Integrated Physiology Test 2: Cardiovascular System
Valve involved in Heart Murmur
AV valve
Formed elements (cells)
About 45% of blood. This % is called the *hematocrit* or hct >RBCs (erythrocytes), bags of hemoglobin, carry gases >WBCs, involved in immune function, smears can tell us about disease >Platelets, important in blood clotting
What increases afterload?
>Vasoconstriction (constriction of blood vessels, which increases blood pressure) >Hypertension (high blood pressure) Basically anything that causes high blood pressure
How does the heart pump?
Cardiac muscle squeezes --> pressure increases --> blood flows from high to low pressure This is called *Bulk Flow* Forward flow direction is ensured by 1-way valves
Circuitry of Blood Flow: Pulmonary Circulation
(Continuing from Systemic) 6) Blood leave alveolar capillaries 7) Travels through pulmonary vein to left atrium --> mitral bicuspid valve to the left ventricle 8) From semilunar aortic valve to aorta to brachiocephalic trunk to common carotid -->subclavian artery --> Whole Circuitry of Blood Flow Process starts all over again @ Systemic Circulation
P-Wave
*Atrial depolarization* 1) Atria = full of blood 2) SA Node fires (note: electrical signal causes contraction to occur later in *P-Q*) 3) Electrical signals speed throughout atria & cause them to *depolarize*
R-Wave
*Ventricular depolarization* >Depolarization of main mass of ventricles
T-Wave
*Ventricular repolarization* >Ventricular repolarization immediately before ventricular relaxation/diastole >AKA ventricles are recovering and taking a breather
3 mechanisms affecting Stroke Volume
1) *Harder to Push Mechanism* (*afterload*): Higher arterial blood pressure will prevent aortic valve form opening as quickly during contraction --> lessens SV >Occurs during *systole* (ventricles are contracting: ejecting blood out of aorta & into pulmonary trunk) >High systemic blood pressure can lead to congestive heart failure by backing up blood into pulmonary system if it can't freely move into the aorta 2)*Frank-Starling Law (preload)*: Larger the ventricle volume just before it begins to contract = end-diastolic volume (EDV) will lead to GREATER SV 3) *Contractility*: Many nerves and circulating hormones have *cardiac muscle cells as targets* --> increases *contractility (more SV for a given EDV)* >This is WAYYY different from Frank Starling Law >Contractility = only mechanism by which brain can control SV
Circuitry of Blood Flow: Systemic Circulation
1) Blood leaves tissue capillaries 2) Enters superior vena cava to right ventricle 3) Pulmonary semilunar valve → pulmonary artery 4) Blood enters alveolar capillaries 5) Blood enters alveoli of lungs
Pulmonary Circulation Blood Flow (Condensed--this is probably the depth of detail that we actually need to know)
1) Blood returns to heart from body, enters right atrium 2) Blood enters right ventricle 3) Blood is pumped from right ventricle to lungs
Blood Movement Requires 3 Pumps
1) Heart 20 mmHg left (venules) to 0 (at atrium) >This is the remaining pressure form the aortic pressure 2) Skeletal Muscle Pump (see attached pic) 3)Respiratory Pump >Inhalation lowers chest pressure, drawing blood back to heart (sucking it in)
Systemic Circulation Blood Flow (Condensed--this is probably the depth of detail that we actually need to know))
4) Blood returns to left atrium from lungs 5) Blood enters left ventricle 6) Blood = pumped from left ventricle to body
Relationship Between Different Pressures
>*Average hydrostatic pressure = about 25 mm Hg* >*Average osmotic pressure = 24 mm Hg inward* for a *net outward push of 1 mm Hg* >A bit more fluid leaves capillaries than enters >This extra fluid = returned to blood by *lymphatic system* To be a little more snazzy... *Fall in pressure as blood moves through capillary:* >Result = net filtration on arterial end & net absorption on venous end
How do molecules enter & leave capillaries: Vesicular transport
>*Particular proteins* can be shuttled across endothelial cells by endo & exocytosis >Needed b/c proteins (being large & polar) CANNOT pass through cell membranes using methods of transport that we've already talked about
