TEST 3: Cardiovascular Flashcards
What is the function of the circulatory system?
P. 1020
-Transports nutrients, oxygen, hormones to the cells and removes waste
-Two branches:
-Right heart pumps blood through the lungs (pulmonary circulation)
-Left heart pumps blood which is everywhere else (systemic circulation)
Blood flow into and out of the heart
( Organizer)
Right heart pumps UNoxygenated blood thru pulmonary circulation—>
This is where oxygen enters the blood and carbon dioxide is exhaled —>
The left heart pumps Oxygentated blood to and from all other organ systems
Blood flow begins at left ventricle —> flows thru the arteries and capillaries and veins to the right atrium —>
Right ventricle—> pulmonary artery—> pulmonary veins —> left atrium —>
Back to the left ventricle
3 layers of heart wall
P. 1022
- Epicardium (smooth layer that minimizes friction between heart walls d pericardial sac)
- Myocardium (thickest layer that is composed of cardiac muscle and is anchored to the hearts fibrous skeleton)
- Endocardium (internal lining of myocardium compounded of connective tissue/ squamous cells and is continuous with the endothelium that line all arteries/veins/ capillaries ensuring a closed circulatory system)
Functions of the pericardial sac
P. 1021
-Provides heart stability in the thorax
-Reduces friction between the heart and mediastinal structures
-Limits the size of heart chambers
-Provides a barrier to prevent spread of infection
-Contains pain receptors/ mechanoreceptors that can cause changes in BP/ HR
Vasculature
(Lecture)
- Arteries: transport blood under high pressure from the heart to the capillary beds (high pressure system with thick muscular walls)
- Arterioles: smaller branches of arteries that are conduits between arteries and capillary beds of tissues (muscular walls and sphincters)
- Capillaries: extensive vessel network that supplies blood to the cells and are areas of substrate exchange (thin walled with pores for permeability)
- Venules: collect blood from capillaries and coalesce to form veins (not muscular)
- Veins: transport blood from venules back to the heart and act as a reservoir (low pressure system with thin walls)
Chambers of the heart
P. 1022
-Right heart is a low pressure system pumping blood through the lungs
-Left heart is a high pressure system pumping blood through the rest of the body
-Atria are smaller than ventricles and have less thick walls
-Ventricles are more structurally complex
Valves of the heart blood flow
P. 1023
Deoxygenated blood enters the right atrium from the body via superior and inferior vena cava —> blood flows through the TRICUSPID VALVE into the right ventricle —> right ventricle contracts and blood exits through the PULMONARY SEMILUNAR VALVE into the pulmonary arteries —> blood picks up oxygen in the lungs and returns to the left atrium via the pulmonary veins—> blood then flows through the MITRAL VALVE into the left ventricle—> left ventricle contracts, pushing blood thru the AORTIC SEMILUNAR VALVE into the aorta, where its circulated throughout the body.
Atrioventricular valves =
-tricuspid (right heart)
-mitral (left heart)
Semilunar valves=
-Pulmonary semilunar (right heart)
-aortic semilunar (left heart)
Mitral and tricuspid complex functions as a unit and is made up of
P. 1023
- Atria
- Fibrous rings
- Valvular tissue
- Chordae tendinae
- Papillary muscles
- Ventricular walls
-Side note: damage to any one of these can alter heart function and contribute to heart failure
Intracardiac pressures of valves
P. 1025
-Pressure gradients ensure that blood only flows one way through the heart
-When ventricles relax, the two AV valves open and blood flows from higher pressure in the atria to lower pressure in the ventricles
-As the ventricles contract, ventricular pressure increases and causes those valves to close and prevent back flow to the atria
-Semilunar valves open when ventricular pressure exceeds aortic/ pulmonary pressures, and blood flows out of the ventricles into circulation
-After ventricular contraction and ejection, pressure decreases and semilunar valves close, preventing back flow to the ventricles
Two main left coronary arteries
(Lecture and p. 1026)
- Left anterior descending artery (supplies the left and right ventricle/ intraventricular septum)
- Circumflex Artery (supplies the left atrium and left lateral wall of left ventricle)
Right Coronary Artery
(Lecture and p. 1026)
-Does have some branches off of it but main artery is right coronary artery
-Branches off into the conus (supplies blood to the upper right ventricle), the right marginal branch (supplies blood to right ventricle to the apex), and the posterior descending (supplies smaller branches to both ventricles)
