Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
87 Cards in this Set
- Front
- Back
|
What is responsible for the resting membrane potential in ventricular/atrial myocytes?
|
- IR K channels (high K conductance, low Na -- RMP near EK = -90mV)
- Only open at very negative membrane potentials |
|
|
What happens to IR K channels when depolarization occurs in ventricular/atrial myocytes?
|
- They are blocked by Mg so no more K flows out
|
|
|
What is responsible for rapid depolarization (phase 0) in ventricular/atrial myocytes?
|
- Na channels activate
- IR K channels become blocked |
|
|
What is responsible for partial repolarization (phase 0) in ventricular/atrial myocytes?
|
- Na channels inactivate
|
|
|
When to I-to K channels activate in ventricular/atrial myocytes?
|
During phase 0 depolarization
|
|
|
What is responsible for the plateau (phase 2) in ventricular/atrial myocytes?
|
- Ca channels open and Ca goes into cells
- I-to K channels are open and K is going out of cells - This causes membrane potential to settle around 0 - Na channels are inactivated |
|
|
What happens during phase 2 to facilitate repolarization (phase 3) in ventricular/atrial myocytes?
|
- Ca channels inactivate slowly
- DR K channels activate slowly - This swings membrane permeability balance in favor of K |
|
|
What is responsible for the transition to resting membrane potential in phase 4 in ventricular/atrial myocytes?
|
As membrane becomes more negative...
- DR K channels close - IR K channels become unblocked |
|
|
When is the absolute refractory period in ventricular/atrial myocytes and what causes it?
|
- Lasts from phase 0 to midway through phase 3
- Na channels are inactivated and Ca channels are activated - Therefore no stimulus could trigger another AP |
|
|
When is the relative refractory period in ventricular/atrial myocytes and what causes it?
|
- Last from midway through phase 3 to beginning of phase 4
- Na channels are still inactivated, but Ca channels slowly recover from inactivation - A strong stimulus could activate these available Ca channels to cause slowly depolarizing AP (because Ca channels open slowly) |
|
|
What is the normal maximum diastolic polarization in pacemaker cells and why is it lower?
|
-60 to -70mV
- It is lower because there are fewer IR K channels than in ventricular myocytes |
|
|
Why do action potentials in pacemaker cells propagate slower and what is the effect?
|
- Virtually no Na channels are involved b/c it never gets repolarized enough for them to reactivate
- Propagation is due to Ca channels which open/close more slowly - This allows time for ventricular filling |
|
|
What are the main results of Na channels not being involved in pacemaker cell APs?
|
- Phase 0 is slower
- No phase 1 |
|
|
What are I-h channels and where are they involved?
|
- Channels permeable to both Na and K that open at negative membrane potentials
- Responsible for phase 4 depolarization in pacemaker cell action potentials - Driving force for Na to come into the cell is higher than for K to leave cell, so membrane potential creeps toward E-Na |
|
|
What causes the slow depolarization of phase 4 in pacemaker cell action potentials?
|
- The DR K channels that were open in phase 3 close slowly
- So K is still leaking out as Na moves in through I-h channels |
|
|
What sets the threshold in pacemaker cells?
|
- Activation of Ca channels
- Leads to slow phase 0 depolarization |
|
|
Why does action potential propagate more slowly in pacemaker cells?
|
- Activation of Ca channels is slow (responsible for phase 0 depolarization)
|
|
|
What causes the delay at the AV node?
|
- Pacemaker potential is set to slower rate (longer phase 4)
- Fewer gap junctions |
|
|
What are three ways to increase the rate of phase 4 depolarization in pacemaker cell action potentials and what will the result be?
|
1) Increase I-h channel activity
2) Increase DR K channel closing 3) Increase activation of Ca channels - Results in increased HR |
|
|
What effect will increasing I-h channel activity have in pacemaker cell action potentials?
|
- Increase rate of phase 4 depolarization
- Increases HR |
|
|
What effect will increasing rate of DR K channel closing have in pacemaker cell action potentials?