HR Control
>*nerve fibers* from cardiovascular control center (CCC) in brain + *hormones* from different organs go to *SA Node* >Modulate HR when they go to myocardium (muscle fibers) they alter strength of contraction (contractility) >If all nerves = cut, HR will rise from resting rate from 70 to 100 -- tells us that during resting state, nervous stimulation is slowing HR
The Heart
>2 pumps in series; pump from 5-6 to 30 L/minute (exercise dependent); through 60,000 miles of vessels, left pumps against a pressure of 100 mmHg; right, 30 mmHg in *thoracic cavity (chest)* along w/ lungs >surrounded by sac called *pericardium* -- low friction sac w/ pericardial fluid in sac -- sides attached to hear & thoracic cavity, lungs, Secure attachment > Low pressure in fluid keeps volume small
Blood Vessel Tour
>All vessels have an *endothelial cell layer* next to blood & a *basement membrane* >Basement membrane makes a proteinacious billo pad of *fibrous tissue* on the outermost surface to prevent blowouts >Except for capillaries, all have *elastic tissue* & *smooth muscle between those layers*
ISF and Lymph
>Blind End vessels have lower pressure on inside & higher pressure on outside >Back pressure closes minivalves >If ISF pressure = greater, then blood flows in! >If ISF pressure is less, then the valves close!
How do molecules enter & leave capillaries: Bulk Flow
>Blood (hydrostatic) pressure in capillaries = greater than ISF (ECF) pressure, therefore any leaks cause flow (think of a soaker hose!) >These leaks include gaps between cells & aquaporins (water channels)
Chart of Resistance in Blood
>Blood follows path of resistance >If more blood is needed in a lot of organs, then new *parallel circuits* will open up and TPR will fall While emptying a swimming pool, the more siphons ya use, the faster the pool will empty! There is less total resistance to flow! >Now during fall of TPR, if CO stays constant, what would happen to MAP? It would fall, as MAP = controlled variable in the CV system >If TPR falls, the CO must increase to keep MAP constant CO = MAP/TPR MAP = CO * TPR
Bulk Flow in Vessels
>Blood moves or flows *en masse* >It is 1 dynamite mass-transit system
Edema can also be caused by...
>Breakage of capillaries,*lowering resistance to bulk flow out of capillary* >Histamine release, which enlarges gaps between endothelial cells, again enhancing bulk flow >Blockage of lymph flow (e.g. elephantitis -- see photo)
Relationship between Intrinsic Frequency & Electrical Signal Speed
>Cell w/ highest intrinsic frequency starts process of electrical signaling >This cell lives in SA node in the right atrium >Since SA node always starts wave of depolarization, when we need to alter HR, nerve fibers to this cluster of cells in SA node & release substances that change slope of rise of membrane potential toward threshold >Reaching threshold quicker incereases heart rate & vice versa
Relationship between Vasoconstriction and Blood Flow
>Constricting a blood vessel (vasoconstriction) = less blood goes past >Where does fluid resistance come from? Think of a small slow-moving stream! >Water by edge is barely moving & water in center is moving along at a good clip! SAME W/ BLOOD VESSELS! >@ edge where blood is rubbing against vessel wall, (AKA resistance), it is barely moving >As it moves out to center it speeds up Concentric rings metaphor >As each ring is traveling @ diff speed, they are rubbing against each other
Capillaries & Exchange
>Dependent on location, have different exchange requirements >Due to differences in tightness of junctions holding endothelial cells to one another >NOTE: capillary cross-section has evolved just to fit a RBC
Slope of Pacemaker Potential
>Determines heart rate >Affected by nerves & hormones acting on certain pores or channels
What controls blood flow?
>Either through the whole system or through a particular capillary bed; the 2 main variables are 1) *Difference in pressure* (How strong the push is) 2) *Resistance* to flow
How does the signal rocketing over cell membrane (change in Vm) get *inside* cell to the actual contractile machinery?
