1
Q
syncope
A
loss of consciousness with loss of postural tone and spontaneous return to baseline neurologic function with no resuscitative efforts
2
Q
underlying mechanism of syncope
A
global hypoperfusion of both cerebral cortices or focal hypoperfusion of reticular activating system
3
Q
presyncope and true syncope are what
A
spectrum of same condition
4
Q
syncope can be manifestations of what
A
tachyarrhythmias
bradyarrhythmias
neurocardiogenic syncop
OR
unrelated to any arrhythmia
5
Q
treatment if diagnosis is certain
A
treat based on severity and frequency of episodes
6
Q
treatment if diagnosis uncertain
A
additional evaluation
7
Q
history suggestive of arrhythmic cause
A
palpitation and lack of neuro deficits preceding or following event
8
Q
event longer than 4-5 minutes raises concerns of what
A
seizure or other causes of mental status
9
Q
syncope with exertion can suggest what
A
arrhythmia or obstruction of cardiac flow
-eval with CXR, EKG, echo
10
Q
extra heart sounds (S3, S4) can suggest what
A
heart failure
11
Q
dyspnea or chest pain aggravated by exertion can alert physician to what
A
cardio-pulmonary issues
12
Q
carotid bruits can suggest what
A
aortic stenosis radiating to neck
13
Q
jugular venous distension can suggest what
A
heat failure
14
Q
atrial septal defect murmurs
A
systolic - increased flow through pulmonic valve so heard in pulmonic area
diastolic - left to right atrial shunt causing low pitched murmur at LLSB
15
Q
increases preload
A
bradycardia, hypervolemia, squatting, passive elevation of legs
16
Q
decreases preload
A
tachycardia, hypovolemia, standing up, valsalva, venodilating drugs
17
Q
increased afterload
A
hang grip, squatting, vasoconstrictor drugs, hypervolemia
18
Q
decreased afterload
A
hypovolemia, vasodilating drugs
19
Q
increasing preload does what
A
increase sound of murmur
EXCEPT mitral valve prolapse, hypertrophic obstructive cardiomyopathy
20
Q
increasing afterload does what
A
increases sound of murmur
EXCEPT mitral valve prolapse, hypertrophic obstructive cardiomyopathy, aortic stenosis
21
Q
right hear lesions do what in respiratory cycle
A
inspiration - increase
expiration - decrease
22
Q
left heart lesions do what in respiratory cycle
A
inspiration - decrease
expiration - increase
23
Q
patent ductus arteriosis murmur heard in what part of the cardiac cycle
A
it is continuous (systole and diastole)
24
Q
why do rectal exam with syncope
A
stool guaiac test can identify GI bleeding (can occur in syncope)
25
why do oral exam in syncope
lacerations to lateral tongue suggest seizure
26
common injuries with syncope
facial fractures, hip fractures, wrist fractures, subdural hematomas
27
cardiac syncope
arrhythmias, AV blocks, cardiac disease
increased risk of sudden death
sudden without warning or prodrome (chest pain/dyspnea)
28
patients with prodromes are more likely to have what
neurogenic syncope and typically at low risk
29
reflex syncope
neurocardiogenic (vasovagal)
carotid sinus syndrome
situational (cough, sneeze, swallow)
generally have prodrome
30
syncope while sitting or supine is suspicious for
arrhythmia
31
reflex syncope
autonomic response
significant bradycardia and/or hypotension
1. cardioinhibitory response - increased parasympathetic activation
2. vasodepressor - inhibited sympathetic pathway
3. mixed
often genetic predisposition
often have prodrome
32
orthostasis
decrease in systolic BP of 20, decrease in diastolic BP of 10 within 3 minutes of standing
heart rate increase on standing of 30+ beats per minute
33
seizure clues
prodrome (aura), abrupt onser associated with injury, tonic phase, head deviation, biting, loss of bladder or bowel control, postictal phase
34
medications that commonly cause syncope are what
CCB, BB, alpha blockers, nitrates, antiarrhythmics, diuretics, QT interval alteration (antipsychotics and antiemetics)
35
transcutaneous pacing
electrical pasing of heart through skin
in symptomatic bradycardia (sinus bradycardia, higher degree heart blocks)
anterior pad (-) in apical area
posterior pad (+) placed in mid upper back area
36
first degree heart block
one P to each QRS
prolonged PR intercal
37
second degree heart block
type 1 - PR interval progressively lengthens, 1 nonconducted beat
type 2 - constant PR interval in conducted beats but have dropped beats
38
third degree heart block
PP and RR constant
no relation between P and QRS
39
brugada syndrome
autosomal dominant
resemble RBBB, ST elevations in V1-3
structurally normal hearts but mutation in voltage gated sodium channels
vantricular arrhythmias but more commonly atrial fibrillation
40
rule out hypoglycemia in who
all patients with altered mental status
41
get electrolytes in who
critically ill, patients with suspected electrolyte abnormalities from volume loss or diuretic use
42
hematocrit for what
active bleeding or suspected anemia
43
pregnancy test on who
any female of child bearing age
44
carotid sinus syndrome
dizziness, presyncope, or syncope precipitated by any maneuver which causes mechanical stimulation of carotid sinus
tx - permanent pacemaker
45
sinus node dysfunction
abnormalities of SN impulse formation causing inappropriate atrial rates
