cardiology Flashcards
pr interval
0.12-0.20
left atrial enlargmenet
m shaped- biphasic p wave in lead II
right atrial enlargement
tall p wave in lead II more than 3m
bundle branch block
both have wide QRS
acetylcholine
regulated by the vagus nerve- decreases force of contractio, decreased SA node
anticholinergics
increase heart rate
sick sinus syndreom
permanent pacemaker is treatment- or brady with v tach- permanent pacemeaker with automatic implantable cardioverter-defib (AICD)
sinus brady
atropine , less than 60
afib
no p waves, beta blockers tx
tx: calcium channel blockers: NON DHP!!- diltiazem and verapamil
DIGOXIN- RATE CONTROL IN patient with HYPOTENSION OR CONGESTIVE HEART FAILURE!!
unstable: sycnhorinzed cardioversion
Rhtyhm control: start heparin, cardiovert within 24 hours, and then anticoag for 4 weeks
AMIODRAONE for rhythm control
dabigatran
direct thrombin inhibitors
factor XA inhibitors (binds to antithrombin III)
rivaroxabana, apixaban, edoxaban
warfarin INR goal
2-3
long QT syndrome
TCA, macrolides
paroxysmal supraventricular tach
more than 100, regularly with narrow QRS complexes
rhtyhm from above ventricles.
WPV is a form- both one accessory pathway is outside the AV node and 1 within the av node
COMMON ONE: both pathways within av node( one slow one fast)- most common
tx for SVT
vagal maneuvers adenosine- first lien MEDICAL beta block or calcium channel dont use adenosin in patients with asma//copd- bronchospasm amiodarine
TX for WPW
PROCAINAMIDE
MAT
3 p wav morphologies- SEVERE COPD association
calcium channel blockers or Beta blockers used
WPW
delta waves (slurred QRS upstroke) WIDE QRS SHORT PR interval
STABLE:tx: procainamide
Adempsome. BETA. CAlcium, DIGOXIN
unstable:::: SYNCHORNIZED CARDIOVERS
def management: radiofrequency ablation
junctional
p waves inverted, or negative- like I, II, avf leads. NARROW QRS 40-60 for junctional 60-100 for accelerated juctional tacy: more than 100
pvc - premature venticular complex
no treatment needed usually
V Tach
prolonged QT interval common predisposing condition
TORSADES dE pointes
MC due to hypomagnesemia, HYPO kalemia, - twists around baslene
STABLE VT
amiodarine
unstable vt with a pulse
synchronized cardioversion
VT (no pulse)
defib and cpr
trosades de pointes
IV MAG
pulsesless electrical activity
rhtyhm on monitor but pulseless person- CPR and epi and check for shockable rhythm every 2 mins
acute pericarditisi
concave ST elevations in the precordial leads (v1 to v6)
pr depresisons in the same leads iwth ST elevations
phyaiological split
inspiration separates S2 into A2 followed by P2.
pulsus paraoxus
more than 10 mm hg decline in SBP with inspiration
treatmill test
+ if hypotension or hypertension, arrhytmias, or st elevation,
CI: can’t exercises, LBBB, WPW, baseline ST changes, pacing
pharmaco stress test
if patients can’t exericse- do this
ADENOSINE or dipyridamole: CORONARY vasodilators OF ONLY THE NORMAL arterities- used for people with baseline ecg abnromaltieis like LBBB or ventricular pacing
CI: bronchospastic disease
stress echo
USES DOBUTAMINE!: stimulates increased hr/ contractiliity
CI: v. arrthytmias, severe aortic stenosis, SBP more than 180, aortic dissection or patients on beta blockers
coronary artery disease
ATHEROsclerosis: MC
fatty streak formation: lipid in the white blood cells: then formation of an early plaque, formation of fibrous plaque- narrows coronary arterial lume and calicficiation- uaully more than 70% will cause symptoms
angina pectoris
usually short in duration- less than 30 mins, leveines sign, pain relieved with rest,
anginal equivalent: dyspea, epigatric or sholuder pain
ST depression
coronary angiography: definitive diagnosis/gold standard
PTCA
1 or 2 vessel disease not involving the lefft main coronary artery and v function is normal- stents
CABGL
LEft main coronary artery disease- 3 vessel disease, ejection fraction less than 40% on left
beta blockers (Cardioselective- metoprolol and atenolol)
prolongs coronary artery filling times, reduces o2 requirement
ca blockers
prevents/terminates ischemia idnuced by coronary vaspospasm- coronary vasodilation
pain at rest for heart disease
indicates more than 90% occlusion
inferior wall MI
chest pain and BRADYcardia- may be suggestive of an inferior MI , +s4!!!
