertensive emergencies and
congestive heart failure
carvedilol
Non-selective β-receptor antagonist; has
some capacity to block α1-receptors
Stronger ability to antagonize catecholamines
at β-receptor
Antioxidant properties
Contributes to clinical benefit in chronic heart
failure
Racemic mixture with stereoselective
metabolism: (R)-carvedilol
avoid beta blockers in patients with asthma
nodal dysfunction (SA or AV)
diabetes
beta blockers WITHOUT Intrinsic sympathetic activity
(adverse effects)
increased triglycerides in plasma
lower HDL cholesterol
beta receptor blockers WITH ISA have little
effect on blood lipids
how to discontinue beta blockers
taper off 2 weeks to avoid tachycardia,
hypertension, and/or ischemia
NEVER STOP ABRUPTLY
Stimulating β1 receptors will do what to the force and
rate of contraction of the heart?Increase
Stimulating M receptors will do what to the force and
rate of contraction of the heart?Decrease
Stimulating α1 receptors will cause most arteries to do
what?Vasoconstrict
Stimulating α2 receptors will cause veins to do what? Vasoconstrict
Stimulating β2 receptors will cause arteries in skeletal
muscle to do what?vasodilate
this drug can be used to treat reflex vagal discharge or
hyperactive carotid sinus reflexesatropine (M2 antagonist)
this drug can cause a decrease in blood pressure as
peripheral vascular resistance and venous return are
decreased.
mecamylamine (ganglionic blocker)
This drug increases peripheral resistance, diastolic and
systolic BP. it is an agonist at β1 and α receptors.Norepinephrine (AKA. Levarterenol)
This drug can be used in the treatment of shock
Adverse Effects - precipitation of angina, cardiac
arrhythmias and myocardial ischemia
Norepinephrine (AKA. Levarterenol)
The overall effects of this drug include
-Increased cardiac contractility, decreased peripheral
resistance (due to balance between α-mediated
vasoconstriction and β2 mediated vasodilation)
-Little change in heart rate and does not require a
Dobutamine
greater oxygen demand on myocardium
Dobutamine
receptor/action?
Primarily considered β1 selective synthetic
catecholamine, but has activity at both α and β
receptors
Clinically prepared as a racemic mixture
(+) isomer is a potent β1 agonist and an α1
antagonist (partial agonist)
(-) isomer is a potent α1 agonist (causes
significant vasoconstriction when given alone)
This drug is used for heart failure NOT ACCOMPANIED
BY hypotension
-Useful only short-term due to receptor downregulation
Adverse Effects - tachyarrhythmias ventricular
arrhythmias
Dobutamine
This drug is contraindicated in the elderly (start at low
dose)
Drug Interactions - MAOIs may cause hypertension
Dobutamine
Phenylephrine
receptor/action?
α-agonist (favors α1 over α2)
used for hypotension, supraventricular
tachycardia
This drug can be used to raise BP and terminate
episodes of supraventricular tachycardia
Adverse Effects - hypertension, reflex bradycardia,
hypertension headaches
phenylephrine (α-agonist)
Phenylephrine
Contraindications and drug interactions
Contraindications - hypertension, within 14
days of MAOIs
Drug Interactions - MAOIs
This drug is used in the treatment of orthostatic
hypotension due to impaired autonomic nervous system
function (chronic)
It increases peripheral resistance
Midodrine; a prodrug hydrolyzed to
desglymidodrine (α1-receptor agonist)
Adverse effects, contraindications and drug interactions Adverse Effects - Supine hypertension, urinary
of Midodrine
urgency, retention, polyuria, dysuria
Contraindications - pheochromocytoma,
thyrotoxicosis, persistent and significant
supine hypertension, severe organic heart
disease and acute renal failure
Drug Interactions - β-blockers, Ca2+ channel
blockers, digoxin
This drug
-Activates α and β receptors
-Enhances the release of norepinephrine from
sympathetic neurons
-Stimulates heart rate and cardiac output and increases
peripheral resistance
-Ultimately raises BP (both systolic and diastolic)
Ephedrine
This drug is used to treat idiopathic orthostatic
hypotension & anesthesia-induced hypotensionEphedrine
Adverse Effects - hypertension, arrhythmias, insomnia
Contraindications - cardiac arrhythmias, elderly
(crosses BBB causing confusion), diabetes, thyroid
dysfunction, seizures
Drug Interactions - MAOIs --> increased hypertension
Ephedrine
This drug:
Reduces peripheral resistance decreasing blood
pressure
Reduces RENAL vascular resistance
May also reduced heart rate and cardiac output
α-methyldopa
Pro-drug metabolized centrally to α-methyl-
norepinephrine which stimulates α2 receptors
This drug is used to treat pregnancy-related
hypertension
α-methyldopa
Pro-drug metabolized centrally to α-methyl-
norepinephrine which stimulates α2 receptors
Which drug?
Adverse Effects: sedation (at onset), lactation due to
increased prolactin secretion (both men and women),
α-methyldopa
Pro-drug metabolized centrally to α-methyl-
norepinephrine which stimulates α2 receptors
impotence
Positive Coomb's test in 10 - 20% of pts. after 1-yr
-Complicates cross-matching of blood for transfusion
-Can cause hemolytic anemia
Potential for serious hepatotoxicity, hemolytic anemia,
hepatitis and drug fever
This drug binds covalently to α receptors (primary
action; irreversible blockade for ~ 2 days)
-Also inhibits the reuptake of released norepinephrine
by presynaptic adrenergic nerve terminals. This block
impairs the normal feedback inhibition of norepinephrine
release increasing the baroreceptor reflex increase in
heart rate (an undesired side effect of the non-selective
α antagonists)
-Also blocks histamine, acetylcholine and serotonin
receptors (at higher doses)
phenoxybenzamine
this drug is used to treat Pheochromocytoma
Adverse Effects: orthostatic hypotension and reflex
tachycardia, nasal stuffiness, inhibition of ejaculation
Phenoxybenzamine
Attenuates catecholamine induced
vasoconstriction
-Reduces BP when sympathetic tone is high
(upright position or low blood volume)
All 216 termsPrint new! Export Combine
Terms Definitions
What is a positive stress testFlat or Down sloping St-segment depression >1 mm occurring 80 msec
after j point
When to stop a stress testSt segment depression > 2 mm, ventricular tachycardia, drop in SBP >
15, chest pain, dyspnea, lightheadedness
Stress test of choice with a
LBBB or ventricular pacing?Myocardial perfusion imaging with adenosine,NOT exercising!
