First Aid Flashcards
Things that increase inotropy (4)
catecholamines
inc intracellular Ca
dec extracellular Na
digitalis
Things that decrease inotropy (5)
Beta blockade heart failure acidosis hypoxemia/hypercapnia non-dihydropyridine CCBs
Things that increase SV (3)
anxiety
exercise
pregnancy
Hydralazine
VASOdilator, reduces afterload
Things that increase preload (3)
Exercise (slightly)
increased blood volume
sympathetics
Things that increase O2 demand (4)
increased afterload
inc contractility
inc heart rate
inc heart size (inc wall tension)
R =
(viscocity x length)/radius^4
x 8/pi
Things that increase viscosity (3)
polycythemia
hyperporteinemic states (eg multiple myeloma)
hereditary spherocytosis
Where is S1 loudest?
Mitral area
Where is S2 loudest?
Left sternal border
When is S3 normal?
children
pregnant
Causes of wide S2 split
RBBB
pulmonary stenosis
Causes of paradoxical S2 split
LBBB
aortic stenosis
What murmurs heard in aortic area?
Systolic murmur
- AS
- flow murmur
- aortic valve sclerosis
What murmurs heard in pulmonic area?
Systolic ejection murmur
- PS
- flow murmur (ex. ASD)
What murmurs heard in tricuspid area?
pansystolic -TR -VSD diastolic -TS -ASD
What murmurs heard in mitral area?
Sysolic
-MR
Diastolic
-MS
What murmurs heard in L sternal border?
Diastolic -AR -PR Systolic -hypertrophic cardiomyopathy
What is the ASD murmur?
Flow across actual ASD doesn’t cause murmur
- pulmonary flow murmur due to inc flow through pulmonary
- diastolic rumble due to inc flow across tricuspid
- progression –> louder diastolic murmur of pulm regurg from dilatation of PA
Dicrotic notch
Dip in aortic pressure at end of systole (right when aortic valve closes); due to blood flowing back into valve cusps
What does inspiration do to heart sounds?
increases intensity of R heart sounds
What does expiration do to heart sounds?
increases intensity of L heart sounds
What does hand grip do & what does this do to heart sounds?
- inc systemic vascular resistance
- inc MR, VSD murmurs
What does valsava do & what does this do to heart sounds?
- decreases venous return
- most murmurs dec in intensity
- MVP & hypertrophic cardiomyopathy murmurs increase
What does rapid squatting do & what does this do to heart sounds?
- inc venous return, inc afterload
- dec MPV, hypertrophic cardiomyopathy murmurs
Where is MR murmur loudest & where does it radiate?
loudest at apex
radiates to axilla
Quality & timing of MR & TR murmurs
Holosystolic, high pitched, blowing
What increases MR murmur?
increased by increased TPR (squatting, handgrip)
or increased LA return (expiration)
Common causes for MR
ischemic heart disease
MVP
LV dilatation
Where is TR murmur loudest & where does it radiate?
Loudest at tricuspid area
radiates to R sternal border
What increases TR murmur
increased by increased RA return (inspiration)
Common causes for TR
RV dilatation or endocarditis
RF causes both
What extra sound does AS have?
ejection click at start of murmur (due to abrupt halting of valve leaflets)
What is “pulsus parvus et tardus”?
In aortic stenosis
= weak pulses compared to heart sounds
VSD murmur - where, and what?
Loudest at tricuspid
harsh holosystolic
MVP murmur - what?
midsystolic click followed by crescendo murmur, loudest at S2
What can MVP predispose to?
IE
Common causes of MVP
myxomatous degeneration
RF
chordae rupture
What worsens MVP
decreasing venous return (standing, valsalva)
AR murmur - quality and timing
Begins immediately at S2
high pitched
blowing
Clinical features of AR
wide pulse pressure when chronic
can have bounding pulses & head bobbing
Common causes of AR
aortic root dilatation
bicuspid aortic valve
RF
What decreases intensity of AR murmur?
vasodilators
What extra sound is heard with MS?
opening snap
-due to abrupt halt of leaflet motion after rapid opening due to fusion at leaflet tips
What does MS murmur sound like?
rumbling
What increases MS murmur?
