Week 1 Flashcards
(244 cards)
1
Q
ductus venosus
A
shunts oxygenated blood from umbilical vein past the liver and to the IVC/R atrium
2
Q
foramen ovale
A
blood from RA via IVC passes through this foramen to bypass the lungs and go straight to the LA
3
Q
ductus arteriosus
A
blood from SVC enters RA, RV, out through PA but manages to bypass the lungs via this channel into the aorta distal to the L subclavian artery
4
Q
2 important characteristics of the intrauterine circulation
A
increased PVR and decreased RV diastolic compliance (hypertrophy from elevated PAP)
5
Q
circulatory changes at birth
A
decrease in PVR (with lung inflation), increased venous return from lungs (opposes FO flow), closure of DA (increased O2 & PGE2), RV atrophies
6
Q
CO
A
HR x SV–volume of blood pumped per unit time
7
Q
cardiac index
A
CO/BSA–CO normalized to body SA
8
Q
Heart rate
A
number of cardiac cycles per minute
9
Q
stroke volume
A
volume of blood ejected during each beat by the heart (N=100ml/beat)
10
Q
systemic arterial pressure
A
the pressure in the arterial system. recorded as the highest pressure during systole and the lowest pressure during diastole (N=120/80)
11
Q
vascular resistance
A
the resistance to flow through a vascular system.
12
Q
LVEF
A
the percent of the blood volume in the LV at end diastole that is ejected during systole. A crude measure of LV contractile performance. N=55-70%
13
Q
LVEF equation
A
SV/EDV
14
Q
compliance
A
change in volume over change in pressure. low=rigid, high=distensible (require less pressure to increase in volume)
15
Q
Bernoulli Equation
A
P=v^2
pressure at obstruction<pressure downstream, but greater velocity
16
Q
LaPlace Equation
A
wall stress=(pressure*radius)/wall thickness
as cavity gets bigger, wall stress does too
important in LVH and aneurysms
17
Q
Poiseulle equation
A
flow=r^4, 1/viscosity
why radial changes at arterials regulate flow
18
Q
Ohms Law
A
R=P/flow
19
Q
anterior heart
A
RV, RA
20
Q
aortic dissection
A
tear in wall, presents as chest pain
21
Q
regurgitation
A
valve doesn’t close during systole=retrograde leakage
22
Q
order of aorta offshoots
A
brachicephalic trunk, L common carotid artery, L subclavian artery
23
Q
relationship of subclavian veins to subclavian arteries
A
anterior (why central lines are accessible)
24
Q
thoracic duct start and end
A
cisterna chyle, left subclavian vein
25
injury to phrenic nerve
hemi-diaphragm elevation
26
injury to recurrent laryngeal nerve
hoarseness
27
injury to CN X (vagal)
delayed gastric emptying
28
injury to sympathetic chain
Horners syndrome (anhydrosis, ptosis, meiosis)
29
starlings law
the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume) when all other factors remain constant
30
what structures can be well seen with TEE?
valves and cardiac chambers, ascending & descending aorta
31
what structures can't be seen with TEE?
aortic arch, PA, PVs (trachea carina/air is in the way)
32
most common structure damaged during PDA ligation?
recurrent laryngeal nerve (hoarseness)
33
which approach should one take for mitral valve surgery?
right chest incision so it's not obscured by LV
34
right border of heart
RA
35
inferior border of heart
LV
36
posterior border of heart
LA
37
where do the coronary arteries lie?
epicardium, below the visceral layer
38
endocardium
lines the chambers, valves (monolayer), and vessels
39
fibrous skeleton of heart
separates the atria from the ventricles. dense aponeurosis. annuli fibrosi
40
purkinje fibers
specialized myocytes with few myofibrils and many intercalated disks and gap junctions
41
intercalated disks
connect myocytes in series, but also contain complex branching pattern.
