Cardiovascular Flashcards
functions of the cardiovascular system
- bringing nutrient into the body (e.g. from the intestine to liver)
- bring fuel to cells
- bringing O2 to cells from lungs
- removal of waste products
- circulation of hormones
- circulation of immune cells and antibodies
- regulation of electrolytes
- regulation of pH
- H2O balance
- thermoregulation
- …….transport, transport, transport
Does an amoeba need blood
No
Fish Circulatory System
- Closed circulation
- Single loop circulation
- 2 chambers
- has gill capillaries + systemic capillaries
Amphibian & Reptilian Circulatory System
- 3 chambers
- double-loop circulation
- closed circulation
Mammalian Circulatory system
- 4 chamber heart
-double-loop circulation
-closed circulation
Right side
-pulmonary circulation
Left side
-Systemic Circulation
Septum
Part of the heart that separates the two sides
Haemodynamics
- the branch of physioology dealing with the forces involved in the circulation of the blood
- the circulation and movement of blood in the body and the forces involved therein
Volume (blood)
- 75% of weight is blood (75 kg man)
- 60% of blood is in the veins, why venous system is called capacitance
- Arterial system is called resistance, less blood flowing
Flow (blood)
- purpose of the card. system is to create flow
- flow coming into the heart has to be equal to flow coming out of the heart
- Flow = Volume/Time
- Flow = area x (mean)velocity
Flow = perfusion pressure/resistance
Flow from the left Heart
Cardiac Output
Flow from the right heart
Venous return
Total Cross Sectional Area and Flow Velocity
- Total cross section area increases as you go closer to the capillaries
- crs. sct. area decreases as you go towards the vena cava from the capillaries.
- Crs. Sct. area determines the pressure of the flow.
- Low flow velocity allows a more efficient transfer of oxygen
Pressure (blood)
-Pressure = Force/Area
S.I. unit: pascal(Pa) = newton/m^2
-n.m. 120/80 mmHg
Hydrostatic Pressure
Volume = area x height Mass = density x volume F= mass x acceleration due to gravity Pressure = Force/Area
Perfusion Pressure
Perfusion pressure = inlet pressure - outlet pressure
- The thing that will drive the flow is the difference between pressure
= arterial pressure - venous pressure
P = Pa - Pv
Resistance (blood)
Resistance = Perfusion pressure/ flow
Laminar or Parabolic Flow
- Smooth flow: lamiar or parabolic flow
- near the wall velocity decreases
- highest velocity is at the midline of the vessel
Friction losses in a viscous flow
generation of heat –> fall in pressure down the vessel.
Control of vessel resistance
- Vessels can contract or relax
- This changes the radius, thus affecting the flow of blood
Vessels in Series
Resistance = R1 + R2
Vessels in Parrallel
1/R = 1/R1 + 1/R2
Cardiac Valves
- all of the valves sit in the fibrous ring (connective tissue)
- bicuspid = two leaflets
- tricuspid = three leaflets
Injection Phase of the Heart
Ventricle contraction –> pulmonary valve opens –> valve then closes because the pressure in the ventricle falls as the heart stops its contraction process, at this point the pressure in the pulmonary track will be higher.
Chordae Tendinae
little fibers that attach the muscle to the cardiac valves
Sino Atrial (SA) Node
pacemaker of the heart. Activates a small amount of cells.
Endocaridium (enothelium)
muscle on the inside of the heart, closest to the blood
Epicardium
muscle just outside of the heart, second
Activation Sequence of the Heart
- need contraction of the atrium then the ventrile
- SA node sends signal that depolarizes the cells, sending electrical signals through the right atrium. The wave will die at the fibrous ring but will contrinue through the AV node –> then enter the bundle of HIS –> break into two bundles –> keep breaking up into very fine fibers –> purkinje fibers.
- These fine fibers tend to be in the endocardial muscle in the ventricle (NOT IN THE EPICARDIAL MUSCLE).
Muscle that first gets activated
Endocardial muscle then to the epicardial muscle, This creates a contraction.
Intercalated Disc
-Dark lines between cells
Nexus or Gap Junction
- as you go along the intercalated disc, you will run into a gap junction.
