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564 Cards in this Set

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Stages of Atherosclerosis
1: smooth lumen
2: fatty streaks, early immune response
3: cholesterol, calcium crystals, cellular debris. intima bulges into lumen
4: thrombus formation, embolus
diet/atherosclerosis
decrease sodium, increase Mg, Ca, K, fiber, folate, vit K, antioxidants, fish oil
Atherogenic
LDL, lipoprotein, homocysteine, hypertension, diabetes mellitus, artery harden, vitamin K deficiency, male over 55, female over 65, FH(x) coronary heart disease, smoking
thrombogenic
low fish, low fruit, low veggie, high fat, obesity
atherogenic LPs
chylo remnants
LDL
VLDL remnants
nonatherogenic LPs
chylomicrons
HDL
VLDL
chylomicrons
intestine to other organs
carry TGs, cholesterol, Vit A, D, E, K
pancreatic lipase
cleaves dietary fat in small intestine
increase in TGs
independent risk factor for CHD
high fat diet
saturates chylo remnant clearance, prolongs circulation
VLDL
TGs, cholesterol, Vit E from liver to other organs

half converted to LDL, half taken up in receptor mediated process
cholesterol raising
myristic, (butter, milk, meat, coconut)
palmitic (shortening)
trans fats (partially hydrogenated)
neutral fats
stearic (beef, chocolate)
oleic (olive, canola, almond)
palmitoleic (palm oil)
decrease cholesterol fats
linoleic (seeds, veggies, walnuts)
alpha-linolenic (flaxseed, linseed)
epa/dha (fatty fish)
left axis shift
hypertrophy
bold lines ekg pulse
300-150-100-75-60-50-40
p>5 blocks
first degree heart block
no P wave
av impulse, no SA
normal axis
-30 to +120
right axis deviation
negative in lead I
normal axis leads I, II, III
upright
RVH
positive R wave in V1
right axis deviation
pulmonary hypertension

negative in I, II, AVF (rt axis shift)

positive AVR (should be negative)
LVH
left axis deviation

positive I
negative II, III, AVF

aortic stenosis, HTN

huge R waves in V leads
Flipped T waves (ischemia)
Determine LVH
add amplitudes V1 and V5, >35 = LVH
flipped T waves
ischemia
tissue hypoxia
infarction
paradoxical wall motion
Inferior STEMI
STE in II, III, AVF
Wall Injury
Q wave 1mm x 1mm or 1/3 height QRS
Lateral STEMI
I, AVL, V5, V6
Anterior STEMI
V3, V4
Septal STEMI
V1, V2
RCA occlusion
inferior stemi
acute septal MI
V1, V2
irregularly irregular
atrial FIB
hard time finding P waves
saw tooth pattern
atrial flutter
atrial rate 300bpm
ventricle 1/2 (150bpm)
Dig Toxicity
salvador dali mustache, depression ST segment
single chamber pacemaker
huge spikes, looks like left axis shift
dual chamber pacers
double spikes
hyperkalemia
peak T
wide QRS
renal failure
give Calclium
hypokalemia
U wave instead of T wave
repolarizing abnormality
biphasic P waves
atrial enlargement (left, right, biatrial)
LBBB
biphasic R waves
QRS widened
V5, V6
pericarditis EKG
STE everywhere because enflamed pericardium
AV valves mumurs
vegetation systolic
damage diastolic
left atrium dilated
MS
LVH
AS
functional regurgitation causes
dilated ventricle causes papillary muscle to be pulled down and out

dilated aorta or PA pullls valve commisures apart, prevents closure
MCC valve disease
acquire MS/AS
Calcific AS
MC valve abnormality
acquired
calcific cusps hard to open
LV pressure overload

ischemia, angina, CHF
Rheumatic AS, Congenital AS
commisural fusion
AS prognosies
ASx, good

Sx, bad

high pitched systolic murmur
COngenital Bicuspid AV
MC congenital cardiac malformation

calcific
mitral annular calcification
calcium deposits cause stony nodules

doesnt usually affect Fx

can cause Sx

nodules can embolize, be nidus for infx, ringlike opacities CXR
myxomatous degeneration mitral valve
MVP, young women, midsystolic click, chorda tendinae long, thin, depot mucoid material
secondary changes to MVP
fibrous leaflets, thickening endocardium from friction injury by leaflets, thrombi on atrial surface leaflets,focal calcifications

marfan
rheumatic fever
follows group A strep pharyngitis
IgG cross react with tissue glycoproteins in heart, joints, etc (M proteins)

takes 20 years to develop in western individuals, happens in children in 3rd world

pancarditis

MV Most commonly

migratory polyarthritis
erythema

sydenham choria (involuntary rapid purposeless movements)

jones criteria
group A pharyngitis
fever, athralgias, acute phase reacts
aschoff bodies

acute RF
fibrinoid necrosis surrounded by mononucleocyte infiltrates
anitschow cells

RF
large histiocytes with vesicular nuclei, basophilic cytoplasm, owl eye ross section
chronic RF
irreversible valve deformity, increased vascularity, lymphocyte infiltrates, chordae fibrous and fused, valvular annular calcification

mv MC
women more than men
fish mouth deformity
Left atrium dilation, mural thrombi, arrythmias,
carotid upstroke
sound during-systole
sound before-diastole
S1
closure MV, TV, hear at TV
SPLIT S1
RBBB
INcreased S1
MS, Increased CO, short PR
Decreased S1
long PR, decreased CO, MR
S2
closure PV/AV
splits on inspiration
hear at PV
SPlit S2
AS,LBBB, PUlmonary HTN, Trans Venous PAcers
wide splitting
volume overload, AR (diastolic murmur, Eccentric Hypertrophy (heart folds back in on itself)), PDA
Systolic murmur aorta
AS
S4
diastolic mumur
over ventricle with bell Left Lateral Decubitus
separate S1 (inspirate) from S4 (hand grip)