sick sinus syndrome
symptomatic - pacemaker
asymptomatic - no therapy
46
ambulatory monitoring
for sporadic intermittent symptoms
47
holter monitors
continuous record of EKG for 12-24 hours
48
event monitors (loop recorders)
record intermittent episodes during long periors
only during specific events (patient activated or event triggered)
49
implantable loop recorders
small devices w integrated leads implanted in small subcutaneous pocket
useful with infrequent episodes, elderly, or cannot otherwise wear event recorder
50
tilt table testing
confirm neurogenic syncope
positive = sudden and precipitous fall in BP and HR w concurrent reproducibility of symptoms
51
exercise testing
assess arrhythmias especially if symptoms exercise related
52
how is antiplatelet therapy for ACS given
orally
53
antiplatelet drug options
cyclooxygenase inhibitors: aspirin
phosphodiesterase inhibitors: dipyridamole and cilostazol
GP IIa/IIIb inhibitors: eptifibatide and tirofiban
P2Y12 receptor inhibitors: clopidogrel, prasugrel, ticagrelor, and cangrelor
PAR1 receptor inhibitor: vorapaxar
54
what do antiplatelet drugs target
arterial thrombi
55
cyclooxygenase inhibitors
aspirin
irreversibly bind COX 1 which inhibits synthesis of thromboxane 2A which inhibits platelet aggregation
can cause GI, tinnitis, hypersensitivity
56
phosphodiesterase inhibitors
dipyridamole
cilostazol
57
GP IIa/IIIb inhibitors
block receptor on platelet surface which inhibits fibrinogen binding which decreases platelet aggregation
not typically used unless large thrombus or as bailout
not recommended w fibrinolytic
cant use with stroke, renally adjusted, causes dyspnea
58
P2Y12 receptor inhibitors
prevent activating GP IIa/IIIb which prevents platelet aggregation
CYP metabolism
clopidogrel - TTP and hypersensitivity side effects
prasugrel - contraindicated with stroke/TIA, higher bleeding risk
ticagrelor - bleeding risk, dyspnea
cangrelor - if unable to be treated with oral P2Y12 inhibitor before PCI
59
anticoagulant route for ACS
usually parenteral
60
what do anticoagulant drugs target
arterial and venous thrombi
61
anticoagulant drug options
inhibit clotting factors: heparin, enoxaparin, deltaparin. fondaparinux
inhibit clotting factor synthesis: warfarin
direct thrombin inhibitors: bivalrudin, argatroban
62
inhibition of clotting factors
heparin - inhibit thrombin, factor Xa, IXa, XIa, XII a (causes thrombocytopenia and HIT)
LMWH's = more selective for Xa
enoxaparin, deltaparin, fondaparinux (most specific and doesnt cause HIT but not used for primary PCI)
63
direct thrombin inhibitors
bivalrudin - bind thrombin in clots and prevent activity
argatroban - not routinely used in STEMI but is used in NSTEMI with history of HIT
64
fibrinolytic therapy target
arterial and venous thrombi, clot dissolution
activate plasmin to degrade fibrin
65
fibrinolytic drugs
alteplase - good specificity
reteplase - longer half life, less specific
tenecteplase - long half life and greater binding affinity
contraindicated: stroke in past 3 months, uncontrolled HTN, cerebral vascular lesion
66
STEMI treatment
first line - primary PCI in 90 minutes
alternate - fibrinolytic in 30 minutes
adjunct therapy for both: (dual antiplatelet) + anticoagulant
67
primary PCI adjunct options
(aspirin + P2Y12) + (UFH or bivalrudin)
aspirin - loading dose 162-325 mg, long term 75-100 mg
P2Y12 - loading dose as early as possible, maintenance for 1 year, no prasugrel with a history of stroke then you will use ticagrelor
anticoagulant - heparin unless HIT then bivalrudin
68
P2Y12 choice
PCI - prasugrel or ticagrelor
CABG - ticagrelor or clopidogrel
no invasive evaluation - ticagrelor
fibrinolytic - clopidogrel
69
fibrinolytic adjuncts
(aspirin + clopidogrel) + (UFH or enoxaparin or fondaparinux)
70
dual antiplatelet therapy duration
12 months unless bleeding risk
71
anticoagulation duration
uncomplicated and no indication - stop after PCI
with indication - continue until can start DOAC/warfarin
72
NSTEMI and unstable angina treatment
(aspirin + P2Y12) + (UFH or biovalrudin or enoxaparin or fondaparinux)
antiplatelet - ticagrelor or pasugrel for invasive, ticagrelor for noninvasive
anticoagulation - UFH for invasive, other for noninvasive
73
diuretics for HTN
thiazides - first line with normal renal function, decrease PVR
furosemide - in malignant HTN and CKD
spironolactone - in hyperaldosteronism
74
Sympatho Drugs in HTN
clonidine - central acting antiadrenergic, presynaptic activation of alpha 2, decrease HR/venous tone/PVR, CNS effects in elderly and rebound HTN if stopped
methyldopa - transformed into alpha 2 receptor agonist, same effects as above
prazosin - alpha blocker, decrease venous tone/PVR, can cause pastural hypotension
propranolol/esmolol - decrease HR/CO, avoid in restrictive airway disease or HR <60 unless IHD or HF
labetalol - beta and alpha blocker, decrease HR/CO/venous tone/PVR
75
vasodilators for HTN
hydralazine - arterioles
nitroprusside - arterioles and veins, produce NO, hypotension/rebound HTN/increased intracranial pressure
minoxidil - arterioles, K channel opening, increase renal flow
amlodipine and nifedipine - DHP CCB, increase HR/CO, decrease PVR