|
- Increase rate of phase 4 depolarization
- Increases HR |
|
|
What effect will increasing activation of Ca channels have in pacemaker cell action potentials?
|
- Increase rate of phase 4 depolarization
- Increases HR |
|
|
What are two ways to raise (make more positive) the MDP (maximum diastolic polarization) and what will the result be?
|
1) Decrease the activity of IR K channels
2) Decrease the activity of DR K channels - Results in increased heart rate |
|
|
What effect will decreasing the activity of IR K channels have in pacemaker cell action potentials?
|
- Makes MDP more positive
- Increases HR |
|
|
What effect will decreasing the activity of DR K channels have in pacemaker cell action potentials?
|
- Makes MDP more positive
- Increases HR |
|
|
Why does sympathetic innvervation increase DR K channel activity in order to increase heart rate?
|
- Seems counterintuitive because it would seem to lower MDP
- However, the purpose is to get membrane negative again so that it can respond to stimulus and create another AP |
|
|
Why is MDP not lowered when the sympathetic nervous system increases DR K channel activity in order to increase heart rate?
|
- The increased I-h activity counters the MDP lowering effect of increased DR K activity
|
|
|
What does the parasympathetic nervous system do to lower the heart rate in pacemaker cells?
|
1) Inhibits Ca channel activity
2) Inhibits I-h channel activity 3) Stimulates K channels (similar to IR K channels, but these are G-protein coupled = GIR K channels |
|
|
What is the IR K channel analog targeted by the parasympathetic nervous system to lower the heart rate?
|
GIR K channels
- These are stimulated to lower MDP and cause a slower phase 4 depolarization |
|
|
What is the main difference in cardiac muscle compared to skeletal muscle with excitation-contraction coupling?
|
- Cardiac muscle uses calcium induced calcium release from SR
- Influx of Ca through voltage-gated Ca channels is necessary for contraction (versus voltage sensors in skeletal muscles) |
|
|
What are three ways in which sympathoexcitation increases contractility in cardiac muscle cells?
|
1) Increased extracellular Ca entry
2) Increased intracellular Ca release 3) Increased Ca reuptake to speed relaxation |
|
|
What is the big difference in cardiac muscle compared to skeletal muscle with strength of contraction?
|
- Cardiac muscle is graded contraction based on Ca concentration while skeletal muscle is fixed contraction per AP
|
|
|
How is Ca concentration increased in smooth muscle cells?
|
1) Activate voltage-gated Ca channels
2) Increase Ca release from SR 3) Increase stretch activated Ca channels |
|
|
What is the GPCR receptor and its steps in vasoconstriction?
|
1) G-alpha Q
2) IP3 3) Ca release from SR 4) Vasoconstriction |
|
|
What is the GPCR receptor and its steps in vasodilation?
|
1) G-alpha S
2) PK A or PK G 3) Activates K channels or Ca pumps 4) Ca concentration decreases 5) Vasodilation |
|
|
How is intracellular Ca concentration regulated in smooth muscle?
|
Voltage gated Ca channels signal G-protein coupled receptors
|
|
|
What favors a reentry arrhythmia?
|
1) Two pathways
2) Dispersion of refractoriness (conduction travels slower in one of the pathways, usually the less refractory one) |
|
|
Where is the re-entry pathway in paroxysmal SVT?
|
- Around AV node (AVNRT)
- In a bypass tract (AVRT) |
|
|
Where is the re-entry in atrial flutter or atrial fibrillation?
|
- Atria
|
|
|
What causes re-entry in v-tach?
|
- Scar tissue from MI or injury
|
|
|
On the Wiggers diagram, what happens when the AV valves close?
|
- Isovolumetric contraction
- Ventricular pressure begins to increase - S1 heart sound |
|
|
On the Wiggers diagram, what happens when the aortic valve opens?
|
- Ventricular volume rapidly decreases
- Aortic pressure begins to increase |
|
|
On the Wiggers diagram, what happens when the aortic valve closes?