left anterior descending (LAD)
anterior wall-septal v1 through v4
circumflex
LATERAL WALL- I, AVL, v5, V6
inferior
2, 3, avf- RIGHT CORONARY artery
myoglobin
first cardiac marker to increase
adp inhibitors (clopidogrel)
good for patients with aspirin allergy- inbhiits aDP mediated platelet ggreagation
GPIIb/iIIA inhibitors
inhibits teh final pathway for platelet aggreagatio (eptifbatid, tirofiban, abciximab)
unfractioned heaprin
binds to and potentiates antithrombin IIi ability to inactivate factor XA, inactivates thrombin (IIA). Low molectular weight heaprin- more specific to factor XA-
unstable angina or NSTEMI
- antithrombotic therapy, and adjunctive anti-ischmic therapy
anti thrombotic: aspirin, clopidogrel, gPIIb/IIIa
heparin - as anticoag
adjuncts: beta blockers, nitrates, morphine, ca blockers (
St elevations management
- reperfusion therapy- most important
DONE WITHIN 12 hours- either PCI or thrombolytics
pci: best within 3 h of symptoms PCI is better than thrombolytics - thrombolytics: TISSUE plasminogen activateors (alteplase, tenecteplase)- dissolves clot by activating tissue plasminogen to plasmin
streptokinase: only given once
thromblytics dissolve existing clots
adjunctive: BETA blockers, ACE inhibitors, NITRATES, morphine
ACE
slows progression of CHF and decreases VENTRICULAR remodeling
cocaine
DONT GIVE BETA blockers
USE CALCIUM channel blockers, benzo, aspirin, heparin
heart failure
most common cause is cad
systolic failure
decresed ejection fraction, thin ventriular walls, dilated LV chamber, +s3
diastolic failure
increased ejection fraction or normal
thick ventriicular walls
SMALL lv chamber
+s4
high output failure
severe, anemia, thyrotoxicosis, av shutning, beriberi
ejection fraction
most important determinant of progrnosis in heart failure
use BNP- to identify CHF as the cause of dyspnea in the ER
beta blockers
DONT USE during decomponsated HF
HF: vasodilators (decrease afterload)
ACe inhibitors, ARBs, beta blockers, hydralazine and nitrates)
decrease preload during HF
diuretics, potassium sparing diuretics, hydrochlorthiazides
sympathomimetics
SHORT TERM IN SEVERE ACUTE CHF: dobutamine, digoxine and dopamine: positive ionotropes
digoxin
double/blurred vision/green yellow halos around lights), seizures, dizziness,
DECOMPENSATED HEart failure
LASIX, morphine, nitrates, oxygen, position
reducing preload
acute pericarditis
aspirin or NSAIDS for 7-14 days
Dressler: ASPOIRIN or colchicine
pericardial effusion
low voltage Qrs complex, electric alternans
pericardial tamponade
pulsus paraodxus: more than 10 mmhg decrease in systolic blood pressure with inspiration!!
HYPOTENSION, JVP , muffled heart sounds
constrictive pericardi
:thickened, fibrotic, calicfied pericardium- restricts diastolic filling- percardiectomy is tx
acute pericarditis
mc idiopathic
virus: enterovirus: coxackie
myocarditis
C viral: enteroviruses like coxsackie, parvo too
gold standard: endoyocardial biopsy-
CXR: dilated cardiomyopathy!
+cardiac enzymes
restrictive cardiomyopathy
amyloisodosis MC cause
sarcoidsosis
diastiolic function imparied
kussmaul’s sign: jvp increses with INSPIRATION
hypertrophic cardiomyopathy
SYSTOLIC crescendo-descredo murmur
handgrip, INCREASED VENOUS return by squatting or lying supine- DECREASES mURMUR
DECREASED VenOUS return such as valsalva and standing- increases murmur intesnsity- assymettriacal wall thickeness- esp septal
TX : beta blockers, CCB
rheuamtic fever
migratory polyarthritis active carditis nodules (subcutaneous) erythema marginatum syndenham's chorea
plus recent strep infection
tx for rheumatic fever
antiinflammatory: aspirin, and penicillin G
if pcn allergic: erythromycin
ejection clinck
mitral valve prolapse
harsh rumble sounds
THINK STENOSIS
bllowing sound
think REGURG
aortic stenosis
congenital heart disease (bicuspid aov)
angina, syncope, congestive heart failure
systolic ejection!