- Nexus = a connection or series of connections linking two or more things.
Hemi-channel or Connexon
- Channels that connect two cells
- If the membranes are close enough they will dock
- Through these channels, action potential can travel.
Local Circuit Currents
- Cells usually sit at -90mv
- Action potential is moving left to right
- Resting cell is negative compared to the outside
- Activated cell –> +40mv
- Potassium ion will move into resting cell due to opposite charge attraction
- Sodium ion will move into newly activated cell from unactivated
- Negative charges leave about to be charged cell
- Need both intra and extra-cellular flow
- Causes depolarization across the membrane
ECG Waves and Complexes
- P wave
- Q wave
- QRS complex
- R wave
- T wave
- amplitude ~1mV (vs 100 mV for an intracellular recording)
P wave
-indicates activation of both atrium. Only until the AV node do you see the Pwave
QRS complex
Activation of ventricles
Q –> Atrial Relaxation
RS –> Activation of the ventricles propagation
T wave
-repolarization from the ventricular muscles. (ventricular relaxation)
Ionic Basis Underlying Ventricular AP
- At rest, permeability to K is relatively high, permeability to sodium and calcium are low.
- When a membrane is only permeable to K it will reach close to -100mV.
- This is why at the start the membrane is close to -100mV
- The local currents is what causes the initial spike in potential
- Action potential will change the permeability to Na
- The positive Na ions will be attracted to the negative charge on the inside of the cell. Influx of Na ions.
- There is also a higher conc. gradient of Na outside the cell forcing ions in.
- Both conc. force and electrical force, will force ions into the cell
- This will depolarize the cell
- Fast inward Na current = quick turning off and on of Na Channels
Ionic Basis Underlying Ventricular Ap continued
- One class of K channel closes as result of depolarization –> permeability of K decreases
- Ca channels will notice increase in voltage, Ca channels activate slowly
- Ca channels are slow to open and close
- Conc. of Ca outside the cell is very high –> high force to push Ca ions into the cell
Another class of K channels that are lazy will wait till the end after recognizing the voltage increase, to open -This causes the cell to repolarize (more negative)
SA node Action Potential
- Instead of going back to resting potential after firing, it slowly depolarizes
- will slowly hit the threshold and fire
- no resting membrane potential in the Sinus node
- Here the influx of Calcium is what causes the depolarization
Purpose to why conduction velocity in the AV node is slow
the atrium needs to finish contracting before the ventricle begins contracting. Hence delay between the contraction of ventricle and atrium.
Sinus Bradycardia
rate
Sinus Tachycardia
rate > 100/min
Sinus arrhythmia
- on inspiration rate goes up
- on expiration, rate goes down
2:1 Atrioventricular Block
- Two p waves for one QRS and T
- P wave gets blocked somewhere in the AV, bundle of his or further down.
- Problem is that the ratio of P wave blocks may increase causes of failure of ventricle contraction
- Treatment: place an electronic pace maker in the heart.
Complete Atrioventricular Block
- P wave gets blocked somewhere in the heart.
- No QRST at all
- Treatment: “odds are you put in a pacemaker”
What happens in the ventricles during a complete atrioventricular block
- somewhere in the ventricles there is an area that has become a pacemaker
- spontaneously creating action potentials (thought to be in the purkinje fibers)
- SA node and atria are working together, whilst the ventricles are working at their own rate.
Premature Ventricular Contraction
- Ectopic beat because it comes from an ectopic pacemaker
- Ectopic means it is in the wrong place
Ventricular Tachycardia and Fibrillation
- Heart pumps sporadically, ventricles pump out blood, atria do no not pump blood into ventricles. Blood does not circulate body
- can be caused by a pre ventricular contraction (PVC)
Top of the heart is known as
the base
Bottom of the heart is know as
the apex
Left side of the heart
epicardial sack
Circus movement reentry
Action potential keeps traveling around the heart non-stop. Purkinje fibers must going into the atrium, or there is some sort of connection.
Pulmonary Vein Isolation For treatment of atrial Fibrillation
- cells are frozen to stop propagation of premature stimulus.