verapamil and diltiazem - non DHP CCB, decrease PVR
fenoldapam - arterioles, D1 receptor activation, renal vasodilation
76
RAAS inhibitor in HTN
aliskiren - decrease plasma renin activity
captopril/enalapril/enaprilat - ACEi, decrease venous tone/PVR
losartan - ARB - similar to ACEi
77
hypertensive crisis
BP >180/120
severe HTN or
hypertensive emergency (has end organ damage)
78
elevated BP
120-129/<80
79
stage 1 hypertension
130-139/80-89
80
stage 2 hypertension
>140/>90
81
what should the BP goal be`
<130/80
82
treatment for stage 2 HTN
2 drugs in 1 pill and reassess in 1 month
83
stage 1 HTN treatment
10 year risk <7.5% = lifestyle changes and reassess in 3-6 months
10 year risk >7.5% = 1 drug and reassess in 1 month
84
elevated BP treatment
lifestyle changes and reassess in 3-6 months
85
treatment for hypertensive emergencies
nitroprusside
nitroglycerine
labetalol
esmolol
fenoldopam
nicardipine
enalaprilat
86
management of resistant HTN
3 drug regimen (RAS blocker, CCB, diuretic)
then
substitute thiazide diuretic for another at optimal dose
then
add MRA
then
add BB (as long as not bradycardic)
then
add hydralazine
then
substitute hydralazine for minoxidil
87
potential culprits for essential hypertension
blood vessel
CNS
pressure/volume receptors
adrenals
kidneys
88
what happens to CO as we age
it decreases (possibly due to LVH)
89
what happens to TPR as we age
it increases (due to medial hypertrophy)
90
fixed risk factors for HTN
CKD, family history, age, low socioeconomic status, male, obstructive sleep apnea, psychosocial stress
90
modifiable risk factors for HTN
smoking, DM, dyslipidemia/hypercholesterolemia, obesity, inactivity, diet
91
primary or essential hypertension
gradual increase in BP with slow rate of rise
often due to lifestyle factors or family history
92
secondary hypertension
related to underlying pathologic process, drugs, interactions, or withdrawal
93
white coat hypertension
elevated office BP but normal out of office
94
masked hypertension
normal office readings but elevated out of office
95
sustained hypertension
elevated in and out of office
96
out of office BP monitoring
ambulatory - best
home - more practical
97
basic labs for HTN pt
fasting blood glucose
CBC
lipids
serum creatinine with eGFR
serum sodium, potassium, calciu,
TSH
urinalysis
EKG
98
consequences of HTN
heart failure
myocardial ischemia and infarction
aortic aneurysm and dissection
stroke
nephrosclerosis and renal failure
99
primary agents in treatment of HTN
thiazide diuretics, ACEi, ARBs, ARNIs
100
factors that can affect the accuracy of blood pressure readings
device used
technique or bias of examiner
noisy environment
101
symptoms associated with hypertension
weakness/lethargy
lightheadedness
dizziness
syncope
palpitations
pulsus paradoxus
102
physical exam for hypotension
visualize patient
auscultate chest
check pulses and confirm low blood pressure
if unstable lower head of bed, place on monitor, evaluate for shockable rhyth, or bradyarrhythmia which might require atropine or pacing
103
causes of hypotension
reduced cardiac output
hypovolemia
blood volume redistribution
reduced systemic vascular resistance
vascular obstruction
104
orthostatic hypotension
reduction of 20 in systolic BP or 10 in diastolic BP
105
non pharm treatment of orthostatic hypotension
increase salt and water intake
arising slowly
sleep with head of bed raised
engage in seated or recumbant exercised
avoid straining/valsalva
limit exposure to hot humid environments
use compression garments
106
first line meds for orthostatic hypotension
midodrine and fludrocortisone
107
chest pain in children and adolescents is usually what
benign and self limited
108
key warning signs for serious causes of chest pain are
chest pain associated with fever, syncope, family history
109
myocarditis
viral febrile illness with pericarditis
SOB, non specific chest pain, malaise
possible S3 gallop
CXR possibel cardiomegaly, possible ST depression and nonspecific t wave changes
110
pericarditis
viral febrile illness
acute sharp chest pain lessened by sitting up and leaning forwards
friction rub, may progress to tamponade
diffuse ST elevation/PR depression, may have electrical alternans
111
aortic and subaortic stenosis
chest pain during exercise associated with significant murmur
harsh systolic murmur radiating to carotids with possible palpable thrill
may have LVH
112
hypertrophic cardiomyopathy
inhereted autosomal dominant disorder
systolic murmur increased wtih valsalva
113
coronary artery anomalies
mutliple possible with anomalous origin of left coronary from pulmonary artery
chest pain from ischemia
kawasaki disease - coronary aneurysms complication can cause MI
114
arrhythmia
palpitation can be perceived as pain in children
chest pain with dizziness or syncope may indicate something more serious
ECG to assess
refer patients with prolonged QTc syndrome
115
supraventricular arrhythmias
most frequent pathalogic arrhythmias
PAC's and SVT
116
ventricular arrhythmia
medical emergency
wide QRS complec
117
mitral valve prolapse
usually asymptomatic
mid to late systolic click and possible systolic murmur