increased LA return (ex expiration)
PDA murmur - timing and quality
continuous machine like murmur
loudest at S2
Common causes of PDA
congenital rubella
prematurity
Resting potential of ventricular myocyte
-85mV
ERP of ventricular myocyte
100msec
resting potential of nodal cells
-70mV
How does Ach/adenosine affect HR
dec rate of diastolic depolarization –> dec HR
How do catecholamines affect HR
inc depolarization –> inc HR
How does sympathetic stimulation affect HR?
increases the chance that If channels are open
Normal PR interval length
<200msec
Normal QRS duration
<120msec
What causes a U wave on ECG?
hypokalemia
bradycardia
Order of speed of conduction:
purkinje > atria > ventricles > AV node
How long is the delay through the AV node?
100msec
What can congenital long QT present with?
severe congenital sensorineural deafness
jervell + lange-nielsen syndrome
A-fib treatment
BB, CCB, or digoxin
prophylaxis against thromboemoblism w/ warfarin, aspirin
A-flutter treatment
attempt to convert to sinus rhythm use class IA, IC, or III antiarrhythmics, BBs
When and from where does ANP get released?
released from atria in response to increased blood volume & atrial pressure
Actions of ANP:
causes generalized vascular relaxation
constricts efferent & dilates afferent renal arterials (cGMP mediated), promoting diuresis & contributing to “escape from aldosterone”
What do peripheral chemoreceptors respond to?
dec PO2 (<60mmHg)
inc PCO2
dec pH of blood
What do central chemoreceptors respond to?
changes in pH and PCO2 of brain interstitial fluid, which are inflected by arterial CO2
(don’t respond directly to PO2)
Cushing reaction
Baroreceptors responsible
inc incracranial P constricts arterioles –> cerebral ischemia –> hypertension (sympathetic response) –> reflex bradycardia
Cushing triad
hypertension
bradycardia
respiratory depression
Normal RA pressure
<5
Normal RV pressure
25/5
Normal PA pressure
<25/5
Normal PCWP/LA pressure
<12
Normal LV pressure
130/10
Normal aortic pressure
130/90
Heart autoregulation is via:
local metabolites: CO2, adenosine, NO
Brain autoregulation is via:
local metabolites: CO2 (pH)
Kidney autoregulation is via:
myogenic & tubuloglomerular feedback
Lung autoregulation
hypoxia causes vasoconstriction (so only well ventilated areas are perfused)
(in other organs, hypoxia causes vasodilation)
Skeletal m. autoregulation is via:
local metabolites: lactage, adenosine, K+
Skin autoregulation
Sympathetic stimulation is most important (temp control)
Net fluid flow at a capillary =
(Pnet)x(Kf)
Kf is filtration constant (capillary permeability)
Pnet is from starling forces
Causes of edema:
inc Pc (heart failure) dec PIc (dec plasma proteins in nephrotic syndrome, liver failure) inc Kf (inc cap perm due to toxins, infections, burns) inc PIi (lymph blockage)
R –> L shunts
5 Ts:
tetralogy (most common), transposition, truncus, tricuspid atresia, total anomalous pulmonary venous retrun
Tricuspid atresia
absence of tricuspid valve
hypoplastic RV
requires both ASD & VSD for viability
Total anomalous pulmonary venous return
pulmonary veins drain into right heart circulation (SVC, coronary sinus, etc.)
What is the most common congenital cardiac anomaly?
VSD
How to close a PDA?
indomethacin
What improves tetralogy symptoms & why?
squatting
compressing the femoral aa. increases TPR –> directs less blood through the shunt and more through the lungs
What causes tetralogy?
anterosuperior displacement of the infundibular septum
Maternal diabetes associated defects
transposition
Marfan’s associated defects
aortic insufficiency (late complication)
Turner associated defects
preductal coarctation
rubella associated defects
septal defects, PDA, PA stenosis
Downs associated defects
ASD, VSD, AV septal defect (endocardial cushion defect)
22q11 associated defects
truncus, tetralogy
consequnces of PDA
RVH (rarely RH failure)
Unocrrected can lead to late cyanosis in lower extremities (differential cyanosis)
What keeps PDA open?