42
transverse portion of intercalated disks
adhering junctions-interdigitate to provide stable syncytium under distending forces (mechanical junction)
43
longitudinal portion of intercalated disks
gap junctions-electrical junctions that permit solute flow
44
why do the ventricles "wring" with contraction?
the superficial myocardium is made of oblique fibers. middle are circumferential, deep are longitudinal. systole=longitudinal and circumferential shortening
45
titin-origin and end
M to Z lines
46
importance of titin
acts as a spring, the source of passive tension when stretched.
47
difference between cardiac and skeletal titin?
cardiac is shorter and stiffer. resting tension increases faster so that muscle doesn't stretch and contractions therefore remain strong with each beat
48
how many capillaries does each myocyte contact?
7
49
myocyte nuclei
central
50
what is special about atrial myocytes?
they can act as endocrine cells: in response to distention, they release natriuretic peptides (ANP)
51
what blocks gap junctions?
increased intracellular Ca. mechanism of protection that limits the spread of damage
52
tropomyosin
encircles actin to stiffin it
53
troponin
binds actin, tropomyosin, and Ca
54
relationship between sarcomere length and developed force
always a positive relationship
55
which organelle surrounds the myofibrils?
mitochondria
56
three layers of vessels
tunica intima, media, adventitia
57
which layers do capillaries contain?
only the tunica intima
58
tunica intima
contains endothelial cells, basal lamina, internal elastic lamina
59
tunica media
contains smooth muscle cells, elastic fibers
60
tunica adventitia
contains external lamina, smooth muscle, vasa vasorum, nerves
61
three types of arteries
elastic, muscular, arterioles
62
larget type of arteries?
elastic (think aorta)
63
elastic artery function
conducting vessels that propel blood during diastole.
64
elastic artery composition
high elastic fiber content in thick tunica media.
65
benefit of high elastic fiber content in elastic arteries?
allows systolic expansion to store energy for diastolic propulsion
66
which vessels contain the external elastic lamina?
arteries only
67
muscular artery function
distrubuting vessels that control regional blood flow
68
muscular artery composition
lots of smooth muscle in tunica media (fine control of diameter)
69
arterioles function
determine resistance and therefore pressure
70
arterioles composition
only contain the intima
71
function of veins
capacitance (can stretch and store blood)
72
difference between vein and artery composition?
via tunica media: thinner than the adventitia in veins with wavy or collapsed contour.
73
vein adventitia
no external elastic lamina
74
how do veins propel blood if they don't have thick tunica media or high elastic content?
semilunar valves propel against gravity
75
function of capillaries
exchange vessels (duh)
76
how are capillaries regulated?
smooth muscle sphincters are located at the entrance of each
77
three types of capillaries
continuous, fenestrated, discontinuous
78
continuous capillaries
endothelial cells are closed via tight junctions and a complete basal lamina. transport occurs via diffusion or pinocytosis
79
fenestrated capillaries
basal lamina is complete but endothelial cells have pores. used for areas of extensive fluid and metabolite absorption
80
discontinuous capillaries
incomplete basal lamina and endothelial lining. sinusoids of the liver and spleen
81
portal circulation
2 sets of capillaries joined by arteries or veins
82
arteriovenous anastomosis
shunts blood past capillaries
83
venule function
site of egress of inflammatory cells to tissues
84
endothelial thrombotic properties
naturally inhibitory, but with injury promotes platelet activation via tF and vWF
85
endothelial vasodilation properties
releases NO for dilation, endothelin for constriction
86
which nervous system stimulates vascular smooth muscle?
sympathetic
87
organization of vascular smooth muscle
no sarcomeres, t tubules, troponin, actin is anchored at dense bodies, myosin and actin have opposite polarity at sarcomeres
88
vascular smooth muscle contraction
calmodulin and increased Ca= activates MLCK= phosphorylates RLC=myosin and actin interact=contraction
89
Lymphatic circuit
a one way circuit that prevents back flow
90
where is blood flow velocity highest?
in the aorta (all the capillaries have a greater CSA overall)
91
what determines the normal tone of the vascular smooth muscle?
constant stimulation by the SNS
92
actin:myosin in smooth muscle
actin>myosin, which allows for myosin to change which actin it interacts with at different degrees of distention=greater contraction
93
Functions of the Endothelium (TGIF)
Tone, Growth, Inflammation, Fluidity
94
Rheology
the study of deformation and flow of blood.