long term HTN and organ disease
S3
diastole
increases with hand grip, ventricular overload
increase venous return
squatting, inhalation
decrease venous return,
standing, expiration
handgrip
increase left sided murmurs
inspirate
increase right sided murmurs
opening snap
MS, calcification
ASD murmur
systolic murmur
MS murmur
diastolic rumble
Normal S3
up to 40 years of age
S4 normal
never
into non compliant ventricle
need atrial contraction to augment CO
extra beats
PAC hear it fear it
PVC, hear dont feel, could be benign
inspiration
S2 moves from S1
S3
inspiration increases over sternum, handgrip increases left lateral decub, big heart

filling problem
S4
handgrip with bell left lateral decbuoitus

small heart
PV, TV, IHSS, MS
MR
handgrip, apical
AS
bilateral carotid bruits, 2nd right intercostal, handgrip, angina, shortness breath,
PS
2nd left intercostal, doesnt radiate, shortness breath angina, increased volume acomodated,neck vein distension, longer with inspiration
ASD
neck vein distension, doesnt respond to maneuvers, incomplete RBBB,
VSD
hand grip exaggerate, 4th intercostal, left sternal border

Ddx-TR, inspiration increases this
PDA
only holosystolic murmur, heard best over clavicle, machinegun murmur
AR
two and blow
handgrip
2nd left or 2nd right intercostal
MS
diastolic murmur
chronic aortic valvulitis
males, mitral valvulitis, LVH, thick adherent cusps OR fibrosis and retraction
calcific AS
LVH, ASx, fibrosis with calcification
Non Bacterial Thrombotic Endocarditis
aka marantic endocarditis, in pts with sepsis or cancer, small nodules on valve, no inflammation no damage but embolize

happen in endocardial trauma

valve free of inflammation and bacteria.
associated with cancer,mucin producing carcinomas,
resolve spontaneously

AV most commonly involved
carcinoid heart disease
endocardium, right sided valves

cardiac manifestation systemic syndrome

tumors, malignant potential

produce products called carcinoid

cardiac, wheezing, rash, gi, diaphoresis

plaquelike thickenings on cardiac chambers
major right side blood vessels, valves
acid/mucopolysaccaride rich matrix

thicken from serotonin and histamine

inactivated in pulmonary system, so the lesions stop in right side of heart
Endocarditis of SLE
libman-sachs endocarditis

sterile, pink warty vegetations
valve, chords, mural endocardium
artificial valves
infx at tissue, prosthesis interface, hemoloysis, overgrowth of tissue
infective endocarditis
bulky friable vegetation, microbe, fibrin, bacterial, destruction common,

IVDA

ricekttsiae, fungi aslo possible

infx occurs during bacteremia

IVDA, prosthetic valves, cardiac abnormalities
acute endocarditis
highly virulent organisms

destructive infx in previously normal
difficult to treat

necrotizing, ulcerative, invasive lesions
subacute endocarditis
lower virulence, previously abnormal valves, recovery with antibiotics
IE previoulsy damaged valves
strep viridans
prosthetic valves IE
staph epi
IVDA IE
staph aureus, TV (usually MV/AV in IE)
IE difficult to treat
avascular valves
IE morphology
ring abcesses, veg erodes into myocardium, fungal causes larger, systemic infarcts possible
IE clinical
fever, janeway lesions (purpura soles/palms),, osler nodes (tender pulp digits), roth spoths (retinal hemmorages), splinter hemmorages
SLE IE
undersurface of AV valves
NBTE
depot platelets, fibrin, hypercoagulable state, sterile, debilitated patients
artificial valves complications
up to ten years post op, hemolysis, exuberant, inappropriate healing, mech. valves need anticoagulation, bioprosthesis degrades
paronychia
inflammation around nail bed
pupura
purple-brown-red discoloration of skin greater than .5cm
vegetation
tissue/blood clot

fungating-spongy
MCC IE
staph aureus
2nd-viridans
clinical indication IE
febrile illness, no resolve and murmur
staph bovis
if isolated check colon
IE e. feacalis
GI surgeru
MCC culture negative antibiotics
early antibiotic dosage
RHD IE
young, group A strep pyogenes, beta hemolyric, genetically susceptible hosts or those in 3rd world, Ig to M protein,

licks the joints bites the heart
IE elderly
no fever
peripheral IE
splinter hemmorage, janeway, oslers, roth spots, conjunctival petechiae, sudden blindness in one eye, clubbing fingers (scharoth's sign)
HACEK organisms
gm negative

Heamophilus
actinobacillus
Cardiobacterium hominus
Eikenella Corrodens (human bites)
Kingella (children arthritis)
prophylactic tx for IE
prosthetic valve, previous IE< CHD, invasive dental procedure, resp tract incision, surg procedures with INFX tissue
strep pyogenes
developing countries
MCC acquired heart disease kids developing world
kawasakis
pericarditis clinical
uncomfortable laying down, prefer to sit upright
PVC/VPC
PQRST + abnormal wave

opposite widened axis
prolonged QT
T wave is 1/2 distance between Rs
P wave close to T wave
atrial depolarizes when ventricle is sensitive-->vfib
antihistamine and decongestant
prolong QT, add coughing fit, VTACH/VFIB
pulmonary emobolus
S1Q3(enlarged 1/3 height complex)T3 (flipped)
Right Atrial Enlargement
bigger P wave
RBBB
R and R'