aortic regurg
Endocaritis, MARFAN syndrome, syphillis, aortic dissesction,
AUSTIN flint murmur
bounding pulse
wide pulse pressure
water hammer pulse: radial pulse upstroke and rapid fall
corrigans’ pulse: carotid artery
de musset’s : head bobbing
traube’s sound: pistol shot femoral artery
quinke’s pulse: fingernail bed pulsations
PULSUS bisferins: double pulse carotid upstroke
a
tx of aortic regur
afterload reduction with ace, arbs, nifiedipine, surgical
mitral stenosis
mc rheumatic heart disease
pulm symptoms: pulmonary htn, dyspnea, atrial fib, OPENING SNAP!!!!
left atrial enlargement +Afib
percutaneous blaloon valvulopasty
mitral regurg
most common cause: mitral valve prolapse, or ISCHEMIA/infarction
mitral valve prolapse
MC in young women
most asymptomatic
mid late systolic EJECTION CLICK!
pulmonic stenosis
congenital and disease of the young
htn
sysotlic more than 140
diastolic more than 90
95% primary- idiopathic etiology
secondary: mc reason is renovascular mc- renal artery stenosis
goal is less than 140 /90 for diabetecs and chronic renal disease!
spirinolactone
Side effect: hyperkalemia and gyenocmastia
hydrochlorthiazides
side effect: hypercalcemia, hyperglycemia, hypercalcemia, hyperuricemia, hypokaemia
alpha blockers
used tfor BPH-
se: dizzines, headache-
calcium channel
dont give for CHF or 2/3rd heart block
african americans
do well with thiazides, cCB
DM
do well with ACEI, ARB
htn urgency
increased bp , but no acute organ damage- oral agents used - clonidine, captopril, furosemide, labetalol, nicardibine
htn emergency
with acute end organ damage- usually more than 180 and diastolic more than 120
neuro /cardiac. renal /
if its retial damage: malignant htn- papilledema
INIATE statin therapy
type 1 or type 2 between 40-75 with LDL-C levels of 70 to 189 mg per dL
cardiovasc disease 40-75 and 7.5 % risk of heart attack or stroke in 10 years
peaople more than 21 with ldl levels of more than 190
any form of clinical atherosclerotic cardiovasc disease
increase hdl
niacin0 best drug- increases HDL
se: hyperuric, hyperglycemia
lower elevated trigliceride
fibrates - decreases hepatic production of tiglyceride
seE: myositis, and yalgias esp with statin, gall stones
lower ldl
statins: increases ldl receptions
se: myositis/.myagias, hepatitis
bile acid sequestrants
used for pruritis associated with biliary obstruction
ONLY MED SAFE IN PREGNANCY!!!!
removes LDL from the blood
-sE: causes increased trigly
endocarditis
MC valve: MITRAL valve
IN IV drug users: TRICUSPID VALVE
acute bacterial endocard
s. aureus- for normal valves
subacute bacterial endocard
ABNORMAL VALVES- s. viridans
endocarditis in IV drug users
MRSA
prosthetic valve endocarditis
STAPH epidermis MC- early
late: staph aureus
hacek organizesm
hemophilus, actinobaci, cardiobacterium, eikenella, klingella- gram neg organizesm- large vegetables
janeway
painless macules on palms and soles (endo)
roth spots
retinal hemorrhages with pale centers
osler’s nodes
tender on pads of the digits
blood culture for endcard
3 sets at least 1 hour apart, use TEE- more sesntiive.