Know the algorithm for stress
testingSee page 5-3,figure 5-1
When to not use doutamine
for stressHistory of VT, severe HTN, Low BP, poor echo images
When to not use adenosine
for stress
Bronchospasm, severe valvular dysfunction, severe carotid stenosis,
2nd degree heart block, theophylline dependent
Normals for PA catheter
pressuresRA <7, RV 30/7, PCWP 3-11
PA cath findings in
tamponade or restrictive
pericarditis
Diastolic pressures elevated and equalized in all chambers, low BP
PA cath findings with RV AMIElevated RA and PA pressures, decreased or nl PCWP, hypotension,
and inferior MI. R side is decompensated, cannot fill L side of the heart
PA cath findings in
cardiogenic shockElevated PCWP, RA pressure, and decreased SBP/cardiac output
PA cath findings in mitral
stenosis with RV failureElevated RA, PA (very elevated), PCWP, nl SBP
PA cath findings in pulmonary
HTNElevated PA, RA pressures, nl PCWP, SBP
Pulsus paradoxus
decrease in systolic BP of more than 10mmHg with normal inspiration;
palpated as weakened pulse with inspiration along with more heart
contractions to pulse beats
What conditions give you
pulsus paradoxus?Constrictive or restrictive pericarditis, asthma, tension pneumothorax
What gives you pulsus
bisferiens (two systolic peaks
per cycle)
Aortic regurgitation, HOCM
What causes pulsus alternans Severe LV dysfunction
What causes pulsus tardus Aortic stenosis
How do positional maneuvers -standing/valsalva - decreased cardiac filling, decreases most murmurs
affect blood flow and murmurs
except MVP and HOCM
-squatting/ lying down - increase cardiac volume, increased murmurs
except MVP, HOCM
-sustained handgrip - increases systemic resistance, decreases murmur
in HOCM, AS
What causes a physiologic
split S2
Increased blood volume in the RV prolongs systole and delays
pulmonary valve closure
What causes a fixed split S2Pulmonary stenosis, PE, LV pacer, RBBB, MR (early AV closure), ASD,
RV failue
What causes a paradoxic split
S2LBBB, RV pacing, HOCM
What causes an S3? Rapid LV filling - acute ventricular decompensation, severe AR or MR
KNOW - S3 with LV
dysfunction is a poor
prognostic factor
...
What causes a S4?
Decreased ventricular compliance during atrial contraction - ischemic
heart dz, AS, MR, HOCM, hypertrophic or diabetic cardiomyopathy,
HTN heart dz, concentric LVH
Can you have a S4 with atrial
fibrillation?No - no atrial contraction
What are the parts of the
venous waveform?
A wave - atrial contraction
X descent - atria relax, RV fills rapidly
Bottom of x descent is TC valve closure
V wave - ventricle contacting against closed TC valve
Y descent - TC valve opens, passive emptying into ventricle
What gives elevated a and v
wavesPulmonary HTN, RV infarction
Large r side v waves Septal rupture
Large v waves TR (right), MR (left)
Rapid x and y descentConstrictive pericarditis, restrictive cardiomyopathy, tamponade (x
descent only, loss of y descent)
Large a waves TS,severe RVH (on right), MS
Cannon a waves AV disassociation - complete heart block, ventricular pacing
Slow Y descent Delayed atrial emptying - TS
Most important prognostic
factor with CADDegree of LV dysfunction
Causes of resting ST
elevation
MI, pericarditis, LV aneurysm, LBBB, ventricular pacing, LVH, early
repolarization
Hibernating myocardium
myocardium near the infarction may be underperfused but not necrotic-
the metabolism of the cells adapts to low energy supplies and are
nonfunctional until perfusion is restored
Reperfusion injury
the re-establishment of blood flow after a coronary artery is blocked,
which may further damage the heart tissue due to the formation of
oxygen free radicals
Stunned myocardiumprolonged post ischemic dysfunction, salvaged by reperfusion, several
days
Giving nitrates causes severe
decompensation in a IWMI pt.
What happened?