QRS bigger than 3 boxes
PR elevated
primary av block
PR 6,8,10,12,6,8,10,12
wenkebachs
T close to P
prolonged QT
Supraventricular Tach SVT
suspect if HR greater than 150
Rate dependent ST depression
ischemia with tach
VTACH
ectopic electrical impulses, ventricle firing away, poor blood flow, doesnt repolarize, deep troughs, concordance (superimposable waves)
Wolf Parkinson White Syndrome
Q-R slope instead of spike
normal intervals
PR less than 5
QRS less than 3
QT less than 1/2 R to R
long PR
first degree block
STE II, III, AVF
inferior MI
STE I, AVL, V5, V6
Lateral MI
Peak Ts
hyperkalemia
U waves
hypokalemia
circumflex occlusion MI
lateral
LAD MI
anterior (v3,v4)
right coronary MI
(posterior, st depression v1,v2)
right/left cornoary MI
inferior
hypocalcemia
prolonged PR


hypercalcemia
shortened PR
VFIB
pulseless, squiggly
Torsades de Pointes
VFib Up/down/up/down like party streamer (rhythm exists but difficult to visualize)
cpr?
asystoly
Murmurs characteristics
Timing, grade, location, duration, pitch, radiation, intensity, shape, maneuvers
MCC rupture papillary muscle
posteromedial papillary receiving blood supply from posterior descenidng branch of a dominant RCA associated with inferior MI

anterolateral papillary has dual blood supply and less common to ruptire
MCC valvular lesion
AS 1, MR 2
MCC mitral abnormalities
myxomatous degeneration
MCC MR third world
rhd
MR relations
not diabetes, dyslipidemia.

female, lower bmi, old age, renal, prior mi, ms, mvp
acute MR
sudden volume overload on left atrium and left ventricle

no hypertrophic compenation, SV decreases because TSV increased but FSV is same

severely Sx
normal LV because not hypertrophic
hyperdynamic systolic Fx of left ventricle on TTE in patient with acute CHF
suspect acute severe MR
acute MR tx
nitroprusside
increase aortic flow, if normotensive

if hypotensive
nitroprsside and inotropic
chronic MR
LA/LV, sufficient time to dilate and accomodate volume
tsv/fsv preserved by hypertrophy
LV dilates, pulls MV leaflets, worsens MR
indications for MV surgery
patients with poor heart function but no Sx

severe cardiac dysfx will not do well
AS
obstructive murmur
syncope
angina
dyspnea

radiates to carotid, consistent with gallalvardin effect

prominent S4 (left atrium contracting into stiff ventricle)

crescendo-decrescendo (mid to late peaking)

increased squatting, reduced valsalva
MCC AS
caclific

calcification of annulus can lead to heart blocks
pulsus parvus et tardus
delayed carotid pulse
gallavardin
mimics MR, doesnt radiate to axilla
MCC congenital AS
bicuspid
Rheumatic AS
commisures fuse, fibrosis, aortic insufficiency from retracted leaflets, mitral and aortic valvular disease
aortic sclerosis
calcification not hemodyanamically significant
mortality from onset of symptoms
angina 5 years
syncope 3 years
heart failur 2 years
AS heyde syndrome
gi bleeds due to angiodysplasia or other vascular malformation b/c enhanced vWF-platelet interactions increases shear stress
signs AR
muller sign (pulsation uvula)
musset sign( bobbing head)
water hammer pulse
corrigan pulse (pulsating filling cap bed under fingernail)
pulsus bisferiens( dual impulse in same cardiac cycle


fatigue, angina, dyspnea,
TX valve stuff
echo, cath, CXR.

acute-pressor/inotropic/vasodilator, avoid beta blockers to not disrupt compensatory mechs)
ischemia beyond 30 minus
irreversible cell injury begins (down ATP, up lactate)
activate PKCE before ischemia
cardioprotective, upregulates Katp channels
inhibit PKC after ischemie
cardioprotective
eNOS and BH4
coupled, cardioprotective, produce NO
eNOS and BH2
uncoupled, produce SO anion, bad
increases bh2
atherosclerosis, HTN, DM
LNAME
not cardioprotective, blocks NO
VIt E
promote couples eNOS, Ig to adhesion molecules, cytokines, complement
statins
antiinflammatory, reduce plaques, augment enos
BH4 and PKCE during reperfusion
good
BH2 and PKC inhibitor
increase NO, cardiprotective
decrease phase 4 slope
Na, Ca, Beta blockers
increase threshold potential
Na Blockers
increase maximum diastolic potential
adenosine (hyperpolarize cell, open K+)
increase action potential duration
K+ blockers, longer ERP
digoxin
risk of arryhtmias, calcium buildup
gen anesthesia
arryhtmia isk
80% MI patients
at risk for later arryhtmia
automaticity
slope phase 4
increases slope/automaticity
SNS, ischemia
decreases slope, automaticity
PNS
IA/IC agents
increase APD
IB agents
increase ERP
abnormal automaticity
SA node up-tach
SA node down-brady

digoxin triggers automaticity (eartly/delayed afterpolarizations)
conduction block
ischemia
SVT
ectopic atrial foci
PVC
ectopic foci
VTACH
ectopic foci, torsades de pointes
class I antiARR
NA blockers
decrease phase 0 upstroke rate (increase threshold)
class II antiARR
beta blockers
decrease phase 4 slope
class III antiARR
k+ blockers

increase APD
class IV antiARR
K+ blockers
increase APD
adenosine
increase diastolic potential, open K+ channels
IB agent
lidocaine, up ERP
affinity for inactivated channels
IA/IC agents
open channels, on upstroke, low affinity for resting or closed channels
IA agents
quinidine, procainamide, dispoyramide
also block K+
increase HR
hyperkalemia toxicity
increase QRS, QT
Quinidine
PO
IA
chronic control
alpha blocking, cause hypotension

ADRS
cinchonism
increased DIg toxicity
Procainamide
short T1/2,
PO/IV
sides:

