cardiac 2 Flashcards
(112 cards)
1
Q
beta 1 stimulation
A
activates adenylate cyclase- converts ATP to cAMP
cAMP increases activation of protein kinase A (pka)
2
Q
what does activated pka do
A
phosphorylates proteins and accomplishes 3 tasks
- activation of L type ca channels (more ca enters the cell)
- stimualtion of ryanodyne 2 receptor to release more ca
- stimulation of serca2 pump to increase ca uptake (faster rate of ca uptake in the SR) with subsequent enhanced ca release
3
Q
net effect of beta 1 actvation (pka)
A
more forceful contraction over shorter time - pos inotropy with enhanced relaxation (pos lusitropy) between beats)
4
Q
afterload
A
the force the ventricle must overcome to eject its stroke volume
5
Q
loook at pressure volume loops
A
6
Q
ejection fraction
A
-informs us about hearts ability to pump blood
-% of hearts ability to pump blood- how much blood is pumped by heart during each beat
7
Q
L and R coronary arteries rise from
A
aortic root
8
Q
L coronary artery
A
emerges from behind pulmonary trunk, divides into LAD and circumflex
9
Q
LAD perfuses
A
anterolateral and apical walls of LV and anterior 2/3 of interventricular septum
10
Q
circumflex artery supplies
A
LA and lateral and posteior walls of LV
11
Q
RCA perfuses
A
RA, RV, intraarterial septum and posterior 3rd of interventricular septum
12
Q
PDA perfuses
where does it origionate?
A
posterior descending artery- infrior wall- origin of this defines coronary dominance
70-80% it comes from RCA - R dominant
the rest comes from rca or circumflex- L dominant
13
Q
what are the main coronary veins
A
great cardiac vein (LAD)
middle cardiac v (PDA)
anterior cardiac v (RCA)
run enxt to the A in ()
14
Q
coronary sinus
A
located on posterior aspect of RA, superior to tricuspid valve
most of the blood returning from LV drains into here
15
Q
thebesian v
A
small amount of blood empties directly into all four cardiac chambers via thesbian veins- contributes a small amount of anatomic shunt. dilutes pao2 of oxygenated blood that passes through lungs
16
Q
which ones are epicardial vessels and what does that mean
A
rca, lad, cxa
lay on top of ht surface
these are the ones that are usually affected by vascular stenosis
17
Q
what is the best view on tee for diagnosing LV ischemia
A
mid papillary muscle level in short axis
18
Q
what supply oxygenated blood to myocardium
A
LCA and RCA
19
Q
at rest myocardium consumes o2 at a rate of
A
8-10 ml/min/100g with extraction rate of 70%
20
Q
coronary blood flor is __ ml/min or __% of co
A
225; 4-5
21
Q
coronary vasculature autoregulates between a map of
A
60-140
out of this range cbf is dependent on cpp
22
Q
what is coronary reserve
A
difference between coronary blood flow at rest and maximal dilation. degree of margin allows cbf to increase in times of hemodynamic stress or exercise
23
Q
the most important determinant of coronary vessel diameter is
A
local metabolism
24
Q
as mvo2 increases
A
the coronary endothelium releases adenosine as well as a variety of other vasodilator substances, including nitric oxide, prostaglandins, hydrogen, K and co2
25
myogenic response
refers to a vessels innate ability to maintain a constant vessel diameter. when vessels diameter increases, it will have the tendency to contract, when diameter decreases it will have tendency to dilate
26
what does tachycardia do to supply and demand
decreases supply and increases demand
27
what does increased aortic diastolic pressure do to supply and demand
increases supply and demand
28
increase preload does what to supply and demand
decreases supply and increases demand
29
what plays a critical role in regulation of peripheral vessel diameter
calcium- increased ca causes vasoconstriction; reduced causes vasodilation
30
g protein cAMP pathway->
vasodilation
31
nitric oxide cGMP pathway->
vasodilation
32
phospholipase C pathway->
vasoconstriction
33
describe the g protein cAMP pathway
in cardiac myocyte: inc cAMP and pka increases intracellular calcium
in vascular muscle cell: inc cAMP and PKA decreases intracell calcium
34
how does pka affect excitation contraction coupling
-inhibition of voltage gated ca channels in the sarcolemma
-inhibition of ca release from the SR
-reduced sensitivity of the myofilaments to ca
