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Peds Cards Boards > Cardiovascular Physiology and Complex CHD > Flashcards

Cardiovascular Physiology and Complex CHD Flashcards

1
Q

What does adenosine do to coronary artery flow

A

Causes coronary artery vasodilation

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2
Q

Where is calcium stored in a mature myocyte and how is it released

A
  • Sarcoplasmic reticulum
  • Calcium enters through L type voltage gated channels when then activates the ryanodine receptor and causes calcium release from the sarcoplasmic reticulum
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3
Q

How does renin get released from the kidney

A
  • In response to lower renal perfusion pressure from the juxtaglomerular apparatus
  • Leads to cleavage of angiotensinogen to angiotensin I and then angiotensin II by ACE
  • Angiotensin II then induces vasoconstriction and stimulates ADH (vasopressin) secretion
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4
Q

Most common abnormal coronary arrangement in TGA

A

Anoamlous circ from the RCA (16% of patients) but most have normal coronaries

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5
Q

ANP effects on the kidney

A
  • ANP is released in response to atrial stretch and leads to increased GFR
  • Also decreases sodium resorption in the distal tubules
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6
Q

What causes shifting to the right in the hemoglobin/oxygen dissociation curve

A
  • Acidosis
  • Increased temperature
  • Increased 2, 3 DPG
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7
Q

What is the systemic arterial response to decreased oxygen

A
  • Systemic vasodilation due to attempts to get more oxygen delivery through increased flow
  • Local vasodilation is also caused by increasing pCO2, increasing acidosis or increasing K
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8
Q

Least saturated blood in the fetus

A

Coronary sinus and SVC

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9
Q

The dominant resting conductance of the myocyte is dependent on which ion

A

Potassium
- Keeps the myocyte negatively polarized until an action potential arrives to activate the cell into phase 0

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10
Q

What happens in phase 0 of action potential

A

Rapid depolarization due to Na entry into the cell

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11
Q

What happens in phase 1 of action potential

A

Early repolarization with K efflux from the cell

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12
Q

What happens in phase 2 of action potential

A

Influx of calcium into the cell through L-type calcium channels (voltage dependent)

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13
Q

What happens in phase 3 of action potential

A

Repolarization phase and is dominated by K efflux from the cell

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14
Q

What happens in phase 4 of action potential

A

Return of the resting membrane potential and is maintained by Na/K ATPase channels

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15
Q

What is the role of fibroblasts in the heart

A
  • Structural integrity, remodeling, development
  • Deposition of extracellular matrix
  • Involved in secretion of cytokines and growth factors
  • Most common non-myocyte cardiac cell in the heart
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16
Q

What is the function of intercalated discs

A
  • Connect cardiac myocytes end to end
  • Transmit electrical impulses
  • Made of desmosomes, adherens junctions, gap junctions
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17
Q

What is the process of calcium uptake during relaxation phase

A

80% done by Ca-ATPase SERCA pumps on the sarcoplasmic reticulum

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18
Q

Fetal hemoglobin subunits and relative oxygen affinity compared to adult

A
  • Fetal is alpha and gamma
  • Adult is alpha and beta
  • Fetal has higher affinity for oxygen and becomes adult by about 3 months of age
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19
Q

How does norepinephrine activate B1 adrenergic receptors

A
  • Activates the Gs subunit of the G protein complex which activates adenylate cyclase to convert ATP to cAMP and activates protein kinase A
  • PKA phosphorylates multiple proteins involved in muscle contraction and action potentials of the heart
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20
Q

Functions of troponin C

A

Binds to calcium and allows tropomyosin to change positions to allow actin and myosin to bind and lead to muscle cell contraction

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21
Q

Baroreceptors location and response to arterial stretch

A
  • Carotid sinus and aortic arch
  • Send impulses to brain and decrease BP by decreasing HR and causing vasodilation
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22
Q

How does troponin lead to cardiac contraction

A

In systole calcium binds to troponin C which binds to troponin I and moves it from the ATP site on actin. Troponin T binds to tropomyosin which changes the conformation and allows cross bridging of actin and myosin leading to ATP becoming hydrolyzed and myosin and actin pulling the filament inward (power stroke)

In diastole troponin inhibits binding of myosin to actin

23
Q

Path of oxygen rich blood from mom in fetus

A

Placenta –> umbilical veins –> ductus venosus –> Eustachian valve across PFO –> L heart –> ascending aorta

