ACOM > Cardio Block 2 > Flashcards

Cardio Block 2 Flashcards

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1
Q

what is VTE

A

DVT + PE
DVT may lead to PE and treaments overlaps

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2
Q

what is DVT

A

detachment of a thrombus carried to remote vessels

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3
Q

hyper coagulability risk factors

A

inherited - factor V leiden mutation, prothrombin gene mutation, low protein C/S, family history
acquired - age, smoking, obesity, malignancy, hormone replacement, pregnancy, infection, atherosclerosis, antiphospholipid antibodies

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4
Q

virchows triangle

A

risk for DVT
stasis (immobility, air trave)
venous injury/endothelial damage (trauma, sx, catheter)
hyper coagulability

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5
Q

DVT presentation

A

cramp in lower calf that persists/worsens over several days
leg/foot swelling, tenderness, erythema, palpable cord like veins

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6
Q

testing if low likelihood of DVT

A

d-dimer (cleaved fibrin cross links, appears 1 hour after thrombus formation)

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7
Q

testing if high likelihood DVT

A

skip d-dimer and get imaging (ultrasound shows loss of vein compressibility)

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8
Q

treatment for DVT

A

ALL ANTICOAGULATION MEDS
unfractionated heparin
low molecular weight heparin
argatroban
fondaparinux
bivalirudin
warfarin
direct oral anticoagulants

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9
Q

complications of anticoagulation

A

intracranial hemorrhage bc UFH or LMWH give protamine sulfate
warfarin effects give vitamin k and fresh frozen plasma
dabigatran effects give idarucizumab
andexxa and kcentra for factor Xa effects

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10
Q

duration of anticoagulation

A

3-6 months for initial episode of provoked DVT
indefinite for idiopathic unprovoked DVT
with cancer use LMWH and DOAC as monotherapy indefinitely

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11
Q

what to do if recurrent venous thrombosis despite anticoagulation

A

IVC filter
can be reversed up to several months after insertion
becomes permanent after a few months

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12
Q

DVT prophylaxis

A

hospitalized without obvious risk factors do not need pharmacologic thromboprophylaxis (can do early ambulation)
hospitalized with 1+ risk factor use pharmacologic thromboprophylaxis
very low risk - no methods
low risk - mechanical methods
moderate risk - LMWH
high risk - LMWH and mechanical

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13
Q

localized edema

A

limited to particular organ or vascular bed

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14
Q

unilateral extremity edema

A

venous or lymphatic obstruction (stasis edema of paralyzed lower limb)

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15
Q

facial edema

A

angioedema and superior vena caval obstruction

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16
Q

bilateral lower extremity edema

A

inferior vena cava obstruction, compression due to ascites, abdominal mass

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17
Q

ascites

A

fluid in peritoneal cavity
from cirrhosis, nephrotic syndrome, CHF

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18
Q

hydrothorax

A

fluid in pleural space

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19
Q

periorbital edema

A

renal disease and impaired Na excretion

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20
Q

idiopathic edema

A

recurrent rapid weight gain and edema in women of reproductive age

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21
Q

hypothyroidism

A

myxedema in pretibial region

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22
Q

treatment of edema

A

Na restriction
bed rest for salt restriction
stockings and elevation of lower extremities
if hyponatremia then limit water intake
diuretics for marked peripheral edema, pulmonary edema, CHF
loop diuretics first, if resistant add distal diuretics or metolazone

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23
Q

fever of unknown origin

A

over 101
over 3 weeks
not immunocompromised
diagnosis uncertain after thorough history, physical, and labs
if all above are met its likely FUO and outpatient workout is allowed and common

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24
Q

recurrent fevers

A

repeated episodes of fever interspersed with fever free intervals of at least 2 weeks
can be of known or unknown causes
if this lasts more than 2 years its unlikely it is due to infection or malignancy
relapsing fevers same thing but often refer to bacterial infections