usually doesnt require endocarditis prophylaxis
118
aortic root dissection
unrelenting chest pain radiating to back
children with Marfan syndrom and other connective tissue diseases
119
postpericardiotomy syndrome
1-12 weeks post open heart surgery
chest pain, fever, pericardial and pleural effusions
tachycardia and pericardial friction rub
often self limited with symtpomatic treatment
120
pain worsens with deep breathing
pleuritic
121
sharp sudden pain relieved by deep breath
pleural cathc
122
localized pain reproducable with movement or palpation
musculoskeletal/costochondritis
123
diffuse, pre or post prandial, deep or burning pain
GI
124
myoglobin
elevated in 30 min to 4 hours
peak 6-12 hours
normal in 24-36 hours
125
CK-MB
elevated in 2-4 hours
peak at 24
back to normal in 72 hours
126
troponin
elevated in 2-4 hours
peak 24-36 hours
normal in 7-10 days
127
lactate dehydrogenase
elevated by 24 hours
peak 3-6 days
normal in 8-14 days
128
reperfusion therapy
primary PCI 9percutaneous coronary intervention)
fibrinolytic if PCI not available
no fibrinolytic in UA or NSTEMI
129
TIMI scores
0-2 low risk
3-4 medium risk
5-7 high risk
130
when to use early invasive strategies for UA or NSTEMI
TIMI score of 3 or more
angiography within 48 hours (within 12 hours if score is 5 or more)
131
HEART score
do not use if new ST segment elevation requiring immediate intervention or clinically unstable
<4 low risk = discharge
4-6 moderate risk = medical optimization and further workup
>6 high risk = early invasive testing
automatically consider elevated troponin high risk
132
use of beta blockers in STEMI/NSTEMI/UA
typically considered appropriate
avoid if cocaine induced ACS. second or third degree AV block, HR < 50
133
use of nitrates
useful in ACS, especially with heart failure or sever hypertension
avoid in suspected RV infarct, SBP < 90 or > 30 below baseline, recent use of 5' phosphodiesterase inhibitors
134
use of non DHP CCB
no mortality benefit for patients with ACS
reserved for those with persistent ischemia despite use of BB and nitrates or with BB contraindications
135
use of ACEi
reduce incidence of heart failure, recurrent ischemic events, and mortality following MI
especially favorable in higher risk patients (anterior infarcts and LV systolic dysfunction)
136
use of statins
reduce mortality rates of patients with CAD
137
use of MRA's (spironolactone and epleronone)
decrease mortality following MI in patients with left ventricular dysfunction
left ventrical ejection fraction less than 40% and symptoms of heart failure
138
how to limit ventricular remodeling
reperfusion therapies
drugs that interfere with the renin angiotensin system
139
tricuspid stenosis
diastolic
140
tricuspid insufficiency
systolic
141
pulmonary stenosis
systolic
142
pulmonary insufficiency
early diastolic
143
mitral stenosis
diastolic
144
mitral insufficiency
systolic
145
aortic stenossi
systolic
146
aortic insufficiency
early diastolic
147
black patients
more presenting with angina
fewer treated urgently
similar for hispanics and those with medicaid/uninsured
148
south asian
often missed diagnosis or delayed diagnosis
149
women
moderate to severe ischemia more symptomatic than men
less likely to have timely appropriate care
more likely to experience prodromal symptoms
often have accompanying symptoms
150
older patients
more likely to have comorbidities
require more extensive work up
151
cardiovascular collapse
sudden loss of effective circulation due to cardiac and/or peripheral vascular factors that may reverse spontaneously
includes cardiac arrest and transient events like syncope
152
cardiac arrest
abrupt cessation of cardiac function resulting in loss of effective circulation that may be reversible by prompt intervention
rare spontaneous reversion
Vfib, vtach, asystole, bradycardia, pulseless electrical activity, noncardiac mechanical factors
153
sudden cardiac death
sudden unexpected death attributed to cardiac arrest which occurs within 1 hour of symptom onset
same causes as cardiac arrest
154
what is the amin cause of sudden cardiac death
coronary heart disease
then cardiomyopathies
then valvular disease
then inherited arrhythmias
then idiopathic
155
death certification
all physicians in patient care must participate per statutes and expectations
expected role of attending physician to certify cause of death
some cases it is mandated (determine cause of death)
156
who can certify cause of death for non natural deaths
medical examiners
157
cause of death
sequence of events that directly led to death
sequence of events is listed
158
manner of death
homicide, accident, suicide, undetermined
physicians can typically only list natural causes
159
causes of acyanotic defects
shunt lesions - atrial septal defects, ventricular septal defects, patent ductus arteriosus
obstructive lesions - coarctation of the aorta, aortic stenosis, pulmonary stenosis
160
define acyanotic
no central cyanosis
O2 > 95%
shunt lesions (ASD, VSD, PDA)
obstructive lesions (CoA, AS, PS)
volume or pressure overload
long term = eisenmenger syndrome
161
eisenmenger syndrome
long term pulmonary hypertension causes right to left shunt instead of left to right
