1
Q
diabetes
A
tissues that contain aldose reductase - cataracts (lens), microaneurysms in the eye (pericytes), peripheral neuropathy (Schwann cells)
NEG makes BM permeable to protein - hyaline within vessel wall
2
Q
aneurysm
A
weakening –> outpouching of vessel wall
[compare this to a process in the lung? = bronchiectasis
- ex CF pt –> infection –> weakening of elastic tissue and dilatation of bronchi
GI “aneurysm” - weakening, outpouching of mucosa through a weak point in the muscular wall]
Law of Laplace - wall stress increases as radius increases –> all aneurysms will burst
P = 2T*thickness/r
abd aortic aneurysm: no vasa vasorum to aorta below the renal arteries –> outer part of the wall is most susceptible –> atherosclerosis occurs here –> rupture
-rupture triad = left flank pain (SADPUCKER), hypotension, and pulsatile mass
arch of aorta aneurysm - most common cause is tertiary syphilis (vasculitis of arterioles, arterioles surrounded by plasma cells with lumen completely occluded –> necrosis of overlying tissue, death of nerves)
key factor for causing aortic arch rupture
- HTN
- elastic tissue fragmentation
- cystic medial necrosis - GAGs turn into cysts
proximal dissection is the most common one
- closes lumen to subclavian = absent pulse left
- death by cardiac tamponade
- retrosternal tearing chest pain
- Marfans - most common cause of death is mitral prolapse and conduction disruption, second most common cause of death is dissection
- most common cause of death in Ehlers-Danlos
- pregnancy - dissecting aortic aneurysm is a catastrophic aortic disease, increased plasma volume –> weakening of wall –> dissection
- side note - can get dilated CM in pregnancy
3
Q
pt with lung cancer comes in complaining of headaches
A
you see retinal veins are engorged, he is congested
ddx - SVC syndrome –> death
radiation to shrink tumor restore some blood flow
4
Q
Sturge-Weber formation
A
vascular malformation in the face in the trigeminal nerve distribution
+ AV malformation
+ mental retardation
5
Q
spider angioma
A
= AV fistulas (bypass venule)
normal in pregnant women - spider angiomas occur in pregnant women
- or in alcoholics - w/ cirrhosis
- in alcoholics - you will also see gynecomastia, palmar erythema, warm skin
- another reason you see these in alcoholics - cant metabolize 17-ketosteroids –> will aromatize those in adipose –> more estrogen
blanchable
6
Q
muscular vessel vasculitis
A
consequence is infarction
polyarteritis nodosa - males
- necrotizing inflammation –> can get bead-like aneurysm formation (esp in mesenteric circulation)
- p-ANCA
- scenario - IVDA with chronic hep B who has a nodular, inflammed mass on LE + hematuria
- chronic hepB means pt has HbSAg
Wegener’s granulomatosis (with polyangiitis)
- saddle nose defomity (bridge of nose can collapse due to perforated septum), sinusitis, glomerulonephritis
- c-ANCA
- treat with cyclophosphamide –> hemorrhagic cystitis (prevent with MESNA) and bladder cancer
Kawaski disease - coronary artery vasculitis –> most common cause of MI in kids
+ mucocutaneous inflammation, desquamation of skin, LAD
7
Q
elastic artery vasculitis
A
in arch vessels –> pulseless disease, strokes
Takayasu’s arteritis - young, Asian lady with absent pulse
8
Q
temporal arteritis
A
granulomatous vasculitis of temporal artery
-can also involve ophthalmic branch –> blindness
associated with polymyalgia rheumatica - no elevation in serum CK
- v.s. polymyositis = inflammation of muscle, elevated CK
corticosteroids on hx alone (for 1 year)
9
Q
Henoch-Schonlein purpura
A
14 yo with URI last week - presents with joint pains, hematuria, palpable purpura of buttock and lower extremities
most common vasculitis in children
IC = IgA-(anti-IgA)
10
Q
Rickettsial organisms
A
infect endothelial cells –> petechiae
RMSF - extremities to trunk, other rashes do the reverse
11
Q
Mucormycosis
A
DKA
mucor in frontal sinuses –> invade through cribiform plate –> brain
12
Q
Raynaud’s phenomena
A
100s of diseases can cause this
1) cold reacting antibodies (IgM agglutinins) and cryoglobulins (associated with hepC) - Raynaud’s in cold weather
2) scleroderma, CREST syndrome - first Raynauds, then digital vasculitis and eventually fibrosis
- C - calcinosis, centromere antibody
- R - Raynauds
- E - esophageal dismotility
- S - sclerodactyl (finger stuck in a pencil sharpener)
- T - telangiectasia
3) vasoconstriction - common in pts who take ergot derivatives for migraines
- migraines are are cause by vasodilation…
13
Q
HTN
A
most common causes of death
1) MI (MI is also the most common cause of death in diabetes)
2) stroke - in BG!
3) renal failure - hyaline arteriolar sclerosis
most common abnormality in HTN - LVH
HTN (esp in AA and elderly) is a condition increased Na –> increased blood volume
- Na likes to go into smooth muscle cells - peripheral resistance arterioles
- Na enters muscle - opens up Ca2+ channels –> peripheral resistance arterioles are constricting
- -> blood is being squeezed out arterial system –> increases diastolic pressure
- treat this population with HCTZ
- if pt has HLD - cant use HCTZ or b-blockers (they can produce HLD), use ACEI instead
- low renin HTN - because of high plasma volume
otherwise - in primary HTN, 60% have normal renin levels and 25% have increased renin levels, 15% have low renin levels
HTN: 90% is essential
10% due to fibromuscular dysplasia (irregular thickening of large and medium sized arteries, string of beads appearance), others
HTN predisposes to many things - one of which is afib
thiazides - first line in HTN
HTN with HF - b-blockers must be used with caution, contraindicated in cardiogenic shock
HTN in pregnancy - hydralazine, labetalol, methyldopa, nifedipine
- hydralazine - increased cGMP in smooth muscles –> vasodilator
- compensatory tachy (so you would NOT use it in an hypertensive ermergency, can give b-blocker to counteract), fluid retention, headache, Lupus-like syndrome
HTN emergency - clevidipine, fenoldopam, labetalol, nicardipine, nitroprusside
- nitroprusside - increased cGMP via direct release of NO, can cause cyanide tox
- fenoldopam - D1 agonist –> stimulates adenylyl cyclase –> raises cAMP –> vasodilation of most arterial beds (renal..)
