Physiology Flashcards
Effect of Resting Potential on AP
- membrane potential determines how many channels are open
- closer you are to RMP, the more channels will be available
Factors that lead to arrythmias
- Impulse Formation
2. Impulse Conduction
Altering pacemaker
Slowing (ACh, beta-blocker) - alter slope of diastolic interval - hyperpolarize diastolic interval Speed up (SNS, fiber stretch) - alter slope of diastolic interval
Afterdepolarizations
- membrane voltage oscillations that result in transient, abnormal depolarizations of cardiac myocytes during phase 2, 3, 4
- EAD or DAD
Early Afterdepolarizations
- occurs DURING AP and interrupts orderly repolarization of myocyte
- exacerbated by SLOW HR
1. late phase 2 = opening more Ca2+ channels
2. early phase 3 = opening Na+ channels
3. Both = inhibition of K+ channels
Delayed Afterdepolarizations
- occurs AFTER AP but before another AP is supposed to occur
- exacerbated by FAST HR
1. elevated cytosolic Ca2+ levels - overload of SR -> spontaneous release of Ca2+
Block
- occurs if electrical signal is slowed or disrupted as it moves thru heart
- can be partial or complete
Reentry
- impulse reenters and excites areas of heart more than once
- TIMING IS EVERYTHING
In order to occur
1. Must have obstacle (anatomical or physiological)
2. Must be unidirectional block
3. Conduction time must exceed effective refractory period
Wolf-Parkinson-White Syndrome
Bundle of Kent -> abnormal electrical accessory connection between atria and ventricle
- allows impulse to be conducted without going through AV node -> premature contraction
Classes of Antiarrythmic Drugs
Class I - Na blockers, alters AP duration
Class II - beta-blockers, blocks SNS effects
Class III - K blockers, prolongation of effective refractory period
Class IV - Ca blockers - slows conduction where depolarization is Ca dependent
Drug Usefullness
- bind readily activated/inactivated channels
- bind poorly to resting channels -> prevents binding and promotes dissociation
Warning of Antiarrythmias
- can be a lack of channel specificity with higher doses
Sonogram Technique
- images made by sending pulse of ultrasound into tissue
- sound reflects and echoes off
- longer time between wave transmission and return -> deeper tissue
Doppler Electrocardiography
- useful for detecting valve stenosis or insufficiency
- as sound moves toward probe, increase in perceived frequency/pitch due to compression of wave front
- Red -> toward
- Blue -> away
Cardiac/Coronary Angiography
- used to visualize interior of heart chambers and blood vessels
- inject radio-opaque contrast agent into blood vessels and imaging using xray
End-Systolic Pressure-Volume Loop
- assesses contractility
- Plot ESV vs ESP on PV loop
- decrease contractility = downward shift of ESPVR
Fick Principle
- calculates rate at which substance is being added to or removed from blood as it passes through organ
- Q= X(tc) / ([Xa]-[Xv])
Cardiac Index
CI = CO/body surface area
ECG Regions of NO voltage
End of PR interval - atria depolarized, ventricles resting ST segment - no rapid changes in membrane - atria resting, ventricles depolarized NO CURRENT IMPULSE - nothing happens until next SA impulse
T wave has positive deflection
-negative wave front approaching negative lead -> double negative signal is translated as a positive deflection
Axial Deviations
Normal = 0-90 degrees Left Axis Deviations = <0 - physical displacement of heart to L - L ventricular hypertrophy - loss of electrical activity to R ventricle Right Axis Deviation - physical displacement of heart to R - R ventricular hypertrophy - loss of electrical activity to L ventricle
ECG Timing
PR Interval = 120-200 msec
QRS = 60-100 msec
QT Interval = <380 msec
SV and Ejection Fraction
SV = EDV-ESV
EF = SV/EDV
- normal is >55%
Stenotic Valves
don’t open fully –> increases “pressure” work –> leads to hypertrophy
Insufficient Valves
don’t close fully –> increases “volume” work –> leads to chamber dilation
What does cardiac valve abnormalities do to capillary hydrostatic pressure?