Pressures in circulatory system
(Lecture)
-Systole = contraction of heart
-Diastolic = relaxation and filling of the heart
-Right side of the heart should have lower pressure than the left side of the heart
-Left ventricle has highest pressures
-Elevated right heart pressures usually indicate back up/ congestion (ie pulmonary edema)
Flow (Q) through a blood vessel
Determination and Considerations
(Lecture)
-Is determined by:
-Pressure difference (^P) between 2 ends of a vessel
-Resistance (related to diameter of a vessel)
-Viscosity (n) of the blood
-Length (l) of the vessel
Consider
QP : QS ratio
(Flow of blood to the lungs) : (flow of blood to the body)
-Helpful in pulmonary hypertension metrics
Conduction System Review
(P. 1029)
-Sinoatrial Node (SA) : pacemaker of the heart; Carries action potential to both atria to contract, beginning systole (located at the junction of the right atrium and superior vena cava above the tricuspid valve)
-Atrioventricular node (AV) : receives action potential from SA node and carries it to the ventricles (located on the right atrial wall and above the tricuspid)
-Bundle of HIS (AV bundle) : conducting fibers from the AV node converge to form this; this then gives rise to the right and left bundle branches (located in the interventricular septum)
-Right bundle branch: thin and travels without much branching to the right ventricular apex (because it’s thin it’s susceptible to interruption of impulse)
-Left bundle branch: divides into two branches —> left anterior bundle branch (passes thru papillary muscle) and left posterior bundle branch (posterior papillary muscle) LBB is more protected than the right
-Purkinje Fibers: the terminal branches of the RBB and the LBB (they extend from the ventricle apexes to to the outer myocardium) this extensive network of fibers promote the rapid spread of impulses to the ventricle apexes)
Quick overview of cardiac excitation
(P.1029)
-From the SA node, the impulse that begins systole spreads throughout the right atrium —> the action potential is delayed at the AV node (the delay between the atrial and ventricular excitation gives an extra boost to ventricular filling by atrial contraction which is your “atrial kick”) —> from the AV hide the impulse travels from the AV bundle and thru its branches to the purkinje fibers (conduction velocities in the AV/ Purkinje are the most rapid in the heart) —> the interventricular septum is activated by the RBB and LBB (travels left to right) and the extensive network of purkinje fibers promotes the rapid spread of impulses to ventricular apexes
The Electrocardiogram quick overview
(P. 1031, lecture)
-P wave: atrial depolarization (SA node)
-PR interval: pause of conduction; a measure of time from the onset of atrial activation to the onset of ventricular activation (represents the necessary time for electrical activity to travel from the sinus node, thru the atrium, AV node, and His-Purkinje system to activate the ventricular myocardial cells)
-QRS complex: represent the sum of all ventricular muscle cell depolarization/ atrial repolarization
-ST interval: the entire ventricular myocardium is depolarized
-QT interval: called the “electrical systole” of the ventricles (time it takes varies inversely with the heart rate)
-T wave: ventricular repolarization
Automaticity
(P. 1031)
-The property of generating spontaneous depolarization to threshold
-What enables the SA and AV nodes to generate cardiac action potentials without any external stimulus
Rhythmicity
(P.1031)
-The regular generation of an action potential by the hearts conduction system
-SA node sets the pace (60-100)
-If SA is damaged, AV takes over (40-60)
-Eventually conduction cells in the atria take over from the AV
-Purkinje fibers are capable but much slower than the AV node (last resort)
PVR vs. SVR
(Lecture)
-Pulmonary Vascular Resistance (pressure within the lungs)
< 8 weeks = 8-10 woods units/ m2
> 8 weeks = 1-3 woods units/ m2
-Systemic Vascular Resistance (pressure within the body)
Infant = 10-15 woods units/ m2
1-2 year old = 15-20 woods units/ m2
Child to adult = 15-30 woods units/ m2
Determinants of vascular resistance
(Lecture)
-Compliance (how easy is it for blood to flow through the arteries)
Controlled by:
-Sympathetic nervous system (releases catecholemines)
-Local tissue metabolism (hypoxia as a stimulus to increase oxygen to that area)
-Hormones (thyroid)
-Changes in chemical environment
Vascular compliance
(P.1045)
-The increase in volume a vessel can accommodate with a given increase in pressure
-Compliance = Delta V / Delta P
-Depends on factors related to the nature of a vessel wall (ex ratio of elastic fibers to muscle fibers in the wall)