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25
cardio causes of FUO
tumors (myxoma, lymphoma) infections (infective endocarditis, graft infections, aortopathies) collagen vascular vasculitis thrombosis transplant/immune conditions aneurysms/dissections pulmonary embolism
26
if still FUO after extensive workup what is the prognosis
western countries generally good most FUO deaths related to malignancy
27
how to treat FUO
avoid antibiotics, steroids, or antituberculosis agents unless condition is rapidly deteriorating
28
endocarditis
inflammation of endocardium usually affects valves
29
endocarditis symptoms
fever, anemia, abnormal heart beat \abdominal or side pain petechia over upper body and fingernails enlarged spleen (subacute) almost always fever and murmur splinter hemorrhages, oslers nodules, janeway lesions
30
endocarditis mortality
20-50% with treatment causes - mitral valve prolapse, aortic sclerosis, bicuspid aortic vulvar heart disease
31
common causes of endocarditis
native valve - oral strep viridans (enterococcus) IV drug users - staph aureus prosthetic valves (early) - coagulase negative staph prosthetic valves (late) - oral strep (enterococcus)
32
HACEK group infections
normal oral flora, cause subacute endocarditis, hard to diagnose Aggregatibacter aphrophilus (haemophilus) aggregatibacter actinomycetemcomitans cardiobacterium hominis eikenella corrodens kingella kingae more typical to have oslers nodules
33
septicemia
fever, hypotension, hypovolemia
34
rheumatic fever pathogenesis
strep antigens cross react with cardiac/host antigens m protein cross reacts with glycoprotein in heart valves
35
rheumatic fever prevention
penicillin for strep long term prophylaxis for 5 years or until 21
36
myocarditis
persistent inflammatory process following an infection of the myocardium can be asymptomatic or have fever, malaise, fatigue, arthralgias, myalgias, skin rash viral infection most common cause in US
37
myocarditis triphasic disease process
1 - viral infection and replication (direct injury to cardiomyocytes) 2 - autoimmunity and injury (dysregulated immune response causes cardiac damage) 3 - dilated cardiomyopathy (cytokines play a role, cause remodeling and progressive heart failure)
38
myocarditis physical exam
tachycardio, hypotension, fever narrow pulse pressure murmurs of mitral or tricuspid regurg S3 and S4 gallops distended neck veins, pulomonary crackles, wheezes
39
myocarditis diagnostic studies
endomyocardial biopsy (at least 4 or 5) CBC, ESR, rheumatology screen, cardiac enzymes, serum viral antibody titers for viral myocarditis echocardiography cardiac angiography gadolinium enhanced MRI nuclear imaging electrocardiogram
40
myocarditis causes
viral - coxsachievirus B mouth is portal of entry replicate in oropharynx and intestine incubate 1-2 weeks and virus is spread in throat and feces for 1 and 3 weeks
41
Chagas disease
american trypanosomiasis transmitted through feces of triatomid bug parasites infect cardiac, smooth, and skeletal muscle flagellated form - infectious (trypomastigote) amastigote - tissue form (replicative form) cardiomyopathy and damages autonomic nervous system congestive heart failoure and arrythmia
42
increasing bloof flow through the affected valve does what to a murmur
increases the sound
43
decreasing blood flow through the affected valve does what to a murmur
decreases the sound
44
how to increase preload
bradycardio, hypervolemia, squatting, leg raise
45
hot to decrease preload
tachycardia, hypovolemia, standing up, valsalva, vasodilating drugs
46
how to increase afterload
hand grip, squat, vasoconstrictor drugs
47
how to decrease afterload
hypovolemia, vasodilating drugs
48
increasing does what to a murmur
increases the sound except in mitral valve prolapse and hypertrophic obstructive cardiomyopathy
49
increasing afterload does what to a murmur
increasesthe sound except in mitral valve prolapse, hypertrophic obstructive cardiomyopathy, aortic stenosis
50
murmurs in right heart do what during the respiratory cycle
increase with inspiration decrease with exhalation
51
murmurs in the left heart do what during the respiratory cycle
increase with exhalation decrease with inhalation
52
pure stenosis
valve does not open fully, flow obstructed
53
pure regurgitation
valve does not close completely, backward flow occurs
54
isolated disease
only one valve
55
combined disease
more than one valve
56
functional regurgitation
valve becomes incompetent due to dilation of ventricle, dilation of aorta or pulmonary artery
57
most frequent acquired valvular diseases are what
stenosis of aortic and mitral valves
58
infective endocarditis
infection of cardiac valve or mural endocardium by microbial agent formation of bulky vegetations composed of thrombotic debris mom - mitral actually - aortic can - combined take - tricuspid pictures - pulmonic
59
acute endocarditis
most commonly staph aureus major organism for IV drug users (tricuspid valve) acute onset fever, chills, weakness
60
subacute endocarditis
most common strep viridans (oral procedures) presthetic valves also can be staph epidermidis colon can be strep gallolyticus HACEK organisms prolonged course most recover w antibiotics
