Kin 132 CV unit Flashcards
Explain what a positive and negative feedback loop are
Positive: Brings the change back towards the midline
Negative: Accelerates the change away from the midline
Explain the reaction pathway to a stimulus
A change in a controle variable caused by a stimulus is detected by receptors which send an afferent signal to a control centre which chooses a reaction. efferent signal is sent out causing a response which can cause positive or negative feedback loops.
What is plasma composed of?
- Water
- 90% - Proteins
- circulate in a inactive state - Other solutes
- Electrolytes, gases, Nutrient…
What is blood composed of?
- Plasma
- Cellular elements
What are the types of cellular elements found in blood?
- Erythrocytes: red blood cells
- Thrombocytes: Platelets
- Leukocytes: White blood cells
Explain what Erythrocytes are. Explain hemoglobin
- Biconcave disk shaped
- No nucleaus
- Contains high amount of hemoglobin (protein that helps with transport of gas)
Hemoglobin structure:
- 4 global chains with 4 heme disks that contain a iron core
- Oxygen and CO binds to iron in the heme disk for transport
- CO2 and Hydrogen bind to the globin chains for transport
In homeostasis, what are the points that trigger the increase or decrease of the variable in a negative feedback loop?
- Upper tolerance level
- Lower tolerance level
What is Erythropoiesis? How does it work?
- Stimulus of low Red blood cells is received
- The control variable is hypoxia at the kidneys. Receptors at kidneys detect this
- Kidneys, sensing a low level of oxygen, increase the secretion of eurethropointin (EPO) which is released into the blood
- EPO travels to red bone marrow which stimulates it to speed up the production of the erythrocytes
- More red blood cells are produced, increasing the oxygen transport sending the system back into its homeostatic range
What is hypoxia
Low oxygen delivery to the tissue
What is Hematocrit? How is it determine
What percent of the blood volume is red blood cells? Blood is spun in a centrifuge and separated into RBC and platelets + white blood cells
What does being anemic mean? How is it developed?
Anemia leads to having a lower bed blood cell count (lower hematocrit) when compared to the average leading to hypoxia.
Developed by:
- Blood loss,
- lack of iron,
- damage to critical development areas such as red bone marrow or kidneys,
- RBC destroyed (sickle cell anemia)
What does being polycythemic mean? how is it developed?
- Polycythemia leads to having a higher red blood cell count (higher hematocrit) when compared to average.
- can be true: Increased RBC count
- Can be relative: Decreased plasma level, same RBC level
Developed by:
- Bone marrow tumor
- Elevated living conditions
- Athletics
Explain how altitude training helps athletic performance
At higher altitudes, less oxygen is available. This means that less oxygen is being delivered to the kidneys resulting in increased erythropoiesis. When returning to sea level it takes time for the increase in RBC production to return to normal.
Explain what blood doping is and how it increases performance
Blood doping is when blood is removed from body, separate the RBC which are frozen. Before competition frozen RBC are reinfected increasing the oxygen delivery capability.
Another way is to inject EPO directly, skipping the kidney hypoxia step fully. Increased EPO results in short increase in red blood cell count.
Explain what thrombocytes are
- they are platelets
- Platelets are fragments of a megakaryocyte that have broken off
- No nucleus
- live for 5-9 days
- Main roll: Contain vesicles that store substances important for blood loss
What are the terms called for blood loss and storage of blood loss
Hemorage= blood loss
Hemostasis = stop of blood loss
Explain the process of Hemostasis with platelets
- Von willebrand factors are secreted by the damaged endothelium. This causes platelets to stick to the damaged tissue triggering step 2
- Vesecles in the platelets are opened releasing their content into the blood.
- ADP and serotonin: change the shape of the platelets
Thromboxan A2: attracts more circulating platelets to the damaged site. Once it attracts more platelets it triggers step 3 - Platelets become sticky to each other, attaching together and forming a plug (blocks hemorrhage in small injuries)
- PGI2 and nitric oxide is released from healthy endothelium preventing the first 3 steps from occurring. Only the damaged area releases thromxin A2. This helps keep the plug from forming at unwanted locations.