-Compliance determines a vessels response to pressure changes
-Stiffness is the exact opposite (most common are aging and atherosclerosis)
Catecholamines in vascular resistance—
Epinephrine (lecture, p. 1032)
Epinephrine
-Mainly released by Adrenal medulla and reaches the heart thru the blood stream
-Epi has a greater effect on the beta receptors, HR, CO, and Systolic BP than NorEpi
-Stimulation of both beta 1 and 2 receptors gives you increased HR (chronotropy) and force of muscle contraction (inotropy)
GEM: overall cardiac structures have more beta than alpha receptors therefore effects mediated by the beta receptors predominate
Catecholamines in Vascular Resistance—
Norepinephrine (Lecture, p.1033)
-NorEpi is released by post synaptic sympathetic nerve endings in the heart
-NorEpi has a greater effect than Epi on the alpha receptors (which causes vasoconstriction)
Really interesting sh** on beta receptors in the heart
(P.1032)
-Heart is predominantly made of structures with more beta receptors than alpha, so effects mediated by the beta receptors dominate
B1 receptors: found mainly in the heart (specifically conduction system, AV/ SA nodes, Purkinje fibers)
B2 receptors: found in the heart and also on vascular smooth muscle
-Stimulating BOTH B1 and B2 receptors is going to increase your HR (chronotropy) and force of myocardial contraction (inotropy)
-Stimulation in B 2 receptors= vasodilation
-Overall, Beta 1 and 2 stimulated enables the heart to pump more blood, and B2 increases coronary blood flow
Stimulation of B3 receptors opposes the effects of B1 and B2 and acts as a safety mechanism to prevent overstimulation of the heart by the SNS
Really interesting sh** on alpha receptors in the heart
(P. 1033)
-Alpha receptors cause smooth muscle contractions, thus VASOCONSTRICTION
-Subtype of alpha 2 receptors effect is to inhibit more release of NorEpi to prevent excessive elevated BP
Preload
(lecture, p. 1036)
-The volume and pressure inside the ventricle at the end of diastole (blood returning to the heart from systemic circulation)
-Determined by 2 primary factors:
1. The amount of blood left in the ventricle after systole
2. The amount of venous blood returning total be ventricle during diastole
-Is estimated by your right atrial pressure (CVP) and the pulmonary artery wedge pressure for the left side
-Gives you a sense of someone’s volume status
-In HF, elevated preload can cause decreased SV
Afterload
(Lecture, p. 1038)
-The pressure the heart must pump against to get the blood out of the ventricle; the load the muscle has to move during contraction.
-Mean arterial pressure (MAP) is a good indicator
-Increased pressure is usually the result of increased SVR
In those with HTN, the increased SVR means that the afterload is chronically elevated (which makes the ventricular work harder and causes hypertrophy of myocardium
-Changes in afterload can also be the result of aortic valvular disease
Cardiac Muscle
(Lecture, p.1033)
-Lattice of cells with myofibrils (contraction units), a nucleus, mitochondria, internal membrane (sarcoplasmic reticulum), cytoplasm (sarcoplasm), and a plasma membrane (sarcolemma) that encloses the cell.
-Lattice is composed of:
ACTIN: thin protein filament, light band, or I band (isotropic)
MYOSIN: thick protein filament, dark bands or A bands (anisotropic), small projections from sides form cross bridges
-Z discs connect myofibrils (connect actin and myosin together)
-Sarcomeres: portion of the myofibril between 2 Z-disks
Actin Filament
(Lecture)
-Has 3 protein components with a helix backbone
Two types:
1. F actin (when activated, causes contraction of the heart)
2. G actin (active site for cross bridges with myosin)
Tropomyosin
(Lecture, p. 1034)
-Is a relaxing molecule
-White bands that wrap around the actin
-the reason that the heart isn’t continually contracting
-Blocks F actin strands, causing cardiac muscle to relax
The way tropomyosin knows whether to relax or contract
(Lecture, p. 1034)
- TROPONIN (relaxing protein)
-3 types that attach to tropomyosin
- Troponin I : affinity for actin (inhibits ATPase of actomyosin—
- Troponin T: affinity for tropomyosin (aids in binding of the Troponin complex to actin and tropomyosin)
- Troponin C: affinity for calcium (contains binding sites for calcium ions involved in contraction)
Summary: when it’s time to contract, the influx of calcium causes the affinity of tropomyosin to bind with actin and activate it, causing heart contraction. When it’s time to relax, the calcium has left the cell, Troponin T will cause the myosin to block the F actin strand, causing relaxation of the heart.