SLE
Disopyramide
IA
2nd line drug
inotropically negative
ADR urinary retention, constipation
Lidocaine
IB
inactivated channels
NOT K block
IV only

DUAL CNS effects adr

mixilitine/tocainide
-po lidocaine for vtach
IC agents
mortality
popafenone, morcizine, flecainide
beta blockers
propanolol, esmolol, metoprolol, acebutolol
prevent MI
esmolol
emergency IV tx
K blockers (class III)
increase plateau, APD
Sotalol
class III wit BB properties
increase RP
ventricular arrthymias
bretylium
class III
iv emergency, VFIB
ibutilide
atrial fib/flutter
dofetilide
PO, atrial fib, inpt setting
amiodarone
class III with I,II,IV effects
thyroxine iodide analog
for V/SV tach
loading doses

ADR
skin, eye neuro deposits
increase tox dig, warfarin
Class IV calcium blockers
supraventricular tach

slows SA-AV conduction

ADR Gi/CHF
adenosine
av node tach
open k channels
increase max diastolic potential
short T1/2
decrease AV node conduction
vasodilator, can cause bronchospasm
magnesium sulfate
diuretics cause MG def. arrythmias
Adenosine
for acute aV tach
lidocaine
MI, VTACH
cause of ILLNESS
SNS
traube-herring-meyer wave
central-->interstitial-->veins/lymph
raynauds syndrome
peripheral reaction to cold, vasoconstrict, worse with previous hypersympathetic tone
scleroderma
fibrosis, slow with fascial release
largel lymphatic vessels
contrlled by SNS
T2-T7
upper extremity
T9-L3
lower extremity
unilateral issue
muscle trap
bilateral issue
lymph ducts
primary lymphadema uncommon, 2ndary common
mastectomy, radiation, infx, parasite, crush injury, cancer, surgery
AV/Lymph/CSF
primary, secundary, tertiary circulation systems
right lymph duct vs left lymph duct
right arm, right chest, right head/neck

left-everything else
lymph flow
respiration plus heart pump plus muscle
false diaphragms
popliteal fossa etc
lymph anchoring filaments
keep vessel open/closed depending on pressure
cisterna chyli
congestion problems, false diaphragm
lymphatic ducts connect to thoracic ducts
multiple places in subclavian venous trunk
thoracic duct control
sympathetic
50% plasma proteins and salts
return via lymphatics
na blockers
faster heart rates
esmolol
iv emergency atrial flutter
bretylium
vfib
ibutilide
afib
dofetilide
afib
amiodarone
vtach, svt
ca blockers
svt, vt
PSVT, AV tach acute
adenosine

hyperpolarizes, prevents AV conduction
increase PR interval
verapimil
VTACH
lidocaine
TV IE
IVDA
IE MC VALVE
AV,MV
IE gp a strep
uncommon
IE more common
immunocompromised
MCC IE in native valve
staph aureus

2nd viridans
MCC in prosthetic valve
staph epidermidis
MCCIE in IVDA
s. aureus

ivda greatest risk factor patients under 40
HACEK
assoc w endocarditis
HIV infx IE
indpendent risk factor
3/4 IE patients have a structural abormality
yes
Major criteria IE
+ blood culture (3 every 12 hours)
echo evidence endocardial involvement
minor criteria IE
predisposition, fever, vasc/immunologic phenomenon
microbio/echocardio evidence not meeting major

glomerulonephritis
rheumatic fever
oslers nodes
roth spots
janeway lesions
positive echo IE
oscillating mass on valve/structure or in path of regurgitant jets with absence of alternate explanation

abcess
partial dehiscience of prosthetic valve (w/ or w/o veg)
valve regurgitation (new)
less common IE risk factors
pregnancy, central lines, shunts, av fistulas, ulcerative colon lesions
native valve IE in MVP
coagulase negative staph

subacute

staph lugdanensis can attack heart valve with no previous abnormality
group B strep IE
aortic valve

large friable veg

VHD, DM, EtOH, Neoplasia, GUinfx, Abortion, cirrhosis, ivda

pneumococcal IE
-rare
austrians triad-meningitis, pneumonia, IE
assoc with EtOH
gram negative bacillary IE
IVDA. Nosocomial

persistent baceteremia despirt antibiotic tx

unlikely on prosthetic valve
PHV IE
50% patients with nosocomial bacteremia/fungemia had PHV endocarditis
HACEK
hemophilus,actinobacillus, cardiobacterium, eikenella, kingella

large friable veg

frequent emboli, frequent valve replacement
sub acute clinical presentation
IE clinical
fever, murmur, petechia, skin, conjunctiva, oral mucosa, anorexia, wt loss, malaise, night sweats, splenomegaly, splinter hemmorages, osler nodes, janeway lesions


goes to areas of previous trauma
MCC culture negative endocarditis
previous antibiotic treatment
Hx most important part of diagnosing IE
yes.
TEE
better than TTE
indications for surgery
CHF, persistent/uncontrolled infx, recurrent emboli, fungal, highly resistant organism


if neuro, wait until sterile b/c heparin during bypass
IE prophylaxis
invasive dental procedures, other situations only if high risk

previous IE
prosthetic valve
congenital cyanotic heart disease with prosthetic shunts first six months after repair

repaired CHD with residual defects
cardiac transplant with valvular disease
acetazolamide
carbonic anhydrase inhibitor

pct

glaucoma

ADR metabolic acidosis
mannitol
osmotic agent
PCT
for cerebral edema
worsen CHF
furosemide
loop agents
thick ascending limb
for acute chf
HCTZ
thiazide
DCT
mild pulmonary edema
spares calcium
carbonic anhydrase inhibitors
increases loss HCO3
PCT
Sulfonamides
Urine alkaline/blood acidic
for glaucoma, to alkanalize urine
mannitol
osmotic diuretic
IV
increased urine volume with little NA loss
PCTcause fluid overload CHF
extracts intracellular water
decreases ICP