Explain blood clotting
- Occurs if the platelet hemostasis isn’t enough
- Clotting factors (type of plasma proteins) are circulating inactively in blood, but become active when in contact to damaged area. Fibrinogen gets converted to fibrin which forms a mesh at damage site
- Mesh traps material. plug from platelet steps plus the material collected in the mesh form a blood clot which seals the wound
- Clot dissolving (fibrinolysis):
- Plasminogen (inactive plasma protein) was incorporated in the clot. release of plasminogen activator from the health tissue causes it to break up the clot
What are thew 2 types of intravascular clots (clots in blood vessels). What’s the biggest risk with them?
- Thrombus: blood clot in a blood vessel that’s fixed in a location
- Embolus: Free floating blood clot in the blood vessel
Risks: The biggest risk is occlusion which is the blockage of a blood vessel. can cause heart attack, stroke, deep vein thrombosis
More likely if more plaque is built up on blood vessel walls as it narrows blood vessel
Explain the parts of a action potential
Resting membrane potential: membrane potential before a action potential
Depolarization: becomes less negative
Overshoot: membrane potential becomes positive
re-polarization: membrane potential comes more negative
Threshold: voltage required to trigger a action potential
What is the contraction and relaxation of the heart called?
sistole: contraction
Diastole: relaxation
explain the composition of the heart
- 99% cardiac muscle are contractile
- 1% are conduction system (generation and movement of AP)
Explain the sinoatrical node (SA node)
- Generation site of action potentials. Other parts of heart can send AP, but the SA node produces the most dominant one. considered pacemaker of heart
- Has no resting membrane potential: once re-polarized depolarized immediately
What is it called when a action potential is generated somewhere other than the SA node?
Ectopic focus
Explain the steps of a action potential in a SA node
- Ions slowly depolarize the cell until it hits the threshold triggering a AP
- Ca2+ voltage gate opens causing calcium to rush into cell rapidly depolarizing it
- K+ voltage gate channel opens + Ca2+ gate closes, causing K+ to rush out of the cell causing rapid re-polerization
Explain atrial muscle systole
- The action potential generated in the SA node travels to the atrial contractile cardiac cells which sits at a resting membrane potential of -90mv
- AP causes the Na+ voltage gate to open allowing for sodium to rush in cause a rapid depolarization
- Ca2+ gate opens as well as the K+ gate. Calcium rushes in, but potassium rushes out creating a plateau in the membrane potential. Ca2+ in flow causes the contraction of the atrium
- Ca2+ channels close, K+ channels stay open causing repolerization
- action potential speeds to next atrial contractile cell so quickly that they appear to contract together
Explain ventricular systole
- When Action potential travels to atrium to contract, it also propagates to the atrioventricular node (AV node)
- The atrioventricular node delays the signal ~0.1 sec letting atrial systole Finnish before ventricular systole begins
- After delay AP propagates (study pathway of this) to the ventricle causing ventricle systole
What are the differences in the Action potentials in atrial systole and ventricular systole?
- Atriol systole has begins before ventricular systole and has a smaller plateau
What is a EGC?
A graph that represents all of the ventricular and atrial Action potentials together.
- Amplitude = mv distance = time
What do the different parts of the EGC represent?
P wave: depolarization of the atrium
QRS complex: depolarization of the ventricle and atrium re-polerization
T wave: re-polerization of the ventricle
PR segment: AV node delay
ST segment: ventricular systole
TP segment: ventricular distole
What is the cardiac cycle
1 heart beat
Explain when atrial and ventricular systole begin and end during a electrocardiogram
Atrial systole begins at the P wave and ends during QRS complex beginning atrial diastole
Ventricular systole begins during the QRS complex and ends at the the end of the T wave. diastole then begins
What causes the blood flow to happen in the heart
Pressure differentials
What are the 2 types of valves in the heart and what are they? How does the valve work?
Atrioventricular valves:
- Bicuspid valve: between left atrium and ventricle
- Tricuspid valve: between right atrium and ventricle
Close by: Papillary muscles contract pulling the c horde tendinae closing the valve
Semilunar valves:
- Aortic valve: left atrium to the aorta
- Pulmonary valve: connects right ventricle to the pulmonary artery
Closes by: Backflow of blood get caught in cusps causing the valve to close
What phases do ventricular systole include?
- Ventricular isovolumetric contraction: Ventricle contracts but blood isle ejected because valves are closed. This causes the ventricle pressure to increase in oder to make the valves open
- Ventricular ejection: Blood is ejected from the ventricle through the now open valve
What phases does ventricular diastole include?