162
atrial septal defect
normally ostium secundum
flow from LA to RA
increased size of RA and RV and increased pulmonary blood flow
PE - increased RV impulse, systolic ejection murmur (pulmonary area), fixed split S2
tx - cardiac catheterization with atrial septal occlusion device, open heart surgery, risk atrial arrhythmias after repair
163
ventricular septal defect
25 - 30% CHD
types - inlet, trabecular (muscular), membranous, outlet
presentation - depends on size and degree of pulmonary HTN, small = little shunt and may close spontaneously, medium = CHF symptoms, large = CHF less turbulent
PE - harsh holosystolic murmur, large has left or biventricular hypertrophy
tx - large = early surgical closure (3-6 months)
164
patent ductus arteriosus
connects pulmonary artery to aorta (usually closes 24-48 hours after birth)
in PDA blood flows from aorta to pulmonary artery increasing pulmonary flow
small = no symps, large = CHF symptoms
PE - constant machine like murmur at upper left sternal border, if L to R shunt is large may have diastolic rumble from mitral valve at apex and bounding pulses
tx - asymptomatic = observed until transcatheter closure, symptomatic = digoxin and furosemide
165
coarctation of aorta
narrowing of aortic arch just inferior to left subclavian artery
severe may depend on R to L PDA to perfuse descending aorta
initially asymptomatic but as PDA closes symptoms of CHF develop
PE - HTN noted in right arm and reduced BP in extremities, bruit may be audible at left upper back, bicuspif aortic valve or aortic stenosis 50% of patients
3's sign and rib notching
tx - IV prostoglandin E, ionotropic meds, low dose dopamine, sx for newborns or infants, ballon angioplasty with or without stent for school age
166
aortic stenosis
more females, most common abnormality is bicuspid aortic valve
15-20% have PDA, coarctation of aorta, VSD
diagnosed on fetal echo, severe diagnosed by 2 months bc onset CHF
mild = no symps, severe = fatigue/chest pain/syncope, severe = heart failure
PE - systolic ejection murmur at right 2nd intercostal often with click (radiates to neck), thrill RU sternal border
increased risk sudden death
degree often progresses with growth and age
tx - balloon vulvoplasty and surgical management
167
pulmonary stenosis
leaflets can be partially fused
area above or below valve can be narrowed
severe often seen on antenatal ultrasound and has cyanosis due to R to L shunting through foramen ovale
increased RV pressure and decreased RV output
PE - can have S2 splitting, systolic ejection murmur at left 2nd intercostal, thrill may be palpable at 2-3 intercostal
tx - balloon dilation, valvotomy, valvectomy, patch enlargement
168
long term tx
lifelong cardio follow up
endocarditis prophylaxis
exercise restrictions
pregnancy counseling
late complications - arrhythmias, valve dysfunction, myocardial dysfunction
169
primary hear field is established when and from what
day 18
splanchnic lateral plate mesoderm
170
what is the primary hear field induced by
pharyngeal endoderm
171
what is the secondary heart field specified by
splanchnic mesoderm
172
cardiogenic progenitors of the primary heart fiels coalesce into what
endocardial tube
173
what surrounds the endocardial tube
splanchnic mesoderm myocardial cells secreting cardiac jelly
174
how is the heart tube connected to the dorsal pericardium
dorsal mesocardium
175
what brings the heart into the thoracic region
craniocaudal folding
176
regions of the heart tube
aortic sac = connection to aortic arch
truncus arteriosus = ascending aorta and pulmonary trunk
conus arteriosus/conus cordis = infundibulum/aortic vestibule
primitive ventricle = r/l ventricles
primitive atrium = r/l atriua
sinus venosum = coronary sinus and sinus venarum
veins = vena cava
177
actopia cordis
failure of sternum to fuse producing heart outside thoracic cavity
178
what influences the twisting of the heart tube
laterality of the secondary heart field
179
what forms the septum transversum
portions of the mesoderm
becomes part of diaphragm
separates thoracic and abdominal cavities
180
dectrocardia
reverse roatation
no problem = situs inversus totalis
big problem = situs inversus ambiguous (only some organs reversed)
181
endocardial cushions
epithelial to mesenchymal transition
conotruncal - separates aortic sac and primitive ventricle (neural crest cells)
dorsal/ventral - separate primitive atria and ventricle (AV septum)
182
formation of AV valves
mesenchymal tissue comes toward each other
muscular cords attached to muscle wall and cavitation occurs
AV valves are present (mesenchyme) with chordae tendinae (muscular cords) and papillary muscles (muscular wall)
183
atrial septation
septum primum forms (containing foramen primum and foramen secundum)
septum secundum forms over septum primum (cover the foramina in septum primum but has its own foramen ovale)
184
ventricular septation
muscular ventricular septum present
conotruncal ridges form bulbar ridges
proximal part forms outflow tract septation
distal part forms membranous ventricular septum
185
semilunar valve development
conotruncal ridges split pulmonic and aortic trunk
