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october exam > cardiac 2 > Flashcards

cardiac 2 Flashcards

1
Q

beta 1 stimulation

A

activates adenylate cyclase- converts ATP to cAMP

cAMP increases activation of protein kinase A (pka)

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2
Q

what does activated pka do

A

phosphorylates proteins and accomplishes 3 tasks

  1. activation of L type ca channels (more ca enters the cell)
  2. stimualtion of ryanodyne 2 receptor to release more ca
  3. stimulation of serca2 pump to increase ca uptake (faster rate of ca uptake in the SR) with subsequent enhanced ca release
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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)

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4
Q

afterload

A

the force the ventricle must overcome to eject its stroke volume

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5
Q

loook at pressure volume loops

A
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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

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7
Q

L and R coronary arteries rise from

A

aortic root

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8
Q

L coronary artery

A

emerges from behind pulmonary trunk, divides into LAD and circumflex

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9
Q

LAD perfuses

A

anterolateral and apical walls of LV and anterior 2/3 of interventricular septum

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10
Q

circumflex artery supplies

A

LA and lateral and posteior walls of LV

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11
Q

RCA perfuses

A

RA, RV, intraarterial septum and posterior 3rd of interventricular septum

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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

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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 ()

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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

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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

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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

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17
Q

what is the best view on tee for diagnosing LV ischemia

A

mid papillary muscle level in short axis

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18
Q

what supply oxygenated blood to myocardium

A

LCA and RCA

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19
Q

at rest myocardium consumes o2 at a rate of

A

8-10 ml/min/100g with extraction rate of 70%

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20
Q

coronary blood flor is __ ml/min or __% of co

A

225; 4-5

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21
Q

coronary vasculature autoregulates between a map of

A

60-140

out of this range cbf is dependent on cpp

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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

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23
Q

the most important determinant of coronary vessel diameter is

A

local metabolism

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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

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25
Q

myogenic response

A

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

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26
Q

what does tachycardia do to supply and demand

A

decreases supply and increases demand

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27
Q

what does increased aortic diastolic pressure do to supply and demand

A

increases supply and demand

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28
Q

increase preload does what to supply and demand

A

decreases supply and increases demand

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29
Q

what plays a critical role in regulation of peripheral vessel diameter

A

calcium- increased ca causes vasoconstriction; reduced causes vasodilation

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30
Q

g protein cAMP pathway->

A

vasodilation

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31
Q

nitric oxide cGMP pathway->

A

vasodilation

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32
Q

phospholipase C pathway->

A

vasoconstriction

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33
Q

describe the g protein cAMP pathway

A

in cardiac myocyte: inc cAMP and pka increases intracellular calcium

in vascular muscle cell: inc cAMP and PKA decreases intracell calcium

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34
Q

how does pka affect excitation contraction coupling

A

-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

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35
Q

describe the nitric oxide cGMP pathway

A

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

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36
Q

describe vasoconstriction phospholipase c pathway

A

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

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37
Q

the AV valves (__ and ___) seperate __ from ___

A

mitral and tricuspid; atria from ventricles

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38
Q

AV valve leaflets are anchored to the inferior of the ventricles by

A

chordae tendinae and papillary

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39
Q

semilunar valves (___ and ___)

A

aortic and pulmonary

both have mercedes benz look on tee

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40
Q

how are semilunar valves anchored

A

not attached to chordinae tendinae or pap muscles

blood gets propelled by pressure gradients

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41
Q

stenosis leads to what kind of issue with the heart

A

pressure overload-> concentric hypertrophy

ht compensates by adding sarcomeres in parallel - chamber wall becomes THICKER, reducing chamber radius

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42
Q

regurgitation leads to what kind of heart issue

A

volume overload-> eccentric hypertrophy

heart compensated by increasing radius- DILATES

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43
Q

normal valve area for aortic valve

A

2.5-3.5

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44
Q

severe aortic stenosis

A

</= 0.8 cm (some say 1)

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45
Q

causes of aortic stenosis

A

bicuspid aortic valve and calcification of valve leaflets (most common)

rheumatic fever

ineffective endocarditis

46
Q

how does concentric hypertrophy eventually fail

A

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
Q

classic presentaiton of aortic stenosis

A

syncope, angina and dyspnea on exertion

48
Q

anesthetic management of aortic stenosis

A

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
Q

aortic insufficiency etiology

A

incompetent valve or dilation of aortic root

50
Q

conditions to avoid that will worsen aortic regurg

A

bradycardia (prolongs diastolic filling)
inc SVR (inc aorta LV pressure gradient)
lg valve orfice (lg area for blood to return through)

51
Q

how do you inject cardioplegia in a pt with aortic regurg

A

retrograde!! or directly into coronary ostia

52
Q

cause of acute AI

A

usually endocarditis; can cause LV failure

53
Q

chronic AI

A

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
Q

anesthetic management of AI

A

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
Q

normal mitral valve area

A

4-6

56
Q

severe mitral stenosis

A

< = 1 cm

57
Q

causes of mitral stenosis

A

rheumatoid fever, endocarditis, calcification of mitral annulus secondary to atherosclerosis

58
Q

what happens initally with increased LA pressure and mitral stenosis

A

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
Q

how does the body compensate to the underfilled LV that happens with mitral stenosis

A

by increasing SVR to maintain BP

60
Q

what happens with the increased LA pressure with mitral stenosis

A

it backs up into the pulmonary venous system. chronic pulmonary fluid overload-> pulmonary HTN-> RV failure