ADR hyponatremia, hypokalemia
furosemide
loop diuretics
high ceiling diuretic
excretes everything
for severe chf, renal failure, hypercalcemia

ADR Ototoxic
contraindicated with aminoglycosides
Increase LDl/TGs
Sulfa Rxns
Hs
hyponatremia
hypotension
hypokalemia (arr)
hypocalcemia (muscle excitabilityi)
hypomagnesia(convulsions)
hypochloremic alkalosis (excessive loss Cl)
hyperuricemia
hyperglycemia
thiazides
DCT
lower ceiling
calcium sparing

ADR
sulfa
LDL.Tg

for moderate CHF, hypocalcemia, diabetes inspidsus,

decreasing URINE calcium to decrease kidney stones

K+ sparking diruetics
spironoloactone, amiloride
spironolactone
aldosterone antagonist
collecting ducts
aldosterone dependent diuretic

for 2nd aldosteronism to CHF, cirrhosis, hypokalemia


ADR hyperkalemia, impotence, gynecomastia
amiloride
triamterene
not dependent on aldosterone
K+ sapring
combo with other diuretics

sides hyperkalemia
ADH antagonists
conivaptan/demeclocycline

collecting tubule
conivaptan
PO
adrenal insuff, hypothyroid, too much ADH

ADR
hypokalemia
demeclocycline
ADR Diabetes inspidus, renal failure, photosensitivity, no children under 12
acute CHF tx
furosemide
moderate chf tx
HCTZ
cause of hypercalcemia
HCTZ
decreases urine Ca
HCTZ
tx renal failure, hyper kalemia
HCTZ
need to void calcium?
furosemide
need to get Ca out of urine
HCTZ
have a metabolic acidosis? what did you take
acetazolamide
for acute CHF
furosemide
systolic dysfunction
younger, pump dysfunction, decrease CO
diastolic dysfunction
older, TPR, renal HTN, vascular
increase sodium in SMC
increase calcium, increase sensitivity to NE/EPI/ANGII with increase in calcium -->vasoconstriction
diuretics antihypertensives
decrease NA, CA, TPR

k sparers paired with loops

interfere with compensatory reflexes, baroreceptors, RAA
protect against osteoporosis
HCTZ
spironolocatone useful in chf 2nd aldosteronism
k+ sparing
beta blockers
NS propanolol, B1 Atenolol and metoprolol

decrease CO, Renin (B1)
use with younger patients with increased SNS tone, hyperkinetic circulation

decrease LVH

ADR depression, fatigue, TG.Chol, IMportence
labetalol/carvedolol
alpha 1 and non specific BB

decrease TPR and CO


IV in HTN emergency, pheochromocytoma
alpha 1 blockers
prazosin
decrease pre/afterload
maintain RBF
increase CO in CHF, decrease LVH

ADR postural hypotension, impotence, tachycardia
alpha 2 agonists
presynaptic in PNS/CNS exerts negative feedback, decrease NE release

postsynaptic in CNS
inhibit SNS outflow from vasomotor/cardiac centers
decrease vasomotor tone, BP, HR
Clonidine
alpha 2 agonist
decrease BP HR CO, increase PNS, vagal
PO, transdermal
ADR cns depression, sedation
abrupt cessation, rebound effect
methyldopa
alpha 2 agonsit
decrease BP, less HR and RAA than clonidine
useful with diuretic
safe in preg but cause hemolytic anemia
cns sedation, disturbances
hydralazine
arteriolar vasodilator
decrease diastolic more than systolic, decrease TPR
activates baroreceptor/RAA reflect
diuretic and BB in severe HTN
ADR excessive vasodilation, edema, flushing, SLE, arthalgia
minoxidil
arteriolar dilator
open K+, decrease SMC contraction

ADR relfex tach, edema, chf, tamponade, hair growth


used for severe htn w diuretic
HTN crisis
nitroprusside, diazoxide
nitroprusside
IV, increase HR, decrease BP,
adr flushing
diazoxide
K+ channels
arteriolar dilator
increase HR
used with BB
antiHTN Ca blocker verapimil diltaizem
arteriolar dilators, decrease CO
too much cause CHF
ADR av block, constipation
nifedipine, dihydropyradines
cal channel more potent but reflex tach,
adr excessive vasodilator, chf, edema
minoxidil
increase hair and heart rate
dose dependent HR decrease
verapimil
ACEI
decrease angiotensin II, decrease TPR, decrease vasoconstriction

increase bradykinin (vasodilator) (decrease pre/afterload)

increase CO in CHF, maintain renal Fx in diabetic neuropathy

no metabolic, no impotency issues

ADR hypotension, hypokalemia, cough
contraindicated in preg
captopril
aceI, fast, short t1/2
enalapril/lisinopril
prodrugs, long t1/2
losartan
ang II inhibitor

ATI blocker
long t1/2
arterial SMC, kidney, adrenal effects
does not increase bradykinin