95
laminar flow
all the fluid is moving in the same direction, although there may be some differences in the velocity of flow due to the effect of pipe friction on fluid near the wall
96
turbulent flow
blood flows in several directions at once
97
which vessels control vascular flow?
arterioles
98
list of vasodilators
NO (EDRF), PGI2, bradykinin, ACh
99
intact endothelium's rxn to ACh
vasodilation. levels too low to produce contraction & opposed by NO. but at high levels, will override NO and cause vasoconstriction
100
damaged endothelium's rxn to ACh
vasoconstriction. no NO to counteract
101
NOS
NO synthase. stimulated by shear stress or by ACh
102
NO tone mechanism
diffuses from endothelial cell to VSMC, where it stimulates generation of cGMP, which causes vasodilation via relaxation
103
PGI2
produced by the endothelium in response to shear stress, receptor binding=increase cAMP=relaxation/dilation
104
bradykinin-vascular tone
acts on B2 endothelial receptors causing release of NO & PGI2.
105
what inhibits bradykinin?
angiotensin 2
106
list of vasoconstrictors
endothelin, angiotensin 2, TxA2, ACh
107
most potent natural vasoconstrictor
endothelin. elevated in hypertension and CHF
108
ACh & atherosclerosis testing
patients with atherosclerosis vasoconstrict with administration of ACh
109
angiogenesis factors
VEGF, fibroblast GF, PDGF
110
when does capillary growth occur normally?
during embryonic development, menses, wound healing
111
pathologic angiogenesis
retinopathy, tumorigenesis
112
specification in vessel growth
angioblasts and EPCs produce angiogenesis factors which lead to vasculogenesis
113
angiogenesis
maturation of immature, unstable vessels
114
relationship of EPCs to vasodilation
fewer EPCs=decreased ability to vasodilator and grow/heal
115
HHT
genetic disorder of TGFb receptors that leads to abnormal vascular formation=telangiectasias, bleeding, paradoxical emboli in lungs
116
endothelium anti-clot properties
fibrinolytic (t-PA), anti-thrombin (thrombomodulin, heparin), antiplatelet (NO, PGI2)
117
endothelium pro-clot properties
antifibrinolytic (plasminogen activator inhibtor PAI-1 stimulated by angiotensin 2)
118
fibrinolysis pathway
removes thrombi by proteolytically degrading fibrin. plasminogen activator increases plasmin after binding with t-PA
119
virchow triad
hypercoaguable state, endothelial injury, circulatory stasis
120
venous thrombi
RBCs enmeshed in fibrin with few platelets=red thrombi. usually caused by stasis since its a low flow/pressure system. treated with anticoagulant
121
arterial thrombi
form under shear stress, platelet activation, or damage. composed predominantly of platelets=white thrombi. treated with antiplatelet
122
characteristics of dysfunctional endothelium leading to thrombosis
increased vWF increases platelet activation. increased synthesis of PAI-1 results in impaired fibrinolysis
123
cell adhesion molecules on endothelium
ICAMs and VCAMs are unregulated in times of inflammation and bind to integrins on leukocytes
124
VCAM and plaque
oxidized LDL stimulates production of VCAMs so hypercholesterolemia induces inflammation
125
angiotensin 2 & atherosclerosis
acts as a pro-inflammatory factor by stimulating NFkB which causes expression of VCAM, monocyte recruitment protein, and IL6
126
microparticles
membrane bound vesicles that have been budded from cell surface and stimulate IL release and I/VCAM expression
127
where does atherosclerosis occur?
