Chapter 12: Cardiovascular Physiology Flashcards
12.4-12.5
- Cardiovascular System Overview
* 3 principal components:- the heart (the pump)
- the blood vessels (the pipes)
- the blood (the fluid to be moved)
- function is impacted by:
- endocrine system
- nervous system
- kidneys - there are 2 “loops”
- function is impacted by:
- systemic
- pulmonary
- systemic loop
- carries blood from the heart to the rest of the body - pulmonary loop
- carries oxygen-poor blood to the lungs and back to the heart
- systemic loop
- Heart Anatomy
- superior vena cava for heart up
- vena cava for heart down
- the heart venus blood through the coronary sinus
- all three dumps into the right atrium- takes the oxygen-lacking blood
- the ventricles are pressurizing from bottom to top to push the blood- subendocardial network
- EPICARDIUM- superficial
- visceral serous membrane
- MYOCARDIUM- middle
- mostly cardiac muscle
- most of the heart
- ENDOCARDIUM- inner
- continuous with blood vessels
- CONDUCTION SYSTEM
- doesn’t need nerve impulse to start contractions
- action potential is initiated by autorhythmic cells
a. SA node
b. AV node - ANS signals can alter rhythm
- Heartbeat Coordination
- A. Excitation of the SA Node
* action potentials in the excitable membranes of the SA node
* non-contractile
* stimulate heartbeat
* RMP for the heart is -45, which is good for preventing random depolarization
* PACEMAKER POTENTIAL- initial depolarization by Na+ entry
- further depolarization to threshold by Ca2+
- rapid depolarization to peak by major influx of Ca2+
a. AP is created - repolarization by K+ exit
* 4 VOLTAGE GATED CHANNELS - F-TYPE (funny)
a. open when membrane potential is negative
b. Na+ enters - T-TYPE (transient)
a. Ca2+ channel
b. brief entry of Ca2+
c. to threshold - L-TYPE (long-lasting)
a. Ca2+ channel
b. rapid entry of Ca2+
c. to peak of AP - K+ CHANNELS
a. K+ EXITS
b. repolarization - F→T→L→K the relay race of voltage-gated ion channels helps potentiate the action potential
- B. Systemic Regulation of the Heart
* autorhythmic cells create an action potential and send it to the cells
* as we send the action potential, we send a wave of depolarization
* the gap junctions send the AP and there is continuous conduction through the sarcolemma
* NEURAL- innervated by both SNS & PNS nerve fibers
- PSNS
a. innervates the node cells
b. releases ACh that binds muscarinic AChR - SNS
a. innervates the entire myocardium and node cells
b. releases NE that binds β-adrenergic receptors
* HORMONAL - released from adrenal medulla
- travels through blood
- binds β-adrenergic receptors
- C. Sequence of Excitation
* the ventricles are pressurizing from bottom to top to push the blood-subendocardial network - D. Cardiac Action Potential
* in the cardiac muscle cell membranes
* low resting membrane potnetial due to K+
* depolarization by nodes/fibers opens voltage-gated Na+ channels- rapid Na+ entry
* depolarization to peak opens voltage-gated Ca2+ channels ( L-type)
* plateau phase - Ca2+ entry & K+ exit
- balanced
* depolarization causes contraction of myocardial cell via Ca2+ - the contraction lasts the entire time the cell is depolarized
* repolarization - Ca2+ channels close
- K+ outflow increases
- rapid Na+ entry
- Refractory Period of the Heart
* no summation in myocardial cells
* absolute refractory period- long (20-200ms)
- due to Na+ channel inactivation
* contractions lasts 250 ms - second contraction cannot be stimulated
- produces irregular heartbeat
- Electrocardiogram
* a graphic record of the heart’s electrical activity
* the leads must be placed correctly to get a proper reading
* the reading is a composite of the electrical activity, not a single action potential
* P WAVE- depolarization wave from SA node to AV node
- atria contract 0.1 second after start
* QRS COMPLEX - ventriular depolarization
- precedes ventricular contraction
* T WAVE - ventricular repolarization