- Isovolumetric relaxation
- ventricular filling prior to atrial systole
- Ventricular filling during atrial systole
Explain the cardiac cycle
- Left atrium P > Left ventricle P
- Bicuspid valve is open
- Left Ventricle fills
- Left atrium systole pushes final blood volume into ventricle
- Left atrium P < Left ventricle P
- Bicuspid valve closes causing 1st heart beat (S1 Lub)
- Left ventricle filling is done
- -Left ventricle P < Aortic P
- Aortic valve closed
- Isovolumetric systole occurs driving the left ventricle P up - Left ventricle pressure > aortic pressure
- Aortic valve opens
- Blood ejects into aorta
- Left ventricle P rapidly decreases
- Pressure drops so Left ventricle P < Aortic P
- Aortic valve closes creating 2nd heart sound (S2 Dub)
- Left ventricle emptying ends
- Volume ejected from the left ventricle is the stroke volume (end diastolic volume - end systolic volume)
- Left ventricle P > left atrium P
- Left ventricle does isovolumetric relaxation causing a drop in pressure
- Left atrium P > Left ventricle P
- Bicuspid valve is open
- Blood that’s been collecting in the left atrium flows to the left ventricle (rapid at first then slow)
- Atrium systole pushes final volume into ventricle
- Repeat cycle
Explain what the end diastolic and end systolic volume is
The highest and lowest amount the ventricle is filled with blood
Which ventricle needs to produce more pressure. Left or Right? What does this result in?
- Left ventricle as it needs to push blood out to the parts of the body
- This results in the left ventricle to have much larger muscle thickness
What does strength train vs endurance training affect the ventricles
Strength training: thicker muscles in the left ventricle
Endurance training: Larger ventricle cavity
What is cardiac output (Q). What creates it?
Volume of blood pumped out of each ventricle (L/min). Created by multiplying stroke volume by heart rate
What’s heart rate
Beats per minute
What’s stroke volume?
Amount of blood ejected by the ventricle per beat
How does cardiac output (Q) change as exersize increases
In a linear fashion
What 2 categories is heart rate broken down into?
- Intrinsic heart rate:
- SA node firing without any other influences - Extrinsic heart rate:
- Other influences from outside the heart can either: - Positive chronotropic: Increase HR
- Negative chronotropic: Decrease HR
How are these influences in extrinsic hear rate being triggered?
Positive chronotropic: Sympathetic neural activation
Negative chronotropic: Parasympathetic neural activation
What is a “centre”
A group of neurons that receives info, anilines that stimulus and then sends out a efferent signal
What are the 3 smaller centres in the larger centre of the medulla oblongata?
- Cardioacelaritory center
- Cardioinhibitory center
- Vasomotor center
Explain the cardio acelitory pathway
- The cardioacceleratory centre sends out a signal to release norepinephrine which binds to beta receptors on SA node and AV node. This causes there SA node to increase firing rate and to shorten the AV node delay increasing heart rate.
- The cardioacceleratory centre also sends a signal to the adrenal gland to produce epinephrine which then binds to beta receptors on the SA and VA node, doing the same process as norepinephrine
Explain the cardioinhibitory centre
The cardioinhibitorary centre sends a signal to release acetylcholine which binds to musirinic receptors on the SA and VA node. This causes a increase in SAnnode firing and a delay on VA node delay which increases heart rate
The cardio accelerator and inhibitory pathways are types of what?
Positive and negative chronotrtpics
What is the trend between stroke volume and exercise?
Linier positive relationship until moderate intensity where it begins to plateau
What are the two categories stroke volume is separated into?
- Intrinsic Stroke volume:
- Stroke volume of SA node without any other influences - Extrinsic stroke volume:
- Stroke volume is affected by external factors primarily Preload and Contractility
What is Ejection fraction?
It’s the percent of the end diastolic volume ejected by the heart. It’s a way to express stroke volume as a fraction.
Ejection fraction = Stroke volume / end diastolic volume
Explain preload
- Definition: Volume in the ventricle before ventricular systole (same as end diastolic volume)
- Determined by venous return
What is frank sterlings law of the heart?
The heart contracts stronger during systole when it was filled more during diastole
What is venous blood return? What determines it?
- Amount of blood returning to the ventricle. More blood returned the stronger systole will be.