- when the action potential is released it would die in the ring of dead cells created.
Excitation-Contraction Coupling
- Action potential will run down the membrane
- The increase in voltage will be noticed by the Ca channes
- Ca will flood into the cell
- Ca that gets into the cell will bind to a receptor(ryanodine receptor) on the sarcoplasmic Reticulum
- SR is fucll of Ca at high concentration
- Ca that leaves the SR and goes into the cytoplasm
- The Ca will then combine with the troponin on the actin (in muscle)
- Thus resulting in contraction
*there is a Ca pump that keeps the SR concentration high
Pulseless electrical activity
action potentials are being sent off but no mechanical activity or pulse
Systole
-Ventricles start to contract –> atria ventricle valve opens –> the ventricle does not need to contract for very long until the pressure inside exceeds the pressure in the atrium –> atrial valves close.
- Systole refers to the fact that the ventricle is contracting
- At some point the pressure in the ventricle exceeds the pressure in the aorta –> the aortic and pulmoary valves open and blood is ejected.
- The ventricle is still contracting, the pressure is still going up
-The ventricle will then relax and the pressure drops.
Isovolumetric Ventricular Contraction
the blood volume is fixed, ventricle contract, so the pressure inside increases.
Diastole
- Filling of the heart
- The pressure in the ventricle is less than that of the aorta and pulmonary arteries –> the upper valves close –> the volume inside the ventricles is fixed –> enter the third phase –> the pressure in the ventricle falls lower than than the atrium.
-Blood enters the ventricle at relaxation and at atrial contraction.
Stroke Volume
Stroke Volume = End Diastolic Volume - End Systolic Volume
e.g. SV = 120mL - 50mL = 70 mL
Ejection Fraction
EF = Stroke Volume/ End Diastolic Volume
e.g.
EF = 70mL/120mL = 0.6 (60%)
Cardiac Output
CO = Heart rate x Stroke Volume
e.g.
CO = 70 per min x 70mL
=4900 mL/min
= 5 L/min
End diastolic volume
volume when the ventricle is filled
End systolic volume
volume when the blood is ejected
Starlings Law of the Heart (Frank-Starling Mechanism)
- If you increase the filling of the ventricle, then it contracts, the stroke volume will increase.
- The muscle will contract more forcefully because it is more stretched
- Stroke volume increases with volume increase.
-Right Atrial pressure is used as an indicator for pre-load
Abnormal Valve (Stenotic valve)
- fucked up valve
- narrowed valve
- turbulent flow = murmur
Abnormal valve (Insufficient valve)
- valve allows backflow of blood
- leaky valve
- Turbulent backflow = murmur
Total Peripheral Resistance TPR (Systemic Vascular Resistance)
- resistance of all the arteriole, etc.
- TPR = (Blood Pressure Mean (BPM) - Pressure in the right Atrium (Pra) )/ CO
Blood Pressure Mean (BP mean)
= CO x TPR
or
= HR x SV x TPR
*usually around 100 mmHg
Control of Vessel Tone
- Local factors: depending on what organs are around it. (local or metabolic)
- Neural: all vessels have some type of neural innervation
- Hormonal : hormones that flow through the blood
- Vessel tone: state of constriction of the vessel.
Pulmonary Vascular Resistance
- this is the resistance of the blood going through the lungs
- perfusion pressure is 10x smaller in the lungs, but the flow is the same
- Resistance is smaller than systemic
Systemic vs Pulmonary Circulation
Systemic Circulation - High Pressure, High Resistance
Pulmonary Circulation- Low pressure, low resistance
*flow is same for both
Coronary Arteries
-Heart feeds itself first. First arteries that come out of the aorta are the coronary arteries
Coronary Autoregulation
- when perfusion pressure decreases, the coronary flow will also decrease.
- coronary flow will bounce back up via decrease or increase of resistance depending on the state of the Coronary Perfusion Pressure (CPP)
Two mechanisms of Autoregulation
- Metabolic
- Myogenic (muscle)
- When flow of blood decreases, the O2 decreases to the tissue. Increase in waster products
- Vessel wall stretch decreases
- Metabolites act on the tissue relaxing it in turn –> decreasing resistance
- Resistance of the flow decreases –> flow increases
- Smooth muscle will recognize the fall in stretch –> decrease in resistance.