Pt had R side infarction as well, the preload reduction from the nitrate
now meant little flow getting to the L side of the heart
St segment elevation during a
stress signifies what?Coronary artery spasm
NSTEMI have _____ initial
mortality, but have the _____
one year mortality as a STEMI
Lower, Same
NSTEMI have a higher risk of
these vs. STEMIPersistent angina, reinfarction, and death within several months
MI without chest pain is more
likely to happen in theseElderly, diabetics, women
MR due to papillary muscle
rupture is most common with
MI in this region
Inferior
VSD is more likely with MIs
hereAnterior, inferior
Types of arrythmias with Junctional escape, Mobitz I, and they are usually temporary
IWMI
Types of arrythmias with
AWMI
,Mobitz II, BBB. More of the myocardium
Is involved
After 12 hrs., pt has no more
CP, nl trop and EKG. What's
next
Stress test. If nl, can dc
What do all Pts with ACS get
Continuous EKG, ASA, NTG prn for pain or continuous IV gtt if
continued ischemia or HTN, oxygen if sats < 90, morphine is pain not
better with NTG, B-blocker, ACE if still with HTN or LV dysfunction
Contraindications for B-
blockers
Bradycardia, hypotension, 2nd or 3rd degree AVB, pulmonary edema,
asthma. NOT DM
When to use non-
dihydropyridne CCBs in ACS
Contraindications to B blockers, continued ischemia, but NO LV
dysfunction
What anticoagulant to use
with ACS
Enoxaparin good, but have to stop 12-24 hrs before CABG
Fondaparinux is increased risk of bleeding, do not use if going to do PCI
- increased risk of catheter thrombosis and coronary complications
If using Fondaparanux and decide to do PCI, change to heparin or
bivalirudin
What are the platelet P2Y12
receptor blockersClopidogrel or plavix, ticlodipine or Ticlid, prasugrel or effident
When to use clopidogrel with
ACS
All Pts if proven ACS, hold until after CABG or PCI, or for those
intolerant of ASA for conservative treatment
Prasugrel vs clopidogrel Faster onset, more anti platelet activity, more risk of bleeding
GP IIb/IIIa inhibitors, action
and use
Abciximab, eptifibatide, tirofiban, limifiban
Block platelet aggregation
Use in any ACS pt going to cath for probable PCI
When to use fibrinolytics in
ACS
Not with UA/NSTEMI - increases mortality
Use in STEMI, new LBBB if no contraindications and immediate PCI not
available
What to give pt with
UA/NSTEMI
Anti-platelet therapy (plavix) - use at least 1 yr with drug eluting stent, up
to a year even without stent
Lipid and BP control
DC NSAIDs except ASA
ASA, O2, B-blocker, nitrate prn
Heparin, enoxaparin, Fondaparanux, or bilavirudin
Monitor
Gp IIa/IIIb (abciximab, etc) if immediate PCI planned
NO FIBRINOLYTICS!
When to do urgent PCI with
UA/NSTEMI
CHF or hemodynamic instability, recurrent or refractory angina, life
threatening arrythmias
When to use invasive therapy
within 48 hrs with UA/NSTEMI
elevated troponin, dynamic ST changes, DM, GFR < 60, EF < 40%,
Early post-MI angina, PCI in last 6 months, prior MI, prior CABG,
intermediate/ high risk score
When to use conservative
therapy with UA/NSTEMI
no indications for invasive therapy, good response to initial treatment,
low risk post-ACS stress testing. Has the same 1 yr mortality
Cocaine/ meth use and
UA/NSTEMI
give NTG and CCBs
If no better, do cath
If cath not available, give fibrinolytics
No cath is no ST/T changes, negative stress, and negative biomarkers
Anti-platelet therapy after
UA/NSTEMI
no stent - ASA 75-162mg lifelong + Clopidogrel x 1-12 month
Bare metal stent - ASA 162-325 x 1 mo, then 75-162 for life +
Clopidogrel x 1 mo-1 yr
Drug eluting stent - ASA 162-325 x 3-6 mo, then 75-162 for life +
Clopidogrel x 1 yr minimum
Initial therapy for STEMI/new
LBBB MI
Same as NSTEMI, but can use fibrinolytics if PCI not available within 90
minutes of ER arrival
EKG findings with posterior
MIST depression in V1, V2, tall R waves in V1+2
PCI vs. fibrinolytics
Better outcome if experienced practictioner, done within 12 hrs of
symptoms, 90 minutes from ER; substantially better patency of infarcted
vessels
When to use fibrinolytic
therapy
ST elevation in 2+ contiguous lead, new LBBB, under 75 yo, within 12
hrs of symptoms, no capabilty to do PCI
Contraindications to
fibrinolytic therapy
absolute - previous hemorhhagic CVA, cerebrovacular event in last yr,
intracranial neoplasm, active internal bleeding, suspected aortic
dissection
Relative - persistent BP > 180/110, remote CVA, INR > 2-3, bleeding
disorders, recent (2-3 wks) major trauma, non-compressible venous
puncture, previous exposure to streptokinase or antistreplase,
pregnancy, active peptic ulcer, chronic HTN
This class of drugs interacts
with Clopidogrel and should
be carefully watched
PPI's - interfere with Plavix metabolism, increases levels
What vessel for RV infarct
and IWMIRAD; if RV is also infarcted, much worse prognosis
Triad of RV infarct in setting
of IWMIHoTN, clear lung fields, elevated JVD; also often have Kussmauls sign
R heart cath findings of RV
infarctelevated PA pressure > 10 + > 80% of PCWP
Treatment for RV infarctAvoid nitrates and preload agents, fluid support, may need inotropic
support with dobutamine
AVB and bradycardia are
most common with this MI
IWMI. If with AWMI, it means a large part of the intraventricular
myocardium is destroyed, is with high mortality, and usually require
permanent pacer
Indications for temporary
pacing with MI
Asystole, symptomatic bradycardia (sinus brady or AVB with
hypotension not responsive to atropine), complete AVB, Mobitz type II
Mechanical complicatons of
MI's