-facilitation of ca reuptake into the SR via the SERCA2 pump
35
describe the nitric oxide cGMP pathway
nitric oxide is a smooth muscle relaxant that induces vasodilation
its production is increased by ach, substance p, bradykinin, serotonin, vasoactive intestinal peptide, thrombin and shear stress
-nitric oxide synthetase (NOS) is an enzyme that catalyzes the conversion of L-argine to nitric oxide
-NO diffuses from endothelium to sm muscle
-NO activates guanyl cyclase
-GC converts guanosine triphosphate to cGMP
-increased cGMP reduces intracellular calcium, leading to sm muscle relaxation
-phosphodiesterase (type5 ) deactivated cGMP to GMP
36
describe vasoconstriction phospholipase c pathway
activators of PLC pathway include phenylephrine, NE, angiotensin2, endothelin 1
plc activation increases production of 2 second messengers: IP3 and DAG
IP3 augments ca release from SR and DAG activates PKC
this opens voltage gated ca hannels in the sarcolemma and increases ca influx
37
the AV valves (__ and ___) seperate __ from ___
mitral and tricuspid; atria from ventricles
38
AV valve leaflets are anchored to the inferior of the ventricles by
chordae tendinae and papillary
39
semilunar valves (___ and ___)
aortic and pulmonary
both have mercedes benz look on tee
40
how are semilunar valves anchored
not attached to chordinae tendinae or pap muscles
blood gets propelled by pressure gradients
41
stenosis leads to what kind of issue with the heart
pressure overload-> concentric hypertrophy
ht compensates by adding sarcomeres in parallel - chamber wall becomes THICKER, reducing chamber radius
42
regurgitation leads to what kind of heart issue
volume overload-> eccentric hypertrophy
heart compensated by increasing radius- DILATES
43
normal valve area for aortic valve
2.5-3.5
44
severe aortic stenosis
45
causes of aortic stenosis
bicuspid aortic valve and calcification of valve leaflets (most common)
rheumatic fever
ineffective endocarditis
46
how does concentric hypertrophy eventually fail
law of laplace- LV compensates with concentric hypertrophy (thicker wall, decreased compliance, smaller chamber radius)
this comepnsatory mechanism- reduces myocardial oxygen supply (compression subendocardial)- increases mvo2 (increased heart mass)-> myocardial ischemia, LV failure and pulmonary edema
47
classic presentaiton of aortic stenosis
syncope, angina and dyspnea on exertion
48
anesthetic management of aortic stenosis
slow tight full
HR lower/ NSR
any loss of atrial kick (junctionalor afib)- reduces filling and SV
tachy- reduces filling
brady- reduces CO
increase PL- need to fill LV
maintain contracility
SVR- maintain or increase
avoid increase in PVR
avoid regional- hypotenion/ sympathomectomy
49
aortic insufficiency etiology
incompetent valve or dilation of aortic root
50
conditions to avoid that will worsen aortic regurg
bradycardia (prolongs diastolic filling)
inc SVR (inc aorta LV pressure gradient)
lg valve orfice (lg area for blood to return through)
51
how do you inject cardioplegia in a pt with aortic regurg
retrograde!! or directly into coronary ostia
52
cause of acute AI
usually endocarditis; can cause LV failure
53
chronic AI
LV will compensate; eccentric hypertrophy
chamber increases more than the wall thickness
preserves SV and contracility
valve calcification, marfan syndrome, ether danlos, ankylosing spondylitis
54
anesthetic management of AI
full, fast, forward
PL: maintain or increase- avid hypovolemia- some of SV is lost to LV
HR: increase with NSR- faster HR reduces regurg volume and increases AoDBP and CPP; slower HR gives more time for SV to flow back to LV
maintain contractility( if lv failure; inotrope and vasodilator)
decrease svr
maintain pvr
regional good
55
normal mitral valve area
4-6
56
severe mitral stenosis
< = 1 cm
57
causes of mitral stenosis
rheumatoid fever, endocarditis, calcification of mitral annulus secondary to atherosclerosis
58
what happens initally with increased LA pressure and mitral stenosis
initially the increased LA pressure maintains LV filling
but as the valve orfice narrows more, the pressure gradient between LA and LV increases, LV becomes chronically underfilled. Net result is an overfilled LA and underfilled LV