GEM *Troponin I and T are released into the bloodstream during myocardial injury *
Myosin Filament
(Lecture)
-Made of a tail (2 polypeptide chains wrapped in spiral forming double helix) and a head (globular polypeptide with associated light chain proteins)
-Myosin filaments are individual myosin molecules bundled together to form the body where the cross bridge hangs (myosin heads moving is what helps move the cardiac muscle and is what drives the physical movement of cardiac muscle contraction)
think of a rowboat with oars
-Cross bridge: flexible hinge and arm connected to myosin heads
-ATPase: enzyme in myosin head for energy production (ie what you need to be a en to move the cardiac cell)
Myofilaments and Actin
(Lecture)
-At rest, active sites on actin filaments are blocked by TROPONIN and tropomyosin complexes (preventing myosin attachment to actin)
-During action potential, as calcium enters the cell, Troponin C binds with ten calcium moves the complexes off of the active actin site, so actin and myosin can interact (which allows for contraction)
Actin-Myosin Cross - Bridge
(Lecture)
Aka the “Walk Along Theory”
-After the head of the myosin cross bridge can attach to the actin filaments at the active site—> intermolecular forces cause the myosin head to tilt forward on a flexible hinge and drag the actin filament with it (power stroke) —> myosin head breaks away and then interacts with the next active actin site-> the Z disc pulls filaments together at the sarcomeres —> this produces muscle contraction
-ATP is needed for this process
Action potential
(Lecture, p. 1030)
-An electrical stimulation that causes a change in charge across a cell membrane
How sodium/ potassium contribute to cardiac action potential
(Lecture)
-Potassium is high inside the membrane and low outside the membrane, so when it diffuses out of the cell you get a NEGATIVE INTRACELLULAR CHARGE
-Sodium is low inside the membrane and high outside the membrane, so when it diffuses into the cell you get a
POSITIVE INTRACELLULAR CHARGE
Generating an action potential
(Lecture)
-At rest, negative intracellular charge
-Depolarization: sodium leaks into cell and decreases the intracellular negativity, this opens the voltage gated ion channel to generate more positive ions (NA/CA) entry
-Inside of the cell becomes more positive and an action potential is triggered
-Repolarization: when potassium rapidly diffuses out of the cell and the intracellular negativity increase to resting state
Quick review of action potential phases
(Lecture, p. 1030)
Phase 0: Depolarization (resting phase, K inside cell, NA outside cell)
electrical stimulus
Phase 1: Early repolarization (rapid Na entering the cell; triggers contraction)
Phase 2: Plateau (aka repolarization; Ca and Na slowly enter the cell)
Phase 3: K moves out of the cell trying to get back to depolarization
Phase 4: Return to resting potential (K is intracellular again and Na is extracellular)
GEM
Refractory period= refractory to additional cardiac stimulation
BUT strong excitatory signal may generate a depolarization during this period
Excitation pathways
(Lecture, p. 1032)
-Network of excitatory/ conductive fibers that cause contraction in heart
-SA node=site of automaticity
(due to the slow leak of Na ions intracellularly that slowly increase intracellular charge until action potential is fired)
-electrical current generated releases calcium from the muscle fibers to cause myosin/ actin to contract
Pump function of the heart
Definitions
(Lecture, p. 1036)
-End-diastolic volume: amount of blood in a heart chamber AFTER filling, BEFORE systole
-End-systolic volume: amount of blood that REMAINS in the chamber after systole (when it contracts)
-Stroke volume: amount of blood ejected with each contraction of the heart (volume of blood ejected during systole)
-Ejection fraction: percent of blood in chamber that is ejected with each systole (% of total and diastolic volume ejected per beat); is increased by factors that increase contractility
-Cardiac output: the amount of blood pumped into the aorta each minute
(HR x SV)
