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Apex- Cardiac A&P Flashcards

1
Q

Does hypokalemia increase or decrease RMP?

A

Decrease

hyperkalemia increases RMP (just think, physically increases it closer t

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2
Q

Hypocalcemia (increases/decreases) threshold potential

What is TP?

A

decreases

TP = -70mV

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3
Q

T/F: the wave of depolarization throughout the heart is facilitated by t-tubules

A

False - gap junctions

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4
Q

T/F- ventricular myocytes contain more mitochondria than skeletal myocytes

A

True

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5
Q

Which phase of the ventricular action potential is associated with the GREATEST calcium conductance?

1,2,3,4

A

2

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6
Q

What happens during the 5 phases of the myocytes action potential? (0-4)

A
  • Phase 0- Depolarization → Sodium in (+++)
  • Phase 1- Inital repolarization → Cl- in and K+ out (-)
  • Phase 2- Plateau → Calcium in and K+ out
  • Phase 3- Repolarization → K+ out (—)
  • Phase 4- Maintenance of TP → (K+ out & NA/K-ATPase function)
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7
Q

Match with Phase 0, 1, 2, 3, 4

  • ST segment
  • Potaassium Leak
  • Plateau
  • Isoelectric EKG
  • Q wave
  • Final Repolarization
  • Depolarization
  • Potassium Efflux
  • Calcium influx
  • T-Wave
  • Sodium influx
  • Resting phase
A

Phase 0 - Q-Wave, depolarization, NA++ influx
Phase 2 - ST segment, plateau , Ca++ influx
Phase 3- final repolarization , K+ efflux, T-wave
Phase 4 - potassium leak, isoelectric ECG, resting phase

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8
Q

Which current is responsible for sponatenous phase 4 depolarization in the SA node?

A. I-NA
B. I-K
C. I-Ca
D. I-f

A

D (I-funny channels)

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9
Q

How can volitale anesthetics cause a junctional rhythm?

A

By depressing automaticity of the SA node

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10
Q

What are the 3 phases of action potential in the SA and AV node?

A

Phase 4 = Spontaneous depolarization → Na+ in (I-f) then Ca ++ in (T-type)
Phase 0 = Depolarization → CA++ in (L-type)
Phase 3 = Repolarization → K+

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11
Q

Where are action potentials propagated after the SA node (course through the heart)

A

SA node → internodal tracts → AV node → Bundle of His → Left and Right Bundle Branches → Purkinje Fibers

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12
Q

What is the intrinsic firing rate of the SA node vs AV node vs Purkinje fibers?

A

SA node → 70-80
AV node → 40-60
Purkinjes → 15-40

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13
Q

What is the Keith-Flack node and where does it reside?

A

It’s the SA node and it resides in the right atrium

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14
Q

What is the expected o2 delivery of a 70kg adult?

A. 20ml/dL
B. 1000ml/min
C. 250ml/min
D. 15ml/dL

Can you identify the other numbers? They are signify something lol

A

B. 1,000 mL/min

A. 20ml/dL = Arterial o2 content (CaO2)
B. 1,000mL/min = Oxygen delivery (DO2)
C. 250ml/min = O2 consumption (VO2)
D. 15ml/dL = Venous o2 content (CvO2)

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15
Q

How do you calculate o2 delivery (DO2)?

A

CO x CaO2 x 10

CaO2 = O2 bound + O2 dissolved

CaO2 = (Hgb x SaO2 x 1.34) + (PaO2 x 0.003)

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16
Q

The amount of oxygen dissolved in blood (PaO2) follows what law?

A

Henrys

-at a constant temp, the amount of gas that dissolves in a solution is directly proportional to the pressure of that gas

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17
Q

Blood flow is inversely propostional to:
A. Body temp
B. Vessel Diameter
C. Afrteriovenous pressure difference
D. Hematocrit

A

D. Hematocrit

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18
Q

What 3 things does poiseuille’s law consider?

which one impacts blood flow the most?

A

Vessel diameter (R^4)
Viscosity
Tube length

*changing diamater is best way

Doubling radius → flow increase 16 fold ; Tripling radius → increases 81 fold ; Quadrupling → 256 fold

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19
Q

What reynold’s number predicts that flow will be mostly laminar vs mostly turbulant vs transitional?