labetalol - a1, b1, b2
- can be used in cocaine intox
14
Q
CCBs
A
amlodipine (dihydropyridines), diltiazem, verapamil
- block L-type Ca channels
- amlodipine/nifedipine best for vascular smooth muscle
- verapamil best for heart
non-dihydropines - can also be used for afib/flutter
ADRs
- pines - peripheral edema, flushing, dizziness, gingival hyperplasia
- non-dihydropyridines - cardiac depression, *AV block, hyperprolactinemia, constipation
15
Q
nitrates
A
venodilation > vasodilation (especially arteries and not arterioles) - decrease preload
used in angina, coronary heart syndrome, pulm edema
cGMP –> decreased intracellular Ca and activation of myosin light chain phosphatase –> myosin light-chain dephosphorylation
ADRs
- reflex tachy, hypotension, headaches, flushing
- Monday disease in industrial exposure - tolerance during week, loss of tolerance over weekend –> ADRs when re-exposed
- contraindicated in RV infarct
- cyanide tox = with nitroprusside infusion
- cyanide inhibits cytochrome C –> lactic acidosis and bright red venous blood
- normally metabolized by rhodanese - enzyme that transfers a sulfur to cyanide
- in cyanide tox - give sulfur donors (sodium thiosulfate) or something that can bind to cyanide (sodium nitrite –> metHb will bind to cyanide, hydroxocobalamin)
b-blockers and nitrates are good anti-anginal therapy - reduce myocardial O2 consumption
16
Q
lipid-lowering agents
A
HMG-coA reductase inhibitors - blocks HMG-coA –> mevalonate –> cholesterol
- *decrease LDL, increased HDL, decrease TGs
- hepatotox, myopathy esp when used with fibrates or niacin
bile acid resins - cholestyramine, colestipol, colesevelam
- prevent intestinal absorption of bile acids - liver must use cholesterol to make more
- decrease LDL, increase HDL and TGs
- GI upset, decreased absorption of drugs and fat-soluble vitamins
ezetimibe
- decrease LDL
- prevent cholesterol absorption at small intestine brush border
- rare LFTs, diarrhea
fibrates - gemfibrozil, -fibrates
- decrease LDL, increase HDL, *decrease TGs
- upregulate LPL –> increased TG clearance, activates PPAR-a to induce HDL synthesis
- myopathy, cholesterol gallstones
niacin - decrease LDL, increase HDL, decrease TGs
- inhibits lipolysis (HSL) in adipose tissue, reduces hepatic VLDL synthesis
- red flushed face, hyperglycemia, hyperuricemia
PCSK9 inhibitors -mabs
- *decrease LDL, increased HDL, decrease TGs
- inactivation of LDL-R degradation –> increases amount of LDL removed from blood
- myalgias, delerium/dementia
17
Q
digoxin
A
binds to K+ site of Na/K ATPase - hypokalemia can lead to tox (more digoxin binds)
- decreases APD - can cause short QT interval
also stimulates vagus nerve –> AV nodal conduction –> decreased HR
uses: HF, afib (decreases conduction at AV node, depresses SA node)
- when AV conduction is slowed, atria will continue to fibrillate/flutter but ventricles will contract at a normal rate (enough time for diastolic filling)
tox: hyperkalemia, cholingeric side effects (blurry yellow vision - Van Gogh), arrhythmias and AV block
- can cause delayed afterdepolizations (because it increases intracellular Ca) –> v.tach and death
verapamil, amiodarone, quinidine can cause decreased clearance
antidote - slowly normalize K+, cardiac pacer, anti-digoxin Fab fragments, Mg2+
18
Q
rheumatic fever
A
antibodies to M protein of S. pharyngitis…
- ddx by evidence of prior group A strep infection (anti-streptolysin O or anti-DNase B titer)
myocarditis - most common cause of death in the acute phase
- Aschoff bodies = granuloma with giant cells in myocardium
- Anitschkow cells - enlarged macrophages with caterpillar nucleus
acute attack- vegetations on mitral valve –> mitral valve regurg (can also have aortic valve involvement)
- chronic disease = valve scarring –> mitral stenosis
- occasionally, aortic valve stenosis (fishmouth)
- and the complication is endocarditis
19
Q
heart failure
A
ACEI/ARB, b-blockers, and spironolactone decrease mortality (other diuretics provide symptom relief)
- can add hydralazine and nitrate therapy
b-blockers - decreases cardiac work, but only use in STABLE HF
1) slows ventricular rate
2) reduces peripheral resistance by decreasing circulating levels of NE, renin, endothelin
orthopnea - due to increased venous return
pulm edema - HF cells (hemosideran-laden macrophages in lungs)
20
Q
shock
A
shock = low perfusion to tissues –> lactic acid accumulation
- additionally - liver is the primary site of lactic acid clearance (converted back to glucose), hypoperfusion will affect liver
hypovolemic - …burns, cold and clammy, give IV fluids
cardiogenic/obstructive - cold clammy, decreased CO (more so than in hypovolemia), inotropes, diuresis, relieve obstruction
distributive -
- sepsis, anaphylaxis- warm, increased CO and decreased SVR
- septic shock is distributive shock - means blood is trapped in small vessels rather than large - that is why you have a low PCWP and CVP but high CO - CNS injury - dry, decreased CO and SVR
- pressors and fluids
21
Q
HLD signs
A
cholesterol in the skin
xanthomas (lipid-laden macrophages), tendinous xanthoma (Achilles), corneal arcus (white ring around iris, common in elderly)
familial hypercholesterolemia
- absent LDL receptor - put you on an HMG-coA reductase inhibitor
- Achilles tendon xanthoma
- death by age 20 by coronary attack
22
Q
congenital cardiac defect associations
A
Septal defects:
fetal alcohol syndrome - septal defects, tet of Fallot
DS - AV septal defect (endocardial cushion defect), other septal defects
congenital rubella - PDA, pulmonary artery stenosis, septal defects
Valve defects:
Marfan - mitral valve prolapse, aneurysm/dissection/aortic regurg
Li - tricuspid displaced towards apex