acute (native valve )Endocard
naficillin and genta X 4-6 weeks, vanco for mrsa and genta
subacute (native valve)
pen or ampi, plus genta, VANCO in IVDA
protsthetic valve
VANCO+genta, +rifampin (staph aureus)
fungal (Endocard)
amphotericin B
prophylaxis for endocarditis
prosthetic, heart repairs, prior history of endcard, congenital heart disease, cardiac valvulopathy
DENTAL- gums, roots of teeth, oral mucosa
respir: rigit dbronchoscopy , respiratory mucosa surgery
INFECTED SKIN/musculoskeleta tissue : abscess incision and draining
AMOX 30-60min sbefore surgery
clinda if penc allergy
leriche’s syndrome
claudication (buttock, thigh pain), impotence, and decreased femoral pulses
acute arterial emoblism
paresthsais, pain, pallor, pulseless, paralysis, poikilothermia
PAD
lateral malleolar ulcers, atrophic skin changes,
USE ABI +pad if less than 0.90
arteriorgraphy: gold standard
CILOSTAZOL tx
AAA
mc risk factor, atherosclerosis, smoking!!!, marfan’s, syphillis, HTN
_tender, pulsatile abdominal mass, syncope or hypotension
more than 5 cm is rupture risk
ultrasound: imagin study of choice
CT SCAN: test of choice for THORACIC aneurysm
ANGIOGRAPHY: gold standard
Aortic dissection
TEAR IN THE INNERMOST LAYER OF AORTA (INTIMA)
65% ascending, ascending- high mortality
HYPERTENSION- RISK FACTOR! MOST IMPORTANT!
variation in pulse between right and left arm
acute NEW onset- AORTIC REGURG
GOLD STANDARD: MRI angiography!
CT scan with contrast- test of choice??
XR: widening mediastinum
surgical management for debakey I or II/stanford A
medical: descending without complications
debakey
type I: aortic arch and beyond it distally
type II: ascending aorta- confined
type III: descending aorta
buerger’s disease (THROMBOANGIITS OBLITERANS)
superficial migratory thrombophlebitis, ischemic ulcers or gangrene finger/toe ischemia, raynaud’s phenomena
ABNORMAL allen test: assesses patency of radial and ulnar arteries
tx: CCB, STOP SMOKING!
DVT
virchow triad: venous stasis, endothelial damage, hypercoagulability
VENOUS DUPLEX ULTRASOUND- first line
D dimer - for low risk patients- can rule it out
venography: gold standard
tx: heparin and then WARFARIN!
warfarin
inhibits protein C and S, 2,7,9,10
postural hypotension (orthostatic)
impaired autonomic reflexes or reduced intravascular volume
fall in the systolic blood pressure of more than 20 mm or fall of the diastolic blood pressure more than 10 mm with changes in position
if due to hypovolemia: increase in pulse rate of more than 15
ciruclatory shock
low cardiac output OR low systemic vascular RESISTANCE
inadequate tissue perfusion, autonomic nervous sytem activation- increases SVR and contracitilyt when NE, DOPAMINE and cortisol relesed, RAAS activation- decreased urine output
systemic effects of shock: ATOP depletion, metabolic acidsosi, lactic acid, multisystemic organ failure
hypovolemic shock
vasoconstriction, increased SVR, hypotension, decreased CO, and decreased pulmonary capillary pressure
tX: crystalloids, normal saline, control hemorrahge
cardiogenic shock
increased pulmonary capillary wedge pressure, increased SVR (Vasoconstrict), hypotension, decreased CO
ONLY SHOCK WHERE LARGE AMOUNTS OF fluids aren’t given
ionotopic support: DOBUTAMINE, epinephrine, treat underlying
obstructive shock
MASSIVE PE: ECG: S1Q3T3
perciardial tamponande
tension pneumo
aortic DISSECTION!
Distributive shock
maldistribution of blood and vasodilation- shunt of blood away from vital to nonvital organs!
decreased cardiac output , decreased SVR (this is diff from other shocks), decreased pulmonary wedge pressure
But if warm extremities: increased CO, decreased SVR- early septic shock
(septic shock, anaphylactic shock, neurogenic shock, endocrine shock)
septic shock (distributive shock)
infectiev organism activates immune system: host produces systemic inflammatory response
SIRS: temp, pulse high, RR high, wbc high or too low
sepsis: incresed lactate, and sirs
severe sepsis: sirs and multi system organ failure
septic shock: sepsis and refractory hypotension
- BROAD SPECTRUM abx
iv fluid resusciationt,
VASOPRESSORS if no response to iv fluids
anaphylactic shock
ige mediated severe systemic hypersens reactivity
epinephrine, air way management, antihistamines, iv fluids
neurogenic shock
acute spinal cord injury- brady and hypotens- wide pulse pressure
endocrine shock
adrenal insufficiency - tx with hydrocortisone