1. Papillary muscle rupture - IWMI, 3-7 days out, short early systolic
murmur, sudden onset of shock. Dx with echo, treat with urgent CT
surgery
2. VSD - 3-7 days out, anterioseptal MI, sudden shock, loud holosystolic
murmur. Oxygen step up 10% from RA to PA on RHC. Dx with echo, tx
with urgent CT surgery. High mortality
3. Free wall rupture of LV - 3-7 days out, large AWMI, usually elderly
HTN women. Sudden syncope, neck veins engorged, tamponade. Few
survive with urgent surgery
ICD's post MI - indications EF < 35%, baseline episodes of VT
What affects HDLincreases - exercise, small amounts of EtOH, niacin, estrogens
Decreases - tobacco, andogens
True/false - cholesterol levels
are accurate around the time
false - can be falsely low for up to 2 months
of MI/ surgery
Indications for CABG
1. significant LMA or LMA equivalent (proximal LAD + proximal LCA)
2. 3 vessel disease - survival benefit even greater with EF<50
3. 2 vessel + prox LAD + EF <50% or ischemia on non-invasive testing
4. 1-2 vessel dz w/o significant prox LAD, but have a lareg area of viable
myocardium and high risk stress
5. Can use PCI for others
CABG improves survival in
which groups
1. L main dz or L main equivalent (2 vessel, one is LAD)
2. 3 vessel with LV dysfunction
3. DM
Does not improve survival in 1-2 vessel dz, but does improve symptoms
Stent vs. angioplasty
Less plaque dissection
Less elastic recoil
Lower restenosis rate
Restenosis rates
Angioplasty- 30-50% on 6 mo
Bare metal stent - 25%
Drug eluting stent - 5%
Causes of PAD
Arteriosclerosis (risks DM, smoking)
Arteritis (CTD, Takayasu's)
Trauma
Buerger's disease (males <30, smokers, affects wrists, hands)
Entrapment
Best test for functional
imparement in PADpre and post exercise ABI
Non-invasive tx of PAD
1. Exercise
2. Stop smoking
3. Pletal (Cilostazol) - cannot use with grade III or IV CHF
4. Pentoxyfylline (Trental)
S/Sx spontaneous internal
carotid dissection
Unilateral HA, TIA or dilated pupil, unilateral neck pain in a HTN pt.,
cholesterol emboli on fundoscopy
No treatment needed (occasionally needs stent or anticoagulation
Risks for Thoractic aortic
aneurysm
HTN, cystic medial necrosis, bicuspid aortic valve, coarctation of the
aorta, 3rd trimester of pregnancy, Marfan's syndrome
Side effects of proximal TAA Aortic regurgitation, hemopericardium, MI from involvement of the
coronary artery takeoff. Presents as severe anterior chest pain and inter
scapular pain
Treatment of TAA dissection
Decrease BP with B Blockers, nitroprusside
Surgery for all ascending TAA due to risk of complications
Surgery for descending if persistent pain, evidence of end-organ
damage (renal insufficiency, limb compromise)
Size for TAA surgery 5.5 for ascending, 5.0 if Marfans, 6.5 for descending
Surgery for AAA
Monitor with q6mo CT or US if <5.5 cm
Surgery if larger or if increase in size >0.5cm every 6 months
Do cardiac testing pre op if two or more cardiac risks. Heart issues
cause 70% of the mortality
Classification of endocarditis
1. Acute vs. subacute
2. Native valve vs. prosthetic valve vs. assc. with IVDU vs. culture
negative
Bugs with endocarditis
Acute - S. aureus, broup B strep, gram negatives
Sub-acute - strep (60-80% of all), enterococcus (older men post GU
surgery), staph epi
Types of bugs in IVDU and
prosthetic valve endocarditisS. aureus, S epi, gram negs
Physical findings with
endocarditis
new murmur, Oslers nodes (painful, fingers), Janeway lesions
(nontender, palms, soles), splinter hemorrhages, Roth spots
when to replace prosthetic
valve with endocarditis
Less than 2 months from surgery, valve ring infection, myocardial
penetration (new HB or BBB)
Indications for surgery in
endocarditis
CHF, extension into the myocardium, perivalvular abscess, failure of
medical therapy, large vegetation with septic emboli
Indications for endocarditis
prophylaxis
Prosthetic valves, H/O endocarditis, congential HD (unrepaired cyanotic
CHD, repair within 6 months, repair with residual defects), cardiac
transplant with valve lesions
Drugs for endocarditis
prophylaxis
Dental - Amox, Amp, Cefazolin, Ceftriaxone; allergic - Clinda, Azithro,
Clarithro
GU/ GI - not needed!
Respiratory tract procedures, skin or muscle infection - staph, strep
coverage
Jones criteria for rheumatic
fever
Major criteria, Major: Carditis, Polyarthritis, Chorea, Erythema
marginatum, Subcutaneous nodules
Minor: Arthralgia, Fever, Elevated Acute Phase Reactants, Prolonged
PR, Previous History of Group A Strep Infeciton or rheumatic Fever.
2 Major or 1 major 2 Minor
Aortic stenosis info
Etiol - age related calific degeneration or bicuspid valve
S/Sx - LV failure, syncope, angina
Exam - slow upstroke to pulse (pulsus tardus), sustained apical impulse,
diamond shaped SEM at RUSM with radiation to neck, S4 gallop,
decreased or absent S2 (AV doesn't move well), ejection click
Have a higher rate of CAD, so cath before fixing
Severe AS = area < 1.0 cm, gradient >50
Treat all symptomatic pts with AoVR
Post AovR, anticoagulation to INR 2-3 (2.5-2.5 with MVR)
Chronic aortic regurgitation
info
Etiol - valve deformity (bifid, rheumatic fever, endocarditis, degenerative
valve dz) or abnormal aortic root (Marfans, senile aortic dz, giant cell
arteritis, relapsing polychondritis, syphilis)
Causes LV volume overload ->LVH -> LV dysfunction
Exam - decrescendo diastolic high pitched blowing murmur, RUSB (root
dz) or LUSB (leaflet dz), wide bounding pulse (water hammer), can give
low pitched rumble (Austin-Flint) with flow against mitral valve; Becker's
sign (pulsatile retinal arteries), de Musset's sign (bobbing head with