Turner - bicuspid aortic, coarctation of aorta (esp in between aortic branches and PDA) –> blood from pulmonary trunk will enter the aorta (low pressure area downstream of coarctation)
- coarctation of aorta - eventually, intercostal arteries enlarge due to collateral circulation –> erode and notch ribs
- in adults, coarctation is not associated with PDA and lies distal to aortic arch
- associated with bicuspid aortic valve
- collateral circulation across intercostals
Williams syndrome - supravalvular aortic stenosis
Other:
infant of diabetic mother - transposition of great vessels
22q11 (Digeorge) - truncus arteriosus, tet fallot, transposition of great vessels
23
Q
ECG abnormalities
A
AV node supplied by RCA - 100ms delay
Pacemaker rates: SA > AV > ventricular system
conduction velocity: Purkinje > atria > ventricles > AV node
PR = 200 ms QRS = 120 ms
T wave inversion - recent MI, ischemia U wave (mini wave that follows T wave) - hypokalemia, bradycardia
Afib = irregularly irregular
- no P waves, irregularly spaced QRS
- can have fine fibrillatory waves in between the QRS complexes
- risk factors - HTN, CAD
- precipitated by illness or increased sympathetic tone, or excessive alcohol consumption (holiday heart syndrome)
A flutter - 4:1 sawtooth pattern
- 3 P waves + 1 QRS + 1 T = 4:1 sawtooth
- treat like afib, definitive treatment is catheter ablation
Vfib - SCD
- SCD is associated with CAD (70%), HCM, long QT, Brugada, cocaine abuse, mitral valve prolapse
- prevent with implantable cardioverter-defibrillator
Torsads - can progress to v fib
- long QT predisposes to torsades
- drug-induced - anti-arrhythmics (1A, 3), macrolides, haloperidol, TCAs, ondansetron
- metabolites - hypokalemia, hypoMg
- congenital
- treat with MgSO4
24
Q
AV block
A
first degree - PR > 200, benign and asymptomatic
second degree
Mobitz 1) progressive lengthening of PR until beat drops - P is NOT followed by QRS, regularly irregular (RR interval)
2) dropped beats, PR interval stays constant - may progress to 3rd block
- treat with pacemaker
third degree = complete
- atria and ventricles beat independently of each other
- atrial rate > ventricle rate
- treat with pacemaker
- can be cause by Lyme disease
25
coronary circulation
left coronary --> LAD, LM, LC
- LAD - anterior surface, anterolateral papillary muscle
- LC - lateral and posterior walls, anterolateral papillary muscle
right coronary - PDA (85% of time), RM
- RCA - SA and AV nodes
- PDA - ...posteromedial papillary muscle, usually rises from RCA (can arise from LCX, or codominant circulation)
coronary blood flow during diastole: aortic pressure > IV pressure
RCA occlusion --> inferior wall MI --> *RV dysfunction*
26
pericardium
innervated by phrenic nerve (C3-C5) - pericarditis can cause referred pain to shoulder
acute pericarditis
- aggravated by inspiration
- relieved by sitting up and sitting forward
- sensitive to movements - coughing, radiates to neck (phrenic nerve)
- widespread ST-segment elevation and/or PR depression
- causes - unknown viral, Coxsackie, neoplasia, autoimmune (SLE, pericarditis), uremia, STEMI (due to transmural infarct and inflammatory exudate), Dressler syndrome, radiation therapy
fibrinous pericarditis in the 2-3 days following a STEMI - disappears with 1-3d of ASA
27
organs are arranged in parallel
mean pressure in each major artery will be approx same as the mean pressure in the aorta
- nephrectomy will increase TPR and decrease CO
systolic pressure and pulse pressure are higher in large arteries than in the aorta because of inertia of blood - pressure waves travel at a higher velocity than blood itself
28
compliance
C = dV/dP
aging decreases compliance of arteries - increased arterial pressures in the elderly
29
systolic and pulse pressures
systolic and pulse pressures are increased - ...OSA (due to increased sympathetic tone)
30
S2
A2, P2 - pulmonic valve closes after
inspiration delays closure of pulmonic valve - decreased intrathoracic pressure --> venous return to RA/RV is increased --> take longer to empty RV
- also pulmonary vessels have increased holding capacity during inspiration
wide splitting - when RV emptying is delayed (pulmonary stenosis, RBBB)
fixed splitting in L --> R shunt
paradoxical splitting - when closure of aortic valve is delayed (aortic stenosis, LBBB)
- split is eliminated during inspiration
31
threshold potential
potential difference where there is a NET inward current - depolarization becomes self-sustained
32
ventricular AP
0) upstroke - Na enters cells (inactivation gates close at 20 mV)
- dV/dt depends on resting membrane potential - lower is better
- the larger the inward current --> the more rapidly local currents will spread to adjacent sites and depolarize them (does NOT depend on AP duration)
1) initial repolarization - inward Na has ceased, outward K
2) plateau - inward current = outward current
- Ca in through dihydropyridine channels (nifedipine is the inhibitor)
- Ca entry --> Ca-induced Ca-release
- K is moving out
- 150 ms in atria < ventricles < Purkinje cells
3) repolarization - slow K channels open
4) resting membrane potential = -85mV
- high K permeability, leak channels, ATPases
things that are different from skeletal muscle - plateau, Ca-induced Ca-release, gap junctions
contraction
1) as myosin head binds ATP - it detaches from actin
2) ATP is hydrolyzed --> conformational change --> actin is rebound
- cardiac muscle has high resting tension - difficult to stretch cells beyond Lmax so will only operate on ascending limb of length-tension curve
inotropy
- positive inotropes increase tension, also cause faster relaxation (more time for filling)
- SNS --> P-L-type Ca channels...