61
infective endocarditis physical exam findings
new murmur or change in old murmur petechia, splinter hemmorhages, osler nodules, janeway lesions, roth spots
62
infective endocarditis pathophys
friable vegetations on valve cusps that can extend onto chordae tendinae acture inflammatory cells, fibrin, platelets, bacterial colonies sometimes chronic inflammatory cells, fibrosis, calcification
63
noninfected vegetations
nonbacterial thrombotic endocarditis endocarditis of systemic lupus erythematous (libman sacks)
64
non bacterial thrombotic endocarditis
deposition of small masses of fibrin, platelets, and other blood components on cardiac valve leaflets malignancy and cachexia, endocardial trauma, debilitating conditions single or multiple vegetations along the lines of closure of valve leaflets often on mitral valve and can lead to mitral regurg bland thrombus without accompanying inflammatory reaction
65
libman sacks endocarditis
associated with SLE sterile vegetations mitral and tricuspid valves (can lead to regurg) can cause serious valve deformity requiring surgery single or multiple granular pink vegetations on either or both sides of the valve leaflets, may extend onto chordae tendinae, papillary muscles, or mureal endocardium intense inflammation, fibrinoid necrosis, fibrosis
66
concentric hypertrophy
increased afterload wall thickness increases bc sarcomeres added in parrallel
67
eccentric hypertrophy
increased preload chamber dilates bc sarcomeres added in series wall thickness can be normal, increases, or decreased
68
degenerative calcific aortic valve stenosis
most common valvular abnormality most age related 70s for tricuspid aortic valve 40-60 for bicuspid aortic valve systolic ejection murmur - crescendo decrescendo at right upper sternal border
69
degenerative calcific aortic valve stenosis characteristics
heaped up calcific masses within aortic cusps fibrosis and calcification of valve
70
mitral annular calcification
degenerative most common in women over 60 normally doesnt affect valvular function stony hard nodules can cause mitral regurg, mitral stenosis, or infective endocarditis
71
mitral valve prolapse
most common cause mitral regurg most cases sporadic and cause unknown marfan and ehler danlos common valve is floppy and incompetent
72
mitral valve prolapse characteristics
ballooning of thickened mitral valve leaflets chordae tendinae elongated attenuated fibrosa layer thickening spongiosa layer with deposition of mucoid material
73
mitral regurgitation
blood flows back from left ventricle into left atrium during systole systolic murmur best hear at apex and often radiates to axilla
74
rheumatic fever
after untreated Strep A pharyngitis usually 5-15 years old 10 days - 6 weeks after throat infection
75
what type of hemolysis does strep A do
beta
76
pathogenesis of rheumatic fever
genetic susceptibility GAS M protein has antibodies produced against it that cross react with glycoprotein antigens in human tissues (type II hypersensitivity)
77
rheumatic fever lab findings
elevated antistreptolysin O (ASO) and/or DNASE B titers
78
major jones criteria
J- joints = polyarthritis O - heart = carditis N - subcutaneous Nodules E - erythema marginatum S - syndenham chorea
79
minor Jones criteria
arthralgia fever elevater ESR or CRP prolonged PR interval on EKG
80
morphology of rheumatic fever
pancarditis small warty vegetations along lines of closure of valves mom - mitral actually - aortic takes - tricuspid pictures - pulmonic aschoff bodies - inflammatory lesions, focal fibrinoid necrosis of collagen alongside blood vessels, plump histiocytes (anitschkow cells) which are pathogenic for RF fibrinous or serofibrinous exudate
81
chronic rheumatic heart disease
increased risk with repeated GAS infections and recurrent acute rheumatic fever organization of acute inflammation and fibrosis - valve leaflet thickening, commissural fusion, thick fused chordae tendinae, aschoff bodies replaced by fibrinous scar, fish mouth stenosis most frequent cause of mitral stenosis
82
aortic regurgitation
due to abnormality of valve leaflets or aortid root dilation leads to primary volume overload causing eccentric hypertrophy early diastolic decrescendo at third intercostal space adjacent to left sternal border widened pulse pressure bounding pulses, dancing carotids, head bobbing
83
tricuspid stenosis
opening snap and diastolic murmur heard at tricuspid area
84
tricuspid regurgitation
usually due to right ventricular enlargement causing distorted valves systolic murmur best heard at tricuspid area
85
pulmonic stenosis
systolic ejections murmur can lead to splitting of S2 due to delayed P2 usually due to congenital deformity of valve
86
pulmonic regurgitations
usually due to pulmonary hypertension enlarging pulmonic artery and distorting valve diastolic decrescendo murmur
87
dilated (congestive) cardiomyopathy
all 4 chamber dilated and have hypertrophy most common cause idiopathic can be end stage of remote viral endocarditis age 20-50 S3 gallop mitral and tricuspid regurgitation, mural thrombi, cardiac arrythmias sudden emotional stress
88
hypertrophic cardiomyopathy