PGE synthesis & low O2 tension
Coarcation, info:
infantile type associated with turner syndrome
check femoral pulses
can result in AR
most commonly associated with bicuspid aortic valve
Transposition prognosis
not compatible with life unless a shunt is present (VSD, PDA, or PFO)
Die within first few months w/o surgery
Risk factors for HTN
inc age, obesity, diabetes, smoking, genetics
black > white > asian
malignant HTN =
severe & rapidly progressing
HTN predisposes to:
atherosclerosis, LVH, CHF, stroke, renal failure, retinopathy, and aortic dissection
Hyperlipidemia signs:
atheromas
xanthalasmas & xanthomas
corneal arcus
atheroma
plaque in vessel wall
xanthomas
plaque/nodule composed of lipid laden histiocytes, commonly in achilles tendon (tendonous xanthoma)
xanthelasma
plaque/nodule composed of lipid-laden histiocytes int eh skin, esp. eyelid
corneal arcus
lipid deposit in cornea, nonspecific (arcus senilis)
Monckeberg arteriosclerosis
calcification in media
esp radial or ulnar aa.
usually benign, not obstructive to blood flow, intima not involved
“pipestem aa”
ateriolosclerosis
hyaline thickening of small aa in primary htn or diabetes mellitus
hyperplasting “onion skinning’ in malignant htn
Atherosclerosis, about:
fibrous plaques & atheromas form in intima of ateries
disease of elastic aa and lg & med muscular aa
Atherosclerosis risk factors:
smoking, htn, DM, hyperlipidemia, FH
Atherosclerosis pathogenesis:
endothelial cell dysfunction –> fatty streaks –> macrophage & LDL accumulation –> foam cell formation –> fatty streaks –> smooth muscle cell migration (involves PDGF + TGF-B) –> fibrous plaque –> complex atheroma (can see cholesterol crystals)
Atherosclerosis complications:
aneurysms, ischemia, infarcts, peripheral vascular disease, thrombus, emboli
Atherosclerosis locations:
abdominal aorta > coronary aa. > popliteal a. > carotid a.
Atherosclerosis symptoms:
angina, claudication
can be asymptomatic
What is abdominal aortic aneurysm associated with?
associated with atherosclerosis
What is thoracic aortic aneurysm associated with?
associated with HTN, cystic medial necrosis (Marfan’s)
Who is AAA most frequent in?
male smokers >50
What is aortic dissection associated with?
htn, cystic medial necrosis (Marfan)
What does aortic dissection feel like?
tearing chest pain radiating to the back
Stable angina
mostly secondary to atherosclerosis
ST depression
retrosternal chest pain with exertion
Prinzmetal’s variant angina
at rest
secondary to coronary a. spasm
ST elevation
Unstable/crescendo angina
thrombus but no necrosis
ST depression
Worsening chest pain at rest or with minimal exertion
What is an MI most often due to?
acute thrombosis due to coronary a. atherosclerosis –> myocyte necrosis
Chronic ischemic heart disease
progressive onset of CHF over many years due to chronic ischemic myocardial damage
MI artery frequency:
LAD > RCA > circumflex
MI sxs
diaphoresis, n/v, severe retrosternal pain, radiating to L arm & jaw, SOB, fatigue, adrenergic sxs
MI gross changes 4-24hrs
dark mottling
pale with tetrazolium stain
MI gross changes 2-4 days
hyperemia
MI gross changes 5-10 days
hyperemic border
central yellow-brown softening
Maximally yellow & soft by 10 days
MI gross changes 7 wks
recanalized .
gray white
MI LM changes 4-12 hrs
early coagulative necrosis, edema, hemorrhage, wavy fibers
MI LM changes 12-24 hrs
contraction bands, release of necrotic cell content into blood, beg. of neutrophil emigration
MI LM changes 2-4 days
extenive coagulative necrosis, tissue surrounding infarct shows acute inflammation, neutrophil emigration
MI LM 5-10 days
granulation tissue appears at margins
MI LM 7 wks
contracted scar complete
MI risk from onset to 4 days
arrhythmia
MI risk 5-10 days
free wall rupture, tamponade, papillary m. rupture, septal rupture due to macrophages that have degraded important structural components
MI risk 7 wks
ventricular aneurysm
MI dx in first 6 hours
ECG = gold standard in first 6 hrs
Transmural MI ECG findings
ST elevation, pathologic Q waves
Subendocardial MI ECG findings
ST depression
Troponin I
rises after 4 hrs, elevated for 7-10 days
most specific
CK-MB
can also be from skeletal m.