* atrial repolarization is obscrued by the QRS complex
- Clinical Issues
* ARRHYTHMIA- irregular heartbeat
- caused by a defect in the conduction system
- premature contractions in atria or ventricles
* FIBRILLATION - rapid and irregular (usually out of phase) contraction
- SA node is no longer controlling myocardium
* ATRIAL FIBRILLATION - clotting (embolus) → inefficient filling of ventricles
- VENTRICULAR FIBRILLATION
- typically deadly
- pump without filling → reduced/zero circulation
* DEFIBRILLATION - application of an electrical stimulus to shock the heart back into a normal SA rhythm
* PACEMAKERS - chronic issues
- deliver the electrical stimulus rather than the SA node
* if SA node is damaged - AV node can take over
- ~60 beats per minute
- adequate for normal circulation
* if AV node is damaged - heart block
- no communication between atria and ventricles
- treated with a pacemaker
KNOW PULMONARY CIRCUIT, SYSTEMIC CIRCUIT, AND EVERYTHING
(BLOOD VESSELS) GOING INTO THE HEART AND OUT OF THE HEART THAT IS MAJOR
LOOK AT THE THREE TYPES OF APS AND KNOW THEIR MECHANISMS
12.1 Components of the Circulatory System
- Cardiovascular System Overview
* 3 principal components:- the heart (the pump)
- the blood vessels (the pipes)
- the blood (the fluid to be moved)
- function is impacted by:
- endocrine system
- nervous system
- kidneys - there are 2 “loops”
- function is impacted by:
- systemic
- pulmonary
- systemic loop
- carries blood from the heart to the rest of the body - pulmonary loop
- carries oxygen-poor blood to the lungs and back to the heart
- systemic loop
- CIRCULATORY SYSTEM COMPONENTS:
- heart (the pump), blood vessels (set of interconnected tubes), blood (fluid connective tissue containing water, solutes, and cells that fills the tubes)
- circulatory system aka cardiovascular system transports molecules and other substances rapidly over long distances between cels, tissues, and organs
- BLOOD/PLASMA COMPOSITION:
- plasma is composed of water, proteins, nutrients, metabolic end products, hormones, and inorganic electrolytes (ions)
- HEMATOCRIT- the percentage of blood volume that is erythrocytes; tends to be 45% in men and 42% in women; plasma is greater in volume than erythrocytes
- PLASMA PROTEINS:
- synthesizes in the liver
- many functions in the blood (e.g., osmotic pressure and clotting)
- 3 broad groups of plasma proteins- ALBUMINS, GLOBULINS, and FIBRINOGEN
- blood is composed of FORMED ELEMENTS (cells and cell fragments) suspended in liquid called plasma
- SERUM- plasma with fibrinogen and other proteins involved in clotting
- plasma proteins constitute most of the plasma solutes by weight; they play a role in exerting osmotic pressure and favor the absorption of extracellular fluid into capillaries
- BLOOD CELLS:
- MULTIPOTENT HEMATOPOIETIC STEM CELLS- undifferentiated cells capable of giving rise to precursors (progenitors) of any of the different blood cells; when the multipotent stem cell divides, the first branching yields either bone marrow lymphocyte precursor cells (give rise to lymphocytes) or committed stem cells (give rise to basically everything else)
- ERTHROCYTES- OXYGEN TRANSPORT TO TISSUES AND CELLS; 99% of blood cells; carry oxygen bound to iron within HEMOGLOBIN- which binds iron and reversibly binds oxygen and carbon dioxide; major function in gas transport; produced in the BONE MARROW; young name is RETICULOCYTE (due to residual presence of ribosomes which gives webbed aka reticular appearance); lack nuclei and most organelles; major breakdown product of hemoglobin is BILIRUBIN which is returned to circulation; 120 day lifespan and so are rapidly replaced; biconcave disc shape of erythrocytes allow for high surface area to volume ratio for quick diffusion of gasses between the plasma and cytosol; cannot reproduce