most common form idiopathic hypertrophic subaortic stenosis from asymmetric interventricular septal hypertrophy left ventricle outflow tract obstruction most causes familial mutation in genes that encode proteins of sarcomere may cause syncope in exertion, sudden death in young athletes murmur increase with valsalva or standing murmur decrease with squating, hand grip, or elevating feet
89
arrhythmogenic right ventricular cardiomyopathy
familial autosomal dominant with variable penetrance RV thin and replaced with fat
89
restrictive cardiomyopathy
myocardium infiltrated with material causing impaired ventricular filling amyloidosis and hemochromatosis decreased ventricular compliance causing decreased QRS amplituted
90
rheumatic fever progression
simple strep throat scarlet fever rheumatic fever
91
rheumatic fever treatment
penicillin G or amoxicillin (also anti-inflammatory, heart failure management, secondary prophylaxis)
92
tempo of infective endocarditis
acute - most likely staph aureus and treat empirically subacute - most likely strep sp can wait for cultures
93
infective endocarditis treatment
gentamicin and beta lactams
94
septic shock treatment
empiric with heavy hitting broad spectrum antibiotics
95
those susceptible to infective endocarditis and need primary prophylaxis
prosthetic heart valves prior history of infective endocarditis unrepaired cyanotic congenital heart disease completely repaired congenital heart defect w prosthetic material in first 6 months after procedure valve regurgitation cardiac transplant recipients with cardiac valvular disease
96
primary prophylaxis for dental procedures
amoxicillin 500 mg 4 capsules
97
primary prophylaxis for dental and respiratory procedures
penicillin or amoxicillin if cant take bc bc penicillin allergy take azithromycin, clarithromycin, cephalexin
98
duke criteria for diagnosing infective endocarditis
major - positive blood cultures x 2, evidence of endocardial involvement minor - fever, predisposition for infective endocarditis, vascular phenomenon, immunologic phenomenon, microbiologic evidence
99
for acutely ill pts with s/s strongly suggestive of IE empiric therapy may be necessary
target staphylococci, streptococci, enterococci give abx after blood cultures have been obtained
100
general rules for treating infective endocarditis
bactericidal treatment IV for 6 weeks after engative cultures
101
empiric IE treatment with native valve
vancomycin + ceftriaxone
102
empiric IE treatment with prosthetic valve
vancomycin + cefepime or pip/tazo +/- gentamicin (+ rifampin for biofilm protection)
103
MSSA IE treatment with native valve
nafcillin or oxacillin OR cefazolin
104
MRSA IE treatment for native valve
vancomycin (daptomycin if cant take vanc)
105
viridans strep or S. bovis IE treatment for native valve
penicillin or ceftriaxone +/- gentamicin if allergic desensitize with PCN plus gentamicin
106
enterococcal IE treatment with native valve
ampicillin + ceftriaxone
107
gram negative HACEK group IE treatment for native valve
ceftriaxone
108
MRSA or S epidemidis IE treatment for prosthetic valve
vancomycin + gentamicin + rifampin
109
MSSA IE treatment for prosthetic valve
nafcillin +gentamicin + rifampin
110
secondary prevention of rheumatic fever without carditis duration
5 years or until 21
111
secondary prevention of rheumatic fever with carditis but no residual heart disease (no valvular disease)
10 years or until 21
112
secondary prevention of rheumativ fever with carditis and residual heart disease (persistent valvular disease)
10 years or until 40
113
adult sepsis treatment when source is unclear
"penem" and vancomycin OR pip/tazo and vancomycin
114
adult sepsis treatment if suspect community acquired pneumonia
ceftriaxone and azithromycin OR cefepime and azithromycin and vancomycine if suspect pseudo and MRSA
115
adult sepsis treatment if suspect intra abdominal source
pip/tazo or meropenem
116
adult sepsis treatment if suspect urinary souce
ceftriaxone or ertapenem or pip/tazo
117
pulmonary hypertension
pulmonary artery pressure over 20 mm Hg
118
P2
normally soft and only heard at pulmonic region but even in this region A2 is usually louder
119
increased intensity of P2
pulmonary hypertension atrial septal defect
120
pulmonary artery catheterization
catheter floated into right side of heart and wedged into pulmonary arteriole wedged and pressure measured PCWP reflects left atrial pressure which reflects ventricular end diastolic pressure which reflects left end diastolic volume
121
measuring preload
right side of heart - right atrial pressure or central venous pressure left side of heart - PCWP
122
normal right atrial and ventricular pressures
atrial - 2 - 6 mm Hg ventricular - 15-25 mm Hg (systolic) 0-8 mm Hg (diastolic)
123
normal pulmonary arterial pressure
15-25/8-15 mm Hg mean - 10-20 mm Hg
124
normal PCWP
6-12 mm Hg
125
congestive heart failure
cardiac output insufficient for metabolic requirements of body abnormality in structure or function forward failure = increased perfusion nackward failure = passive congestion of organs
126
systolic heart failure
decreased myocardial contractility decreased ejection fraction
127
diastolic heart failure