INTIMA
128
mechanism of atherosclerosis
at site of injury, monocytes adhere to adhesion molecules, undergo diapedesis into vessel wall intimal space where lipids accumulate into plaque
129
location of main coronary trunks
sub epicardial
130
origin of main LCA
left sinus of valsalva
131
course of main LCA
behind the pulmonary artery to the L anterior inter ventricular groove where it bifurcates into the LADA and LCX
132
LADA
courses in the anterior inter ventricular groove. supplies anterolateral wall of LV via diagonal branches and uppers 2/3rd of septum via septal perforators
133
LCX
courses in L AV groove. supplies the lateral wall of LV via marginal branches and the LA
134
origin of main RCA
right sinus of valsalva
135
course of main RCA
through the R AV groove. supplies RV via marginal branches and inferior LV/lower 1/3 of septum via PDA (also RA, SAN, AVN)
136
coronary dominance
90%: RCA supplies PDA
| 10%: LCX supplies PDA (therefore RCA only supplies the RV)
137
supply to anterolateral papillary muscle
dual supply: marginal branches of LCX and LDA
138
supply to posteromedial papillary muscle
PDA. more susceptible to ischemia
139
coronary venous drainage
coronary arteries drain into the coronary sinus, located in the L AV groove. drains into the RA.
140
will the heart beat if all nerve connections are severed?
yes bc myocardial contraction is myogenic, initiated by the SA node. hormones and neural connections just regulate rate/strength. This is actually what the situation is in a heart transplant
141
what mediates upstroke of AP
Na channels opening
142
phase 1 repolarization
Na channels inactivate and transient outwar K channels open
143
plateau phase of AP
slow repolarization of membrane towards Vm.
| Due to L/T type Ca channels inactivating slowly and the opening of delayed rectifier K channels
144
phase 3 repolarization
Ca channels totally inactivate, delayed & inward K activate
145
which channels maintain Vm (phase 4)?
inward K rectifiers
146
effect of increased extracellular K (such as in ischemia)
depolarizes the Vm, thereby decreasing the AP excitability and conduction velocity--> leads to arrhythmias
147
T type Ca channel
transient (in SA/AV nodes): activate around -60 but do so less quickly, inactivate more quickly
148
L Type Ca channel
long lasting: activate around -30, inactivate very slowly (maintain plateau),
149
inward rectifier K channel
outward K current, maintains Vm, off during the plateau
150
delayed rectifier K channel
activation increases very slowly when membrane is depolarized (maintains the plateau for slow repolarization)
151
why don't the pacemaking APs have a stable Vm?
the delayed rectifier K channels turn off slowly=diastolic depolarization
152
what causes the upstroke in pacemaking cells?
L/T Ca channels
153
t tubule
extension of the surface membrane. brings the AP down into the cells to the DHPR L type Ca channels that interact with the RyR channels of the SR
154
myocardial contraction flow
AP down t tubule--DHPR Ca channels open with depolarization-- Ca flows into cell-- binds to RyR on SR-- RyR open-- Ca flows out of SR-- binds to troponin C-- tropomyosin moves-- myosin can bind actin--contraction
155
myocardial relaxation flow
Ca is removed two ways: SR Ca ATPase pumps it back into SR or Na/Ca exchanger pumps it out of cell
156
which part of myocardial contractive is an active process?
TRICK QUESTION. both require energy
157
how to change pacemaking rate (HR)
1. change rate of phase 4 depolarization
2. change depolarization threshold
3. change the Vm
158
what is the predominant control point for HR?
the diastolic interval-most sensitive to regulation
159
sympathetic stimulation of SA node
increase HR via NE &E. increase the rate of diastolic depolarization due to increased Ca current (switch on L/T Ca channels)
160
positive chronotrophic effect
increase HR
161
parasympathetic influence on SA node
ACh from vagus nerve decreases HR by increasing K permeability via muscarinic receptor--slows diastolic depolarization (if levels are high enough, will hyper polarize and stop AP altogether)
162
how to change strength of contraction
1. change Ca concentration (more=stronger)
2. change Ca sensitivity (more sensitive=right shift)
3. alter strength relative to Ca (more force=upwards shift)
163
why can we use Ca concentration as means to alter contraction strength?