useful for reinfarction after acute MI
AST
nonspecific
in cardiac, liver & skeletal muscle cells
ECG MI locations:
LAD –> ant: V1-4, ant-sept: V1-2
LCX –> ant-lat: V4-6, lat: I, aVL
RCA –> inf: II, III, aVF
MI complications:
arrhythmia, LV failure + pulmonary edema, cardiogenic shock, rupture, aneurysm, post infarction fibrinous pericarditis, Dressler’s syndrome
Dressler’s syndrome
several weeks post MI
autoimmune phenomenon resulting in fibrinous pericarditis
What is hypertrophic cardiomyopathy associated with?
Friedrich’s ataxia
What to treat hypertrophic cardiomyopathy with?
BB or non-dihydropyradine CCB
Causes of restrictive/obliterative cardiomyopathy:
sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastosis (thick fibroelastic tissue in endocardium of young children), loffler’s syndrome (endomyocardial fibrosis w/ a prominent eosinophilic infiltrate), hemochromatosis (dilated cardiomyopathy can also occur)
If isolated right heart CHF, usually due to what?
Cor pulmonale
CHF drugs - which reduce mortality, which for symptom relief only?
ACE, ARB, BBs, Spironolactone reduce mortality
Nitrates & diuretics (thiazide or loop) for symptom relief
What causes dyspnea on exertion?
Failure of CO to increase during exercise
What are heart failure cells?
Seen with left sided heart failure
They’re hemosiderin-laden macrophages found in the lungs
What causes orthopnea in heart failure?
increased venous return when supine –> exacerbates pulmonary vascular congestion
Nutmeg liver
Can see with R sided heart failure
increased venous pressure –> inc resistance to portal flow
rarely leads to “cardiac cirrhosis”
Bacterial endocarditis
FROM JANE
Fever, Roth spots, Osler’s nodes, new Murmur
Janeway lesions, Anemia, Nail-splinter hemorrhages, Emboli
Roth spots
round white spots on retina surrounded by hemorrhage
in bacterial endocarditis
Acute bacterial endocarditis
S. aureus (high virulence)
Large vegetations
Sudden onset
Subacute bacterial endocarditis
Viridans strep (low virulence)
Small vegetations
Sequela of dental procedures
more insidious onset
Causes of nonbacterial endocarditis:
malignancy, hypercoagulable sate, lupus
marantic/thrombotic endocarditis
S. bovis
colon cancer
S. epidermidis
prosthetic valves
Most frequent valve affected in endocarditis
Mitral
IV drug abusers - endocarditis –> which valve and which bugs?
Tricuspid valve
S. aureus, pseudomonas, candida
Complications of endocarditis
chordae rupture, glomerulonephritis, suppurative pericarditis, emboli
Rheumatic fever, cause of early deaths?
myocarditis
Late sequalae of rheumatic fever
rheumatic heart disease
mitral > aortic»_space; tricuspid
Early rheumatic fever lesion
Mitral regurgitation
Late rheumatic fever lesion
Mitral stenosis
Rheumatic fever histology:
Aschoff bodies (granuloma w/ giant cell) Anitschkow's cells (activated histiocytes)
Rheumatic fever, mechanism:
immune mediated
hypersensitivity type II raction
Antibodies to M protein
elevated ASO titers
Rheumatic fever mnemonic
FEVERSS
Fever, Erythema marginatum, Valvular damage (vegetation & fibrosis), elevated ESR, Red hot joints (migratory polyarthritis), Subcutaneous nodules, St vitus dance (chorea)
Acute pericarditis - clinical
sharp pain (esp w/ inspiration) relieved by sitting up & leaning forward
Most common pericarditis
fibrinous pericarditis
Causes of fibrinous pericarditis
Dressler’s syndrome, uremia, radiation
Presentation of fibrinous pericarditis
loud friction rub
Cause of serous pericarditis
noninfectious inflammatory diseases (ex. rheumatoid arthritis, SLE)
Cause of suppurative/purulent pericarditis
infectious agents
Tamponade - clinical features
dec CO, equilibrium of diastolic pressure in all 4 chambers, hypotension, elevated JVD, distant heart sounds, inc HR, pulsus paradoxus
Syphilitic heart disease
tertiary syphilis
disrupts vasa vasorum of aorta
dilation of aorta & valve ring
calcification of aortic root & ascending arch
“tree bark” appearance of aorta
can result in aneurysm of ascending aorta or arch & valve incompetence
Myxoma
most common primary tumor
90% in atria (mostly LA)