>Electrical signals coursing over membrane *change their method of encoding info* & *enter cell interior* by using *influx in calcium!* >This is an example of transduction! >Signal changes from electrical event traveling over cell surface to a burst in Ca++ entering cytosol >Accomplished via use of a *voltage-sensitive calcium channel* & *calcium-induced-calcium release*
Physiological control of Erythropoiesis (making new RBCs)
>Erythropoietin: Signal to bone marrow, released by kidney when oxygen delivery is low >Why do we need to make so many RBCs? They only last 120 days (lack nuclei so they can't repair themselves)
New RBCs are Continuously Made
>Factories = in red bone marrow >100 billion cells made each day, 1-2 million per sec >Made from "stem" or "blast" cells called hematopoietic stem cells >These cells differentiate (morph & then commit) into cell types that begin producing hemoglobin; when they've made enough they expel organelles & are well on their way to becoming an RBC >Enter bloodstream as reticulocytes (RBCs that have not yet expelled their endoplasmic reticulum) >Ratio of reticulocytes to older RBCs = good indicator of recent RBC synthesis
What does blood carry? How much?
>Gases, nutrients, messages, & elements of the immune system > 4-6 Liters/human; buffered to pH 7.4
How do the blood flow variables relate to flow?
>Greater pressure difference = greater flow...THUS they are directly proportional >Greater resistance means less flow...THUS indirectly proportional SO... back to our old formula! *Flow = Change in P/R)
Why is Frank-Starling unique?
>Happens automatically >Does not require the cardiovascular center telling it what to do, it's built in (AKA *intrinsic*!)
Why is Dup higher than Lub?
>Heart sounds = caused by valves snapping shut >Rapid shutting causes reverb in the affected blood vessels & heart >Lubb comes from reverb in atrium & vein as a consequence of AV valve closing, very low-pressure compartments >AV valve shuts doe to ventricle beginning its contraction >Dupp = caused by reverb in the aorta due to aortic valve shutting as heart relaxes >Aorta = high pressure area, walls of aorta = tighter, less compliant, & these reverberations lead to higher frequency sound >THINK of frequency difference between plucking guitar strings: 1 is much tighter than the other
Myogenic Control
>Higher anteriolar pressure stretches smooth muscle cells, they respond by contracting >Keeps flow relatively constant in a capillary bed, but it is easily overridden by other factors
Plasma (liquid fraction)
>Water >Proteins -- *Albumin*, from liver, used in osmotic balance -- *Globulins*, transport proteins and antibodies (immunoglobins) -- *Fibrinogen*, and other clotting factors -- Other: e.g. *Nutrients (sugars, fats), gases, electrolytes (salts)*
Excitation-Contraction-Coupling
>How does cell change/transduce nature of the signal? *Electrical signal going down membrane = sensed by voltage-sensitive channel*. It is a *voltage sensitive calcium channel --> responds to change in membrane potential by OPENING causing there to be a huge puff of Ca++ >Then channel in an interior organelle, the *sarcoplasmic reticular* responds to increased Ca++ by opening its channel (also a Ca++ channel) --> causing amplification of signal to a LARGER increase in intracellular Ca++ >Amplification process is called *calcium-induced-calcium release* -- release is from the *sarcoplasmic reticulum*
Volume Flow Rates
>IF Cardiac Output is 5 L/min leaving heart, won't it be 5L/min entering heart? Isn't it also 5 L/min of blood passing through capillaries? >Water speeds up as canyon narrows (linear flow rate) >But didn't the water's volume stay constant? If not, where did the water go? Imagine water moving in center of very large river @ 5 miles/hour & compare volume flow in trout stream w/ 5 mile/hour speed....is same volume of water going by each second? NO While linear speed is same, volume flow rate is super diff... *Average Linear Speed* * *Cross Sectional Area* = *Volume Flow Rate*
Contraction at the Cellular Level
>Image shows intercalated discs (dark) that link cells together, & striations (stripes) >Signal for contraction in muscle cell is *a change* in the membrane potential (AKA group of ionic charges aligned across from one another on cell membrane >It's a change in membrane potential that flows through gap junctions
Cardiac Muscle
>Involuntary (no conscious control) >Contractile cells organized into 2 large networks: *Atrial & Ventricular* by *gap junctions* -- electrical conduits or synapses between cells (see sketch)
Body's Intent
>Keep MAP close to 100 mmHg >Controlled variable in CV is MAP!