|
- Aortic pressure has a hump (from elastic recoil)
- S2 heart sound |
|
|
On the Wiggers diagram, what happens when the AV valve opens?
|
- Rapid ventricular filling (although pressure stays the same)
- S3 heart sound (tensing of chordae tendinae as blood flows across mitral valve) |
|
|
What causes S3 heart sound?
|
Tensing of chordae tendinae as blood flows over these during ventricular filling
|
|
|
What causes S4 heart sound?
|
Contraction of atria against a stiffened ventricle
|
|
|
When are systolic murmers heard in relation to S1 and S2?
|
In between them
|
|
|
What are three causes of systolic murmers?
|
1) Semilunar valve stenosis
2) AV valve regurgitation 3) Ventricular septal defects |
|
|
What are three causes of diastolic murmers?
|
1) Semilunar regurgitation
2) AV valve stenosis 3) Patent ductus arteriosis (continuous murmer) |
|
|
How is compliance formulated and explained?
|
= Change in volume / Change in pressure
- Veins have large compliance: over a given change in volume, they have the smallest change in pressure |
|
|
What does a decrease in compliance do to systolic pressure?
|
Increases it (stiff vessel)
|
|
|
What does a decrease in compliance do to diastolic pressure?
|
Decreases it
- Less expansion of arteries during systole, less passive recoil during diastole (diastolic pump), so pressure decreases more rapidly |
|
|
What happens to diastolic pressure with a decreased heart rate and why?
|
Decreases
- Diastolic pressure decreases because there is more time for blood to leave aorta and go into systemic circulation, lowering the pressure at the end of the contraction |
|
|
What does a decrease in CO do to CVP?
|
Decreases it
- Lower cardiac output leaves more blood in veins |
|
|
What changes and stays the same in a vein when smooth muscle contracts?
|
- Compliance decreases (stiffens)
- Diameter stays the same (no change in resistance so no pressure drop) - Because it is less compliant, CVP and venous return increase |
|
|
What determines blood flow to a specific tissue?
|
Resistance of capillaries
- Determined by radius - Increase blood flow with dilators which cause blood to be flowing through more capillaries |
|
|
What are the three forms of intrinsic control of blood flow through capillaries?
|
1) Myogenic
2) Metabolic 3) Autocoid |
|
|
How does myogenic regulation of capillary blood flow work?
|
- Stretch-activated contraction
- Ex. reduced cerebral blood flow (less stretch) dilates the vessels so more blood flows there |
|
|
How does metabolic regulation of capillary blood flow work and what are the vasodilators - what is it called?
|
- Matches blood flow to local tissue needs
- Vasodilators are metabolic waste products: CO2, adenosine, K - Can also vasodilate in response to metabolic needs: low O2 or pH - "Active hyperemia" |
|
|
How does autocoid regulation of capillary blood flow work?
|
- Vasodilators or vasoconstrictors are released from endothelium
|
|
|
What are the vasodilating autocoids?
|
- NO
- Prostacyclin - Histamine from mast cells |
|
|
What are the vasoconstricting autocoids?
|
- Endothelin
- Thromboxanes - Serotonin |
|
|
What are the extrinsic mechanisms for control of blood flow?
|
1) Neural
2) Hormonal |
|
|
How does neural control of blood flow work?
|
- Release NE
- Effect depends upon density of alpha-adrenergic receptors - Dense in tissues where flow can be sacrificed - Sparse in tissues that need flow (brain, heart, lungs) |
|
|
How does hormonal control of blood flow work?
|
- NE and EPI released into plasma from adrenal medulla
- Fight or flight: NE binds to constrict vessels (alpha-receptors) to increase SVR and MAP - EPI binds to beta-receptors on skeletal muscle and coronary beads (opposes alpha response and allows blood to flow here) |
|
|
What are the four hormones involved in hormonal control of blood flow?
|
1) NE
2) EPI 3) Angiotensin II 4) Arginine Vasopressin (AVP) or ADH |
|
|
What is the origin and effect of angiotensin II and vasopressin?