- the hydrostatic pressure in the capillaries in the venous side will be elevated above the oncotic pressure and the fluid will not be reabsorbed –> edema
First Degree Block
- abnormally long PR interval (slow conduction)
Second Degree Block
- some, but not all atrial impulses transmit thru AV node slower
- not all P waves accompanied by QRS T
Third Degree Block
- no impulses transmitted thru AV node, pacemaker defaults to bundle of His
- V rate slower than normal because of alternate pacemaker
Transcapillary diffusion
- [ ] difference
- surface area for exchange
- diffusion distance
- permeability of capillary
Hydrostatic Pressure
pressure of blood forcing fluid OUT of capillary
Oncotic Pressure
osmotic attraction of water IN to regions of higher protein [ ]
Filtration
- net movement of solutes and fluid OUT OF capillary into interstitial fluid (positive pressure gradient)
- occurs at arteriole end
Reabsorption
- net movement of solutes and fluid INTO capillary from interstitial fluid (negative pressure gradient)
- occurs at venule end
Exception to oncotic pressure rule
Injured tissure –> realeases histamine –> makes capillaries increase permeability –> proteins leak into interstitial fluid –> edema
Vessels in series
resistance is additive
- vessel with highest resistance with have greatest impact on pressure!!
Vessels in parallel
1/R = 1R1 + 1R2 + 1Rn
- overall resistance is less than any of the elements
Laminar Flow
- orderly, streamlined, low friction
Turbulent Flow
- disordered, mixing, high friction
Friction
shear stress, force inside wall of vessels that wants to drag inside surface along with blood flow
Arterioles present a large resistance to flow
OPEN
- high flow velocity, high downstream volume
CLOSED
- low flow velocity, low downstream volume
Total Peripheral Resistance
overall resistance to flow through ENTIRE systemic circulation
- organs are in parallel (adding an organ decreases TPR)
Compliancy - elastic property of veins
C = delta V/ delta P
how much volume changes in a response to change in pressure
Elastic properties of arteries
- store pressure energy in walls during expansion
- converts pulsatile flow coming out of aorta into steady flow thru vascular bed
- arteries recoil to shorter lengths and give up stored potential energy –> this is what drives blood thru peripheral vasculature!!!
MAP
MAP = CO x TPR
*assume CVP is 0, so MAP is delta P
MAP = DP + 1/3(SP-DP)
VSM Contraction differences
- Not arranged in regular repeating sarcomeres
- Actin filaments are much longer
- No Z-lines, but dense bodies instead
- also have Latch state = slow/non-cycling cross-bridges which minimize need for ATP
VSM contractility is Ca dependent
Ca complexes with calmodulin –> complex activates MLCK –> MLCK phosphorylates MLC –> MLC(PO4) enables cross-bridging and cycling to occur with actin to contract
Pathway of contractility in VSM can occur 2 ways
- Membrane depolarizations due to AP (VOC)
- GPCR allowing Ca in and same pathway, or PLC –> IP3 –> causes SR to release Ca (ROC)
VSM Relaxation
- Ca channel blockers –> hyperpolarize the cell membrane
- use chemical vasodilators that target GPCR with secondary messenger cAMP and cGMP –> vasodilation
Vascular tone
characterizes general contractile state of a vessel or vascular region
Arteriole Basal Tone Influences
Local, neural, hormonal
Metabolic influence on tone
- represents the most important means of local flow control
- Stimulate vasodilation
1. low O2
2. high CO2, H+, K+
2. adenosine
Endothelial influence on tone
- line the entire CV system
- produce chemicals that affect tone surrounding smooth muscles
- NO –> cGMP –> vasodilation
Local Chemicals influence on tone
PGE, TXA
- some vasodilators, some vasoconstrictors
Transmural pressure influence on tone
- arterioles actively and passively respond to changes in transmural pressure