Arteries Tour
>Large diameter, therefore little friction, therefore very small pressure drop >Carry blood *away from heart* >Lot of elastic tissue to withstand high pressure
S
>Last phase of ventricular depolarization at base of heart >Atrial re-polarization also occurs during this, but signal is obscured by large QRS action potential
Local Control
>Local activity affects local concentrations of carbon dioxide, oxygen, and acid >These molecules affect the smooth muscle cell tension
Lub!
>Lower pressure >AV valve closes
Relationship between Cardiac Output for Right & Left Hearts
>MUST be matched >Since there is roughly 1/3 the resistance for blood flowing through lungs, we see why arterial pressure in pulmonary circuit is 1/3 as great https://www.khanacademy.org/science/healthcare-and-medicine/the-heart/blood_pressure/v/putting-it-all- together--pressure--flow--and-resistance
Life Cycle of RBC
>Macrophages (big eaters) sense when RBCs are old & then engulf them >These macrophages live in the *liver, spleen, and bone* >Most materials are recycled (amino acids, lipids) >Iron from heme is carried by *transferrin* to liver or spleen, where it is stored, bound to *ferritin* >When needed, iron is sent to bone marrow to make more hemoglobin >Rest of heme is converted to urobilinogen, then to stercobilin, which gives feces their brown color >Bilirubin gives plasma its straw color >Neonatal jaundice: treat w/ UV light -- converts bilirubin to something more easily excreted (Jaundice = yellow skin)
How do precapillary sphincters change resistance?
>Need more flow? *Vasodilation*, relaxation of smooth muscles surrounding arteriole, opening small tufts of muscle that are precapillary sphincters (Warms body) >Too much flow? *Vasoconstriction* tightens smooth muscles, reducing flow (Makes body cold)
Extrinsic/Systemic Control
>Nerves from central nervous system (releasing norepinephrin, or ACh) & various circulating hormones (EPI, AII, ADH) cause resistance & flow to change >Often part of the response in maintaining MAP
Frank-Starling Mechanism
>Occurs during diastole (ventricles being filled with blood) >*Stretching cardiac muscle makes the calcium signal work better*, strengthening contraction >Increase in troponin affinity for calcium (AKA it binds it tighter, leading to more binding sites being taken up) >*Oars contact water better* >Thus, as End Diastolic Volume rises, so will SV; heart only uses left side of curve in health >FS controls matching of right & left hearts >Causes big beat after ectopic focus (heart skipping a beat)
How do Nerves & Hormones affect Heart Rate?
>Open H channels, changing slope of diastolic depolarization or pacemaker potential towards threshold >Nerve fibers also go to AV node & modulate the speed of conduction >@ higher HR, the AV node no longer gives the atria a generous headstart
Control of Blood Flow
>Optimal functioning of cells is dependent on this *Flow = Change in Pressure/R* for ALL Bulk Flow Systems How is this flow regulated? >Bodies maintain *MAP* in all healthy situations...Thus MAP is our controlled variable >Organ flow is controlled by *post arterial resistance* >Main vessels that change resistance are *precapillary sphincters that either open or close*
Blood Vessels Function
>Pipes: Carry blood >Have specialized diffusional exchange areas (capillaries) to exchange materials w/ ISF >*CV System*: 2 pumps in series
S-T Segment
>Plateau in myocardial action potential >This is when ventricles contract & pump blood
Why is resistance WAYY larger in vessels of small cross section, compared to larger?