normally, the amount of Ca released into the myocardium is insufficient to saturate the Ca sites on the contractile apparatus. this allows for fine control by adding or reducing binding sites
164
rate staircase
when heart is stimulated more rapidly, the strength of the contraction increases. diastole is shortened so that cells relax faster and maintain a higher overall Ca level
165
Starlings curve
if muscle is stretched at rest (higher levels of diastolic filling), contraction is stronger. because the sarcomere maintains volume, the filaments are closer when stretched
166
automaticity
property to spontaneously depolarize and reach threshold to trigger an AP
167
sinus rhythm
SA node drives intrinsic HR. N=60-80bpm
168
junctional rhythm
His-Purkinje system drives intrinsic HR. N=30-50bpm
169
overdrive suppression
when cells are driven at a faster rate than they intrinsically generate APs/beats, the NaKATPase pump turns on to restore ions--hyperpolarizes cells and suppresses their pacemaking potential
170
why does the SA node drive the HR?
overdrive suppression of the His-Purkinje system due to its higher intrinsic AP rate
171
what do gap junctions do in times of damage?
close. protective mechanism to non damaged cells. slow conduction can then lead to arrhythmias
172
safety factor
ratio of current generated to minimum needed to sustain contraction. how much you need to knock out before making the cell inexcitable
173
why is the AV node at risk for block?
low safety factor
174
ERF (effective refractory period)
time following depolarization when a stimulus cannot elicit a propagating AP
175
what determines the ERP in fast response tissue?
APD (AP duration)- Na current recovers from phase 1 very quickly so reliant on plateau
176
what determines the ERP in slow response tissue?/
the Ca channel recovery time
177
what does the P wave signify?
atrial depolarization
178
what does the QRS segment signify?
ventricular depolarization
179
what does the ST segment signify?
ventricular plateau
180
what does the T wave signify?
ventricular repolarization
181
significance of the PR interval
represents the delay in the AV node. if >120-200=AV conduction delay
182
normal HR values
60-100
183
QRS duration
should be 120, slow ventricular depolarization=bundle branch block or junctional rhythm
184
significance of the QT interval
duration of AP. shortens with increasing HR
185
why are T waves upright if they represent repolarization?
depolarization moves from endo to epicardium, whereas repolarization moves from epi to endocardium=REPOLARIZATION IS OPPOSITE DEPOLARIZATION
186
how to identify RBBB on ECG
long QRS with RSR' in V1
187
normal sinus rhythm
p wave before every QRS, p wave upright in I, II, biphasic in V1
188
normal range of QRS axis
-30 to +90 degrees
189
pressure-flow paradigm
differences in pressure drive the flow of blood (the CO)
190
diastole
AV valves are open, myocardium is relaxed, chamber wall force/pressure drops, volume increases, fills with blood
191
systole
semilunar valves open, myocytes are depolarized & myocardium is active/contracting, chamber wall force/pressure increases, volume drops, blood is propelled out
192
valves during isovolumetric contraction or relaxation
all closed
193
atrial vs ventricular systole
atrial systole occurs 120ms before ventricular systole. also has a shorter duration. starts at a wave, ends at c wave
194
valve function
allows pressure gradients to be maintained so that compartments with >P during the cardiac cycle allow correct blood flow
195
regurgitation
failure of valves to close properly
196
valve stenosis
failure of valves to open properly, obstructs normal flow
197
what causes heart sounds to be heard?
rapid acceleration of blood due to valve closing/opening or ventricular filling. pathologies are heard due to turbulent velocity
198
heart sound -S1
caused by AV valve closure at onset of systole due to increasing Pv.
199
heart sound -S2
caused by semilunar valve closure at the end of systole. long interval is between S1 & S2 (diastole) when trying to figure out which is which
200
during which phase does the carotid upstroke?
ventricular systole. therefore, this upstroke should correlate to S1
201
heart sound- S3 gallop
after S2, sounds like the "in" in "SLOSH-ing-in", where S1=SLOSH, S2=ing
202
what does the presence of an S3 gallop indicate?
early ventricular filling or disordered diastolic compliance
203
heart sound- S4 gallop
before S1, sounds hard like "a-STIFF-wall"
204
what does an S4 gallop indicate?