ventral valve swelling forms remaining pulmonic valve
dorsal valve swelling forms remaining aortic valve
186
atrial septal defects
interatrial wall
mixing of blood between L and R atria
minor includes probe patent foramen ovale
more severe allows L to R shunting or R to L shunting
common = too large foramen secundum or foramen ovale
rare = endocardial cushion defect, sinus venosus ASD defect, common atrium
187
ventricular septal defect
most common congenital heart defect
membranous VSD = failoure of fusion of interventricular septum with endocardial cushion
small defects = L to R shunt
188
truncus defects
failure of spiral septum of truncus arteriosus
affects ascending aorta, pulmonary trunk, semilunar valves
persistent trunkus arteriosus - failure of septation, no aortic or pulmonic valves, automatic VSD
189
transposition of great vessels
R ventricle pumps to aorta, L ventricle pumps to pulmonary trunk
patent ductus arteriosus, VSD, ASD contribute to mixing of blood
190
tetralogy of fallot
pulmonary stenosis bc unequal division of conus cordis
then
overriding aorta (aorta collects blood from both ventricles)
then
VSD
then
hypertrophy of R ventricle
may have ASD or PDA
boot shaped heart
191
venous flow
anterior cardinal veins = jugular veins
thymic and thyroid veins = brachiocephalic veins
sinus venosus = coronary sinus
vitelline veins = inferior vena cava (R), hepatic sinusoids (L)
posterior cardinal veins = connect azygos
192
subcardinal veins do what
drain medial tissues
connect R vitelline vein to urogenital system
193
supracardinal veins do what
drain body wall
form inferior segment of IVC and azygos system
194
vena cava defects
double inferior vena cava (persistent L supracardinal veins)
absent inferior vena cava
double superior vena cava
195
pharyngeal arch 3
internal carotid artery
196
aortic sac
ascending aorta and R brachiocephalic a
197
pharyngeal arch 6
ductus arteriosus and pulmonary trunk
198
double aortic arch
usually lose R side of aortic arch
here it stays present making the left aortic arch small and cross in front of trachea dn esophagus
199
right aortic arch
left aortic arch disappears instead of the right
200
retroesophageal right subclavian artery
abnormal involution superiorly and persistent inferior portion of right aorta
201
interrupted aortic arch
left side of aortic arch regresses and instead the PDA forms the descending aorta vessels
202
coarctation of aorta
narrowing of aortic lumen
ductus arteriosus can act to supply low oxygen blood to lower extremities
heart failure and shock of PDA closes
adult = postductal
BP in upper extremities increased and lower extremities in minimal
203
changes in circulation at birth
decreased R atrial pressure
more blood flowing in pulmonary circuit
increase return of blood flow to L ventricle
all these cause foramen ovale to close
oxygen tension and other factors cause ductus arteriosus and venosus to contract
204
shock
diminished cardiac output or reduced effective circulating blood volume causing cellular hypoxia
205
hypotension and shock
not synonymous
can have hypotension and normal perfusion or shock without hypotension
206
signs of shock
hypotension
altered mental state
cold, moist skin
weak or rapid pulse
rapid breathing
decreased urine output
207
types of shock
hypovolemic
cardiogenic
distributive
obstructive
208
hypovolemic shock
decreased preload (decreased CVP), decreased CO, increased SVR
can be due to hemorrhage or fluid loss
tx - fluids, O2, uterotonic agents/pack uterus, sx
209
cardiogenic shock
pump failure or decreased SV/CO
can be due to MI, arrhythmia, aortic stenosis, mitral regurgitation, myocarditis
tx - vasopressor/inotropic support/revascularization
210
distributive shock
decreased systemic vascular resistance
septic - infection, increased vascular permeability, may have low oxygen or high oxygen (first hyperdynamic/warm w high CO/low PVR then hypodynamic/cold w low CO/poor perfusion), use fluids and vasopressors
anaphylactic - type 1 hypersensitivity, increased vascular permeability, oxygen may be low or high, give epi
neurogenic - brain injury, spinal cord injury, bradycardia, give fluids/atropine
211
obstructive shock
decreased SV/CO
decreased output due to obstruction (impaired filling or RV output)
can be due to pulmonary embolism, cardiac tamponade, constrictive pericarditis, pulmonary HTN, tension pneumothorax
212
shock is what in many diseases
final preterminal event
213
organ dysfunction due to shock
tissue hypoxia causes loss of membrane integrity, catabolic state, loss of ion pumps/chemical and electrical gradients
mitochondrial energy production falls
localized cellular death and organism death
214
compensated shock
body works to maintain cardiac output and BP
tachycardia, rapid shallow breathing, renin release, vasopressin, epinephrine, reduced capillary hydrostatic pressure, increased glycogenolysis
215
progressive uncompensated shock
tissue perfusion inadequate due to vasoconstriction
anaerobic metabolism causes metabolic acidosis
BP drops
216
irreversible shock
organs completely fail
death
217
coat hanger headache can indicate what
POTS
218
tx for HTn with CKD and albuminuria