>Resistance is proportional as 1/r^4 >Think of a trout system in the Mississippi River For both, @ water's edge, flow is theoretically 0; this is the *unstirred layer* >For both, water speed builds up as one heads away form edge >Mississippi will have greater speed in its middle but if there was a bridge and wood chunks thrown into river, how much would speed change over center 100 ft of Mississippi? NOT MUCH AT ALL! >SO in a large vessel in a wide river, the speeds in center do not vary greatly from one another, yet in a tiny vessel, there's a large diff in speeds between all rings....THUS *greater friction = greater pressure loss*
Control of Stroke Volume
>SV is affected by *3 distinct* mechanisms >Cardiovascular center in brain has control over just one of them to actively control SV (contractility)
Cardiac Muscle & Contraction
>Signal for contraction is *electrical* being a *change in membrane potential*, the *separated charges held apart by membrane* >Membrane channels transiently open, allowing ions to flow and change the # of opposing charges held apart by the membrane, therefore changing the membrane potential >Allows contraction signal, change in membrane potential, to run from 1 cell into the next -- This is called *syncytium* >Function: *gap junctions ensure that ALL cardiac muscle cells in syncytium contract @ SAME time* >If this doesn't happen, you can die within SECONDS (fibrillation)
Relationship between Membrane Potential and Time
>Signal originates @ Sinoatrial (SA) node >Spikes = *action potentials* -- electrical trigger for muscle cells to contract >Dashed horizontal line = *threshold potential* -- when membrane rises to TP, the spike fires >These SA nodal cells are *autorhythmic: their membrane potentials drift up to a threshold potential by themselves* >This is seen in *slow depolarization/pacemaker potential* >When membrane potential reaches threshold, cell fires & spike travels cell to cell via gap junctions >Cell = unique & doesn't need anyone else telling to when to fire; it can do it on its own! That's why it's autorhythmic! >Quicker cell reaches threshold, higher the heart rate
RBCs
>Small biconcave discs, good shape for getting through capillaries >Filled w/ hemoglobin >Lacks all organelles, including nucleus & mitochondria
Rule of Thumb for Vessel Size
>Smaller vessel the rings of fluid near center are going at very different speeds >Larger vessel, the rings in the center are close to same speed, which means less rubbing >This is the reason there's more resistance in smaller diameter vessels, explaining why more resistance in smaller diameter vessels, which explains the large loss of pressure as blood travels through them >Another contributing factor: In both cases, resistance against vessel edge (in unstirred layer) is theoretically infinite >Due to geometry, in a small vessel there's greater proportion of fluid rubbing against wall than in large vessel
Capillaries Tour
>Specialized for diffusional exchange although other exchange is present >Thin-walled; only endothelium and brillo pad basement membrane (fibrous tissue) >Material can move through & between cells, using both diffusion and vesicles >Also have tufts of smooth muscle controlling entry of blood into a particular capillary
Arterioles Tour
>Spigots of system, between arteries & capillaries >Very muscular; control flow by constricting or relaxing smooth muscle to change vessel radius >Function like tourniquets: control how much blood flows into the capillary beds
Electrical conduction pathway
>Starts from SA node 1) Sinoatrial node (pacemaker) 2) Atrioventricular node 3) Atrioventricular bundle (Bundle of His) 4) Bundle branches 5) Purkinje fibers
Arteries in the Cardiovascular System
>Swell/inflammate during systolic ejection due to greater pressure >Elastic recoil of arteries drives blood forward during diastole >Flow from heart is intermittent, then becomes continuous in capillaries
Hemoglobin
>Tetramer, each monomer binds an iron-containing heme group >Heme binds oxygen, when bound heme = bright red, unbound dark red >Each RBC can bind a billion oxygen molecules...think about stickiness; must be just right to bind & release oxygen @ appropriate time & place >Carries & binds CO2 to make carbaminohemoglobin; and protons (acid), which buffers blood >Human genome has 4 diff monomers; there are even more if you consider fetal hemoglobin... arose gene duplication, followed by mutation. >Increases complexity over time as we get diff types of hemoglobin >Some arctic fish have seriously mutated hemoglobin to point of being completely non-functional (fossil DNA)
Forces Responsible for Movement of Fluid Into & Out of Capillary