59
how does the body compensate to the underfilled LV that happens with mitral stenosis
by increasing SVR to maintain BP
60
what happens with the increased LA pressure with mitral stenosis
it backs up into the pulmonary venous system. chronic pulmonary fluid overload-> pulmonary HTN-> RV failure
61
anesthetic management for mitral stenosis
slow/ normal HR
avoid increased PVR
everything else keep neutral (preload, contractility, svr)
62
why is tachycardia bad with mitral stenosis
decreases time for blood to pass through the stenotic MV-> increased LA pressure
drugs that will increase HR: ketamine, anticholinergics
increase CO or HR-> increased LA pressure-> pulm edema
(things that can increase CO/ HR: thyroxicitosis, infection, autotransfusion during uterine contractions)
63
why do you want to maintain PL during mitral stenosis
low PL= decreased CO
hypervolemia will increase LA pressure-> pulmonary congestion
64
why maintain SVR with mitral stenosis
rapid decrease in svr elicits baroreceptor increase in HR (bad)
65
how should you treat hypotension with mitral stenosis
neo or vasopressin
66
avoid increase in pvr
avoid increasing pvr: acidosis, hypercarbia, hypoxia
67
mitral insufficiency causes what kind of hypertrophy
eccentric
68
etiologies of mitral insufficiency
rheumatic fever, ischemic ht disease, papillary muscle dysfunction, endocarditis, LV hypertrophy
69
where do you see volume overload with MR
in LV and LA- blood goes out toward aorta and through incompetent valve into L atria
70
what conditions increase regurgitant volume
-slower HR
-increased pressure gradient - between LV and LA
-increased SVR
-increased size of valve orfice
71
anesthetic manegement of MI
fast full foward
-HR: increased with NSR; faster HR reduces time in systole; reducing regurgitant fraction
-PL: maintain or increase- higher PL helps compensate for low volume
-maintain contractility
-decrease SVR
-avoid increased PVR
- sympathomemctomy from regional can be good- reduces SVR- forward flow and reduces regurg fraction
72
aortic stenosis: systole
-LV generates a high pressure to overcome the stenotic aortic valve
-high velocity through the narrow opening creates a "nozzle" effect
-sound can vibrate intensely to the chest and can be palpated as a thrill
-murmur may DECREASE if very severe- not enough blood passing through valve
73
where is aortic stenosis murmur heard
ASSS - aortic stenosis systolci murmur- heard at R sternal border
74
aortic regurg: diastole
-turbulent retrograde flow across aortic valve
-high pitched blowing murmur
-not as loud as aortic stenosis
75
where do you heard aortic regurg murmur
ARDS- aortic regurg diastolic murmur- heard at R sternal border
76
mitral stenosis : diastole
-LA generates increased pressure to overcome stenotic valve
-opening snap followed by low intensity rumbling murmur
77
where do you hear mitral stenotic murmur
mitral stensis as a diastolic murmur- heard at apex and L axilla
78
mitral regurg systole
-retrograde flow across incompetent mitral valve during ventricular contraction
-holosystolic murmur- loud swishing sound
-similar to aortic regurg but heard during systole
79
where do you heard mitral regurg murmur
MRSA- mitral regurg systolic murmu= apex and L axilla
80
what is a tavr for
transcatheter aortic valve replacement
-minimally invasive method of avr in pt with aortic stenosis
81
what are the 3 approaches for tavr
transfemoral
transaortic
transapical (anterograde)
replacement valve is threaded into position and seated inside native aortic valve
82
what are the benefits of tavr
no sternotomy of CPB
83
anesthetic conditions based on the valve for tavr
-sapian valve:
-need balloon valvuloplasty prior to deploying replacement valve to widen aortic valve area; rapid ventricular pacing (hr 160-200) to make cardiac standstill during valvuloplasty and valve deloplyment- makes it easier to get valve into posiiton
-anticipate profound hypotension b/c co will be near 0 during this part
-good bp/ map before ventricular rate increases
-prophylactic vasopressors
-may need to defib if they dont resume NSR
-apnea needed to minimize pt movement
corevalve- no need for valvuloplasty or rapid ventricular pacing
84
complications with tavr