A

<2,000 = laminar
>4,000 = turbulant
2,000-4,000 = transitional

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20
Q

Why do we combine PRBCs with normal saline anad run it through a warmer? What’s the overall purpose?

A

To improve flow
-adding saline reduces viscosity and improves flow
-warming fluid reduces viscosity and improves flow

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21
Q

2 ways to calculate MAP

A

SBP + (2)DBP / 3

(CO x SVR)/ 80 + CVP

SVR = MAP - CVP/CO * 80

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22
Q

CPP autoregulates between what

A

MAPs between 60-140mmHg

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23
Q

What is PAOP the same as?

A

LVEDP

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24
Q

CPP =

A

DBP- PAOP (or LVEDP)

CPP is the driving force of coronary blood flow

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25
What variables are related by the Frank-Starling mechanism? A. LVEDP and SVR B. Contractility and CO C. PAOP and SV D. CVP and MAP
C. PAOP & SV | remember PAOP = LVEDP = Preload (I think)
26
What is the functional unit of the contractile tissue in the heart?
The sarcomere
27
True or False: The end diastolic volume is called preload
True - the amount of blood in the ventricles just prior to systole
28
Atrical contraction (kick) contributes what percent to CO?
20-30%
29
Define preload
The amountof tension on the ventricle wall at the end of diastole (just prior to systole) ## Footnote *think of it as a rubber band- - increased stretch/tension = greater snap after tension is released
30
Conditions associated with decreased myocardial compliance where these people wouldn't tolerate afib or junctional rhythm as well (4)
1. Myocardial hypertrophy 2. Diastolic HF (HF with preserved EF) → think can't relax, less compliant 3. Fibrosis 4. Aging
31
LVEDP, LAP, and PAOP are all surrogate measures of what
LVEDV
32
What is the primary substance that determines inotropy?
Calcium
33
5 ways to increase myocardial contractility
1. SNS stimulation 2. Catecholamines 3. Calcium 4. Digitalis 5. PDE inhibitors ## Footnote PDE turns off adenylate cyclase which converts ATP → cAMP; so inhibiting this leads to increased concentrations of cAMP
34
A reduction of which factor would MOST likely augement stroke volume? A. Preload B. Contractility C. Afterload D. MAP
C. Afterload | *READ - note REDUCTION in which factor
35
What is afterload and what it is set by?
The tension the heart must overcome to eject its stroke volume. -usually set by SVR (mainly at the arterioles)
36
Normal SVR
800-1500 dynes/sec/cm
37
What 2 major things can reduce afterload
1. Arterial vasodilators → Propofol, Clevidipine 2. Sympathectomy → Regional anesthesia
38
Which phases of the cardiac cycle are associated with an open mitral valve and closed aortic valve? (Select 3) -Isovolumetric contraction -Rapid ventricular filling -Ventricular ejection -Atrial systole -Diastasis -Isovolumetric relaxation
Rapid ventricular filling Atrial systole Diastasis (middle 3rd of diastole)
39
What is the incisura
The dicrotic notch ## Footnote The onset of AV closure causes a short period of retrograde flow from the aorta towards the aortic valve, followed by termination of retrograde flow upon complete AV closure.
40
What does the height of a PV loop signify? | What about the width?
Ventricular pressure | Width = ventricular volume
41
Describe valve positions of the PV loop - bottom/top/left/right corners
Bottom left = MV opens Bottom right = MV closes Top right = AV opens Top left = AV closes
42
Label
43
EF values for normal, mild, mod, and severe dysfunction
Normal = >/= 50% Severe =
44
IV fluid bolus ## Footnote increased preload → increased EDV → increased force of contraction; *note loop gets wider but returns to orginal ESV
45
what would cause a PV loop to get wider but still return to starting ESV?
increased preload
46
What would cause a PV loop to get narrower but still return to the orginal ESV?
Decreased preload
47
What would cause a PV loop to get wider, taller, and shift to the left?
increased contractility
48
What would cause a PV loop to get narrow, shorter, and shift to the right?
Decreased contractility
49
What would cause the PV loop to get narrower, taller, and shift the ESV to the right
Increased afterload (cant fully empty so increased ESV)
50