>There is *hydrostatic blood pressure pushing plasma out* >Most capillaries: *medium to large proteins CANNOT leave* through holes between endothelial cells >As fluid leaves capillary blood, pressure drops from 35 to 15 mm Hg -- This drop lessens outward bulk flow of liquid >Now protein: there's *greater concentration of protein in plasma than ISF* -- This causes *osmotic* (called *oncotic* due to *difference in protein concentration* force that *pulls fluid back into blood*) >Osmotic force = result of water hitting holes @ different rates from 2 sides >There is a battle between *hydrostatic & oncotic forces*! See sketches:
Take Home Messages for Capillary Exchange
>There is an outward filtration pressure >There's inward osmotic pressure caused by greater protein concentrations in the plasma relative to the ISF >Due to liver putting a lot of protein (albumin) into the blood, through very large endothelial gaps, & b/c large proteins are prevented from entering the ISF from normal capillaries....this is called *oncotic pressure* or a *colloid (dissolved large stuff) osmotic pressure* >Net result in normal capillary bed = slight net outward pressure, thus a bit of fluid = constantly lost to ISF...this is picked up by lymph vessels & returned to blood via a large vein
Important things to note about Electrical Conduction pathway
>There's a layer of tissue separating atria from ventricles that does NOT allow electrical conduction >This non-conducting layer is pierced by the *Atrioventricular (AV) node* >*Conduction through AV node is SLOWED* -- allows atria to contract slightly before ventricles >Why? Once mighty ventricles begin contracting, *ventricular pressure* INCREASES so quickly that the AV valves shut, preventing any more blood entry from weaker atria
How are capillaries special?
>Thin-walled >Lots of surface area as each one = tiny in cross section (small things have greater surface area to volume ratio) >Continuous blood flow >Slow flow due to large total cross sectional area >Specialized transport mechanisms
Veins Tour
>Thin-walled, little elastic tissue or muscle >Distensible, compliant >Important blood reservoirs, normally contain 60% of blood in system -- when body needs more blood, smooth muscle surrounding veins will squeeze, moving blood forward, into heart (EDV rises, thus CO rises)
Types of Capillaries
>Varying tightness of biological welding material, tight junctions that join cells, modulate ability of material to move between cells >Matched to function >*Brain & joints*: extremely tight (e.g. Blood Brain Barrier--have very tight junctions between endothelial cells) >*Continuous*: normal capillaries, small molecules can slip between endothelial cells >*Fenestrated*: (e.g. kidney) only small proteins can pass >*Sinusoidal*: (e.g. in liver) all proteins can pass
What determines *resistance to blood flow*?
>Whether it is *laminar* or *turbulent flow* -- Turbulence has eddies, etc. Laminar is straight flow. .*Blood flow = Laminar* >Viscosity: unchanging, except for high hematocrits >Vessel length = unchanging except for obesity >Physiologically, it's the *vessel radius* controlled by smooth muscle surrounding arterioles >*Smooth muscle* can constrict to *make vessel opening smaller* & *increase resistance* & vice versa
Control of Cardiac Function
>output of heart per min, (cardiac output) = product of how many times heart beats per minute (heart rate) & how much comes out w/ each beat (stroke volume) CO = HR * SV >CO @ rest = approx. 5 L/min @ exercising rate = 30 L/min >control of CO occurs via internal & external controls (both nerves & hormones)
Electrocardiogram (ECG)
>since signal for all cardiac cells to contract = electrical change, when charges & conducting fibers are added together, it is sufficiently strong where these signals can be sensed @ body surface >Rationale for ECG >ECG process occurs from sinoatrial node to atrioventricular node
Major compartments seen in centrifuged sample of blood
Plasma, Formed elements (cells), and RBCs/Erythrocytes
Q
Depolarization of interventricular septum
How do molecules enter & leave capillaries: Diffusion, facilitated, active transport
Gases, lipid soluble molecules, sugars, amino acids, ions, etc. can move across & between endothelial cells by methods we have discussed
Dup!
Higher pressure, closing of aortic valve
Contractility
How hard myocardium contracts for a given pre-load. >In contrast to Frank-Starling, this is initiated by commands from the *cardiovascular control center* >*Controlled by nerves & circulating hormones acting on myocardium* >Increase in contractility means *larger SV for a given EDV* >Cause: *Cell releases more calcium into cytosol* per contraction NOTE: this is different from making the given calcium more efficient
Smooth Muscle
Involuntary muscle surrounding arterioles that dilates & constricts to control blood flow
What tells smooth muscle to do the right thing?