61
Q

anesthetic management for mitral stenosis

A

slow/ normal HR
avoid increased PVR
everything else keep neutral (preload, contractility, svr)

62
Q

why is tachycardia bad with mitral stenosis

A

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
Q

why do you want to maintain PL during mitral stenosis

A

low PL= decreased CO

hypervolemia will increase LA pressure-> pulmonary congestion

64
Q

why maintain SVR with mitral stenosis

A

rapid decrease in svr elicits baroreceptor increase in HR (bad)

65
Q

how should you treat hypotension with mitral stenosis

A

neo or vasopressin

66
Q

avoid increase in pvr

A

avoid increasing pvr: acidosis, hypercarbia, hypoxia

67
Q

mitral insufficiency causes what kind of hypertrophy

A

eccentric

68
Q

etiologies of mitral insufficiency

A

rheumatic fever, ischemic ht disease, papillary muscle dysfunction, endocarditis, LV hypertrophy

69
Q

where do you see volume overload with MR

A

in LV and LA- blood goes out toward aorta and through incompetent valve into L atria

70
Q

what conditions increase regurgitant volume

A

-slower HR
-increased pressure gradient - between LV and LA
-increased SVR
-increased size of valve orfice

71
Q

anesthetic manegement of MI

A

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
Q

aortic stenosis: systole

A

-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
Q

where is aortic stenosis murmur heard

A

ASSS - aortic stenosis systolci murmur- heard at R sternal border

74
Q

aortic regurg: diastole

A

-turbulent retrograde flow across aortic valve
-high pitched blowing murmur
-not as loud as aortic stenosis

75
Q

where do you heard aortic regurg murmur

A

ARDS- aortic regurg diastolic murmur- heard at R sternal border

76
Q

mitral stenosis : diastole

A

-LA generates increased pressure to overcome stenotic valve
-opening snap followed by low intensity rumbling murmur

77
Q

where do you hear mitral stenotic murmur

A

mitral stensis as a diastolic murmur- heard at apex and L axilla

78
Q

mitral regurg systole

A

-retrograde flow across incompetent mitral valve during ventricular contraction
-holosystolic murmur- loud swishing sound
-similar to aortic regurg but heard during systole

79
Q

where do you heard mitral regurg murmur

A

MRSA- mitral regurg systolic murmu= apex and L axilla

80
Q

what is a tavr for

A

transcatheter aortic valve replacement

-minimally invasive method of avr in pt with aortic stenosis

81
Q

what are the 3 approaches for tavr

A

transfemoral
transaortic
transapical (anterograde)

replacement valve is threaded into position and seated inside native aortic valve

82
Q

what are the benefits of tavr

A

no sternotomy of CPB

83
Q

anesthetic conditions based on the valve for tavr

A

-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
Q

complications with tavr

A

-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
Q

periop higher CV risk factors

A

-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
Q

when is highest risk of reinfarction

A

w/in 30 days of acute MI

87
Q

when are guidelines for elective surgery in pt with recent MI

A

min of 4-6 weeks

88
Q

high risk surgeries

A

emergency, open aortia, periph vasc, long surgical procedure w/ significant volume shifts and or blood loss

89
Q

intermediate risk surgeries

A

carotid endartectomy, head and neck surgery, intrathoracic, intraperitoneal, ortho, prostate

90
Q

low risk surgeries

A

endoscopic, cataract, superficial procedures, breast, ambulatory

91
Q

nyha classification

A

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
Q

things that cause decreased oxygen delivery

A
  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
Q

things that cause increased oxygen demand

A

tachycardia
htn
sns stimulation
incre wall tension, Lvedv, afterload, contractility

94
Q

what happens to a cell without oxygen

A

dies and releases its contents into systemic circulaiton- a cell needs oxygen to maintain the integrity of its cell membrane

95
Q

infarcted myocardium releases what biomarkers

A

creatine kinase-MB, troponin 1, troponin T

96
Q

what biomarker is more sensitive for the diagnosis of MI

A

cardiac troponins are more sensitive than CK-MB

97
Q

what lead identifies inferior wall ischemia and dysrhythmias

A

lead II (esp narrow QRS)

98
Q

what leads are best for LV ischemia

A

v3, v4, v5

99
Q

what lead is best for detecting ST changes

A

v4 - closest to isoelectric line on baseline ekg

100
Q

if you have hx of cad what should you change about ekg

A

need 5 lead ekg!

101
Q

when do most periop MIs occur

A

in postop period - within 48 hrs after surgery

102
Q

most common cause of R ht failure

A

L ht failure

103
Q

conditions that increase PVR

A

hypoxia, hypercariba, acidosis, hypothermia, high PEEP, nitrous oxide

104
Q

treatment of RV failure

A

-inotropes, milrinone, dobutamine
-pulmonary vasodilators: inhaled nitric oxide or sildenafil (pde-5 inhibitor)
-reversing cause of increased PVR

105
Q

complications of systemic HTN

A

LVH (concentric), ischemic HD, CHF, arterial aneurysm, stroke, ESRD

106
Q

what is more common primary or secondary HTN

A

primary 95% (no identifiable cause)
secondary 5% (has cause)

107
Q

pathophys of primary HTN

A

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
Q

anesthetic considerations with HTN

A

-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
Q

htn crisis

A

bp over 180/120

110
Q

htn urgency vs emergency

A

emergency- evidence of end organ injury

111
Q

examples of secondary htn

A

coarcation of aorta, renovascular dz, hyperadrenocorticoism (cushings), hyperaldosteroism (conns), pheochromocytoma, pregnancy induced htn

112
Q
A

october exam (12 decks)

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