ACEI/ARB
often need 2nd agent like thiazide diuretic
219
tx for HTN w CKD and no albuminuria
thiazide diuretic or ACEI/ARB/CCB
likely will need 2nd agent
220
treatment for RV infarct/ischemia
IV saline
avoid nitrates/diuretics
maintain AV synchrony
cardioversion for hemodynamically significant SVT
inotropic support (dobutamine)
221
complications of MI
sudden death
contractile dysfunction
arrhythmias
myocardial rupture
postinfarction pericarditis
mural thrombus, thromboelbolism
ventricular aneurysm
222
post infarction ischemia
common following MI
percutaneous intervention decreases
myocardium at risk for infarction
tx - catheterization and revascularization
223
arrhythmias
common in post infarct period
electrolyte imbalances, ischemic myocardium, autonomic nervous system imbalances
vfib most common cause of sudden death (defibrillation tx and amiodorone)
occasional PVCs in almost 100% of acute MIs
supraventricular - normally sinus tach (BB/CCB tx)
sinus brady - electrical cardiac pacing
224
acute MI induced shock
coronary artery reperfusion
225
myocardial rupture
typically within 14 days
ventricular free wall (fatal due to pericardial tamponade)
ventricular septal rupture (L to R shunt)
papillary muscle rupoture (severe mitral regurg)
may have pericardial friction rub (fibrinous pericarditis/dressler syndrome)
226
thromboembolism
5-10% all acute STEMI's
can be fatal
arterial emboli originating in left atrial appendage or left ventricle, may cause stroke
venous emboli from leg or pelvis
227
left ventricular aneurysm
months to weeks after infarct
decrease force of contraction
mural thrombus may occur
tx - afterload reduction, ACEI, antiischemic meds, anticoagulant
true - scar tissue
pseudo - LV rupture that is clotted off or plugged w thrombus (very susceptible to rupture and cardiac tamponade)
228
coronary steal
narrowed coronary arteries are dilated already
when vasodilating drug given the other arteries dilate but the narrowed arteries cannot
the normal arteries steal blood from the narrowed arteries causing ischemia
229
commotio cordis
ventricular fibrillation precipitated by blunt trauma to the heart
230
carb/protein cal/g
4
231
fat cal/g
9
232
alc cal/g
7
233
lose 1-1.5 lbs in a week by doing what
reduce daily calorie intake by 500-750 calories
234
consume fewer than how many calories from added sugars
10%
235
consume fewer than how many calories from saturated fats
10%
236
consume less than how much sodium
2,300 mg or 2.3 g
237
upper body obesity
males - waist circumference >40 in and waist hip ratio over 0.9
women - waist circumference >35 in and wasit hip ratio over 0.85
both BMI over 30
238
seafood provides what that is good for us
EPA and DHA which reduced cardiac deaths
239
essential fatty acids include what
omega 3 and omega 6
240
why was there a low reporting for essential fatty acid deficiency before the 1980s
assays had lack of sensitivity
241
what happens before the clinical signs of EFAD
biochemical abnormalities
242
low fat diets
deplete body of polyunsaturated fatty acids
lower HDL
increase TGs
tx = dysglycemia diet, flaxseed oil, primrose oil, chromium picolinate, multivitamin, antioxidant, EPA/DHA capsules
243
therapeutic effects of EFAs
modulate inflammatory conditions
improve insulin resistance
improve lipids
reduce CAD
reduce arrhythmias
reduce cancer
reduce depression/ADHD
244
EFAD and trans FAs contribute to CAD how
reduce cell membrane fluidity
diminish insulin binding and action
increase platelet aggregation and increase proinflammatory eicosanoids
reduce arrhythmia threshold
245
mediterranean diet
plenty of exercise
plant based: fruits, vegetables, whole grains, legumes, nuts
healthy fats - olive oil and canola oil
herbs and spices instead of salt
limit red meat
eat fish and poultry at least twice a week
246
effects of omega3
decrease platelet aggregation
reduce inflammation
suppress cytokine formation
decrease TGs
decrease arrhythmias
decrease BPO
decrease whole blood viscosity
247
primary cardiac tumors
rare
248
most common type of cardiac tumor
metastases
249
myxoma
most common primary tumor in adults
benign neoplasm, often gelatinous
produce IL6 and VEGF
90% in atria (L)
fossa ovalis is favored site
constitutional symtpoms, may mimic infective endocarditis
may cause AV valve obstruction, danger of embolization
diagnose w CT/MRI
sx curative
scattered spindle and satellite cells
250
rhabdomyoma
most common cardiac tumor in children
sporadic or associated with tuberous sclerosis
most often in ventricle protruding into ventricular chamber (potential flow abnormalities causing heart murmurs or heart failure)
gray white myocardial mass
large polygonal cells with abundant vacuoles with glycogen separated by pink cytoplasm
251
angiosarcoma
most common primary malignant tumor
right atrium
cardiac enlargement or abnormal cardiac contour
MRI best
bulky infiltrating mass with variable pink red coloration and areas of hemmorhage and necrosis
usually poorly differentiated anastamosing vascular channels forming dilated sinusoids lined by atypical cells
252
carney complex
autosomal dominant (chromosomes 2 and 17)
associated with pituitary tumors and testicular/ovarian tumors