Local control, Myogenic control, & Extrinsic/Systemic Control!
Mean Arterial Pressure (MAP)
MAP = DP + 1/3 PP
What do ECGs for arrthymias look like?
P-Wave becomes *very* absent
Order of ECG
P-Wave, P-Q, Q, R-Wave, S, S-T, T-Wave
Pulse Pressure Equation
PP = SP - DP
Each of the blood movement pumps cause....
Pressure differences that drive *bulk flow* >In *bulk flow*, fluid always travels from high to low pressure >& while *fluid travels, pressure drops* Why? Fluid movement must overcome *fluid friction* >Greatest pressure drops occur in regions of greatest resistance >These regions include *arterioles & capillaries* (see pressure drops in attached graph SP = Systolic Pressure; peak pressure in large arteries. Occurs when heart is contracting DP = Diastolic Pressure; lowest pressure in large arteries...Pressure falls when the heart is not actively pumping and blood is leaving the arteries to go into capillaries. Heart needs to relax to fill w/ blood
P-Q Segment
Represents *time signals travel* from *SA Node* to *AV node* *Note:* Atrial contraction/systole starts 100 millisecs after P-Wave
QRS Interval
Represents firing of AV node, represents ventricular depolarization
Blood Vessels in Cardiovascular System
Restricted to 1-way flow due to flap valves >Arteries *control flow & regulate Medial Arterial Pressure* >Veins are for *return & storage* via Right Heart >Pulmonary Arteries *control flow* >Lung Cars *exchange gases* >Via Left Heart, Systemic Arteries *carry blood away from heart*
Relationship between SP, DP, Mean Pressure, and Pulse Pressure
SP = Systolic Pressure; peak pressure in large arteries. Occurs when heart is contracting DP = Diastolic Pressure; lowest pressure in large arteries...Pressure falls when the heart is not actively pumping and blood is leaving the arteries to go into capillaries. Heart needs to relax to fill w/ blood
Interpreting Linear Flow Rate
See graph... >Linear flow rate slows as total cross sectional area increases >Speeds up again as blood enters veins Analogy: sitting in canoe... seems as if water isn't moving but it really is moving really fast >Thus linear speeds are very different but volume flow rate is same In graph: >As total cross sectional area of vessels increases, linear speed slows This can be confusing cuz capillaries have tiny cross sections, but the point is that there's millions in our body so total cross sectional area adds up to far more than aorta
Electrical System of Heart Videos to Watch
Short: https://www.youtube.com/watch?v=te_SY3MeWys Long, Well Done Vid: https://www.khanacademy.org/science/healthcare- and-medicine/heart-depolarization/v/electrical-system-of-the-heart
What does calcium do in the Excitation-Contraction Coupling process?
Signal that will trigger contraction
Venules
Small, collecting vessels bringing capillary blood to veins
Why capillary function is soooo important: Edema
There are many clinical implications! Edema = *enlargement of ISF* >High blood pressure or low plasma protein concentration will lead to extra fluid loss to the ISF -- this is called *edema* >Diseased liver or protein malnutrition (not enough protein synthesis) or kidney (protein loss into the urine) might cause this >This should make sense if you understand the model >Edema causes *increased lymph flow*
Through either pulmonary or systemic circuits....
Total flow per minute = Cardiac Output >We already know CO = HR * SV Change in pressure = MAP Resistance = Total Peripheral Resistance (i.e. total resistance either going through pulmonary or systemic circuit) THUS... flow through an entire circuit is: *CO = MAP/TPR* Through a single organ, *Flow = Change in Pressure/Resistance of organ*
Analysis of ECG Diagram
https://www.youtube.com/watch?v=v3b- YhZmQu8&NR=1&feature=endscreen
Capillaries
pipes specialized for material exchange between blood and ISF (NOTE: ISF (interstitial fluid--fluid that cracks between cells) is the ECF excluding the blood and lymph)