- Determined by ventricle filling time and venous pressure
Explain the factors that affect venous return
Ventricle filling time:
- The more in shape you are the lower your heart rate will be allowing for more time for ventricle filling
- Increase in ventricle filling time = increase in venous return = larger EDV = Larger stroke volume
Venous pressure:
- More pressure in veins leads to a higher Venus return = larger end diastolic volume = larger stroke volume
Explain contractility and positive/negative inotropic
- Definition: Strength of the cardiac muscles
- Ionotropic: affects contraction strength
What causes positive inotropic (increase contraction):
- Sympathetic neural signal
- Calcium
What causes negative inotropic (decrease contraction):
- parasympathetic neural signal
- Potassium
What’s the usual end diastolic volume?
130ml
Explain how the sympathetic neural activation causes a positive inotropic to increases stroke volume (atrium)
- Cardioaccelatorary center sends out Norepinephrine and tells the adrenal gland to send out epinephrine
- These neurotransmitters bind to the beta receptors on serial contractile fibers
- This is a positive inotropic affect causing stronger atrial systole = larger EDV = larger stroke volume
Explain how the parasympathetic neural activation causes a negative inotropic to decrease stroke volume
- The cardio inhibitory centre releases acetylcholine which binds to muscarinic receptors on the atrial contractile fibers
- This causes a negative inotropic, decreasing the atrium contraction strength = decreased EDV = decreased stroke volume
Explain how the sympathetic neural activation causes a Positive inotropic to Increase stroke volume (ventricle)
- Cardioacceleratroy centre sends signal to send out norepinephrine and to the adrenal gland to send out epinephrine
- They bind to beta receptors on the ventricle contractile fibers causing a positive inotropic = stronger ventricle contraction = stronger stroke volume = decreased end systolic volume
What is hemodynamics. What are the main factors?
- Factors affecting how blood flows though blood vessels
Main factors:
- Blood pressure
- Only interested in looking at pressure change when looking at blood flow (P2 downstream - P1upstream) - Blood resistance
- Friction as blood flows through vessels
- Equation: 8 x Length x blood viscosity / pie x radius^4
What factor affect blood resistance the most?
Radius since its to the power of 4
How to determine blood flow
F = Change in pressure / Resistance
What is the total peripheral resistance and mean arterial pressure?
TPR- Sum of all resistance in a system
MAP - Average pressure driving blood into tissues
MAP determined by:
- (Systolic pressure /3) + (2 x Diastolic pressure / 3)
What are the two ways to determine cardiac output
- Q = SV x HR
- Q = MAP/TPR
Explain the blood pressure change as it circulates
- High through arteries
- Decreases through arterioles
- low in capillaries
- low in venules
- low pressure in veins
- Pressure decreases with distance from the heart, but still has enough to return to the heart
Explain how resistance changes as it circulates
- Low in arterioles as as the radius is large = low resistance
- As Arteries branch off into arterioles radius decreases = increase in resistance
- Resistance increases dramatically when arterioles branch into capillaries
- Decreases dramatically when capillaries merge into venuoles
Explain velocity of blood flow as blood circulates
- Blood flow velocity constant through arteries
- Begins to drop in arterioles
- Reached lowest in capileries
- Speeds up as the resistance decreases in venuoles and veins
What are the two types of arteries
Elastic arteries:
- Larger to medium arteries
- ventricular systole stretches the elastic artery walls out allowing them to act as a pressure resevoir that recoils during ventricular diastole keeping the blood flow constant
Muscular arteries:
- Medium to small arteries
- Contain more muscle tissue and less elastic tissue
- Helps distribute blood around body
When is blood flow higher? during ventricular systole or diastole?