ADR cough, angioedma, fatigue, hypotension, liver enzymes,
verapimil
constipation, no reflext tach
enalapril
decrease AngII
methyldopa
hemolytic anemia
postural hypotension
alpha receptor blockers
captopril
cough
propanolol
FHx HTN, MI, LVH
lidocaine
increase ERP/APD ration
procainamide
SLE
verapimil
av node tach
ibutilide
reduces k+ repolarizing current, increase APD duration
edema and metabolic acidosis
HCTZ
mannitol
cerebral edema
conivaptan
SIADH
myocardial preconditioning
activation KATP channels helps mediate
PKCE activator before transplant
cardiportecitve
BH2 and PKCEativator
increase H202 during reperfusion
coupled enos
limits reperfusion injury
mcc genetic congenital heart disease
down syndrome
lesion chromosome 22

parathyroid. thymus, heart
digeorge syndrome
asd
Asx until adulthood
irreversible pulmonary HTN can develop

l2r


secundum 90% fossa deficieny or fenestrated

primum adjacent to aortic valve, MV defect too

sinus venosus near entrance to SVC-conection to right pulm veines
cardiac cirrhosis, paradoxical embolization, cor pulmonale
vsd
l2r
most involve membranous septum
others liie beneath PV
some close spontaneously

large defects result in RVH, switches r2l, pulm htn, cyanosis, death
tet of fallot
r2l shunt

vsd w/overriding aorta
RVOTO
RVH
boot shaped heart
transposition of great vessels

need vsd to survive

pulm stenosis protects lungs from RVH
pda
r2l
no issues at birth
machinery like murmur
shunt left to right at birth then pbstructive pulm vascular disease and flow shifts r2l
av septal defect
poor formation of av valves

partial, MR

complete
all four chambers communicate,
four chamber hypertrophy
assoc w down syndrome
transposition of great vessels
PA/Aorta reversed

systems separated, must have shunt to live

vsd=stable shunt

PFA=unstable, needs surgery
truncus arteriosus
fail;ure embryologic TA to separate into aorta and PA

single artery receive blood from both ventricles

VSD

irreversible pulm HTN
cyanosis
tricuspid atresia
TV occlusion
unequal division AV valves

RV atrophy

right to left shunt through PFA or ASD

VSD allows for communication to RV/PA
MCC congenital heart disorder
ASD
2:1 female to male
subtle clinical findings
MC ASD
ostium secundum

ostium primum
sinus venosus
eisenmenger system
chronic L2R shunt causes irreversible pulm HTN and a reversal into R2L shunt
ASD
dyspnea
fatigabnility
palpitationms
atrial arrythmias
syncope
stroke
MI

palpable pulsation of PA and ejection click

S1 split
S2 widely split, fixed

acyanotic, no tx necessary

spontaneous closure is frequent in children

repair not recommended in insignificant shunt, severe PA HTN, Pulm Vascular Occlusion
PDA
female to male 2:1

Thoracic aorta-> pulmonary artery

congenital-rubella

children born at high altitude or premature infants
perinatal asphyxia, low birth wt, siblings of PDA

Recurrant Laryngeal loops around DA

L2R shunt
PDA is repsonible for 60%of CO in fetal life
patency promoted by PGE2
NSAIDS in mother can close

absence of DA contraction--hypoxemia, aspphyxia, renal failure, resp disorders

fetal alcohol
congenital rubella
amphetamine, phenytoin use

DX echo, CXR, catheter to measure O2 sat in RV

IV indomethacin, ibuprofen, coil embolization, ligation
ortners syndrome
pulm htn, left atrial enlargement, impinge on recurrent laryngeal
MC VSD
perimembranous
VSD
L2R shunt
AR
LVH, Dilation
Eisenmengers complex
-VSD. HTN. CYANOSIS

CHF, cardiogenic shock


murmur
systolic, left upper sternal border radiate to back

crescendo-decescendo

ECHO, CATH, MRI diagnose

surgical repair

good prognosis
coarctation of Aorta
constrictioed aortic segment
pre/post ductal
can get post stenotic dilation
M:F 2:1
young: CHF old:htn

LVH

acute right heart dilation if FO is not patent

less severe coarctation will produce collateral circulation

greater than 20mmHg difference in blood pressure between upper/lower extrmity
absent lower extremity pulse
cyanotic lower extremity
R2L shunt

murmur nonspecific infraclavicular under left scapula

delay between femoral and brachial pulses
cath with contrast to see aortic pinch
rib notching from collateral circulation
associationd VSD, Bicuspid AV, Abnormal retinal blood vessels

tx baloon angioplasty

poor prognosis uncorrected
TET of fallot
cyanotic
RVOTO
VSD
overriding aorta
Aorta Dextroposition
RVH
PV stenosis

congenital rubella, poor prenatal nutrition, FAS, older mothers, mothers with PKU, DM

down syndrom related to TET

blue skin during crying

tet spells

squatting is compensatory mechanism

surg repair necessary

cyanosis, clubbbing, systolic thrill, PV closure not heard

polycythemia, embolize, low O2 sat, boot shaped heart


propanolo can correct RVOTO

prognosis sudden death, PE, parradoxical emboli,
MCC cyanotic congenital heart defect
TET
BP
=COxTPR(SVR)

CO=HRxSV
SV low and WET
LVEDV increased
SV low and DRY
LVEDV decreased
RAA stimulated
when kidney is not perfused
NE
drives HR, increases TPR
systolic HF
EF <40%, cant pump

right side of starling curve
diastolic HF
EF>40%, cant fill

left side of starling curver
Systolic and Diastolic HF Sx
dyspnea, edema

age, htn, dm, overwt
systolic Dysfx
enlarged apex, displace ventricle down and to left

S3
kyperkinesis
diastolic Dysfx
S4 (atrial sound, heard best with bell over left ventricle)
volume overload
neck veins up, systolic dysfx
afterload reducer of choice for systolic dysfx
ACEI
reduce preload
furosemide
reduce afterload
beta blockers, block NE, indirect afterload reducer
Tx of choice to prolong life
ACEI BB Diuretic
use hydralazine/nitrates?
ACEI contrindicated, ACEIBBDIURETIC not effective
causes of systolic dysfx
htn, mi, IHD, cardiomyopathy, Valvular heart disease, congenital
Big heart
S3 cant pump
diuretic treatment of choice
CHF and uncontrolled HTN
digitalis
when dont respond to BB ACEI DIURETIC and in CHF
diastolic dysfx
left side starling curver underfilled
small cavitieis
scarred, fibrotic ventricle
cavity constricted from outside