insufficient expansion of ventricular volume leading to insufficient cardiac filling
128
dilation
enlarged chamber size with increase in size of internal cavity
129
cardiomegaly
increase in cardiac size due to hypertrophy an/or dilation
130
concentric hypertrophy
increase in afterload wall thickness increases add sarcomeres in parallel
131
eccentric hypertrophy
increase in preload chamber dilates sarcomeres added in series wall thickness normal, decreased, or increased
132
chronic hypertrophy
hypertrophied tissue may outgrow its blood supply leading to ischemia organ failure may occur
133
CHF body compensation
tachycardia frank starling mechanism (increase stroke volume) nyocardial hypertrophy activation of renin angiotensin aldosterone system increased release ADH increased release of natriuretic peptides (vasodilation so secrete Na and water) release catecholamines (NE) increase oxygen extraction from hemoglobinl
134
left heart failure
dyspnea (pulmonary edema) fatigue (decreased cardiac output) diaphoresis/tachycardia/tachypnea (adrenergic) S3 gallop (systolic dysfunction) S4 gallop (diastolic dysfunction) loud P2 (pulm htn)
135
causes of left sided heart failure
ischemic heart disease hypertension aortic and mitral valve disease myocardial infarction dilated cardiomyopathy restrictive cardiomyopathy
136
pulmonary edema
capillaries in lungs rupture macrophages engulf blood and become laden with iron (prussian blue iron stain) alveolar septal fibrosis
137
atrial natriuretic peptide
released in response to atrial stretch excrete sodium and water, vasodilation, inhibit renin secretion, antagonism of angiotensin II on aldosterone and ADH levels
138
B type natriuretic peptide
released in response to ventricular stretch excrete sodium and water, vasodilation, inhibit renin secretion, antagonism of angiotensin II on aldosterone and ADH levels
139
right sided heart failure
most common cause is left sided heart failure pure right sided with chronic pulmonary hypertension (bc hypoxia constricting lung vessels) causing cor pulmonale (right ventricular hypertrophy and right ventricular dilation) fluid overload JVD hepatomegaly (nutmeg liver bc chronic passive congestion and blood pooling near central veins) lower extremity edema ascites splenomegaly congested kidneys loud P2
140
heart failure treatments that reduce mortality
ARNI - subcutril valsartan ARB - "sartans" ACEi - "prils" MRA - spironolactone and eplerenone SGLT2i - "flozins" hydralazine nitrates
141
heart failure treatments to reduce symptoms
ivabradine - when maximized on BB and sinus rhythm > 70 bpm vericguat - unable to tolerate ACE/ARB/ARNI digoxin - if need positive ionotrope
142
acute decompensated heart failure treatments
fluid overload = loop diuretics (furosemide, bumetanide, torsemide) hypertension = nitroprusside (arteriolar vasodilator) dont respond to diuretics = nitroglycerine (venous vasodilator) hyponatremia = vasopressin agonist (tolvaptan) low output/decreased perfusion = inotropes (dobutamine or dopamine or milrinone)
143
stage A treatment
never had s/s or without functional impairment but have high risk flozins
144
stage B treatment
structural damage and likely to develop heart failure ACE/ARB (if intolerant to ACE) and beta blocker
145
stage C and D treatment
ACE/ARB/ARNI, beta blocker, MRA, SGLT2, diuretics as needed if still persistent use hydral nitrates for AA or other therapies for non AA Iivabradine, vericguat, digoxin) if refractory ise durable MCS, cardiac transplant, palliative care
146
risk factors for pulmonary embolism
cancer obesity smoking systemic arterial hypertension COPD antiphospholipid antibodies pregnancy 6-12 weeks postpartum postmenopause hormone replacement inherited clotting mutations
147
treatment for pulmonary embolism
anticoagulation factor Xa inhibitor standard
148
dyspnea
experience of breathing discomfort
149
differential for dyspnea
asthma, COPD, anemia, kyphoscoliosis, pneumonia, pulmonary HTN, chronic thromboembolic disease, CAD, cardiomyopathy, CHF, constrictive pericarditis, cardiac tamponade, anxiety
150
dyspnea treatment
identify and treat underlying causes supplement with O2 if reston O2 less than 88 or O2 drops to this level when active or sleeping
151
myocardial ischemia
imbalance between supply and demand of heart for oxygenated blood reduced nutrient substrates and decreased removal of metabolites
152
arteriosclerosis
thickening and loss of elasticity of arterial walls 3 types - arteriolosclerosis, moncheberg medial calcific sclerosis, atherosclerosis
153
arteriolosclerosis
hyalin - diabetes and HTN (deposition pink hyalin material in vessel wall, luminal narrowing, can lead to ischemia) hyperplastic - severe HTN (fibrinoid necrosis with concentric deposition of smooth muscle cells and BM causing wall thickening and luminal narrowing, can lead to ischemia)
154
monckeberg medial calcific sclerosis
typically elderly males calcification of tunica media and internal elastic lamina of small/medium sized arteries (often radial or ulnar) usually no luminal narrowing or ischemia
155
atherosclerosis
intimal plaques (lipid core w fibrous cap) obstruct lumen of vessels, weakens wall of vessels, may lead to thromboembolism