24
Q

Path of oxygen deplete blood in fetus

A

SVC –> R heart –> PA –> PDA (decreased SVR and high PVR) –> DAo and body

25
Q

Is fetal cardiac output RV or LV dominant

A

RV - 60% total cardiac output
Only 1/3 RV output goes to lungs
Only 5-10% through aortic isthmus

26
Q

What causes PFO closure

A

Increased LA pressure after birth

27
Q

What properties are specific to fetal myocardium

A
  • Poorly developed sarcoplasmic reticulum
  • Increased interstitial water
  • Already at peak Frank-Starling curve
  • Sensitive to afterload and heart rate
28
Q

What is the sarcomere made of

A

Thick filament myosin, thin filament actin, troponin/tropomyosin complex

29
Q

What happens after L type Ca channels allow calcium influx

A

Activates ryanodine receptor 2 on sarcoplasmic reticulum (Ca dependent release of calcium)

30
Q

Pressure volume loops: Increased preload does what

A
  • Moves end diastolic volume further out on the EDPVR
  • Lusitropy moves EDPVR down
31
Q

Pressure volume loops: Increased afterload and contractility do what

A
  • Afterload moves end systolic pressure up (and decreases stroke volume)
  • Contractility moves slope of ESPVR toward the Y axis (steeper slope)
32
Q

What does thyroid hormone do for the heart

A

Increases expression of adrenergic receptors
Regulates myocyte proteins and mitochondria

33
Q

How is the sympathetic nervous system activated

A
  • Circulating catecholamines (mostly B1 receptors)
  • Increases cAMP which increases calcium and therefore contractility
34
Q

How is the parasympathetic nervous system activated

A
  • Via vagal nerve/acetylcholine
  • Slows pacemaker current and negative inotropy by inhibiting adenylyl cyclase
35
Q

What percent of output comes from the atrial kick

A

20-30%
Probably more in HF and single V

36
Q

What does CO2 control in the brain

A
  • Higher pCO2 and hypoxia causes cerebral vasodilation
37
Q

Where are chemoreceptors and what do they do

A

Carotid, arch, brain and cors
- Respond to low O2 or high CO2 and stimulate vasoconstriction as well as respiratory drive

38
Q

Most common form of HLHS

A
  • MA/AA (40%)
  • MS/AS (20%)
  • MS/AA (20%)
39
Q

Most common great artery relationship in tricuspid atresia

A

Normally related great arteries

40
Q

Most common truncal valve morphology

A

Tricuspid (70%)
Qudricuspid (20%)
Bicuspid (10%)

41
Q

Most common type of truncus

A
  • Type I (main PA trunk off the postero lateral aspect of the truncus)
  • Type II (branch PAs off the posterior surface of the truncus)
  • Type III (branch PAs off the lateral surface of the truncus)
  • Type IV (branch PAs off the DAo)
42
Q

If there’s an absent PA in truncus, what side is it

A

Same side as the aortic arch

43
Q

Most common coronary abnormality in tetralogy

A

LAD from the RCA that crosses over the RVOT
10-15% of patients also have an accessory LAD (large contal branch)

44
Q

If there’s an absent PA in ToF, what side is it

A

Opposite side of aortic arch

45
Q

D-TGA associated lesions

A
  • VSD (40-50%)
  • LVOT obstruction/coarc/arch hypoplasia/IAA in about 5%
  • Leftward juxtaposition of the atrial appendage
  • MV abnormalities in about 20% but often insignificant
46
Q

What decreases the murmur of HCM

A

Anything that decreases the gradient (phenylephrine increases afterload)

47
Q

What increases the murmur of HCM

A

Anything that increases the gradient - exercise, standing (after squatting), straining portion of Valsalva, systemic vasodilation with nitro

48
Q

Most common type of IAA with aortopulmonary septation defects (AP window)

A

IAA type A

49
Q

DORV with cyanosis and mildly increased pulmonary vascular markings

A

DORV with subpulmonary VSD and no pulmonary stenosis

Subpulmonary = cyanosis
Subaortic = no cyanosis

50
Q

Taussig Bing anomaly

A

DORV with subpulmonary VSD, side by side great arteries

Can also have coarc/left sided lesions

51
Q

Anatomic hallmarks of complete AVSD

A
  • Cleft in the anterior leaflet of the left AV valve
  • Lateral rotation of the left ventricular papillary muscles
  • Attachments of the left and right AV valves at the same level at the cardiac crux
  • LVOT is elongated creating a ratio of LV inlet to LV outlet < 1
52
Q

Most common lesion with thoracic type of ectopia cordis

A

Tetralogy

53
Q

Where is AV node located in ccTGA

A

Anterior aspect of atrioventricular ring near the atrial septum

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