Local Metabolic Control
Increase metabolic activity –> decrease in O2 and increase in metabolic waste –> relaxes smooth muscle –> vessel will increase in cross sectional area –> resistance goes down –> flow increases
Activate the parasympathetic on Heart
- Slow the rate of the SA node
- ACh binds to receptor on the SA node –> slow it down
Activate the sympathetic system on heart
- increase rate of SA node
- Atropine, drug to get heart rate up. Binds to the muscarinic receptor. Stops ACh from binding which would have lowered the heart rate.
Sympathetic Control of Contractility
- Pre ganglionic axon, ACh neurotransmitter to nicotinic receptor. Two post ganglionic axons with NE released on the Sinus node.
- Send axons to the ventricular cells –> NE makes the cells contract, increase force of cell (increase size of Ca count)
- B-agonist will bind to Beta receptor and increase the contraction of the cells –> increase stroke volume, increase CO, and BP
- B-antagonist: block receptor –> decrease stroke volume, decrease BP.
What results in increased contractility
Increased Stroke volume
Epinephrine and Norepinephrine
- Both alpha and beta agonists
- Will increase the force of contraction, heart rate, and constrict the veins and arteries.
Baroreceptor Reflex
- In the carotid sinus and the aortic arch there are specialized nerve terminals that can sense stretch in the vessel
- If the arterial pressure increase the rate of firing in the baroreceptors increases
- Also vice versa
- Brain will recognize the decrease or increase in firing
- Will either inhibit the parasympathetic and sympathetic system
Afferent Arc of the Baroreflex
-Every reflex has an afferent arc. Information from receptor is sent up to the brain. Then the brain sends information via the autonomic system.
Afferent Arc - to the brain
Efferent Arc - to the blood vessel/organs/etc
How Baroreceptor Reflex works
Decrease in arterial pressure –> decrease in Arterial Baroreceptors firing –> Decrease in parasympathetic outflow to heart –> increase in sympathetic outflow to heart, arterioles, veins –> thus increase in HR, Contractility, vasoconstriction, vasoconstriction –> Pressure goes up
Effect of Baroreflex
- Increase in HR, SV, and TPR
- Increase venous pressure, during the diastolic phases the atrium will be more full, thus the ventricle will be more full
- End diastolic pressure will increase. Stroke volume goes up, CO goes up.
Autonomic Dysfunction
decreased working of the autonomic system
When baroreceptors are cut
- The systolic and diastolic fluctuate to high levels, resulting in high blood pressure
- no change in mean BP. Baroreceptors do not control the mean BP
Diuresis
kidney takes water out of the blood and puts it into the urine
Renin-Angiotensin-Aldosterone (RAA) system
- Arterial pressure falls, in the walls of the renal arteriole are special cells that make a hormone(actually enzyme) renin, that is dumped into circulation
- Renin will travel in the blood until it finds Angiotensin (created by liver)
- Turns it intro Angiotensin I, then travels to Lungs.
- Ace in lungs turns it into Angiotensin II(will contrict arterioles, increase TPR, and MAP)
- Angio II acts on particular parts of the brain so that it secretes a hormone called Anti-diuretic Hormone (ADH).
- ADH will act on the kidney to decrease the amount of diuresis. Retain water in blood.
Third - Ang. II will bind to cells on the adrenal gland. WHich then secretes aldosterone which causes Na to stay in the blood stream. Causing more water stay in the blood –> BP goes up.
Four major agents to bring down BP
- Aldosterone receptor antagonist: will bind to aldo receptor in the kidney. Will occupy the receptor but not activate it. Will decrease water retention
- Ace Inhibitor: Inhibits the enzyme that turns angiotensin into angio II. Body makes less Ang II –> lower BP
AT-II Receptor Blocker: Block all ang II receptors, stopping any of the above actions from happening
Renin Inhibitor: Inhibits the action of renin on angioten substrate to make Ang. I –> lower BP