What would cause the PV loop to get wider, shorter, and shift the ESV to the left?
decreased afterload (can fully empty)
51
Which coronary artery supplies this area
Circumflex- supplies left lateral wall of Lv LAD- supplies anterior wall of LV, 2/3 septum and small portion of the anterior RV RCA- supplies posterior wall of the LV, most of the RV, and posterior 3rd of the septum
52
Which coronary arteries arise from the aortic root?
Left and Right (LCA & RCA)
53
What does the LCA divide into?
the LAD and circumflex arteries
54
Where does the coronary sinus reside? What does it do?
on the hearts posterior surface -it returns cardiac venous blood to the right atrium * it can be cannulated to administer retrograde cardioplegia solution during CPB
55
When using TEE/TTE, the best view fro diagnosing myocardial ischemia is what?
Midpapillary muscle level in short-axis
56
What does the LAD perfuse ## Footnote EKG leads
LV - anterolateral and apical walls Anterior 2/3 of intraventric septum ## Footnote V1-V4
57
What does the circumflex artery supply? ## Footnote EKG leads
Left atrium LV - lateral posterior walls ## Footnote I, avL, V5-V6
58
What does the RCA perfuse? ## Footnote EKG leads
Right Atrium Right Ventricle Posterior LV Interarterial septum Posterior 3rd of the interventricular septum ## Footnote II, III, aVF
59
Which coronary artery determines coronary dominance?
Posterior descending artery
60
In 70-80% of patients, the ________ gives rise to the PDA, and we call this (left/right) dominance .
RCA (70-80%) *Right side dominance ## Footnote in the reminder of patients, the circ or RCA + circ supply the PDA and we call it LEFT dominance or co-dominance
61
The SA node receives its blood supply from the ____ in 70% of patients ## Footnote what about the remainder of the population?
RCA ## Footnote circumflex in the rest
62
The AV node recieves is blood supply from the ______ in 80% of patients
RCA
63
What supplies blood to the bundle of his and left and right bundle brances?
LCA
64
Most cardiac blood returns to which cardiac vein?
Coronary sinus
65
Match: Great, middle, and anterior cardiac veins with : RCA, LAD, PDA
Great = LAD Middle = PDA Anterior = RCA
66
A small amount of blood empties directly into all 4 chambers via the __________ veins
Thebesian veins - contributes to a small amount of anatomic shunt
67
Label
orange supplied by RCA blue supplied by circ green supplied by LAD
68
II, III, aVF - what leads/ what CA
Inferior/RCA
69
What are the lateral leads and what supplies them?
I, aVL, V5, V6 Circ
70
What are the septal leads and what supplies them?
V1-V4 LAD
71
Mediators of coronary vasodilation include (select 2) - adenosine - beta 2 stimulation - alpha 1 stimulation - hypocapnia
Adenosine & beta 2 stimulation ## Footnote *Alpha-1 and hypocapnia cause coronary vasoconstriction
72
Coronary blood flow at rest ## Footnote what % of CO
225-250ml/min ## Footnote ~ 5%
73
Coronary Blood flow =
Coronary perfusion pressure/coronary vascular resistance
74
Coronary Perfusion Pressure =
Aortic DBP - LVEDP
75
Coronary blood flow autoregulates between a MAP of what?
60-140mmHg
76
What is the most important determinant of coronary vessel diameter?
local metabolism
77
At rest, the myocardium consumes o2 at a rate of ______ml/min/100g with an extraction ratio of _____%
8-10ml/min/100g 70% extraction ratio
78
What is a byproduct of ATP metabolism and is a potent coronary vasodilator?
Adensoine
79
Causes coronary artery constriction or dilation: Histamine 1 Histamine 2 Alpha Beta 2 Muscarinic ## Footnote & How
Histamine 1→ CX (^ intracellular CA) **Histamine 2→ dilate** (^cAMP, decreased MLCK sensitivity to CA++) (histamine- think first is worst, second is the best) Alpha→ CX (^ intracellular calcium_ **Beta 2→ dilate** (^cAMP, decreased MLCK sensitivity to CA++) **Muscarinic → dilate** (increase nitric oxide)
80
T/F- the RV subendocardium is most vulnerable to ischemia ## Footnote Why or why not?
False - the LV subendocardium is most vulnerable to ischemia bc LV contraction compression the endocardial vessels during systole ## Footnote flow through the RV is relatively constant throughout the cardiac cycle
81
Which region on the heart does thsi pressure waveform represent?
LCA *flow greatly decreases during ventricular systole due to the mass of hte LV, contraction dramatically compresses the endocardial vessels decreasing flow during systole