- phosphorylation of phospholamban --> activates Ca2+ ATPase on SR --> faster relaxation
decrease inotropy - ...acidosis, hypoxia/hypercapnia, non-dihydropyridine CCBs
33
SA node
unstable resting membrane potential
0) upstroke - *Ca2+* entry, T-type and L-type Ca channels
- slow conduction velocity - used for delay by AV node
- fast VS-Na channels are permanently inactivated due to higher resting potential of these cells
3) repolarization - K out
4) spontaneous depolarization = longest part of AP
- If - mixed inward Na/K current, turned on by preceding repolarization
- *sets HR* - remember adenosine decreases HR
- sympathetic stimulation increases the chance that If channels are open
latent pacemakers - heart will beat slower if it is driven by a latent pacemaker
34
refractory period
absolute refractory period < effective RP (conducted AP cant be generated)
relative RP - AP generated will have an abnormal configuration
35
autonomic effects on HR
SNS: b1-NE
1) increase If, increased rate of phase 4 depol
2) increase in ICa (less depolarization needed to reach threshold)
- also increases conduction velocity through AV node
- and increases the total amount of trigger Ca2+ that has entered the cells
- positive staircase effect or extra beat
PSNS: M2-Ach/adenosine --> Gk (aka Gi protein)
1) decreases If
2) Gk directly increases K-Ach out
3) decreases ICa
- downstream - less Ca enters the cells
36
ACEIs/ARBs
decrease preload and afterload
37
cardiac work
W = P x V
| - pressure work requires more O2 consumption - so O2 consumption increases more with aortic stenosis than with exercise
38
S4 sound
atrial kick - occurs in late diastole
| - best heard at apex with pt at left lateral decubitus
39
JVP
a wave = atrial contraction (in late diastole)
- a wave disappears afib
- giant a wave in mitral/ tricuspid stenosis and with S4
- giant c (?) wave is tricuspid regurg
c wave = RV contraction (tricuspid bulges/reflects backwords)
x descent = downward displacement of tricuspid during ventricular ejection (reduced in tricuspid regurg, HF)
v wave = RA filling
- corresponds to beginning of diastole
y descent = RA emptying into RV, prominent in constrictive pericarditis, absent in cardiac tamponade
Kussmaul sign - increase in JVP on inspiration (normally decreases during inspiration)
- impaired filling of RV --> blood backs up --> JVP increased
- constrictive pericarditis, restrictive cardiomyopathies, RA/RV tumors
40
atherosclerosis
thickening of intima - intimal plaque
- abd aorta > coronary artery > popliteals > carotid
- note coronary arteries are maximally dilated in an area of stenosis - to maintain resting blood flow
damage to endothelium --> lipid enters intima, gets oxidized, uptaken by macrophages = fatty streak
- damage due to - smoke, oxidized lipid, Chlamydia pneumonia infection, viral infections, homocysteine
fatty streak undergoes inflammation, healing, increased lipid deposition and necrosis, development of fibromuscular cap
- inflammation/healing process leads to ECM and smooth muscle proliferation - involves PDGF and FGF (which are produced by monocytes and platelets)
- note fibroblasts dont contribute much to the formation of atheromas - fibrous cap is due to SMC proliferation
symptomatic after > 70% stenosis
causes thickening of blood vessel wall --> wall atrophy --> weakening --> abdominal aneurysm (no vasa vasorum in abdominal aorta)
- palpable pulsatile abdominal mass - rupture is feared when greater than 5 cm
- rupture triad: hypotension, pulsatile abdominal mass and flank pain
- dilated, calcified aortic wall with crescent shaped non-opacification on CT (flap, clot)
41
arteriolosclerosis
hyaline arteriolosclerosis
- classically produces glomerular scarring due to decreased GBF (arteriolonephrosclerosis) --> shrunken kidney with scarring/nodules on surface
hyperplastic arteriolosclerosis - due to smooth muscle hyperplasia
- consequence of severe/malignant HTN
- onion-skin appearance
- classically causes ARF with flea-bitten appearance - surface of kidney has pinpoint hemorrhages
remember malignant HTN also has fibrinoid necrosis (so histo will show hyperplastic arteriolosclerosis and ring of pink surrounding lumen)
42
Monckeberg medial sclerosis
calcification of internal elastic lamina and media - non-obstructive, not clinically significant
incidental finding on x-ray, mammography - pipestem appearance
thought to cause isolated systolic HTN
43
aortic dissection and aneurysm
DISSECTION
most common cause is **HTN**
- intimal tearing is the inciting event - due to HTN
- adventitia contains vasa vasorum... --> medial degeneration and increased wall stiffness
associated with inherited defects of CT, elastic tissue - Marfans (medial cystic degeneration), Ehlers-Danlos
- other causes include HTN, bicuspid aortic valve
dissection - complication is pericardial tamponade --> most common cause of death
- can have fatal hemorrhage into mediastinum (mediastinal widening on CXR), obstruction of arteries (ex renal artery lumen is squeezed shut)
- blood pressure differences between arms
type A: involves ascending aorta - surgery
- ahead of brachiocephalic artery - specifically in the sinotubular junction (right above aortic valve)
- cant propagate distally
type B: involves descending aorta
- originate close to the left subclavian
- treat medically with b-blockers and vasodilators
ANEURYSM
- thoracic - tertiary syphilis and end-arteritis, tree-bark appearance of aorta
- other risk factors include - bicuspid aortic valve, HTN
traumatic aortic rupture - MVC, aortic isthmus (first descending part of the aorta)
44
Large vessel vasculitides
vasculitides in general present with non-specific symptoms (fevers, fatigue, etc.)
aorta or major branches
temporal (giant cell) arteritis
- associated with polymyalgia rheumatica (flu-like symptoms with joint and muscle pain)
- elevated ESR
- giant cells, intimal fibrosis
- segmental lesions so negative biopsy does not exclude disease
- treat with corticosteroids
Takayasu - same as temporal arteritis, presents in Asian women less than 40
- narrowing of aortic arch and proximal vessels --> pulseless disease
- visual and neuro symptoms
- elevated ESR
- treat with corticosteroids
45
Medium vessel vasculitides
muscular arteries that supply organs
polyarteritis nodosa
- necrotizing vasculitis that involves most organs, lung is spared = GI/melena, HTN and renal damage, neuro damage, etc.
- IC mediated
- associated with *HbsAG* - usually occurs in middle aged men
- string of pearls lesions = early lesions have transmural inflammation with fibrinoid necrosis --> wall of blood vessel weakens --> aneurysm, lesions heal to form fibrosis
- treat with corticosteroids and cyclophosphamide (remember this causes transitional cell carcinoma and SIADH)
Kawasaki dz = mucocutaneous LN syndrome
- CRASH and burn
- conjunctivitis, rash (palms and soles), adenopathy (cervical LN), strawberry tongue, hand and foot changes, fever
- coronary artery involvement - thrombosis, aneurysms
- treat with ASA - decreases risk of thrombus development
- give IVIG - modulates complement activation, saturates Fc receptors on macrophages, suppresses idiotypic antibodies
- disease is self-limited
Buerger dz (thromboangiitis obliterans) - segmental thrombosing vasculitis, necrotizing vasculitis involving digits
- ulcers/gangrene/autoamputation of digits and toes
- associated with Raynaud's (vasospasm in response to cold/stress - white --> blue --> red fingers)
- associated with smoking = pt is heavy male smoker < 40 yo
- treat with smoking cessation
46
Small vessel vasculitides
99% of time due to type 3 HSR
IC deposition --> complement --> fibrinoid necrosis of blood vessels --> *palpable* purpura
- complement is called in via alternate/lectin pathway
Wegners - nasopharynx, lungs, kidneys
- PR3-ANCA/c-ANCA
- large necrotizing granulomas with adjacent necrotizing vasculitis - 1) granulomas in lung and upper airway, 2) glomerulonephritis, 3) vasculitis
- treat with cyclophosphamide and steroids - relapses are common
Microscopic polyangiitis
- lung, kidney (glomerulonephritis), skin, palpable purpura
- distinguish from Wegners - NO nasopharyngeal involvement, NO granulomas
- p-ANCA
- treat with cyclophosphamide and steroids - relapses are common
...........................