“ball-valve” obstruction in LA
associated w/ multiple syncopal episodes
Rhabdomyomas
most common primary tumor in children
associated with tuberous sclerosis
Metastasis
most common hear tumor
from melanoma, lymphoma
Kussmaul’s sign
elevated JVP on inspiration
Varicose veins
due to chronically elevated venous pressure
predisposes to poor wound healing, varicose ulcers
thromboemoblism is rare (compare with stasis of deep veins)
Raynaud’s
arteriolar vasospasm in response to cold or emotional stress
Raynaud’s phenomenon
raynaud’s when secondary to mixed CT disease, SLE, CREST syndrome
Temporal (giant cell arteritis)
elderly women, associated w/ polymyalgia rheumatica, focal granulomatous inflammation
tx w/ high dose steroids
Takayasu’s arteritis
<40, weak upper extremity pulses, fever, night sweats, arthritis, myalgias, skin nodules, occular disturbances
granulomatous thickening of aortic arch & proximal great vessels
Tx w/ corticosteroids
Polyarteritis nodosa
young adults, fever, weight loss, malaise, headache, abd pain, melena, htn, neurologic dysfunction, cutaneous erruptions; typically renal & visceral vessels; transmural w/ fibrinoid necrosis; multiple aneurysms & constrictions on arteriogram
tx w/ corticosteroids, cyclophosphamide
Kawasaki disease
fever, lymphadenitis, conjunctivitis, changes in lips/oral mucosa (“strawberry tongue”), hand foot erythema, desquamation, may develop coronary aneurysms
tx w/ IV immunoglobulin & aspirin
Buerger’s disease (thromboangitis obliterans)
gangrene, autoamputation, superficial nodular phlebitis, segmental thrombosing vasculitis
tx w/ smoking cessation
Microscopic polyangiitis
pauci-immune gn, palpable purpura, no granulomas
Wegener granulomatosis
perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis, hemoptysis, cough, dyspnea, hematuria, red cell casts, triad of focal necrotizing vasculitis, necrotizing granulomas in lung & upper airway, and necrotizing GN
CXR - large nodular densities
tx w/ cyclophosphamide, corticosteroids
Churg-strauss syndrome
sinutitis, palpable purpura, peripheral neuropathy (eg wrist/foot drop), can also involve heart, GI, kidneys; pauci immune, granulomatous vasculitis w/ eosinophilia
Henoch-Schonlein purpura
most common form of childhood systemic vasculitis, triad, abdominal painn, melena, multiple lesions of same age, association with IgA nephropathy
Sturge-weber disease
congenital vascular disorder
affects capillary sized vessels
manifests with port wine stain (aka nevus flammeus) on face, ipsilateral leptomeningeal angiomatosis (intracerebral AVM), seizures, early onset glaucoma
Strawberry hemangioma
benign capillary hemangioma of infancy, appears in 1st few weeks of life, 1/2000 births, grows rapidly & regresses spontaneously at 5-8 yrs
Cherry hemangioma
benign capillary hemangioma of the elderly, does not regress, frequency increases with age
Pyogenic granuloma
polypoid capilary hemangioma that can ulcerate & bleed; associated w/ trauma & pregnancy
cystic hygroma
caverous lymphangioma of the neck
associated w/ turner syndrome
glomus tumor
benign, painful, red-blue tumor under fingernails; arises from modified smooth muscle cells of glomus body
bacillary angiomatosis
benign capillary skin papules found in AIDs pts; caused by bartonella henselae infections; freq mistaken for kaposi’s sarcoma
angiosarcoma
highly lethal malignancy of liver; ass w/ vinyl chloride, arsenic, and ThO2 (thorotrast) exposure
lymphangiosarcoma
lymphatic malignancy associated w/ persistent lymphedema (eg post radial mastectomy)
kaposi’s sarcoma
endothelial malignancy of the skin ass w/ HHV-8 & HIV; freq mistaken for bacillary angiomatosis
Essential HTN therapy:
diuretics, ACE, ARBs, CCBs
CHF HTN therapy
diuretics, ACE/ARBs, BBs (compensated CHF), K sparing diuretics
BBs can be used cautiously in decompensated CHF; contraindicated in cardiogenic shock
DM HTN therapy:
ACE/ARBs (protective against diabetic nephropathy), CCB, diuretics, BBs, alpha-blockers
What does hydralazine do
inc cGMP –> smooth muscle relaxation
arterioles > veins
decrease afterload on heart
What is hydralazine used for?