A. iron- oxygen binds to the element iron on a hemoglobin molecule within an erthrocytes; disruption in iron balance can cause iron deficiency or hemochromatosis; homeostatic control of iron resides primarily in the INTESTINAL EPITHELIUM; iron is also stored in the liver bound in a protein called FERRITIN; in recycling iron, TRANSFERRIN delivers almost all of the iron from old erythrocytes destroyed in the spleen to the bone marrow
B. vitamins (FOLIC ACID and VITAMIN B12)- necessary for the formation of DNA and normal cell division; deficiency in folic acid causes cell division to decrease and thus causes fewer erythrocytes to be produced when folic acid is deficient; small quantities of vitamin B12 are also necessary for cell division because it is necessary for the action of folic acid; the absorption of vitamin B12 from the gastrointestinal tract requires a protein called an INTRINSIC FACTOR which is secreted by the stomach; lack of this proteins causes vitamin B12 deficiency, resulting in erythrocyte deficiency known as PERNICIOUS ANEMIA; THESE MUST BE PRESENT FOR ERYTHROPOIESIS
C. hormones- direct control of erythropoiesis is exerted primarily by a hormone called ERYTHROPOIETIN which is secreted into the blood by a certain connective tissue in the kidneys and then helps to stimulate the proliferation of erythrocyte progenitor cells and their differentiation into mature erythrocytes in the bone marrow; in the case where there is iron deficiency, erythrocyte levels will increase to account of lack of oxygen delivery because less can bind to the iron; ANEMIA- a decrease in the ability of the blood to carry oxygen due to a decrease in the total number of erythrocytes, each having a normal quantity of hemoglobin, a diminished concentration of hemoglobin per erythrocyte, or a combination of both; some people also get POLYCYTHEMIA which is an increase in erythrocytes as a response to low oxygen levels - LEUKOCYTES- PROTECT AGAINST INFECTIONS AND CANCER; neutrophils (phagocytes and most abundant leukocytes that aid in inflammatory or antibacterial response), eosinophils (eukaryotic parasites phagocytosis), basophils (anticlotting factor and allergic and bacterial reaction), monocytes (migrate to tissues and develop into macrophages), and lymphocytes (B and T that help with cancer and viruses and bacteria); involved in immune response to injury and infection
- PLATELETS- AID IN BLOOD CLOTTING; cell fragments essential for blood clotting; colorless, nonnucleated cell fragments that contain numerous granules and are much smaller than erythrocytes; produced in large cytoplasmic portions of bone marrow called MEGAKARYOCYTES
- Circulation
- the circulatory system forms a closed loop so that blood pumped out of the heart returns to the heart by a different set; there are two sets, terminating in the heart which is divided longitudinally into two sections; each half contains two chambers: an upper chamber called the atrium and a lower chamber called a ventricle; the atrium in each side empties into the ventricle on its same side;
- in both circuits, vessels carry blood away are the heart are called ARTERIES
- vessels carrying blood from body organs and tissues to heart are called VEINS
- SYSTEM CIRCULATION:
LEFT VENTRICLE → PERIPHERAL ORGANS/TISSUES → RIGHT ATRIUM- ARTERIES- carry blood away from the heart; the largest arteries branch into ARTERIOLES that branch into CAPILLARIES which unite to form VENULES; collectively, these are called MICROCIRCULATION
- VEINS- carry blood back to the heart
- AORTA- the large artery leaving the left ventricle
- SUPERIOR AND INFERIOR VENA CAVAE- large veins emptying into the right atrium
- flow ensures that systemic tissues receive freshly oxygenated blood and allows for independent regulation of blood flow
- PULMONARY CIRCULATION:
RIGHT VENTRICLE → LUNGS → LEFT ATRIUM- PULMONARY TRUNK- divides to form the PULMONARY ARTERIES, which brings blood to the lungs from the right ventricle