pulse)
Treatment of aortic regurg
Vasodilators (ACE, ARB, diuretics)
Surgery if symptomatic, LV end systolic dimension > 55mm, LV end
diastolic dimension > 75mm, EF <55%
Acute AR
Sx - severe pulm edema, low cardiac output, no bounding arterial pulse
(low EF). If significant AR and CHF without a reversable cause, usually
require immediate surgery
Mitral Stenosis info
Usually from rheumatic fever. Often have a fib. Can have CHF, usually
have pulm HTN. Hemoptysis from pulm congestion
Exam - diastolic murmur, low pitched rumble, accentuated S1, diastolic
opening snap
CXR - triad of prominent pulm art vascularity, enlarged LA, nl LV
Increased fluid state in pregnancy can cause acute exacerbation. Can
use heparin if a fib, cardioversion, procainamine, digoxin, verapamil
Treatment for MSValvotomy or surgical replacement if symptomatic, asx with pulm HTN
(>50 rest, >60 exercising)
Chronic mitral regurgitation
Causes - rheumatic HD, annulus dilation from LVH, endocarditis,
ischemic papillary muscle
Presentation - steady systolic murmur, often a fib, wide split S2, s3 if
severe
Treatment - diuretics, afterload reduction; surgery if symptoms, asx with
EF < 65%, LV enlargement with LVESD>45, a fib, pulm HTN. Prefer
repair to replacement
Mitral valve prolapse
Causes - weak papillary muscles, myxomatous leaflets
Sx - none (do NOT get dyspnea, panic attacks, palps, CP, etc)
Exam - midsystolic click with late murmur if MR. Click louder and earlier
if standing or valsalva
No treatment
Acute mitral regurg
Presents with pulmonary edema
Native valve - from flail leaflet (MVP, endocaditis), papillary muscle
ischemia or rupture, chordae tendinae rupture
Prosthetic valve - from tissue valve rupture, mechanic valve closure
problem (thrombus), paravalvular vegetation
Exam - decrescendo apical systolic murmur, nl size LA on echo, large L
side v waves
Rx - afterload resuction, diuresis; IABP; often need surgery
Tricuspid stenosis
Causes - rheumatic fever, congenital, endocarditis, carcinoid syndrome
(usually with TR as well)
Exam - diastolic murmur, LSB, increase with inspiration, giant a wave;
ascites, edema; EKG - tall peaked P waves in II and V1
Treatment - treat underlying, surgery
Tricuspid regurgitation
Causes - functional RV dilation from end stage LV failure, submassive
PE, pulmonary HTN, rheumatic HD, endocarditis (drug users, staph
sometimes candida), carcinoid, congenital (Ebstein's anomoly)
Exam - holosystolic LLSB murmur, parasternal heave; liver pulsations,
ascites, edema; large v waves
Dx with echo
Tx - treat underlying, rarely needs surgery except candida
Pulmonic stenosis Usually congenital, does not progress, rarely from rheumatic HD or
carcinoid; with Noonan's syndrome (low set ears and hairline)
Exam - ejection click, jugular a wave
May need balloon valuloplasty
Pulmonic regurgitation
usually from pulmonary HTN, can be congenital, rheumatic,
endocarditis.
Occasionally see with WPW, PSVT
Prognostic factors after valve
surgeryEF, symptoms, type of surgery
Three mechanisms for
arrhythmias
reentry, triggered, automaticity. Reentry is most common in PVC, SVT
(2/3rds of cases), A flut/fib, VT.
Automaticity - accelerated ectopic rhythims
Triggered RVOT VT - triggered by exercise or adrenergic stimuli
Sick sinus syndrome
Any combo of SA node problems (sinus brady/ pause/ arrest, tachy
brady)
Good prognosis
Indication for pacer - symptomatic, pt with tachyarrhythmias who
treatment would cause bradycardia
Treatment for atrial flutter
Rarely seen in healthy hearts. tx: 1. Drugs to slow impulse conduction
(BB, CCB, digitalis) 2. Conversion with antiarrhythmic drug (ibutilide,
quinine, procainamide, flecanide, propafenone); 3. Cardioversion; 4.
temporary pacing wire; 5. radiofrequency catheter ablation (to destroy
the reenterant pathway)
Anticoagulate if chronic
Cardioversion in A fib
prefer electrical except <48 hr with EF <40, then give amiodarone
Immediate cardioversion if 1. AF with RVR + ischemia, HoTN, CHF,
angina 2. Preexcitation with RVR or hemodynamically unstable, 3.
Severe symptoms
If slow a fib, put in temporary pacer first - likely has nodal dz, may go
into asystole
Pharmacologic cardioversion
drugs for A fib
If > 7 days: 1st Dofetilide; next choices - amio, ibutilide
< 7 days: 1st line - dofetilide, flecanide, ibutilide, or propafenone; 2nd
line - amio
Maintenance drugs in a fib No or minimal HD: flecanide, propafenone, sotalol. If ineffective, use
amio, dofetilide, ablation
CHF, EF< 35%: amio, dolfetilide; fails - ablation
CAD - dolfetilide, sotalol; fails - amio, ablation
HTN with LVH - amio; fails - ablation
HTN, no LVH - flecanide, propafenone, sotalol; fails - amio, ablation,
dolfetilide
Chronic anticoagulation
decision in a fib
Based on CHADS2 score:
C- CHF (1 pt)
H - HTN (1 pt)
A - Age >75 (1 pt)
D - DM (1 pt)
S - stroke or TIA in past (2 pt)
0 pts - ASA; 1 pt - either ASA or warfarin; 2+ pt - warfarin
Multifocal atrial tachycardia
info
Seen with pulmonary dz, especially on theophylline; also low K, Mg
If due to theophylline and cannot stop theoph, rx with diltiazem or
verapamil
Digoxin can worse it - avoid
Rx with ablation or pacing if refractory
Findings with WPW PR<0.12, QRS > 0.12, delta waves
Treatment of WPW
Narrow complex tachy - vagal, cardioversion, procainamide, verapamil,
adenosine
A fib/ flut - usually wide complex - avoid dig, verapamil, B-blockers - can
cause preferential conduction down accesory pathway and incite VF.
Treat with Procainamide or shock if unstable
Can cure with ablation
Treat PVC's?
