Exam 3 Flashcards
What do intercalated disks contain? For what purpose
- gap junctions: provide electrical continuity bw cardiac myocytes –> allows heart to function as an electrical unit and each muscle fiber to contract in coordinated fashion.
- desmosomes: anchor fibers together
Does cardiac muscle have greater or fewer mitochondria? Why?
- Greater
- Allows for continuous aerobic respiration via ox phos
- uses whatever fuel available (switches metabolic pathways)
Does the heart use motor-unit contraction or organ contraction?
Organ contraction
-Heart contracts as a unit or not at all ( no ‘motor-unit’)
Is the ARP long or short in cardiac muscle?
Why?
- Long
- it prevents tetanus
What is the mech of contraction of myocardial fibers
- depol by opening voltage-gated fast Na+ channels
- transmission of depol down T-tubules causing Ca2+ release (80% of Ca comes from the SR via Ca induced Ca release)
- Calcium spark and decr K+ permeability (prolongs depol – plateau)
- Excitation contraction coupling via troponin binding leads to sliding of filaments.
- Repolarization (relaxation) occurs due to Ca2+ transport out of the cytoplasm and K+ perm incr.
Difference bw ventricular myocyte AP and SA node AP
ventricular: -has phase 0,1,2,3,4 -Has plateau period -solid phase 4 SA: - has phase 4,0,3. -phase 4 (resting pot) is not stable (it's continuously depolarizing), known as funny current. -phase 0 is not as fast bc of opening of Ca channels -NO refractory period
What is the funny current due to?
Where do we see this?
- Due to slow Na channels opening
- We see this in autorhythmic cells (SA node)
Rank in terms of AP length? (shortest to longest)
- Purkinje fibers
- Atria
- Ventricles
1-Atria
2- Ventricles
3- Purkinje
What is the P wave?
Depolarization of both atria (contraction)
-Impulses originate at SA node and spread through both atria
What is the QRS complex?
- Ventricles depolarize and contract
- Normal duration 80-120 ms
Why is the QRS complex larger than the P-wave?
Ventricles have a greater muscle mass
What is the T-wave?
-Repolarization begins at apex of heart and spreads upwards through ventricles
(Represents electrical recovery of ventricles?
What is the PR interval?
- Conduction time from atria to the ventricles (through the bundle of his)
- Helps distinguish arrhythmias
- Signal must pass through AV node, so any block that would show elongation of PR –> 1st degree block
- -Normal duration 120-200 ms
What is the ST interval?
- Hearts electrical activity immediately after ventricles contract
- Even with baseline bc no electrical activity flows
- Normal duration:
Where is the ARP located in the EKG?
From middle of QRS complex to middle of T-wave
What are the inflow valves?
Atrioventricular valves:
-tricuspid and bicuspid (mitral)
What are the outflow valves?
Semilunar valves?
-Aortic and pulmonary
What are the phases of the cardiac cycle?
- diastasis (middle of phase 1)
- Isovolumetric contraction (phase 2)
- Ejection or outflow (phase 3)
- Isovolumetric relaxation (phase 4)
- Rapid ventricular filling (early phase 1)
ESV is in which phase of cardiac cycle?
end of phase 3- isovolumetric relaxation
EDV is in which phase of the cardiac cycle?
End of phase 1 (late diastole)– both sets of chambers are relaxed and ventricles fill passively
What is CO?
volume of blood pumped per ventricle per minute
What is SV
volume of blood pumped by a ventricle per beat
-it’s the diff bw EDV and ESV
What is EDV?
vol of blood in ventricles at end of diastole
-pre-load
What is the cardiac cycle
seq of mechanical and electrical events that repeat with every heart beat
What is SV determined by?
EDV
TPR
FOC
What is TPR?
-Impedance to flow in the arteries (afterload)
part of determination for SV
What influences EDV?
- Venous return
- Bp
- Venous pressure
What is the preload?
Amount of tension in the ventricular myocardium before it begins to contract?
(from EDV)
What is the Frank-Starling Law?
-Strength of ventricular contraction varies directly with EDV
-SV is proportional to EDV (as EDV incr, myocardium is stretched more, causing greater contraction and SV)
(Ventricles pump out all the blood that enters them)
-Describes an intrinsic property of the myocardium
What is contractility?
-FOC at any given EDV (or pre-load)
What is the after-load?
What does an incr in afterload do to SV?
Pressure in the arteries just outside the semilunar valves (pressure in the aorta and pulmonary artery)
-Any incr in afterload reduces stroke vol
List positive inotropic agents
Cause contraction (incr Ca)
- Adrenergic agonists (epi)
- cardiac glycosides
- High extra cellular Ca
- Low extracellular Na
- Incr HR
List negative inotropic agents
Cause relaxation (decr Ca)
- Ca channel blockers
- Low extracellular Ca
- High extracellular Na
Why is Cardiac muscle resistant to developing tetanus? Compare to skeletal?