the sound of late diastolic filling due to atrial kick. can hear it because of abnormal diastolic compliance of the ventricle
205
heart sound-splitting
corresponding valves don't close at the same time (S1=M/T, S2=A/P)
206
murmur
turbulent flow due to abnormally increased flow velocity. louder=higher velocity
207
systolic murmur
associated with ventricular ejection. indicates outflow tract obstruction, AV regurg, inter ventricular communication
208
diastolic murmur
associated with ventricular inflow. indicates semilunar valve regurg, AV valve obstruction
209
continuous murmur
associated with a PDA
210
pulse pressure
systolic-diastolic pressure
211
atrial a wave
first positive deflection due to atrial contraction. just before the end of ventricular diastole
212
atrial x descent
negative deflection after A wave. due to atrial diastolic relaxation. occurs at onset of ventricular systole
213
atrial v wave
positive deflection due to atrial filling initiation that occurs during ventricular systole
214
atrial Y descent
negative deflection after V wave due to rapid atrial emptying at the onset of ventricular diastole. passive emptying
215
LVEDP
P in LV at end of diastole. determines the end diastolic sarcomere length which determines the strength of the contraction
216
estimate of preload
LVEDP
217
why is right side systolic pressure lower than L side?
the lungs are very close to the heart, whereas the head is further away and therefore requires higher pressures
218
why is the right sided diastolic pressure lower than L side?
the RV has lower compliance
219
stroke volume
the volume of blood ejected per cardiac cycle. usually 80-90mL per beat
220
cardiac output
the total amount of blood pumped to the systemic circulation per unit time (SV*HR). Nl=5L/min
221
what determines end diastolic volume
forces filling the ventricle during diastole interacting with intrinsic ventricular mechanical properties (PRELOAD)
222
how does one measure end diastolic volume?
LVEDP
223
what determines end systolic volume?
forces opposing ventricular ejection during systole interacting with intrinsic ventricular mechanical and contractile properties (AFTERLOAD & INOTROPY)
224
how does one measure end systolic volume?
great vessel pressure
225
what determines the maximum sarcomere length?
titin-generally 33% of end diastolic length
226
what determines the minimum sarcomere length?
length of the A band
227
myocardial diastolic force-length relationship
myocardium isn't perfectly elastic so relationship is non-linear=as it stretches, it becomes stiffer and opposes overstretching so that P needed to increase V increases
228
myocardial systolic force-length relationship
linear
229
preload
force available to distend myocardium at end diastole--determines the end ventricular volume (ejection volume) and sarcomere length (contraction attainable)--LVEDP
230
we can increase preload to increase CO. what limits the extent to which we can raise it?
increased LA pressure will eventually impede venous return=pulmonary edema
231
afterload
the load that ventricular muscle must overcome during systole in order to eject (the force opposing muscle shortening). can be thought of as the ventricular systolic pressure
232
major determinant of afterload
systemic arterial pressure
233
inotropy
the property of cardiac muscle to alter its intrinsic contractile force (can shorten more to eject more). shifts the systolic force-length relationship upwards
234
ways to change SV
change preload, after load, or inotropy
235
LVEF
percent of volume in LV at end diastole that gets ejected during systole. Nl=55-70%
236
importance of LVEF
used to approximate LV contractile function. dependent on load and inotropy
237
ischemia
decrease in blood flow that causes a decrease in myocardial contractility and creatine phosphate levels
238
hypoxia
temporary lack of O2. blood flow continues to deliver glucose and wash away byproducts.
239
creatine phosphate
important buffer for ATP concentrations since contractile proteins are very sensitive to ATP. drops before ATP in times of ischemia
240
infarction
region of heart dies. cells permanently no longer have contractility=cardiac failure
241
normal energy metabolism within the cardiac myocytes
predominantly via beta oxidation. CPT1 is key regulatory point.
242
energy metabolism in times of ischemia
glucose metabolism takes over: maintains ion balance, provides ATP, generates fewer radicals
243
stunning
transient, reversible interruption in flow/cardiac function. decreased oxphos, ATP is buffered, acidosis, increased Ca/free radicals
244
hibernation
sustained, sublethal ischemia. adaptive changes to a lower energy consumption state. shift protein isoforms that consume less energy but are also less contractile. increase glycolysis, decrease Box