NAME = nevi, cutaneous and atrial myxomas, ephelides
LAMB = lentinges, cutaneous and atrial myxomas, blue nevi
253
papillary fibroelastoma
surface of cariac valves (aortic) or atrial/ventricular surface
some thrombi and not true neoplasm
can embolize
multiple papillary fronds attached to endocardium by short pedicle
myxoid connective tissue with mucopolysaccharide matrix and elastic fibers
254
cardiac fibroma
second most common cardiac tumor of childhood
ventricles, IV septum, and right atrium
fibrous, white, whorled, well circumcized tumor clearly demarcated from surrounding myocardium
sclerotic collaged w sparse bland nuclei, peripheral parts intermingles w myocardium
255
hemangioma
benign vascular neoplasm
red blue soft spongy mass typically demarcated by sharp border
proliferation of benign endothelial cells that form channel containing blood
256
lipoma
usually on epicardium
circumsized mass of homogenous yellow fat
usually encapsulated, mature adipose tissue and maybe entrapped myocytes
257
lipomatous hypertrophy
atrial septum
usually > 60
proliferation of fat cells
circumsized mass of homogenous yellow fat
enlarged cardiac myocytes with nuclei exhibiting variation in shape and size
right atrial obstruction, intractable supraventricular arrhythmias, sudden cardiac death
258
metastatic tumors
commonly lung, breast, lymphoma
259
risk factors for congenital heart defects
prematurity
family history
genetic syndromes
maternal factors (DM, HTN, phenylketonuria, thyroid disease, epilepsy, fertility treatment, utero infection)
260
4 presentations of congenital heart disease
asymptomatic murmur
cyanosis
gradual progressing symtpoms of heart failure
catastophic heart failure and shock
261
nursery screening
pulse ox in r hand and 1 foot
>95% and difference <3% routine care
if between 90-95% or difference >3% retest in 1 hr
if better after 1 hour routine care
if <90% or next test no better proceed with immediate clinical assessment
262
5 T's
1. truncus arteriosus (1 trunk)
2. transposition of great vessels (2 vessels leaving the heart transposed)
3. tricuspid atresia (tri = 3)
4. tetralogy of fallot (tetra = 4)
5. total anomalous pulmonary venous return (5 words)
263
only what condition presents with severe cyanosis in the first few hours after birth
transposition of great vessels
264
truncus arteriosus
failure of septation of truncus aroud week 3-5 of gestation
one large vessel over large VSD
right to left shunt
valve leaflets can be 2-6 and thickened
most present in first few days w cyanosis or low O2
tx - surgical correction
265
transposition of great vessels
maternal diabetes risk factor, older maternal age, maternal alcohol consumption, fam history
cyanosis at birth
PGE1 required to maintain DA
emergent balloon atrial septostomy to enlarge PFO and improve mixing
egg on a string in CXR
266
tricuspid atresia
down syndrome, pregnancy rubella infection, too much alcohol during pregnancy, meds during pregnancy
complete absence of tricuspid valve
RV hypoplastic or absent, deoxygenated blood returning to LA shunted to LA
tire easily with feeding
PGE1 to maintin DA, sx (modified blalock thomas in days after birth, glenn procedure at 2-6 months, fontane procedure at 2-3 years)
267
tetralogy of fallot
large vsd
right ventricular outflow tract obstruction
overriding aorta
right ventricular hypertrophy
age of presentation depends on degree of right ventricular obstruction
tet spells - hyperpnea, increased cyanosis, gasping, syncope possible
boot shaped heart
268
total anomalous pulmonary venous return
pulmonary veins completely or partially drain into systemic circulation
no pulmonary venous connection to LA
right to left shunt present
snowman appearance on CXR
severe = severe cyanosis and surgical emergency
mild = heart failure as pulmonary vascular resistance falls postnatally
269
other CHD's that present with cyanosis
hypoplastic left heart syndrome
other forms of single ventricle
pulmonary atresia
ebstein anomaly of tricuspid valve
270
hypoplastic left heart syndrome
underdevelopment of left sided cardiac structures (mitral valve, aortic valve, ascending aorta)
dependent on PDA and interatrial flow
PGE1 infusion, respiratory support, inotropic meds
sx - norwood then glen shunt (2-6 months), then modified fontan (2-5 years)
271
ebstein anomaly
inferior displacement of tricuspid valve giving large atria and small ventricle
associated with lithium use in pregnancy
RA enlarges due to tricuspid regurg
increased RA blood volume shunts R to L
marked cardiomegaly on CXR
tx - TV repair, TV replacement, closure of ASD, transplantation
ACOM
flashcards
Decks in class (23)
# Cards
-
Exam Block 2158
-
Molecular Medicine Block 3359
-
anatomy block 3105
-
anatomy block 4215
-
molecular medicine block 4174
-
Anatomy Block 5222
-
Molecular Medicine Exam Block 5299
-
Neuro Block 1123
-
Neuro Block 2102
-
Neuro Block 3198
-
MSK Exam 1206
-
MSK Exam 2344
-
Heme Lymph Exam 1324
-
Heme Lymph Exam 2491
-
Derm Exam 1295
-
Derm Exam 2140
-
Cardio Block 1307
-
Cardio Block 2261
-
cardio block 3272
-
Respiratory Exam 1299
-
Respiratory Exam 2208
-
Respiratory Exam 3190
-
Renal Exam 1216