If structurally normal heart, no - even if couplets, lots of them
Can use B-blocker, should get 80% reduction to call it effective
If H/O MI, EF< 40%, PVC's, especially sequential, are at high risk for
sudden death
DDX of wide complex
tachycardia
VT, SVT with aberrant conduction; WPW, SVT with LBBB, severe
hyperkalemia
EKG changes indicating VT
1. Severe L axis deviation;
2. QRS >0.14 in RBBB, >0.16 in LBBB (usually <0.12 if SVT with
aberrancy);
3. AV disassociation, disassociated P waves (cannon a waves);
4. QR or QS in V6 with LBBB or R axis dev with a LBBB;
5. Fusion beats; 6. Rate > 100; 7. capture beats
Treatment of monomorphic Stable - procainamide or amiodarone
VT
Unstable - shock
Unstable and refractory to cardioversion - IV amio or procainamide
VTwith MI - amio first, can use lidocaine
Treatment of polymorphic VT
same as monomoprhic except:
IV B-blocker if ischemia cannot be excluded
IV amio if no prolonged QT
Cath if ischemia suspected
RVOT VTInduced by exercise
Treat with B-blockers
Causes of torsades
Usually preceded by prolong QT interval, U wave
Causes - quinidine, procainamide, class Ia antiarrhythmics, dofetilide,
class III antiarrhythmics (sotalol), tricyclics, hypokalemia,
hypomagnesemia
Treatment of torsadesIncrease atrial rate (isoproterenol), overdrive pacing, MgSulfate if others
contraindicated (MI, severe ischemic HD), shock is last resort
Rhythms to avoid verapamil
with
A fib/ flut with WPW
Wide complex tachycardia
B-Blockers - both negative chronotropes and inotropes
Indications for ICD
VT with structural HD (esp HCM)
VT and cannot correct CAD
VT with EF < 30%
Indications for pacers
Symptomatic bradycardia
Complete HB
Mobitz II after AWMI
Side effects of quinidine
cinchonism (tinnitus), hemolytic anemia, sudden death(quinidine
syncope) due to QT prolongation, torsade/polymorphic ventricular
tachycardia; fever, rash, ITP, psychosis
Side effects of DisopyramideProlonged QT, QRS, torsades; (anticholinergic and vagolytic) urinary
retention, dry mouth, constipation
Side effects of procainamide
agranulocytosis, lupus (does NOT affect kidneys) with high ANA; also
QT prolongation with torsades/ventricular tachycardia; caution with CHF
- slight myocardial depressant
Side effect of Lidocaine seizures
Side effect of tocainide aplastic anemia
Side effects of amiodarone
corneal microdeposits, optic neuritis, pulmonary fibrosis (severe, fatal in
10%),bluish skin discoloration, photosensitivity, hypothyroids or
hyperthyroids, elevated INRs in warfarin patients, may elevate digoxin
levels; no hematologic effects
Evaluation for
neurocardiogenic syncope
1st episode, young, no suspected HD - observe
Infrequent episodes - tilt table, psych eval
Frequent episodes - continuous ambulatory EKG (event monitor)
Tx - B blockers
Types of cardiomyopathies Hypertrophic, restrictive, dilated
HCM is associated with which
bad occurrence
Sudden cardiac death, likely due to ventricular arrhythmia. Only cure is
transplant. Most frequent in young pts with familial form
Problem in HCM
LVH, especially in the basal ventricular septum, occasionally concentric
See diastolic dysfunction; can see Q waves - pseudoinfarct (also can
see with WPW)
Present with exercise induced syncope or severe dyspnea
Exam with HCM
Harsh, non-radiating aortic midsystolic murmur, increases with Valsalva,
decrease with handgrip; bifid pulse - strong upstroke, then falls off as it
obstructs later in systole
EKG - nl, can have inf to lat Q waves from the hypertrophy, with nl to
high voltage from LVH (if low voltage, consider infiltrative CM - amyloid)
Work up for HCM
Echo with doppler
Exercise nuc stress
Holter to look for ventricular arrhythmias
Risk factors for sudden death
in HCM
Septal thickness >30mm
H/O syncope
Fam hx sudden death in 1st degree relative
NSVT/VT on holter
Failure to increase SBP on treadmill test (<10mm)
Treatment for HCM Surgery (septal myotomy) - decreased symptoms, no change in SCD
risk
B-blocked, Verapamil - improve sx
Amiodarone if high risk for SCD (familial)
RV pacing - can improve obstruction in some pts
Avoid anything that decreases LV volume - diuretics, nitrates, volume
depletion (can us diuretics very carefully if in CHF)
Restrictive CM
Causes - amyloidosis, sarcoidosis, hemochromatosis, lipid storage
diseases
Echo - thickened myocardium, may have granularity
MUST differentiate from constrictive pericarditis - identical s/sx, but
pericarditis is quickly treated with good results, restrictive CM is
irreversable
Treatment - diuretics. Avoid digoxin unless a fib
Dilated CM
Causes - idiopathic (usually viral), alcohol, cocaine, amphetamines,
organic solvents, chemo, late hemochromatosis, possibly selenium or
carnitine deficiency
Sx - R & L HF, slow onset over months. Can form mural thrombi with
arterial embolization. Slow, steady progression to death in 3 years
Rx - anticoagulate for thrombus risk, treat HF sx as usual - diuretics, B-
blockers, ACE/ARB
NYHA CHF classes
I - no limitation in activity
II - slight limitation with activity, no sx at rest
III - marked limitation of activity, comfortable at rest. Sx with even slight
activity
IV - sx at rest
ACC/AHA stages for HF
A - at risk for HF, no structural dz
B - structural dz, but no s/sx HF
C - structural dz with s/sx
D - Marked sx at rest
ACC/AHA stage A CHF -
definition, goal, meds
Def: at risk for HF - includes HTN, ASHD, DM, metabolic syndrome,
cardiotoxins, FH of cardiomyopathy
Goal - treat disorder, exercise, discourage alcohol/ illicit drug use
Drugs - ACE/ARB for all
ACC/AHA stage B - definition,
goal, meds
Def - structural HD, no s/sx of HF - includes prior MI, LV remodeling
from LVH, low EF, asx valvular dz
Goals - same as stage A
Tx - ACE/ARB + B-blockers, ICD if indicated
ACC/AHA stage C - definition,
goal, meds
Def - structural HD with s/sx HF - dyspnea, fatigue, decreased exercise
tolerance
Goals - like A/B, add dietary salt restriction
Rx - ACE/ARB + BB + diuretics. May need aldactone, ARBs with ACE,
dig, hydralazine/nitrate combo. BiV pacing +/or ICD as needed
ACC/AHA stage D HF -
definition, goal, meds
Def - marked sx at rest despite max therapy; frequently hospitalized
Goals - A/B/C + discuss end of life care
Meds - same as C. Discuss hospice vs. extraordinary measures
(transplant, chronic inotropes, permanent mechanical support -
ventricular assist device, experimental treatments)
Poor prognosis in CHFLow EF, hyponatremia, high BUN, hypokalemia, hypo/hyperMg, high
norepinephrine and catacholamine levels
BNP in restrictive CM vs.