156
risk factors of atherosclerosis
age, male, postmenopausal women, fam history/genetics smoking, HTN, dyslipidemia, DM, obesity, physical inactivity, inflammation stress, elevated homocysteine, elevated lipoprotein a, elevated apolipoprotein b, alcohol consumption, elevated plasminogen activator inhibitor, CKD
157
coronary obstruction >70%
chest pain w exercise
158
coronary obstruction >90%
symptoms w rest
159
angina
chest pain due to ischemia without cardiac cell death substernal chest pain, provoked by exertion/stress, relieved by rest/nitroglycerin can have ST depression
160
vasospastic angina
coronary artery vasospasm causes complete occlusion transient ST elevation usually relieved by nitroglycerin or calcium channel blockers
161
acute coronary syndromes
unstable angina NSTEMI STEMI
162
unstable angina
chest pain at rest chest pain w less exertion than before increasing frequency/intensity/duration new onset often relieved by nitroglycerin ST depression and/or T wave inversion
163
MI
death of cardiac muscle resulting from ischemia typically due to atherosclerosis with plaque rupture and superimposed thrombus substernal pain that radiates, SOB, N/V, diaphoresis takes 20-40 minutes for irreversible myocardial necrosis to begin
164
transmural MI
most common involves full or near full thickness of ventricular wall in distribution of single coronary artery
165
subendocardial MI
less common necrosis limited to inner 1/3 of ventricular wall can be bc decreased BP superimposed on noncritical coronary stenoses
166
microvascular angina
clinical angina syndrome in absence of atherosclerotic stenoses thought to be related to inadequate vasodilatory reserve
167
T wave in infarction
initially peaks 2 hours later it inverts
168
concave ST elevation (smiley)
doesnt rule out MI but doesnt as strongly suggeswt
169
convex ST elevation (frowny)
strongly suggests acute MI
170
labs for MI
myoglobin creatine kinase MB troponin I and troponin T lactate dehydrogenase
171
myoglobin
elevated in 30 min - 4 hours peak in 6-12 hours back to normal in 24-36 hours
172
CK-MB
elevated in 2-4 hours peak in 24 hours back to normal in 72 hours
173
troponin
elevated in 2-4 hours peak at 24-36 hours back to normal in 7-10 days
174
lactate dehydrogenase
elevated by 24 hours peak at 3-6 days back to normal at 8-14 days
175
gross changes in MI
0-4 hours none 4-12 h occasional dark mottling 12-24 hours dark mottling 1-3 days mottling w yellow tan central pallor 3-7 days yellow tan central pallor and softening with red border 7-10 days max yellow tan and soft with red tan margins 10-14 days red gray depressed borders 2-8 weeks gray white scar 2 months scar complete
176
microscopic features of MI
0-1/2 h none 1/2 - 4 h few wavy fibers 4 - 12 h early coagulative necrosis 12-24 h coagulative necrosis, pyknosis of nuclei, early contraction bands 1-3 d coagulative necrosis, heavy PMNs, contraction bands, loss of nuclei 3-7 d macrophages w early phagocytosis at border, disintegration of dead myofibers 7-10 d phagocytosis and granulation tissue 10-14 d prominent well developed granulation tissue with some collagen deposition 2-8 w fibrosis w increased collagen deposition 2 months dense collagenous scar
177
angina typically occurs when
major coronary artery stenosis of >70% LCA stenosis >50%
178
unstable angina occurs when
>90% stenosis
179
types of arrhythmias with a pulse
tachyarrhythmia - sinus tachycardia, atrial flutter, atrial fibrillation, ventricular fibrillation, ventricular tachycardia bradyarrhythmia - heart blocks
180
shockable cardiac arrest
ventricular fibrillation and pulseless ventricular tachycardia CPR - defibrillator - epinephrine - amiodorone/lidocaine - treat reversible causes
181
non shockable cardiac arrest
asystole and pulseless electrical activity CPR - epinephrine - treat reversible causes
182
class IA antiarrhythmics
procainamide (ventricular arrythmias) quinidine disopyramide (ventricular arrythmias) moderate Na block (moderate decrease slope of phase 0)
183
class IB antiarrhythmics
lidocaine mexiletine weak Na block (slight decrease slope of phase 0)
184
class IC antiarrhythmics
propafenone flecainide strong Na block (strong decrease in slope of phase 0)
185
class II antiarrhythmics
beta blockers - decrease rate and conduction esmolol propranolol
186
class III antiarrhythmics
amiodorone - Na and K channel blockers sotalol - K channel blocker ibutatilides (K channel blocker and activate slow Na current in) delay repolarization (phase 3)
187
class IV antiarrhytmics
calcium channel blockers - decrease rate and conduction non DHP - diltiazem and verapamil DHP - amlodipine
188
treatment for torsades de pointes
magnesium
189
treatment for supraventricular tachycardia
adenosine (adenosine A1 receptor activator that slows conduction) vagal maneuvers (stable) shock (unstable)
190
treatment for atrial fibrillation
beta blockers and non DHP CCB (stable) shock (unstable)
191
treatment monomorphic ventricular tachycardia
shock (unstable) adenosine, procainamide, amiodorone, sotalol (stable)
192
treatment for polymorphic ventricular tachycardia
shock (unstable) procainamide, amiodorone, sotalol (stable)