-Long ARP
A recording of the SA node AP exhibits a sudden incr in slope of phase. How would you explain this? Permeability to which ion is increasing or decreasing?
- increase in symp tone
- Incr Na influx
During which phase of the ventricular AP would you expect permeability to K to be the highest?
3
How would incr symp activity affect the relationship bw ventricular EDV and SV
-Incr EDV which increases SV
What is bl flow driven by?
a const pressure head across variable resistances
What is the link bw HR and SV?
Symp innervation and epi from adrenal medulla cause incr HR and also cause incr contractility which incr SV
Which side is the volume resevoir?
Venous side
Which side is the pressure resevoir
Arterial side
What influences venous return?
- Bl vol
- Venous pressure
- Urine vol (affects bl vol)
- Vasoconstriction by symps
- Skeletal muscle pumps (affects venous pressure)
- Pressure drop during inhalation
What is delta P equal to?
F * R
What does resistance across a circulatory bed result from?
serial arrangements of resistances
What does TPR result from
parallel arrangement of all the circulatory beds in the body
Relationship bw R and flow?
as R increases, F decr
What are 3 parameters that determine resistance for fluid flowing through a vessel?
L- longer vessel, greater R
viscosity - thicker fluid, incr R ??
r- incr r, decr R
What is the velocity of blood flow affected by?
-Where is bl flow the slowest and fastest?
TOTAL cross-sectional area
- Slowest in the capillaries
- Fastest in the aorta
Which blood vessels play the most impt role in the regulation of blood flow to a tissue and blood pressure
Arterioles
As blood travels from the aorta to the capillaries what increases?
R
bc the radius is decr
As a subjects age increase, his/her arterial compliance _____
decr
As symp tone incr, TPR _____
incr
-bc vasoconstriction
As blood moves from the arteries to the capillaries, bp _______
decr
-highest pressure right when it exits the heart and decr from there
As blood flow from the arteries to the capillaries, velocity of flow ______
decr
-bc R incr bc r decr
As you go from arteries to capillaries, the fluid pressure exerted by blood on the vessel walls _______
decr
As HR decr. diastolic pressure will _____
decr
The majority of the blood volume is contained within the _______
veins
volume resevoir
What factor is most sig in affecting TPR?
radius bc r^4
Brief incr in bp will cause symp ton on the blood vessels to_______
decr
Where is the biggest pressure drop?
-arterioles
(greatest site of vasoconstriction)– incr R so decr P
Which circ has a higher P, pulmonary or systemic?
systemic
C =
compliance
delta V / delta P
What is the major cause of non-linear pressure-flow relationship in vascular beds?
elastic properties of the vessels
-if it’s linear, it’s rigid
What are the 3 types of capillaries
continuous
fenestrated
sinusoidal
continuous capillaries
- most comon
- have inter endothelial junctions (in BBB tight junctions instead)
- numerous exocytotic vesicles
- NO fenestrae
- Continuous with few wall interruptions
Fenestrated capillaries
- Endothelial cells are thin and perforated
- Has fenestrations
Sinusoidal capillaries
- Type of fenestrated capillary
- Also called discontinuous
- VERY leaky –> extremely large fenestrae and have actual gaps bw adj endothelial cells
What travels through cap wall by diffusion?
O2, Co2, lipid-soluble molecules
What travels through cap wall by bulk flow?
H20, electrolytes, small molecules
What travels through cap wall by vesicular transport?
macro-molecules
What travels through cap wall by active transport?
ions, small molecules
What is Kf in the NDF equation?
water permeability of cap wall (hydrolic flux)
When NDF is greater that 0 what is favored?
filtration
What is Pc?
capillary hydrostatic pressure
- higher at arteriolar end than venule end BUT more affected by changes in venous end
- forces fluid OUTWARD
What is Pif?
IF hydrostatic pressure
- Normally neg (due to pumping action of lymphatics)
- opposes filtration
- Inward force
What is Pi p/c
Plasma colloid osmotic pressure (oncotic)
- Plasma proteins are major determinant (albumin is most abundant plasma protein and generates about 70% of osmotic pressure)
- forces fluid inward
What is Pi if?
IF colloid osmotic pressure (oncotic)
- Caused by small amt interstitial proteins (in proteoglycans that leak into IF space (so little loss, so little protein in IF –> why Pi if is low)
- Favors filtration
- Forces fluid outward
As you move from the arterial end of a capillary bed to the venous end, the capillary hydrostatic pressure will ______
decr (bc it’s higher at arteriolar end)
Liver dysfunction would cause capillary osmotic pressure to _____
decr
Dehydration causes capillary osmotic pressure to ______
incr
(T/F) Capillary surface area does not influence the amt of substance which diffuses down a conc gradient
F
(T/F) Transport of small solutes across the capillary wall cannot be described in terms of physical laws
F- small pore effect (small polar molecules can cross wall by water-filled pores)