Eosinophilic granulomatosis with polyangiitis (Churg-Strauss) - necrotizing granulomatous vasculitis with eos
- asthma, peripheral eosinophilia, increased IgE
- peripheral neuropathy - foot drop
- p-ANCA
Henoch-Schonlein purpura - vasculitis due to IgA IC deposition
- common in kids - follows URI
- triad: palpable purpura on LE + butt, GI bleeding, arthralgias
- assoc with IgA nephropathy
- self-limiting but may recur, treat with steroids if severe
47
tumors
most common tumor is melanoma met
- most commonly involves pericardium --> pericardial effusion
myxoma - LA --> ball-valve obstruction --> multiple syncopal episodes
- may hear a tumor plop sound during early diastole
- classically embolizes to leg
rhabdomyoma - kids, think TS
- ventricle
strawberry hemangioma - skin, liver
- initally GROW to proportion of the child, then regress spontaneously before puberty
- v.s cherry hemangioma in elderly
angiosarcoma - malignant proliferation of endothelial cells, aggressive and difficult to resect
- skin, head/neck, breast, liver
- usually on sun-exposed areas, associated with radiation therapy and chronic post-mastectomy lymphedema
- liver angiosarcoma in particular - associated with exposure to PVC, arsenic, throtrast (outdate radiocontrast agent)
Kaposi sarcoma - HHV8
- Eastern European males, AIDS, transplant recipients
- lymphocytic infiltrate
v. s Bacillary angiomatosis - AIDS, neutrophilic infiltrate
- visualize with silver stain, treat with sulfa drug
48
hereditary hemorrhagic telangiectasia
Osler-Weber-Rendu syndrome
blanching skin lesions, recurrent epistaxis, skin discolorations, AV malformations, GI bleeds, hematuria
49
embryology
bulbus cordis - RV/LV outflow tracts
cardinal veins - SVC
endocardial cushion - AV septums, AV and SL valves
left horn of sinus venosus - coronary sinus
right horn of sinus venosus - smooth part of RA
primitive pulm vein - smooth part of LA
heart is the first functional organ in the embryo - beats by week 4
- week 4 = looping to establish L-R polarity
50
septation
atria
1) septum primum grows towards endocardial cushions - narrowing foramen primum
2) septum secundum forms in septum primum (foramen primum disappears)
3) foramen secundum forms
4) septum secundum expands
- residual foramen (between septums) is foramen ovale - septums fuse and FO closes soon after birth because of increased LA pressure
ventricles
1) muscular ventricular septum forms, IV foramen
2) aorticopulmonary septum rotates and fuses with muscular IV septum to form membranous IV septum
3) endocardial cushions grow to separate atria from ventricles
outflow tract formation - *neural crest* and endocardial cells migrate.... --> aorticopulmonary septum
51
congenital cardiac malformations
VSD: most common
- membranous part of septum (from aorticopulmonary septum and endocardial cushions)
- shunt-reversal
- *holosystolic*, harsh-sounding murmur, loudest at tricuspid area
ASD
- defect is that septa are missing (v.s. PFO, where septa dont fuse)
- most common type is ostium secudum, ostium primum is associated with DS
- loud S1
- wide, fixed split S2
PDA - after branches come off aorta
- associated with congenital rubella
- *holosystolic* machine-like murmur, loudest at S2, best heard at left infraclavicular area
- shunt reversal - cyanosis of LE
- treat with indomethacin - decreases PGE
Tet of Fallot
1&2) aorta overriding VSD
3&4) stenosis of right outflow tract and RVH
- R-->L shunt - cyanotic baby
- squatting reverses cyanotic spell
- tet spells are caused by crying, fever, and exercise due to exacerbation of RV obstruction
- boot-shaped heart on XR
Transposition of great vessels - have to introduce a shunt, maintain PDA in the meantime
- associated with mat DM
- due to failure of aorticopulmonary septum to spiral
Total anomalous pulmonary venous return
- pulmonary veins drain into right heart (as do SVC, coronary sinus)
- associated with ASD and sometimes PDA
Truncus arteriosus - early cyanosis
- most pts also have VSD
Tricuspid atresia - no valve
- need ASD and VSD for viability
52
angina
stable angina: >70% stenosis
- reversible injury to myocytes (occurs if blood flow is decreased for <20 min)
- ST depression - endocardium is most susceptible to damage
- why? because coronary arteries begin in the epicardium and dive down
- ST DEPression in V5 = subendocardial infarct
unstable angina - due to RUPTURE of atherosclerotic plaque and incomplete occlusion of coronary artery
- again reversible injury and ST-depression
- high risk of progression to MI - thrombus can easily occlude entire vessel
Prinzmetal angina - vasospasm
- transmural ischemia - blood vessel has completely clamped down - ST elevation
- can also have T wave inversion
- smoking is a risk factor
treat all with nitrates (decreases preload), add CCB for Prinzmetal
Coronary steal syndrome - distal to coronary stenosis, vessels are maximally dilated at baseline
- giving vasodilators dilates normal blood vessels and shunts blood towards well-perfused areas --> diverts flow from stenosed vessels --> myocardial ischemia
- principle behind pharmacologic stress tests with vasodilators
53
MI
necrosis of cardiac myocytes - complete occlusion of coronary artery
presentation - crushing pain...dyspnea (due to blockage of blood flow --> pulm congestion)
- symptoms are not relieved by NG
arteries
- usually LAD, next most common is RCA --> in general, LV is more affected
EKG
- STEMI (V5) - transmural infarct, can also have Q waves
- EKG localization of STEMI:
- anteroseptal (LAD) - V1-2
- anteroapical (distal LAD) - V3-4
- anterolateral (LAD, LCX) - V5-6
- lateral (LCX) - 1, aVL
- inferior (RCA) - 2, 3, aVF
- posterior (PDA) - V7-9 and ST-dep in V1-3 with tall R waves
- NSTEMI- subendocardial infarcts (esp inner 1/3)
- other findings: peaked T waves, T wave inversion, new LBBB, pathologic Q waves or poor R wave progression (evolving or old transmural infarct)
labs/tests:
- EKG is gold standard in first 6 hrs