|
Both constrictors to increase MAP during sympathoexcitation
- AII from liver (angiotensinogen) and kidney (renin) - AVP from posterior pituitary |
|
|
How is blood flow to brain, heart, and lungs spared during sympathoexcitation?
|
- Low alpha-adrenergic receptor density
- Low angiotensin II and AVP receptor density |
|
|
What are the effects on capillary flow from vasodilation and inflammation?
|
- Increased surface area
- Increased permeability to plasma proteins - Increased flow - Pro-edema |
|
|
What is the effect on capillary flow from vasoconstriction of arterioles?
|
- Increases arteriolar resistance which causes a bigger pressure drop
- Cappillary hydrostatic pressure is lower, which favors reabsorption |
|
|
What are the effects of changes in MAP on capillary filtration?
|
Small effects because of myogenic buffering
|
|
|
What are the effects of changes in venous pressure on capillary filtration?
|
Large effects
- Increased venous pressure causes higher overall capillary hydrostatic pressure - This causes increased capillary filtration rate and EDEMA |
|
|
What are the two main factors in repaying the oxygen debt incurred by cardiac myocytes during sytole?
|
1) Diastolic arterial pressure (80% of CoBF occurs during diastole)
2) Diastolic duration |
|
|
What two things put heart at risk for ischemia?
|
- Low diastolic pressure (80% of CoBF occurs during diastole)
- Fast heart rate (shortens diastole and perfusion time) |
|
|
What are the main two factors in control of coronary vascular tone?
|
1) Metabolic regulation (icnreased metabolites from more cardiac work cause vasodilation - CO2, H+, adenosine, K+)
2) Myogenic regulation - Very little sympathetic and hormonal regulation |
|
|
What are the two major threats to cerebral blood flow?
|
1) Decreased MAP
2) Increased ICP |
|
|
What can cause increased ICP?
|
- Tumors, hemorrhage
- Increased capillary permeability (no lymphatics in brain to drain off excess fluid) - CSF aqueduct block - Blocked flow of CSF from SA space into venous vessels (meningitis) |
|
|
Why must pulmonary pressure stay low?
|
- Interstitial space must be kept dry around alveoli for gas exchange
- Capillary hydrostatic pressure is kept low so that Starling forces favor net reabsorption |
|
|
What is unique about control of pulmonary blood flow?
|
- Typically very little control
- However, if an area is getting little oxygen, this area constricts to direct blood to areas with higher oxygen - This is opposite the typical vascular smooth muscle response |
|
|
What happens to CVP with a PE in left pulmonary artery?
|
- Preload to left vent. decreases
- SV of left vent. decreases - Afterload in right vent. increases - Pressure builds up in venous system, CVP increases |
|
|
How does the venous baroreflex differ from the arterial?
|
- Venous has stronger hormonal response and arterial has stronger neural response
- Arterial wins out if competing |
|
|
What is an example of the arterial and venous baroreflexes competing?
|
- CHF
- Decreased CO and MAP - Increased CVP - Arterial reflex overrides, SNS is stimulated |
|
|
What is the cause and general response of the cerebral ischemia reflex?
|
- Stimulated by profound hypotension
- Defends against decreased cerebral blood flow by inducing super sympathoexcitation to save MAP |
|
|
What hallmarks are unique to the cerebral ischemic reflex?
|
1) Strong tachycardia
2) Low or normal MAP |
|
|
What hallmarks are present in the cerebral ischemic reflex and cushings reflex?
|
1) Decreased LOC
2) Irregular respirations (variable) 3) Dilated pupils due to sympathetic response (variable) |
|
|
What is the cause and general response of the cushings reflex?
|
- Stimulated by increased ICP
- Defends against decreased cerebral blood flow by inducing super sympathoexcitation to cause hypertension |
|
|
What hallmarks are unique to the cushings reflex?
|
1) Bradycardia (unknown reason)
2) Profound hypertension (arterial baroreflex interrupted) |