severe HTN, CHF, 1st line for HTN in pregancy (w/ methyl dopa), frequently given with BB to prevent reflex tachycardia
Hydralazine toxicity:
compensatory tachycardia (contraindicated in angina/CAD), fluid retention, nausea, headache, angina, lupus-like syndrome
What do CCBs do?
block L type Ca channels of cardiac and smooth muscle –> reduce muscle contractility
Relative potency of the 3 CCBs on vessels:
nifedipine > diltiazem > verapamil
Relative potency of the 3 CCBs on heart:
verapamil > diltiazem > nifedipine
Verapamil = Ventricle
What are CCBs used for?
HTN, angina, arrhythmias (not nif.), prinzemetal’s angina, Raynaud’s
CCB toxicity
cardiac depression, AV block, peripheral edema, flushing, dizziness, constipation
Nitroprusside
Use to tx malignant HTN
short acting, inc cGMP via direct release of NO
can cause cyanide toxicity
Fenoldepam
Used to tx malignant HTN
dopamine D1 receptor agonist
relaxes renal vascular smooth m.
Diazoxide
Used to tx malignant HTN
K channel opener –> hyperpolarizes & relaxes vascular smooth m.
can cause hyperglycemia (reduces insulin release)
What are nitroglycerin, isosorbite dinitrate used for?
angina, pulmonary edema
also aphrodisiac & erection enhancer
Nitroglycerin, isosorbide dinitrate toxicity:
reflex tachy, hypotension, flushing, headache, “monday disease”
“Monday disease”
With nitroglycerin & isosorbide dinitrate
development of tolerance to the vasodilating during the work week & loss of tolerance over the weekend –> resulting in tachycardia, dizziness, headache on reexposure
Anti-anginal meds:
Nitrates (preload), BBs (afterload)
both dec O2 demand, so together they decrease an extra amount
Pindolol & acebutolol
partial beta-agonists –> contraindicated in angina
What do HMG CoA reductace inhibitors do?
**decrease LDL a lot, increase HDL a bit, dec TG a bit
inhibit cholesterol precursor –> mevalonate
HMG CoA reductance inhibitors - side effects
hepatotoxicity (inc LFTs)
rhabdomyolysis
What does niacin do?
dec LDL, **inc HDL, dec TG
inhibits lipolysis in adipose tissue
reduces hepatic VLDL secretion into circulation
Niacin side effects:
red, flushed face (dec by aspirin or by long time use), hyperglycemia (acanthosis nigricans), hyperuricemia (exacerbates gout)
Bile acid resins - which drugs?
cholestyramine
colestipol
colesevelam
What do bile acid resins do?
dec LDL, slightly inc HDL and TGs
Liver uses cholesterol to make more bile acids
Bile acid resins side effects:
pt hates it –> it tastes bad, GI discomfort
dec absorption of fat soluble vitamines
cholesterol gallstones
Cholesterol absorption blocker - what drug?
ezetimibe
What do cholesterol absorption blockers do?
dec LDL
Cholesterol absorption blockers side effects:
rare inc LFTs
What drugs are fibrates?
gemfibrozil, clofibrate, benzafibrate, fenofibrate
What do fibrates do?
dec LDL, inc HDL, hugely dec TGs
upregulate LPL –> inc TG clearance
Fibrates - side effects
myositis, hepatotoxicity (inc LFTs), cholesterol gallstones
Digoxin
= cardiac glycoside 75% bioavailable 20-40% protein bound half life = 40 hours urinary excretion
How does digoxin work?
direct inhibition of Na/K ATPase (pos ino) & stimulates vagus
Digoxin use
CHF (inc contractility), afib (dec conduction at AV node & depression of SA node)
Digoxin toxicity
cholinergic (n/v/diarrhea, blurring yellow vision), ECG (inc PR, dec QT, scooping, T wave inversion, arrhythmia, hyperkalemia)
What worsens digixon toxicity?