IHSS, AS, LVH, HTN
LVH because HTN
beta blocker

no acei no diuretic
cant give beta?
give ca blockers verapimil/diltiazem, block AV node
cardiomyopathy
chronic systolic dysfx

big hearts, poor pumps, S3, shortness breath
TB
chronic/night sweats, cough, hiv

Dx with TAP fro adenosine deaminase


thickened restrictive pericardium needs to be peeled off
hypothyroidism
after radiation
pericardial effusion
gold paint


over time leads to bradycardia

Tx treat hypo T4
CHF and bradycardia
either thyroid or conduction system block
acute pericardial effusion
X descent
chronic pericardial effusion
y descent
constricitve/restrictive disease Sx
dyspnea, neck vein, X/Y descent, small hearts, edema

gget an echo and doppler ultrasound
restrictive problems
show peak and plateau

RV diastolic pressure <1/3 RV systolic pressure

elevated pulmonary pressures

virus, infx, metastatic breast cancer

tanned skin? could be hemochromatosis and liver dysfunction
constrictive problems
filling pressures elevated
RV/PA pressures not elevated
doppler patterns
Normal. E=Violent, A=atrial contract

Early Diastolic dysfx
cavity thick, e wave smaller, atrial contract harder

very large E very small A =restrictive disease
diastolic dysfunction
arrhythmia, atrial fibrilation
afib can be caused by hypothyroidism
atrial fibrillation with rapid ventiricular respoinse 2nd to hyperthytoidism,
use b blocker because it blocks conversion t4 to t3 in periphery
good ventricle, bad atrial arryhtmia
can walk around for a long time
increased NE levels
chronic systolic dysfx,
HOCM
restriction due to obstructive disease of ventricle when septum is thicker than posterior wall and overall heart thickened

valsalva, murmur ets longer

treat obstruction with BBLocker
if not, ca vlockers

get desperate>? use disopyramide (cant pee, cant poop, no good)
causes heart failure
ischemic
non-ischemic-familial, infx, alcohol, thyroid, acromegaly, thiamine def, HTN

in developing world? CHAGAS
causes myocarditis
viral, fungal, bacterial, parasitic, toxins, anthracycline, cocain, chemo
amyloidosis
deposition of insoluble extracellular fibrillar deposits forming b-pleated cheets

senile-depot transthyretin-better prognosis

firm rubbery
dilated
nodules on atrial endocardium
stains congo red positve (green birfringeringences)
rings around myocytes, capilarrioes
compress lumen, capillaries-->ischemie
iron overload
hemochromatosis or excess blood transfusions
heart dilated
iron in ventricles
systolic dysfx-ROS, mess up enzymes
hemochromatosis-chromosome 6
rusty borwn color
hemosiderin in perinuclearregon
cell degeneration, fibrosis
iron containing lysosomes
long QT
dominant gene
antipsychotic, antiarrhythmic, allergy meds
common genetic cause sudden death
Sx during rigorous activity
Dx with ekg
females more likely to experience symptoms
prolonged ventricle repolarization
Torsades de Pointes/VFib
autopsy normal, test for mutated genes
Brugada syndrome
SE asia
inherited, sudden death
middle aged males
RBBB
defectin sodium channel
autosomal dominant
catecholaminergic Polymorphic Vtach
associated with sudden death with exercise
finnsih/italian
syncopal spells in childhood/adolescence
with exercise/stress
50% mortality by 30, resting ekg normal
short QT syndrome
sudden death, premature atrial fib, adolescence
commotio cordis
sudden blunt impact to prcordial area
abnormal ventricle activity, cardiac arrest sudden death
no structural injury
low speed imapct
VFib
impact coincides with period ventricle repolarization
myxomas
50% of primary heart tumors
sporadic-middle aged females, left atrium single

familial-young males, not left atrium multple
carneys syndrome
myxoma, fibroadenomas breast, sertoli cell tumors, adrenocrotical nodular dysplasia (cushings)
left sided myxomas
MS/MR
Right sided myxomas
dyspnea, syncope, neck vein, emboli, infarcys
myxomas
soft, pale, lobulated, stalk attached to septum,
round stellate cells, loose stroma, mucopolysaccarides, no mitotic figures, arises from mulitpotent stem cells
rhabdomyoma
benign tummor skeletal muscle
early life, congenital
adults-tuberous sclerosis or congenitalnheart disease

regress in childhood
well circumscribed nodiles, spider cells with radial cytoplasmic extensions
cardiac fibroma
solitary, 2nd decade, sudden death, outflow tract obstruction
gorlins syndrom
basal cell carcinoma, cardiac fibroma, rhabdomyosarcoma
sottos syndrome
cerebral gigantism, cardiac fibroma
hamartoma of cardiac myocytes
extensive production
localize hypertrophic cardiomyopathy
myocyte disarray
focal scarring
coronary thickenig of bridging arteries
left ventricle
calcified amorpous tumor of the heart
nodular depot calcium in background of degenerating blood cell elements, chronic inflammation
benign clinical course
pathogenesis obscure
Cardiac MICE
mesothelial/monocyte incidental cardiac excrescences
incidental microscopic findings at time of surgery
can attach to heart, floating in cavity,inside an aneurysm
strips of mesothelial cells, tubular and micropappillary formations surrounded by smaller histiocytes
bengin, non neoplastic, no clincal significance
cystic tumors of av node
developmental abnormality of epithelial nature, endodermal origin
may be associated wit other congenital abnormalities
cause complete heart block
tumors rarely seen grossly
micro ductal structures, cysts, nests of epidermal cells, desmosomes,microvillia