- trop I - rises 2-4 hrs after infarction, peaks at 24hrs, normal by 7-10 days
- CK-MB - rises 4-6 hrs after, peaks at 24 hrs, returns to normal by 48-72 hrs
- CK-MB can also be released by skeletal muscle
treat with ASA/heparin, supplemental O2, nitrates, b-blocker, ACEI
- fibrinolysis or angioplasty
- contraction band necrosis - returning blood returns Ca2+
- reperfusion injury - cardiac enzymes continue to rise
- unstable angina/NSTEMI - medical treatment
- STEMI - meds, percutaneous coronary intervention preferred over fibrinolysis (due to lower rates of hemorrhage and recurrent MI)
changes with time:
- first 4hrs - no microscopic changes, arrhythmia
- arrhythmia is an important cause of death before reaching the hospital and within the first 24 hrs
- 1 day of coagulative necrosis (cells will be eosinophilic) - susceptible to reperfusion injury and contraction band necrosis
- 1 week of inflammation - during macrophage phase, complication is rupture of weakened ventricular free wall or septum --> cardiac tamponade, mitral insufficiency (if RCA is affected), shunt
- ventricular pseudoaneurysm is a contained free wall rupture
- 1-3 weeks - granulation tissue, gross exam will show red border at the edge of the infarct
- months - type 1 collagen scar (which is not as strong as the original myocardium)
- ventricular aneurysm
- Dressler syndrome - inflammation in pericardium exposes new antigens --> pericarditis 6-8 weeks after infarction
- Dressler syndrome can also involve other serosal surfaces (aka autoimmune polyserositis), treat with ASA/NSAIDs/glucocorticoids
54
cardiomyopathy
Dilated cardiomyopathy
- valvular regurg
- causes: idiopathic, genetic (AD), Coxsackie myocarditis, alcohol abuse, drugs (doxorubicin, cocaine), pregnancy, Chagas, hemachromatosis, sarcoidosis, wet Beriberi
- eccentric hypertrophy
- treat .... implantable cardioverter, heart transplant
- Takotsubo cardiomyopathy - ventricular apical ballooning, due to SNS input (stressful situations)
HCM (AD) - genetic mutations in *sarcomere* proteins
- outflow obstruction - septal hypertrophy, mitral valve obstruction outflow tract
- myocyte hypertrophy
- can be associated with Friedrich ataxia
- treat - b-blockers, non-dihydropyridine CCBs, ICD if pt is at high risk
Restrictive cardiomyopathy
- normal ejection fraction
- usually normal wall-thickness but can have increased LV thickness
- decreased compliance of endomyocardium
- causes: amyloidosis, sarcoidosis, endocardial fibroelastosis (kids), Loeffler syndrome (eosinophilic infiltrate + endocardial fibrosis), postradiation fibrosis
- amyloidosis - light chains, mutated transthyretin, wild-type transthyretin (senile systemic amyloidosis
- endomyocardial fibrosis - occurs in tropical regions (Uganda)
- classic finding is low voltage EKG
55
SNS and catecholamines
a1 - NE*, epi, phenylepi
b1 - *Epi, dopamine, dobutamine, isoproterenol
b2 - *Epi, isoproterenol, terbutaline
- b2-- > cAMP-PKC --> augmented Ca2+ uptake by SR --> vasodilation
isoproterenol is stronger than epi on b-receptors
- isoproterenol will increase cardiac contractility and decreased SVR
b-blockers - will decrease contractility, can precipitate asthma attack in pts with asthma or COPD
a-neuron blockers - gaunethidine, inhibit NE rlease
56
endocarditis
disrupted normal endocardial surface --> fibrin-platelet nidus --> bacteriaf]
in general multiple blood cultures necessary for ddx:
S aureus - acute, large vegetations
subacute - S. viridans, small vegetations on susceptible valves
- associated with dental procedures
- adheres to tooth enamel and fibrin-platelet aggregates on damaged heart valves - because it produces dextrans (from sucrose)
culture negative orgs are: Coxiella, Bartonella, and HACEK (Haemophilus, Aggregatibaceter, Cardiobacterium, Eikenella, Kingella)
mitral valve is most frequently involved
- tricuspid in IVDA - S aureus, Pseudomonas, Candida
```
other features:
Anemia, murmur
Fever
Roth spots - round white spots on retina
Osler nodes - raised lesions on finger/toe pads due to IC deposition
Janeway lesions - erythematous lesions on palms, soles
Emboli, splinter hemorrhages
- emboli, Janeway lesions are = embolic
- IC - osler nodes, Roth spots
```
endocarditis can be non-bacterial (aka *thrombotic* or marantic endocarditis)
- secondary to malignancy (mucinous adenocarcinomas), hypercoagulable state, lupus (NOT associated with systemic sclerosis)
- hypercoagulable state and cytokines create a setting where thrombi can deposit on heart valves
57
heart murmurs
Aortic stenosis = wear-and-tear disease, dystrophic calcifications
- compensation leads to prolonged asymptomatic stage - systolic ejection click followed by crescendo-decrescendo murmur
- murmur - loudest heart at base --> radiates to carotids
- pulses are weak with a delayed peak (pulsus parvus et tardus), syncope/etc. on exertion
- complications - ...microangiopathic hemolytic anemia
- treat - valve replacement after onset of complications
Aortic regurg - blowing (descrendo) murmur in early diastole
- can be heard at the left or right (if caused by aortic root dilation) sternal border
- widened pulse pressure - head bobbing, pulsating uvula and nail beds, waterhammer pulse
- recurrent laryngeal wraps around aortic arch --> hoarseness
- LV dilation --> LH failure
- LV dilation allows for an increase in stroke volume to maintain CO (this only occurs chronically)
- in acute AR - LV is not large enough to maintain CO --> decrease in CO, increase in HR
- treatment is valve replacement when LV dysfunction develops
Mitral valve prolapse
- most frequent valvular lesion
- mid-systolic ejection click (due to sudden tensing of chordae tendinae), followed by regurg murmur
- asymptomatic
- valve degeneration (Marfans, Ehlers-Danlos) or papillary muscle rupture
- again treat with valve replacement
Mitral regurg
- holosystolic blowing murmur
- loudest at apex and radiates towards *axilla*
- louder with squatting and expiration
