Cardiovascular Physiology and Complex CHD Flashcards
What does adenosine do to coronary artery flow
Causes coronary artery vasodilation
Where is calcium stored in a mature myocyte and how is it released
- Sarcoplasmic reticulum
- Calcium enters through L type voltage gated channels when then activates the ryanodine receptor and causes calcium release from the sarcoplasmic reticulum
How does renin get released from the kidney
- 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
Most common abnormal coronary arrangement in TGA
Anoamlous circ from the RCA (16% of patients) but most have normal coronaries
ANP effects on the kidney
- ANP is released in response to atrial stretch and leads to increased GFR
- Also decreases sodium resorption in the distal tubules
What causes shifting to the right in the hemoglobin/oxygen dissociation curve
- Acidosis
- Increased temperature
- Increased 2, 3 DPG
What is the systemic arterial response to decreased oxygen
- 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
Least saturated blood in the fetus
Coronary sinus and SVC
The dominant resting conductance of the myocyte is dependent on which ion
Potassium
- Keeps the myocyte negatively polarized until an action potential arrives to activate the cell into phase 0
What happens in phase 0 of action potential
Rapid depolarization due to Na entry into the cell
What happens in phase 1 of action potential
Early repolarization with K efflux from the cell
What happens in phase 2 of action potential
Influx of calcium into the cell through L-type calcium channels (voltage dependent)
What happens in phase 3 of action potential
Repolarization phase and is dominated by K efflux from the cell
What happens in phase 4 of action potential
Return of the resting membrane potential and is maintained by Na/K ATPase channels
What is the role of fibroblasts in the heart
- 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
What is the function of intercalated discs
- Connect cardiac myocytes end to end
- Transmit electrical impulses
- Made of desmosomes, adherens junctions, gap junctions
What is the process of calcium uptake during relaxation phase
80% done by Ca-ATPase SERCA pumps on the sarcoplasmic reticulum
Fetal hemoglobin subunits and relative oxygen affinity compared to adult
- 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
How does norepinephrine activate B1 adrenergic receptors
- 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
Functions of troponin C
Binds to calcium and allows tropomyosin to change positions to allow actin and myosin to bind and lead to muscle cell contraction
Baroreceptors location and response to arterial stretch
- Carotid sinus and aortic arch
- Send impulses to brain and decrease BP by decreasing HR and causing vasodilation
How does troponin lead to cardiac contraction
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
Path of oxygen rich blood from mom in fetus
Placenta –> umbilical veins –> ductus venosus –> Eustachian valve across PFO –> L heart –> ascending aorta
Path of oxygen deplete blood in fetus
SVC –> R heart –> PA –> PDA (decreased SVR and high PVR) –> DAo and body
Is fetal cardiac output RV or LV dominant
RV - 60% total cardiac output
Only 1/3 RV output goes to lungs
Only 5-10% through aortic isthmus
What causes PFO closure
Increased LA pressure after birth
What properties are specific to fetal myocardium
- Poorly developed sarcoplasmic reticulum
- Increased interstitial water
- Already at peak Frank-Starling curve
- Sensitive to afterload and heart rate
What is the sarcomere made of
Thick filament myosin, thin filament actin, troponin/tropomyosin complex
What happens after L type Ca channels allow calcium influx
Activates ryanodine receptor 2 on sarcoplasmic reticulum (Ca dependent release of calcium)
Pressure volume loops: Increased preload does what
- Moves end diastolic volume further out on the EDPVR
- Lusitropy moves EDPVR down
Pressure volume loops: Increased afterload and contractility do what
- Afterload moves end systolic pressure up (and decreases stroke volume)
- Contractility moves slope of ESPVR toward the Y axis (steeper slope)
What does thyroid hormone do for the heart
Increases expression of adrenergic receptors
Regulates myocyte proteins and mitochondria
How is the sympathetic nervous system activated
- Circulating catecholamines (mostly B1 receptors)
- Increases cAMP which increases calcium and therefore contractility
How is the parasympathetic nervous system activated
- Via vagal nerve/acetylcholine
- Slows pacemaker current and negative inotropy by inhibiting adenylyl cyclase
What percent of output comes from the atrial kick
20-30%
Probably more in HF and single V
What does CO2 control in the brain
- Higher pCO2 and hypoxia causes cerebral vasodilation
Where are chemoreceptors and what do they do
Carotid, arch, brain and cors
- Respond to low O2 or high CO2 and stimulate vasoconstriction as well as respiratory drive
Most common form of HLHS
- MA/AA (40%)
- MS/AS (20%)
- MS/AA (20%)
Most common great artery relationship in tricuspid atresia
Normally related great arteries
Most common truncal valve morphology
Tricuspid (70%)
Qudricuspid (20%)
Bicuspid (10%)
Most common type of truncus
- 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)
If there’s an absent PA in truncus, what side is it
Same side as the aortic arch
Most common coronary abnormality in tetralogy
LAD from the RCA that crosses over the RVOT
10-15% of patients also have an accessory LAD (large contal branch)
If there’s an absent PA in ToF, what side is it
Opposite side of aortic arch
D-TGA associated lesions
- 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
What decreases the murmur of HCM
Anything that decreases the gradient (phenylephrine increases afterload)
What increases the murmur of HCM
Anything that increases the gradient - exercise, standing (after squatting), straining portion of Valsalva, systemic vasodilation with nitro
Most common type of IAA with aortopulmonary septation defects (AP window)
IAA type A
DORV with cyanosis and mildly increased pulmonary vascular markings
DORV with subpulmonary VSD and no pulmonary stenosis
Subpulmonary = cyanosis
Subaortic = no cyanosis
Taussig Bing anomaly
DORV with subpulmonary VSD, side by side great arteries
Can also have coarc/left sided lesions
Anatomic hallmarks of complete AVSD
- 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
Most common lesion with thoracic type of ectopia cordis
Tetralogy
Where is AV node located in ccTGA
Anterior aspect of atrioventricular ring near the atrial septum