sudden death
papillary fibroelastomas
small papillary growth on valves, etc
incidental finding
hyperplastic endocardial cells covering core of hyalinized hypocellular stroma
end stage organization of thrombus
seen more frequently after cardiac surgery
paraganglioma
primary cardiac neoplasm
left atrium is most common location
HTn, elevated, urine catecholamine
sarcoma
very rare
highly pleomorphic, difficult to classify
angiosarcoma is most common
usually large mass in right atrium
fibrosarcoma
chf, arrhytmhias, svc obstruction
malignant tumors more likely on right side of heart
synovial sarcoma
biphasic pattern
carcinoma/sarcoma
high grade sarcoma
pleomorphic, high n:c ration, spindle cells, mitotic figures
lymphoma
primary is rare, 2nd more common

associated with aids, large cell lymphomas
metastatic timors
primary usually in thoracic area, mediastinal lymph nodes, hematogenous route (breast, kidney, melanoma, choriocarcinoma)
tamponade
compression of atria and ventricles restricting cardiax filling
pericarditis
almost always viral origin
chronic forms seen in TB, fungal but most is acute

secondary thoracic/systemic issues, cardiac surg, metastasis
serous pericarditis
acute
can be noninfx, RF, SLE, uremia, scleroderma, viral associatied
straw colored fluid
viral infx elsewhere,
few leukocytes
small volume (10-50 normal)
rarely organizes
rich protien content
fibrinous pericarditis
acute, protein adherent pericardium to epicardium
most common
serous with fibrinous exudate
assoc with acute mi
dressler sydrome0autoimmune etiology, weeks to months around acute MI)
uremia, chest radiation, RF, SLE, trauma

dry surface, fine granular roughening
serofibrinous pericarditis
combo of two
thicker fluid
WBCs
can become organized
purulent/suppurative pericarditis
infective organisms, pus
-extension from neighboring inflammation
-seed blood-
-lymphatic extension
-direct induction during surgery
acute inflammatory RXN
-organization is likely (constrictive pericarditis)
resolution infrequnct
hemmoragic peridcarditis
blood w/ fibrinous or suppurative
malignant tumor of pericardial space inovolved
bacterial infx, bleeding disorders, tb
follows surgery, serious blood loss, tamponade
caseous pericarditis
tb fungal
spread through nodes
chronic, constrictive
chronic pericarditis
plaque like fibrous thickneing of serosal membrane called soldiers plaque
adhesions found at autopsy with no clinical significance
in severe cases organization can obliterate pericardial sax, cause stringy adhesions bewtween visceral pareityal pericardiim
called adhesive pericarditis
adhesive mediastinal pericarditis
follow suppurative, caseous pericarditis, cardiac surgery, mediastinal irritation
pericardial sac obliterated
great strain on cardiac fx
RVH mimic cardipmyopathy
constrictive pericarditis
dense, fibrous scar
decrease diastolic expansion, decrease CO
hypertrophy, dilation can occur because dense fibrous scar
pericardial space obliterated
right ventricle
preload pump, conduit, dictates volumes
pulmonary venous resistance
right ventricle afterload
MCC rt atrial failure
left ventricle failure
neck vein, edema, cold distal digits
right heart
starling curve
to the right, volume overload
to the left, dehydration
right side maneuvers
inspire, leg raise squat increases
expirate, valsalva decrease
left side maneuvers
hand grip squat.
left MV
htn dyspnea mid to late systolic murmur at apex
AS
old person, syncope, DM, htn, cigarrettes, parvus et tardus, bilateral carotid bruits, systolic at base of hear
decrease venous return valsalva, stand up
4-6 beats later it decreases volume returning

less venous return, less blood pushing walls out, gradient up, longer murmur
ihss
tx with beta blocker
septum wall thicker than posterior, obstructed at rest in diastole
tee
left side valve lesions
MC etiology of diastolic dysfx
HTN/LVH
RV dysfx
begets lv dysfx
constrictive disease
pericardium, matted on epicardium, doesnt allow filling
restrictive disease
normal fx, normal size
rt side faiilure
heptaomegaly, fatigue, neck vein, edema
visceral and somatic afferents
meet at dorsal horn
sympathetic
red then skin blanch quickly

biochemical stays eed
t1-4
eent heart lungs
t5-9
stomach, gallbladder, liver
t10-11
kidney, intestine, gonads
t12-l2
t2-8
upper extremities
t11-l2
lower extremities
direct stimuli
more nociception is easier facilitated set up
overload, fatigue, cold, trauma, gravity, nutrition, endocrine
indirect stimuli
arthritic joint,visceral afferent, segmental somatic dysfx
type II
hyperextension to side of organ by rotators (sympathetics)
V-S clues
1st-celiac-tightness
segmetnal paraspinal tissues texture changes somatic dysfx

enoough visceral nociception sets up facilitated segment


more tissue texture change than restriction=V-S

S-V more restriction
S-V
type II more likely
postural crossovers
apexes of curver
right pec is a major trigger point
neurologic autonomic
treat FS first
kerr/denslow
more facilitated,, less weight to fire segments
neurological lens
stressors
t5-9
upper gi to ligament of trietz (celiac ganglion)
t12-L2
descending colon, inferior mesenteric ganglion
t10-11
superior mesenterica ganglion
VS TYPE II
more likeley
V primary
more tissue texture recurrence post somatic treatment harder rubber hvla response
s primary
posturally challenged, biomechanically challenged
SNS dysfx
decrease blood flow, gland activity up, pain, sensitivitiy up, more anxiety
tissue drain dysfx
biochemical pH changes
lymph congestion, fibrosis, rediced angiogenesisi
tumor
by the time it sets up FS is probably far along
posterior chapmans reflexes
NLV bundle piercing muscle btween spinous and transverse processes