193
treatment for heart blocks
atropine - M2 receptor antagonist (anticholinergic) dopamine epinephrine isopterenol (beta receptor agonist)
194
what is a common complication of end stage renal failure
uremic pericarditis and pericardial effusion
195
EKG finding of pericardial effusion
electrical alternans
196
DKA can cause what
respiratory compensation for profound metabolic acidosis
197
vocal cord polyps
benign laryngeal tumors usually have progressive hoarseness heavy smoking and vocal abuse common factors may cause acute upper airway obstruction
198
COVID 19 has been associated with what
myopericarditis
199
heart failure symptoms
dyspnea, cough, wheeze, fatigue (ineffective flow from left ventricle) peripheral edema and ascites (right ventrical cant take in enough blood) nausea and lack of appetite (blood shifted from GI tract to vital organs) palpitations (lack of flow accommodated by increased HR)
200
diagnostic tests for heart failure pt
POCUS ECG CXR labs ECHO
201
how to determine NSTEMI or unstable angina
using troponin testing
202
stunned myocardium
prolonged systolic dysfunction after return of normal blood flow function gradually recovers
203
hibernating myocardium
chronic ventricular contractile dysfunction because reduced blood supply function promptly improves when appropriate blood supply restored
204
STEMI can also happen alongside what
LBBB creating ST - T changes
205
right ventricular infarction
often caused by infarction of inferior left ventricle produces signs of right heart failure right coronary artery occlusion can affect electrical conduction ST elevation in V1 and sometimes V2 ST depression in II, III, AVF (III more than II) can use right sided precordial leads that will have ST elevation (V3R, V4R, V5R, V6R) avoid nitrates and diuretics use saline, dobutamine
206
complications of MI
sudden death contractile dysfunction arrythmias myocardial rupture postinfarction pericarditis mural thrombus ventricular aneurysm
207
myocarditis
viral syndrome commonly with upper respiratory or GI symptoms CHF, dilated cardiomyopathy, mural thrombus tachycardia arrhythmias usually self limited tachycardio out of proportion to fever
208
hypersensitivity myocarditis
interstitial inflammatory infiltrate composed of largely eosinophils and mononuclear inflammatory cells
209
giant cell myocarditis
multinucleated giant cells and extensive myocyte necrosis often fulminant treat with immunosuppressive drugs
210
pericardial fluid
usually 15-50 mL clear yellow fluid plasma ultrafiltrate secreted by mesothelial cells lining serosal layer of pericardium
211
pericarditis
inflammation of pericardium
212
acute pericarditis
serous pericarditis fibrinous and serofibrinous pericarditis purulent (suppurative) pericarditis hemorrhagic pericarditis caseous pericarditis
213
chronic pericarditis
constrictive pericarditis adhesive pericarditis
214
drug related pericarditis
caused by procainamide and hydralazine
215
pericardial effusion
abnormal accumulation of fluid in pericardial sac abnormal amount and/or abnormal composition
216
symptoms of acute pericarditis
chest pain fever dyspnea palpations cough or runny nose joint swelling or pain night sweats or weight loss friction rub (loudest at LLSB)
217
EKG of acute pericarditis
acute ST segment elevation some PR segment depression
218
lab findings in acute pericarditis
may have elevated troponin and CK-MB elevated ESR depend on underlying etiology
219
radiology findings for acute pericarditis
may have enlargement of cardiac silhouette on CXR may see pneumonia on CXR may see lung mass on CXR monitor for development of pericardial effusion
220
serous pericarditis
usually non infectious 50-200 ml mild inflammatory infiltrate with scant neutrophils, lymphocytes, and macrophages
221
fibrinous/serofibrinous pericarditis
serous fluid mixed with fibrinous exudate containing plasma proteins including fibrinogen rough shaggy appearance inflammation with lymphocytes, fibrin, erythrocytes develop loud pericardial friction rub
222
purulent/suppurative pericarditis
always due to infection thin to creamy purulent fluid 400 - 500 ml acute inflammation which may organize and scar causing constricitve pericarditis
223
hemorrhagic pericarditis
blood mixed with fibrinous or suppurative effusion may be seen in tuberculosis, other infects, or sx may lead to constrictive pericarditis
224
caseous pericarditis
caseation within pericardial sac from tuberculosis until proven utherwise untreated can cause fibrocalcific chronic constrictive pericarditis
225
pericardial effusion findings
muffled heart sounds friction rub electrical alternans enlarged cardiac silhouette on CXR
226
cardiac tamponade
distant heart sounds distended jugular veins decreased arterial pressure pulsus paradoxus compression of RV and RA in diastole tx - pericardiocentesis
227
constrictive pericarditis
fluid from pericardial effusion organizes and forms a scar inhibits normal filling of heart chambers may have kussmaul sign, may have pericardial knock jugular venous distention, edema, ascites, diastolic expansion and cardiac output impaired tx - pericardiectomy
228
cardiac tamponade
pulsus paradoxus
229