82
Which condition increases myocardial o2 consumption? -decreased diastolic filling time -decreased end-diastolic volume -decreased P50 -decreased aortic diastolic BP
Decrased diastolic filling time | (another way of saying increased HR) ## Footnote decreased end-diastolic volume reduces wall stress and reduces demand; deceased P50 shifts the curve to the left (left = love) , less o2 is released to myocardium which decreases supply; decreased aortic DBP reduces coronary perfusion pressure which reduces o2 supply
83
Which condition increases myocardial o2 consumption? -decreased diastolic filling time -decreased end-diastolic volume -decreased P50 -decreased aortic diastolic BP
Decrased diastolic filling time | (another way of saying increased HR) ## Footnote decreased end-diastolic volume reduces wall stress and reduces demand; deceased P50 shifts the curve to the left (left = love) , less o2 is released to myocardium which decreases supply; decreased aortic DBP reduces coronary perfusion pressure which reduces o2 supply
84
Why is tachycardia detrimental to the iscemic heart?
Bc it s imultaneously decreases O2 supply while increasing o2 demand
85
If an increased afterload increases myocardial o2 demand, why is it mostly benificial?
Bc an increased afterload increases coronary perfusion pressure and typically outweighs the risk of increased wall tension
86
Most perioperative MIs occur when?
24-48hrs following surgery
87
What is it that actually causes chest pain?
lactic acid production due to anaerobic metabolism
88
How does tachycardia decrease o2 supply?
bc the LV is best perfused during diastole, and tachycardia = less time in diastole → less time to deliver o2 to the LV
89
Why shouldnt you increase preload in the cardiac ischemic patient?
increased preload increases wall stress, increased wall stress = increased o2 demand also, increased EDV decreases CPP ( aortic DBP - increased LVEDP = decreased CPP)
90
T/F- inhaled nitric oxide causes hypotension
False- it reduces pulm vascular resistance and RV afterload but is **inactivated** by hemoglobin , explaining it's ultra-short half-life (~5 secs) ## Footnote inactivated before it enters systemic circulation
91
T/F- inhaled nitric oxide causes hypotension
False- it reduces pulm vascular resistance and RV afterload but is **inactivated** by hemoglobin , explaining it's ultra-short half-life (~5 secs) ## Footnote inactivated before it enters systemic circulation
92
Bradycardia is caused by: A. making the RMP more positive B. increasing the slope of phase 4 depolarization C. Increasing potassium conductance D. Making the threshold more negative
C. Increasing potassium conductance ## Footnote PNS stimulation increases K+ conductance; since more K (a positive ion) exits the myocite, its interior becomes more negative. This increases the distance b/t RMP and TP -- so it takes longer fro the cell to reach TP; slowing the heart rate
93
What 3 things cause the SA node to increase it's firing rate?
1. The slope of spontaneous phase 4 depolarization INCREASES 2. TP becomes more negative (shorter distance between RMP and TP) 3. RMP becomes more positive (shorter distance between RMP and TP)
94
Which phase exhibits greatest conductance of which ion conductance? 0-3
Phase 0 = Na+ Phase 1 = Cl- Phase 2 = Ca++ Phase 3 = K+
95
T/F - contractility is depdendent on neither preload or afterload
True! -contractility is the ability of the sarcomeres to shorten and perform work indpendent of preload and afterload ## Footnote *remember- Chemicals affect Contractility - especially Calcium
96
What is the MOST potent local vasodilator substance released by the cardiac myocytes? A. Nitric Oxide B. Carbon Dioxide C. Adenosine D. Prostacyclin
C. Adenosine
97
98
The Sarcoplasmic reticulum releases calcium when: A. calcium stimulates the ryanodine receptor B. Repolarization occurs C. Troponin binds to the actin/myosin complex D. The SERCA2 pump is turned on
A. Calcium stimulates the ryanodine receptor -after this, CA binds to TNC on the actin/myosin complex which causes muscle contraction
99
Transection of the right vagus nerve would MOST likely affect: A. SA node automaticity B. AV node conduction C. Bundle of His
A. SA node automaticity ## Footnote the LEFT vagus nerve innervates the AV node

Cardiac (7 decks)

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