renal failure (dec excretion), hypokalemia (permissive for digoxin binding site on NaK ATPase), quinidine (dec dig clearance - displaces it from tissue binding sites)
Antidote to Dig toxicity
slowly normalize K+, lidocaine, cardiac pacer, anti-dig Fab fragments, Mg2+
Nesiritide
=recombinant B-type natriuretic peptide
causes inc cGMP & vasodilation
use for acute decompensated heart failure
toxicity –> hypotension
class I antiarrhythmics
local anesthetics slow or block conduction (esp in depolarized cells), dec slope of phase 0 depol, inc threshold for firing in abnormal pacemaker cells; state dependant (selectively depress tissue that is frequently depolarized, eg fast tachycardia)
What are the Class IA drugs?
quinidine, procainimide, disopyramide
What do the class IA drugs do?
inc AP duration, inc ERP, inc QT interval, affect both atrial & ventricular arrhythmias, esp reentrant & ectopic supraventricular tachycardia
Quinidine toxicity
cinchonism (headache, tinnitus), thrombocytopenia, torsade de pointes due to inc QT interval
Procainamide toxicity
reversible SLE like syndrome
What are the class IB drugs?
lidocaine, mexilitine, tocainide
phenytoin can fall into IB
What do the class IB drugs do?
IB is Best post MI
dec AP duration, preferentially affect ischemic or depolarized purkinje & ventricular tissue
useful in acute ventricular arrhythmias (esp post MI) & in digitalis- induced arrhythmias
Class IB toxicity
local anesthetic, CNS stim/depression, cardiovascular depression
What are the class IC drugs?
flecainide, propafenone
What do the IC drugs do?
no effect on AP duration, useful in Vtachs that progress to VF and in intractable SVT
usually used as a last resort in refractory tachyarrhythmias; for pts WITHOUT structural abnormalities
**IC is Contradindicated post-MI
Class IC toxicities
proarrhythmic, esp Post-MI (contraindicated), significantly prolongs refractory period in AV node
What can increase toxicity for Class I drugs?
hyperkalemia causes inc toxicity for all class I drugs
Effect of different Class I’s on action potential duration
Class IA lengthens AP duration
Class IB shortens AP duration
Class IC doesn’t change AP duration
What do class II (BBs) drugs do?
dec cAMP, dec Ca currents, suppress abnormal pacemaker by dec slope of phase 4
AV node particularly sensitive –> inc PR
Which BB is very short acting?
esmolol
What to use BBs for?
V-tach, SVT, slowing ventricular rate during afib & aflut
BB toxicity
impotence, exacerbation of asthma, cardiovascular effects (brady, AV block, CHF), CNS effects (sedation, sleep alteration), may mask signs of hypoglycemia
A metoprolol side effect
can cause dyslipidemia, treat overdose w/ glucagon
What are the class III drugs?
K IS BAD ibutilide sotolol bretylium amiodarone dronedarone/dofetalide
What do the class III drugs do?
inc AP duration, inc ERP, used when other antiarrhythmics fail, inc QT interval
Sotolol toxicity
torsades, excessive Beta block
Ibutilide tox
torsades
Bretylium toxicity
new arrhythmias, hypotension
Amiodarone toxicity
pulmonary fibrosis, hepatotoxicity, hypothyroidism/hyperthyroidism (40% iodine by weight), corenal deposits, skin deposits (blue/grey) resulting in photodermatitis, neurologic effects, constipation, cardiovascular effects (brady, heart block, CHF)
**Check PFTs, LFTs, and TFTs*
What is special about amiodarone?
it has class I, II, III, IV effects bc it alters the lipid membrane
What doe the Class IV (CCBs) do?
dec conduction vel, inc ERP, inc PR interval, used in prevention of nodal arrhythmias (eg SVT)
Class IV toxicity:
constipation, flushing, edema, CV effects (CHF, AV block, SA node depression)
Adenosine
inc K out of cells –> hyperpolarizes, dec Ca
drug of choice in diagnosing/abolishing SVT
Very short acting (~15sec)
effects blocked by theophylline
Adenosine toxicity
flushing, hypotension, chest pain
Mg2+
effective in torsades de points & digoxin toxicity