-after valve depolyment: tee and fluro used to assess new valve function, AI or perivaluvlar leak and vascular injury
- if valve not in right position- AI
- coronary occlusion possible if valve obstructs coronary artery
-stroke, perivascular leak, pericardial tamponade, AV block, LBBB
85
periop higher CV risk factors
-emergent surgery, open aortic surgery, periph vasc, long surgical procedures w/ significant volume shifts and or blood loss
-hx of ischemic ht disease (unstable angina is greatest risk of periop MI)
-hx of chf
-hx of cerebrovascular dz
-dm
-serum creatine >2
risk of periop MI:
-> 6 M ago 6%
3-6 M ago 15%
<3 m 30%
86
when is highest risk of reinfarction
w/in 30 days of acute MI
87
when are guidelines for elective surgery in pt with recent MI
min of 4-6 weeks
88
high risk surgeries
emergency, open aortia, periph vasc, long surgical procedure w/ significant volume shifts and or blood loss
89
intermediate risk surgeries
carotid endartectomy, head and neck surgery, intrathoracic, intraperitoneal, ortho, prostate
90
low risk surgeries
endoscopic, cataract, superficial procedures, breast, ambulatory
91
nyha classification
1- no symptoms with activity
2- symptoms during acitvity; none with rest
3- symptoms with less than normal activity; none at rest
4- symptoms at rest
3 and 4 need cardio clearance
unelss mac- then reasonable to proceed if preop eval suggests stable cardiac disease
92
things that cause decreased oxygen delivery
1. decreased coronary flow
-tachycardia
-dec aortic pressure
-dec vessel diameter (spasm or hypocapnia)
-incre LV end diastolic pressure
2. decreased cao2
-hypoxemia
-anemia
3. decreased oxygen extraction
-L shift of hgb dissociaton curve (low p50)
-decreased capillary density
93
things that cause increased oxygen demand
tachycardia
htn
sns stimulation
incre wall tension, Lvedv, afterload, contractility
94
what happens to a cell without oxygen
dies and releases its contents into systemic circulaiton- a cell needs oxygen to maintain the integrity of its cell membrane
95
infarcted myocardium releases what biomarkers
creatine kinase-MB, troponin 1, troponin T
96
what biomarker is more sensitive for the diagnosis of MI
cardiac troponins are more sensitive than CK-MB
97
what lead identifies inferior wall ischemia and dysrhythmias
lead II (esp narrow QRS)
98
what leads are best for LV ischemia
v3, v4, v5
99
what lead is best for detecting ST changes
v4 - closest to isoelectric line on baseline ekg
100
if you have hx of cad what should you change about ekg
need 5 lead ekg!
101
when do most periop MIs occur
in postop period - within 48 hrs after surgery
102
most common cause of R ht failure
L ht failure
103
conditions that increase PVR
hypoxia, hypercariba, acidosis, hypothermia, high PEEP, nitrous oxide
104
treatment of RV failure
-inotropes, milrinone, dobutamine
-pulmonary vasodilators: inhaled nitric oxide or sildenafil (pde-5 inhibitor)
-reversing cause of increased PVR
105
complications of systemic HTN
LVH (concentric), ischemic HD, CHF, arterial aneurysm, stroke, ESRD
106
what is more common primary or secondary HTN
primary 95% (no identifiable cause)
secondary 5% (has cause)
107
pathophys of primary HTN
increased CO or SVR- vascular smooth muscle tone (intracellular ca concentration- increases svr)
possibilities:
sns overreactivity- chronic vasoconstriction- increases raas
vasodilator deficiency (less nitric oxide, prostaglandin) increases svr
collagen and metalloproteinase deposition in arterial intima-> increased vascular stiffness-> increased svr
diet high in na and/ or low k and ca intake
108
anesthetic considerations with HTN
-pt will have exagerated hotn response to induction
-exagerated htn response to intubation and extubation
-volume contracted
-continue BB
-ace-i and arbs- > vasoplegia (unresponsive to pressors and fluids)
-maintain map 20%
-if in sitting arm bp willl overestiate bp in brain
-sugrical sitm is most common cause of intra op htn
109
htn crisis
bp over 180/120
110
htn urgency vs emergency
emergency- evidence of end organ injury
111
examples of secondary htn
coarcation of aorta, renovascular dz, hyperadrenocorticoism (cushings), hyperaldosteroism (conns), pheochromocytoma, pregnancy induced htn
112