- squatting - increased TPR send more blood flowing backwards
- expiration - *increases blood that enters LA and LV*
- bounding pulse with brisk upstroke (due to increased LV volumes)
- functional mitral regurg - transient hemodynamic factors that cause LV dilatation and or papillary muscle ischemia
Mitral stenosis
- opening snap followed by diastolic rumble
- opening snap due to abrupt half in leaflet motion in diastole
- decreased interval between S2 and OS correlates with increased severity - probably because this means valve is more stenosed
- chronic rheumatic fever
- chronic MS can result in LA dilatation
58
maneuvers during auscultation
inspiration - increases venous return
- widens S2 split
hand grip - increases afterload
- increased intensity of MR, AR, and VSD murmurs
- decreases hypertrophic cardiomyopathy and AS murmurs
- MVP - later onset of click/murmur
Valsalva, standing up - decrease preload
- decrease intensity of most murmurs (including AS)
- increase intensity of HCM murmur
- MVP - earlier onset of click/murmur
Rapid squatting - increases venous return/preload, increases afterload
- decreased intensity of HCM murmur
- increased intensity of most other murmurs
- MVP - later onset of click/murmur
MVP - maneuvers that increase LV volume maintain tension on the chordae longer --> click occurs later
59
palpable skin rash
N. gonorrhea infection - meningococcemia or disseminated
- begins on trunk and spreads over entire body
- fever, hypotension, tachy = septic
60
long QT
congenital - due to genetic mutations in K+ channel - decreased K outflow
- Romano-Ward syndrome - AD, pure cardiac phenotype
- Jervell and Lange-Nielsen syndrome - AR, sensorineural deafness
61
conduction defects
Brugada - AD, Asian males
- pseudo RBBB and ST elevations in V1-V3
- increased risk of vtach and SCD (use ICD)
WPW = pre-ventricular excitation syndrome
- fast accessory conduction pathway from atria to ventricle (bundle of Kent) that bypasses the AV node
- ventricles begin to partially depolarize earlier - delta wave (curve where Q should be) and widened QRS
- may result in reentry circuit --> supraventricular tachy
62
cardiac tamponade
equilibration of pressures in all heart chambers
Beck's triad - hypotension, distended neck veins, distant heart sounds
- will see late diastolic collapse of RA - pericardial fluid displaces with ventricular expansion
- HR increased
- pulsus paradoxus - SBP <10mmHg during inspiration, because of increased venous return and RA volume, constant pericardial effusion and RV volume --> septum pushes towards LV...
- also seen in asthma, COPD, OSA, pericarditis, croup
- mechanism in COPD - exaggerated drop in intrathoracic pressure --> transmitted to extrathoracic structures --> excessive drop in BP during inspiration
- Korotkoff sounds (hear when you are taking BP, deflating the cuff) - during inspiration --> increased RH volumes. When you cant expand pericardium --> IV septum blows towards LV --> LV stroke volume and SBP decrease
EKG - low voltage and electrical alternans (swinging movement of heart in effusion)
63
anti-arrhythmics
Class 1 - Na channel blockers
```
decrease conduction (esp in depolarized cells)
- decrease slope of phase 0 depol
```
dissociation of drug occurs during resting state of the channel
binding strength: 1C > 1A > 1B
1A) quinidine, procainamide, disopyramide
- increase AP duration and ERP (in vent. AP), increased QT, slows conduction velocity
- some K channel blocking effects - prolongs APD and QT
- use in atrial and vent arrhythmias, esp SVT and VT
- ADRs: cinchonism (headache, tinnitus with quinidine), procainamide (lups), HF (disopyramide), thrombocytopenia, torsads
1B) lidocaine, mexiletine, phenytoin
- decrease AP duration, no effect on conduction velocity
- good for ischemic or depolarized ventricular tissue
- use in acute VT (esp post MI), digitalis-induced arrhythmias
- 1B is Best post-MI - because these tissues have a reduced resting potential that delays the transition from the inactivated to the resting state --> increased drug-channel binding
- CNS stim/dep, CV dep (think lidocaine)
1C) flecainide, propafenone
- prolongs ERP in AV node and accessory tracts (no effect on ventricles), slows AP conduction velocity
- use in SVTs, afib
- proarrhythmic (esp post MI)
- 1C binds with the greatest affinity --> effects accumulate over many cardiac cycles and effect is enhanced with tachycardia --> delay in conduction speed that is out of proportion to prolonged refractory period --> this is why it is proarrthymic
...................................................................
anti-arrhythmics class 2
b-blockers
slows sinus node discharge rate, slows AV node conduction
[decreases SA and AV node activity (less cAMP), decreases Ca currents (also suppresses abnormal pacemakers, decreases slope of phase 4)]
use in SVT, ventricular rate control for afib and aflutter
```
ADRs:
may mask the signs of hypoglycemia
metoprolol - dyslipidemia
propanolol can exacerbate Prinzmetal
contraindicated in pheo and cocaine tox
```
treat OD with saline, atropine, and glucagon
- glucagon increases cAMP and cardiac contractility
```
...................................................................
anti-arrhythmics class 3
K-channel blockers
```
amiodarone, ibutilide, dofetilide, sotalol = AIDS
block - slow delayed rectifier K channels (Iks)
increase AP duration, ERP, and QT
- does NOT affect AP conduction velocity
used in afib, aflutter, vtach (amiodarone, sotalol)
ADRs:
sotalol - torsads, excess b-blockade
ibutilide - torsads
amiodarone - pulmonary fibrosis, hepatotox, hypo/hyperthyroid (drug = 40% iodine), acts as hapten (eye deposits, skin deposits that are photosensitive, blue-grey skin discoloration), neuro effects, CV depression
- amiodarone - PFTs, LFTs, TFTs
- amiodarone has class 1-4 effects
- interestingly, amiodarone has the lowest risk of torsads
```
...................................................................