constrictive pericarditis
kussmaul sign
230
palpitations
concerning awareness of heart beat may occur without serious underlying heart disease
231
premature atrial beats
turning over or flopping noticed when heart rate is slow and laying on left side can have pounding in the neck bc contraction against closed valve increases with caffeine, nicotine, alcohol
232
sinus tachycardia
adrenergic stimulation fast regular rhythm constant rapid pounding can be exercise, anxiety, hyperthyroidism, pheochromocytoma
233
supraventricular tachycardias (paroxysmal atrial tachycardia)
AV nodal tachycardia most common - may occur in emotional stress (panic attack) atrioventricular reciprocating tachycardia - large macroreenterant circuit like WPW may be caused by excess alcohol, emotional upset, strenuous exertion PAT specifically - rapid irregularly irregular bc acute alcohol excess or healthy heart
234
ventricular premature beat
often felt as consequence of forceful beat that follows a pause and increased ventricular filling after missed beat cannon "A" waves may be felt as impulse in neck
235
ventricular tachycardia
one of most dangerous dysrhythmia nonsustained may occur in otherwise healthy person dangerous vt when have heart disease or hereditary defects prolonged QT syndrome is common cause - can lead to torsades de pointes right ventricular outflow tract - right ventricular origin of VT, may be exercise induced
236
brugada syndrome
hereditary autosomal dominanct mutation in gene important to functioning of hearts sodium channels show RBBB and ST elevation in V1 - V3
237
right ventricular cardiomyopathy
right ventricular muscle replaced wtih fat can cause VT can show RBBB
238
lab studies for patients with arrhythmias
hemoglobin (rule out anemia) TSH (rule out hyperthyroidism) potassium, calcium, magnesium (in underlying heart disease) cardiac glycoside level (digoxin to rule out toxicity) vanillylmandelic acid (rule out pheochromocytoma)
239
ambulatory electrocardiographic monitoring
patients whose palpations are accompanied by evidence of underlying heart disease
240
alcoholic cardiomyopathy
may present as paroxysms of AT triggered by binge drinking abstinence can halt or reverse the condition
241
cardiac surgery
AF common after cardiac surgery onset 2nd - 3rd day postop increases risk of mortality and embolic stroke
242
when can you work up AF outpatient
when no hemodynamic compromise is present
243
adhesive pericarditis
adherence of external parietal layer to surrounding structures may have systolic contraction of rib cage/diaphram and pulsus paradoxus
244
what is the purpose of the preoperative evaluation
to estimate the patients ability to respond to stresses intraoperatively and postoperatively
245
areas of focus for preop eval
cardio respiratory, renal, hematologic, nutritional, and endocrine systems
246
beta blockers block what in surgery patients
normal chronotropic response to infection or blood loss
247
obtain baseline Hb in what patients
undergoing procedures associated with extensive blood loss h/o anemia, malignancy, renal insufficiency, cardiac disease, DM, pregnancy
248
patients with chronic medical disease should also get what
baseline electrolytes including serum creatinine
249
screening CXR for
intrathoracic procedure or s/s of active pulmonary disease
250
screening EKG for
females >50 males >40 CV disease, HTN, DM
251
surgery does what to the cardio patient
increase demand of O2 suppress fibrinolytic system myocardial ischemia secondary to CAD
252
cardiac medications in surgery patients
remain on beta blockers statins should be continued prophylaxis for respiratory or dental procedures
253
index of cardiac risk attributes
high risk surgery h/o ischemic heart disease h/o CHF h/o CV disease pre op treatment with insulin preop serum creatinine >2.0 mg/dL
254
cardiac risk index
class I - o factors class II - 1 factor class III - 2 factors class IV - more than 2 factors
255
surgical patient with mild/moderate HTN
adjust meds during the weeks before surgery acute control not advisable
256
surgical patient with poorly controlle HTN
postpone elective surgery until BP < 180/110 if can bring BP to 140/90 take meds morning of sx (except diuretics)
257
surgical patients with renal dysfunction
preop testing includes EKG, CXR with BUN, creatinine, electrolytes maintain renal perfusion and euvolemia d/c ACEi at leat 10 hours preop dont use opioids or NSAIDs
258
surgical patient with hepatic dysfunction
increased risk for bleeding often deficient in thiamine, folate, potassium, magnesium
259
surgical patient with diabetes
goal is to achieve euglycemia diet controlled - no dextrose or insulin oral agents - hold oral hypoglycemic the day of surgery, if well controlled and short surgery may not need insulin, if poorly controlled give variable rate IV insulin infusion, restart oral hypoglycemic when eating normally aim for glucose of 120-180
260
surgical patient in pregnancy
screen every woman of childbearing age delay until second trimester laproscopic sx in second trimester is safe appendicitis and biliary tract disease most common reasons for GI sx
ACOM
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