constrictive pericarditisElevated in RCM, nl in CPC
Diastolic dysfunction
Causes - ischemia, sever concentric LVH, HCM, diabetic CM
CO is normal, HF develops from decreased relaxation/ increased
stiffness of ventricle
Elevated LVEDP, RVEDP, tachycardia, s4
Effects of ACE/ARB in CHFincrease cardiac output, decrease LV filling, vasodilation, decrease
tachycardia, decrease incidence of VT/VF, prolong survival
B-blockers in HFdecrease remodeling, arrythmias. Coreg decreases mortality 65%,
metoprolol + bisoprolol 35%
Diuretics in HF Help fluid control, symptom control, but no improvement in mortality
Spironolactone/ Eplerenone
in HFeffective only with class III/IV, do decrease mortality
Digoxin in HF
effective only in sever systolic failure - stage C or later; use after other
standard therapies, EF <40, class II/III/IV
Resets baroreceptors, dampens renin-angiotensin effects
Improves symptoms, decreases hospitalization, no effect on mortality
Nitrates + hydralazine in HF Use in class III/IV, african american, still symptomatic despite other txs
Anticoagulation in HF start if EF<25% due to risk of mural thrombus
Meds in severe HF Dopamine - only for renal effects. Higher dose - vasoconstriction,
tachycardia
Dobutamine - inotropic, but no vasoconstriction
Milrinone (Primacor)- inotrope, vasodilator - short term use in HF
Nesiritide (natrecor) - BNP -improves clinical status, decreased PCWP/
PA pressure, improved stroke volume, no increase in HR
Hydralazine+NTG - afterload and preload reduction
CABG - only if acute MR, papillary muscle rupture
Transplant in HF Only at end stage - 65% 5 yr survival, 55% 10 yr
High output failure causesperipheral shunting (AV fistula, severe hepatic hemangioma, Pagets),
low SVR (sepsis), hyperthyroidism, Beriberi, carcinoid, anemia
Effects of azotemia on
diuretics
Avoid spironolactone and triamterene - causes hyperkalemia
Thiazides ineffective
Lasix usually works, higher doses needed
Treatment of acute pulmonary
edema
Sit with legs dangling (decrease venous return)
100% O2, morphine
Lasix - venodilation before diuresis
Digoxin - contraindicated if WPW, severe concentric LVH, restrictive CM
IV NTG/ nitroprusside if BP>100
Dobutamine if BP <90
Aminophyline - occasionally used to improve repiratory muscle function
Causes of non-constrictive
pericarditis
Idiopathic (90%, likely viral), TB, CT diseases, sepsis, renal failure,
cancer, MI (dressler syndrome autoimmune, 1-2 wks after MI),
procainamide, hydralazine
Presentation of pericarditis
severe CP, pleuritic, better leaning forward, fever, tachycardia;
pericardial friction rub (not always)
EKG - diffuse, concave upsloped ST elevation, occasionally depressed
PR in II
Transient increase in CKMB
Treatment for pericarditis
Stop/ treat cause
NSAID's
Steroids only if not idiopathic - higher risk of relapse; definitely use if TB
Colchicine
Causes of constrictive
pericarditis
Usually idiopathic, open heart surgery, radiotherapy, coccidiomycosis,
TB
Exam with constrictive
pericarditis
Loud presystolic knock just after s2 (due to rapid early diastolic LV
filling), pulsus paradoxus
Kussmaul sign - heart encapsulated, can't accomodate extra blood in
inspiration, so don't get usual drop in JVD with inspiration, can actually
increase
Large R sided x+y descent due to brisk collapse of the jugular during
diastole
Kussmauls & large x+y descent are HALLMARKS
Imaging with constrictive
pericarditis
CXR - calcification of pericardium - seem best in lateral over R ventricle
- pathognomic for this
CT/MRI/ echo - measures thickness of pericardium - >5mm suggest this
Treatment for constrictive
pericarditispericardectomy. Fixes problem in 50%
Recurrent pericarditis
problem is chest pain
Does NOT progress to constrictive pericarditis
Rarely gives arrythmias
NSAIDs, colchicine, steroids to treat
Pericardectomy not as effective, only use if other options fail
Best imaging modality for
pericardial effusionCT or MRI are better than echo, and can see small pockets of fluid
When to surgically drain
pericardial effusion
traumatic hemopericadium, post surgical effusion, bacteria or TB
suspected as cause
Hallmarks of tamponade
1. Hypotension and muffled heart sounds
2. Pulsus paradoxus
3. JVD with no collapse during diastole
Ostium secundum ASD
Most common CHD found in adults; SEM at LSB (increased flow across
pulm valve)
occ diastolic murmur (flow across tricuspid valve) and a fixed split S2
(RVH)
enlarged RV on CXR and shunt vasculature
RAD and/or RBBB on ECG, can see A fib
Tx: surgical closure or percutaneous closure (do if > 2:1 left to right
(pulmonic/systemic) shunt
Pulmonic HTN is considered a contraindication to surgery
Ostium primum ASD
loud pansystolic murmur 2/2 MR or TR (regurg because ostium is low
on septum, interfering with function of AV valves or L mitral valve).