anti-arrhythmics class 4
Ca-channel blockers
```
verapamil, diltiazem
same action as b-blockers (class 2)
prevents nodal arrhythmias (SVT), rate control in afib
ADRs: constipation, flushing, edema, CV depression
64
other anti-arrhythmics
adenosine - shifts K+ out of cells --> hyperpolarizes cells and decreases Ica --> decreased AV node conduction
- drug of choice for SVT (certain types)
- 15s acting time
- effects are blunted by theophylline and caffeine (adenosine receptor antagonists)
- ADRs: flushing, hypotension, CP, sense of impending doom, bronchospasm
Mg2+ - torsads and digoxin tox
65
exercise
HR increases, CO increases
PaO2 and PaCO2 unchanged - respiratory rate increases to eliminate the additional CO2 produced and improved V/Q matching
- venous blood concentrations will change!
vasodilators - adenosine and NO during exercise dilate coronary blood vessels
- so increase in HR doesnt limit coronary blood flow
when would arterial blood pH decrease - if you get lactic acidosis
66
carotid sinus massage
carotid sinus --> glossopharyngeal nerve (afferent) --> medulla --> vagal nerve
reflex PSNS simulation of SA node, atrial myocytes, and AV node
can be used acutely terminate PSVT
- Valsava and cold water immersion can also be used
67
ivabradine
selective inhibition of If - prolongs phase 4 and decreases SA node firing
use in chronic stable angina pts who dont take b-blockers, chronic HF with reduced ejection fraction
ADRs: luminous phenomena/visual brightness, HTN, bradycardia
68
skeletal muscle contraction
cardiac and smooth muscle - Ca-induced Ca-release and Ryr
- cardiac muscle - Ca binds troponin
- smooth muscle - Ca binds calmodulin
skeletal muscle
- L-type Ca channels directly interact with RyR --> Ca released from SR --> Ca binds to troponin
- mechanical coupling - so Ca2+ influx across plasma membrane isnt required
- verapamil would have no effect
T-tubules are NOT present in smooth muscle
69
complete AV canal defect
DS - most common congenital cardiac anomaly in DS
failure of endocardial cushion fusion --> ostium primum atrial septal defect, VSD, and single AV valve
--> L-R shunting, AV regurg --> excess pulmonary blood flow symptoms
- increased pulmonary venous return - mid-diastolic rumble
- AV valve regurg - holosystolic, best heard at apex
70
homocysteine
endothelial damage
homocysteine --> cystathionine --> cysteine
methylene THF reductase, FAD - used to regenerate methyl-THF
- MTHFR deficiency is the most common genetic cause of hyperhomocyestinemia
methylmalonic acid = neurotoxic
- lethargy, seizures, paresthesias, hypotonia
71
pregnancy and DVTs
due to increased venous stasis (uterus compresses IVC and internal iliacs), endothelial injury (during delivery), and hypercoagulability
- hypercoag - because of increase in factors 1, 2, 7, 8,9, 10 and a drop in protein S levels
use LMWHs - heparins dont cross placenta, short elimination times
- enoxaparin
72
clopidogrel and aspirin
clopidogrel - blocks platelet adenosine diphosphate receptor --> limits platelet aggregation
ASA - prescribed in preelampsia
73
CXR signs of heart failure
cephalization of pulm vessels (diameter of upper lobe vessels > lower lobe vessels), Kerley B lines (edema of interlobular septa)
cocaine can cause acute decompensated heart failure
74
Ach
acts on M2 and M3 receptors
vasodilates via NO release
75
turbidity of plasma
due to TGs (not cholesterol)
chylomicrons - TGs that you eat
- less than 3% cholesterol in chylomicrons
- have to fast to get an accurate TG level, but not to get an accurate cholesterol and HDL level
VLDL is what we make in the liver from G3P
76
Bohr-Haldane effect
increased pCO2 in tissues --> increased pH in erythrocytes
H+ buffered on histidine residues on Hb - stabilize deoxygenated Hb --> decreased affinity for O2
77
NE v.s isoproterenol
NE: a1 > a2 > b1 --> increased MAP (widened pulse P) --> reflex bradycardia
= CO unchanged/changed
- use in hypotension, septic shock
isoproterenol: b1 = b2 >> a --> increase HR and vasodil (decreased MAP)
= everything but MAP is increased, pulse pressure widens more than with NE or epi
- use to evaluate tachy, can worse ischemia
epi: b > a, doesnt increase HR as much as NE, b2 > a1
= all parameters increased
- a effects predominate at high doses
78
LVH and contractility
contractile function is normal, diastolic function is decreased
79
brachiocephalic vein
aka innominate vein
80
subclavian steal syndrome
subclavian artery is stenosed proximally to the origin of the vertebral artery
most pts are asymptomatic
- when symptoms occur --> arm ischemia or vertobasilar insufficiency (dizziness, vertigo, drop attacks)
retrograde flow through vertebral artery on the affected side - because of the lower pressure in the subclavian downstream of the stenosis
coronary -subclavian steal phenomenon
- in pts who have had coronary bypass surgery with internal mammary artery graft
- blood flow through the IMA reverses during increased demand
- chest pain
81
false aneurysm
breach of all 3 layers of the blood vessel --> hematoma outside the vascular wall, held "in" by the surrounding CT
82
aorta on CT
atherosclerosis --> aortic aneurysm
HTN --> dissection
83
phentolamine
reversible competitive a-antagonist
- drug can still get to Vmax (if you increase the concentration enough)
compare to phenoxybenzamine - irr a-agonist
= will decrease Vmax
84
hypertensive crisis
urgency >180/120 and no end-organ damage
hypertensive emergency
- end organ damage - papilledema, hemorrhage/AKI (elevated serum creatinine)/ACS, encephalopathy
85
strange pulses
seen during severe systolic dysfunction - pulse with 2 peaks
hyperkinetic pulse - rapidly rising pulse with high amplitude
- aortic regurg, high CO
86
pacemaker
biventricular pacemaker
- lead in RA, lead in RV
- lead in AV groove on posterior face of heart
87
dystrophic calcification
occurs upon necrosed tissue - ex aortic valve
- aortic sclerosis - *benign* calcifications in elderly
- aortic stenosis - occurs over time
in the setting of hypercalcemia - calcium will deposit on alkaline tissues
- kidneys, lungs, systemic arteries, gastric mucosa
88
ranolazine
antianginal drug
inhibits late phase inward Na channels in ischemic myocardial cells - during cardiac repolarization
less Na - slows down Na/Ca exchanger --> less intracellular calcium --> reduces myocardial O2 consumption
89
scenario - pt with elevated CVP and moderate dilation of the RV has no edema
why?
moderate increases in capillary fluid transudation can be offset by a compensatory increase in lymphatic drainage
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