MYOGENIC RESPONSE - stretch –> activates contraction
- decrease in pressure –> activates dilation
Hyperemia
Active hyperemia - blood flow closely follows tissue’s metabolic rate
Reactive hyperemia - increase in blood flow following the removal of an obstruction (this is duration dependent)
Autoregulation
all organs keep their blood flow constant, despite changes in arterial pressure
- sustained increase in pressure causes initial increase in flow, but then flow regulates back near steady state
Neural Influence on tone
- most important means of reflex control of vasculature
- increase nerve activity = increase vasoconstriction
Hormonal influence on tone
epi and norepi
- activate cardiac beta-1 –> increase HR and contractility
- activate vascular alpha 1 –> vasoconstriction
- activate vascular beta 2 –> vasodilation
beta 2 more sensitive
Vasopressin
ADH - released in response to low blood volume, acts on collecting ducts to decrease excretion of water
Angiotensin II
regulates aldosterone release from adrenal cortex, also a potent vasoconstrictor
Efferent pathways of baroreflex
SNS and PNS postganglionic fibers terminate on heart and vessels
Influence SV, HR, TPR
Afferent pathways of baroreflex
Sensory receptors located in the walls of the aorta and carotids (mechanoreceptors) sense stretch –> send impluse to the medullary cardiovascular center
IMPORTANT EQUATION????
MAP = CO x TPR
Cardiopulmonary baroreceptors
Located in atria, ventricles, coronaries, lungs
- sense pressure or volume
- exhibit tonic inhibitory influence on SNS activity
Chemoreceptor Reflexes
- Low O2 or High CO2 in arterial blood = increased respiratory rate and MAP
Cushing Reflex
a rise in intracranial pressure will result in a rise in arterial pressure
- prevents collapse of cranial vessels and preserves adequate blood flow
Exercising Skeletal Muscle reflex
Reflex tachycardia and increased atrial pressure elicited by stimulation of afferent fibers from skeletal muscle
Dive Reflex
in response to diving, bradycardia and intense vasoconstriction except the brain and heart
UNIQUE SITUATION
- rare situation when SNS and PNS work at same time
Emotional Reflex
responses originate in cerebral cortex and reach medulla center through corticohypothalamic pathways
EX) blushing (loss of sympathetic vasoconstrictor cutaneous vessels), excitement (increase BP by increased SNS and decreased PNS), fainting (decreased cerebral blood flow by loss of BP, loss of sympathetic tone and increase in PNS)
Central Command
implies an input from cerebral cortex to lower brain centers during voluntary muscle exercise
Same cortical drives that initiate skeletal muscle activity also simultaneously initiate cardio and resp adjustments
Pain Reflex
Superficial or cutaneous pain –> rise in BP
Deep or visceral pain –> similar to vasovagal syncope, decreased sympathetic tone and increased parasympathetic tone
Temp Reflex
controlled by hypothalamus –> dilation of cutaneous vessels promotes heat loss
Urinary Output Rate
Glomerular Filtration Rate - Renal Fluid Reabsorption Rate
Glomerular Filtration
transcapillary fluid movement dependent on hydrostatic and oncotic pressure
Rate of renin release from kidneys influenced by:
Increased sympathetic nerve activity
Lowered G.F. rate
Activation of sympathetic vasoconstrictor nerves to renal arterioles
Anti-diuretic hormone (vasopressin)
primary function - regulate extracellular fluid volume by affecting renal handling of water
- acts on collecting duct –> increases H20 permeability, less urine output, increases blood volume and BP
- also causes vasoconstriction
Myocardial O2 demands??
increase HR = increase O2 demand
increase contractility = increase O2 demand
increase arterial pressure = increase O2 demand
increased afterload = increase O2 demand