ECG has left axis and RBBB
Surgery fixes problem
Eisenmenger syndrome is a contraindication to surgery
Sinus venosus ASD SV: Sup septal area ~ CS: Inf septal area, close to Coronary Sinus,
rare; assc with anomalous pulmonary venous return
Patent ductus arteriosus
Usually asymptomatic
Continuous "machinery" murmur LUSB
CXR with calcification of ductus arteriosus
Develop differential cyanosis - clubbed toes, nl fingers, pulmonary HTN
Consider Eisenminger syndrome if develops pulm HTN
Surgical or percutaneous closure
Ventricular septal defect
Most common CHD in kids, uncommon in adults
80% close in 1st year of life
Large VSD's require surgery
Coarctation of the aorta
bicuspid AoV in 70%
Delayed femoral/ brachial pulse
Upper body HTN, HTN aneurysmal dilations, rupture in circle of willis
CXR - rib notching
Amonalous coronary artery suspect with exertional CP or syncope in a young healthy individual
Causes of sudden cardiac
death in exercising young
people
HCM - 36%
Coronary anomalies
Primary pulm HTN
Eisenmenger syndrome
When the left to right shunts cause pulmonary hypertension, vascular
hypertrophy, and eventually shift the L=>R shunt to a R=>L shunt, and
cause late cyanosis. Heart-lung transplant is only cure
Pulm HTN
Includes sporadic idiopathic - young women, refractory, death in 5-10
yrs
Tx - CCBs, sildenafil, heart lung transplant
Pregnancy heart issues
Contraindication to pregnancy - pulm HTN, eisenmengers
Watch closely - secundum ASD, AoS, dilated CM
Bed rest - AoS, dilated CM
Causes of LAD L anterior hemiblock, so a marker of CAD
Causes of RAD
nl in kids, young adults
L posterior hemiblock, RVH, acute or chronic RV overload (pulm HTN,
PE, pulm stenosis)
If an adult has RAD, work it up!
Formula for QTc QT/square root of RR, all in seconds. Nl 340-430 msec
Estimate by 40% of RR
Causes of prolonged QT
Tricyclic OD, hypocalcemia, hypomagnesemia, hypokalemia, starvation,
CNS insult, Type Ia (quinidine, procainamide), III (amiodarone, sotalol)
antiarrhythmics, non sedating antihistamines + EES, azoles,
ketoconazole, liquid protein diet
Causes of short QT digitalis, hypercalcemia
Retrograde P waveneg in II, pos in aVR - ectopic AV focus in the inferior atrium or AV
junction
RAE findings
Causes - RA enlargement, hypertrophy, overload)
nl P width (<0.12)
Peaked P in II, V1
LAE findings
increased L side of the wave, so wave >0.12, wide P wave, shortened
PR interval
notched P in II, increase neg portion in V1
Peaked T waves
hyperkalemia
Hyperacute MI
intracerebral hemorrhage
V1, V2 in evolving MI
Focally flipped T waves
Ischemia
V1-2 with RBBB, RVH, RV HTN, LVH
Lateral leads (I, aVL, V6) with LBBB
Precordial leads in LVH with strain
Diffuse flipped T's in
pericarditis
Diffuse ischemia, post resuscitation
Metabolic abnormalities
Intracerebral hemorrhage
U waves
Best seen just after T in V2-3
If prominent, risk for torsades - hypokalemia, bradycardia, digitalis,
amiodarone
Negative U wave - caused by ischemia, HTN, AV valve dz, RVH. See in
60% on ant MI, 30% of IWMI
ST elevation causes
MI, prinzmetals angina, pericarditis
Less seen in ICH, early repolarization, HCM, LVH, LBBB, cocaine
abuse, myocarditis, hypothermia
ST depression causes
Subendocardial ischemia
Posterior MI (V1-2)
Reciprocal depression in V1-2 in some IWMI
LVH with LV strain
isolated RV infarction (ST elevation V1, depression in V2)RVH
sometimes in V1
Digitalis toxicity
Hypokalemia
Criteria for LVH
Q in V1+ R in V6 >35
R in V5+R in V6 >25-35
If LAD, use S in III>15
RVH RAD + ST depression + flipped T in V1-2
LBBB criteria
QRS = 120-180
RR' in V6, SS' in V1
T opposite of mean QRS vector in anterioseptal and lateral leads
RBBB criteria
QRS >120
delayed depolarization of RV - RSR' or RR' in V1, slurred S in V5-6
Flipped T in V1, sometimes V2
LAFB criteria
LAD -45 to -90 degrees
Large S in inferior leads
Dominant R in I
No other causes of LAD (LBBB)
Poor R wave progression
LPFB criteria
Small Q, large R in inf leads
Small R in I, large S in I, aVL
R axis +80-+140 degrees
Order of changes with MI
T inversion - ischemia
ST changes - injury
Q waves - cell death
All 13 termsPrint new! Export Combine
Terms Definitions
What does the QRS represent depolarization of two simultaneously contracting
ventricles
What does the P wave represent atria depolarization
What does the T wave represent ventricular repolarization
How long should the PRI be 0.12 - 0.20 s
How long should the QRS be < 0.12 s
Where are positive and negative leads placed
on Bipolar leads I, II and II
Lead I - Right Arm is negative - Left Arm is positive
Lead II - Right Arm is negative - Left Leg is positive
*Lead III - Left Arm is negative - Left Leg is positive
How much is the small box 0.04 s
How much is the large box 0.20 s
What is the 1st positive deflection following
the P waveR wave
What is the 1st negative deflection following
the P waveQ wave
Pathological Q wavePathological Q wave is > 0.04 s or deeper than 1/3 of
the total height of the QRS complex
To be considered significant, S-T segment
has to be >> 1 mm or one small box
What does QT interval represent ventricular depolarization and repolarization