During ventricular diastole due to the elastic arteries acting as a pressure reservoir
Explain mean arterial pressure regulation
- Mean arterial pressure is highly regulated and is kept at at stable value
- Arteriol baroceptors are key receptors that monitor MAP:
- Carotid sinus: monitors MAP to brain
- Aortic arch: Monsters MAp to rest of body
Explain how MAP is regulated in the short term (seconds)
- Either Q or TPR changes in order to change MAP
- The baroreceptors (either the corotid sinus or the Aortic arch) detect a change in the MAP
- Signal gets sent to the cardiovascular centre
- To change Q
- The cardio acceleratory or inhibitory centre send a signal to change the HR (via SA node firing or VA node delay) or the SV (via preload or contractility)
or
- To change TPR
- Vasomotor center sends a signal to change blood vessel radius changing TPR - Change in Q or TPR cause a change in MAP
Explain how MAP is regulated long term (minutes to days)
- The baroreceptors detect a change in MAP
- Sends a signal to the CV center
- Sends out a signal to kidneys to change reabsorption and excretion as well as to the hypothalamus thirst center
- Increase or decrease in blood volume changes blood pressure changing MAP
Explain how the change in arterioles can increase TPR with sympathetic activation. (One of the pathways to change MAP)
- Vasomotor centre sends a signal to release norepinephrine as well as to the adrenal medulla to release epinephrine. It also sends a signal which releases angiotensin 2 which causes the release of antidiuretic hormone
- These neurotransmitters bind to the alpha receptors on the arterial
- this causes a vasoconstriction = increase in resistance
- Increase in pressure = increase ion TPR
Explain how the change in arterioles can decrease TPR with parasympathetic activation. (One of the pathways to change MAP)
- Parasympathetic signal sent to vasomotor center
- Vasomotor center send out signals to send out nitric oxide as well as too the adrenal gland to secrete epinephrine as well as causing the release of atrial natriuretic peptide
- These neurotransmitters bind to the beta receptors on the arterioles
- Causes vasodilation = decrease increase in radius = lower resistance = lower TPR
Do all arterioles have both alfa and beta receptors?
Yes, some have a higher concentration of one of them
What are some local effects on arterioles
- cold temp = vasodilation
- Hot temp = vasoconstriction
Explain what shunting is
- Using vasodilation and vasoconstriction to temporarily control where in the body receives the most oxygen to meet exercise demands
- Shunting causes vasodilation to heart, lungs, and skeletal muscles while vasoconstriction blood away from kidneys and digestive system
Explain how the amount of blood entering the capillaries is controlled
- Vaso dilation or contraction controls how much blood flow their is into the capileries
- Precapillary sphincters can be contracted or relaxed controlling how much of capillary bed is open
Explain the general fluid compartments
- extracellular fluid
- Plasma: outside cells in the blood
- Interstitial fluid: Outside cells in the tissue - Intracellular fluid
- Fluid inside the cells
Explain the 4 sterling pressures
- Osmotic pressures:
- Pushes towards a point in the blood or the interstitial fluid - Hydrostatic pressures
- Push away from a point in there blood or interstitial fluid
What is the net filtration pressure?
The net direction of all of the sterling pressures added together
Explain how the Net Filtration Pressure works at the capillaries
- Filtration
- At the start of the capillaries the NFP favours for movement from blood to interstitial fluid, dropping off O2 and nutrient - Absorption
- At the end of the capillaries the NFP favoured the movement from interstitial fluid into the blood causing the blood to take collect from the interstitial fluid
The venous system is considered a blood reservoir and has a high compliance. What does this mean
- Venous system contains most of the blood in the body
- CP (compliance) = Delta volume / Delta Pressure
What does venoconstiction and venodiloation cause?
- Vasomotor centre sends signal venous system to either vastconstrict or dilate
- This alters the blood reservoir volume which alters the venous pressure which alters the venous return which alters the stroke volume which alters the cardiac output
Explain the sympathetic pathway for the venous system
- The vasomotor center sends a signal to release norepinephrine, to the adrenal gland to secrete epinephrine and to secrete angiotensin 2 which triggers the release of antidiuretic hormone
- These neurotransmitters bind to the alfa receptors on the venous vessels causing venocontriction resulting in increased venous pressure
- this leads to a increase in venous return which leads to a larger end diastolic volume which leads to a larger stroke volume which leads to a increased cardiac output which leads to a larger MAP
Explain the parasympathetic pathway for the venous system
- Vasomotor center sends out a signal to release nitric oxide, tells the adrenal gland to release epinephrine and causes the secretion of atrial natriuretic peptide
- These neurotransmitters bind to beta receptors on the venous vessels causing a vasodialation resulting in a lowering of pressure
- This causes a decrease in venous pressure which leads to a lower end diastolic volume which leads to a lower stroke volume which leads to a lower cardiac output which leads to a lower MAP
Explain how skeletal muscles affect mean arterial pressure
- Contractions of skeletal muscle can squeeze venous vessels causing a local pressure change
- Squeeze of the muscle = increased venous pressure = increased venous return = increased EDV = increased SV = increased Q = increased MAP
Explain how the diaphragm increases mean arterial pressure
- Resperation pushes on the venous system
- This causes a increase in venous pressure causing the cascade of events that lead to the increase of MAP