- FOUR PULMONARY ARTERIES- return blood from lungs to the right atrium
- blood leaves the right ventricle via a large artery called the PULMONARY TRUNK which divides into the two PULMONARY ARTERIES which branch into arteries, arterioles, and capillaries and then blood leaves the lungs by the PULMONARY VEINS
- MICROCIRCULATION- blood vessels between arteries and veins (arterioles → capillaries → venules)
- where the exchange of gases, substrates, and waste products occurs between the blood and the extracellular fluid
12.2 Pressure, Flow, and Resistance
*Pressure, Flow, and Resistance
- the applied relationship between pressure, flow, and resistance of blood is called HEMODYNAMICS
- blood flow is always from high pressure to lower pressure
- the pressure exerted by any liquid is HYDROSTATIC PRESSURE, which denotes the force exerted by the blood
- the units are mmHg, deltaP, and mL/min
- the RESISTANCE to flow is how difficult it is for blood to flow between two points at any given pressure difference; FLOW RATE = CHANGE IN PRESSURE/RESISTANCE
the ultimate function of the circulatory system is to ensure adequate blood flow through the capillaries of various organs
- BLOOD FLOW BETWEEN TWO POINTS:
ANALOGOUS TO ELECTRICAL CURRENT IN OHM’S LAW DESCRIBING ELECTRICAL CIRCUITS- directly proportional to the pressure difference
- inversely proportional to resistance
- RESISTANCE:
- directly proportional to the VISCOSITY of the blood and length of the blood vessel
- inversely proportional to the fourth power of the vessel radius (most important determinant of resistance and blood flow to each organ)
12.3 Anatomy
- Heart Anatomy
- superior vena cava for heart up
- vena cava for heart down
- the heart venus blood through the coronary sinus
- all three dumps into the right atrium- takes the oxygen-lacking blood
- the ventricles are pressurizing from bottom to top to push the blood- subendocardial network
- EPICARDIUM- superficial
- visceral serous membrane
- MYOCARDIUM- middle
- mostly cardiac muscle
- most of the heart
- ENDOCARDIUM- inner
- continuous with blood vessels
- CONDUCTION SYSTEM
- doesn’t need nerve impulse to start contractions
- action potential is initiated by autorhythmic cells
a. SA node
b. AV node - ANS signals can alter rhythm
*BASIC HEART ANATOMY
- the heart is a muscular organ enclosed in a protective fibrous sac the PERICARDIUM in the chest
- another fibrous layer is the EPICARDIUM
- the space between the epicardium and the pericardium is filled with a fluid that acts as a lubricant as the heart moves within the sac
- the wall of the heart, or the MYOCARDIUM, is made of mainly cardiac muscle cells
- the inner surface of the cardiac chamber is lined with ENDOTHELIAL CELLS
- the two ventricles of the heart are separated by a muscular wall called the INTERVENTRICULAR SEPTUM
- located between the atrium and the ventricle in each half of the heart are the one way ATRIOVENTRICULAR VALVES which allow blood to flow from the atrium to the ventricle but not backward; the right AV VALVE is called the TRICUSPID VALVE because of its three flaps while the left AV VALVE is called the BICUSPID VALVE because it has two flaps
- the opening and closing of the valves are passive processes that result due to pressure differences across the valves; when blood pressure in the atria is greater than the ventricle, blood pushes out but it can sometimes occur the other way which is not good lol
*CARDIAC MUSCLE
- most of the heart consists of specialized cardiac muscle cells with good resiliency and stamina
- the cells of the myocardium are arranged in tight layers that encircle blood filled chambers; when they contracted, they come together like a fist squeezing a fluid filled balloon and exert pressure on the blood they enclose
- cardiac muscle is an electrically excitable
tissue that converts chemically stored energy in the bonds of ATP into force generation, APs propagate along cell membranes, Ca2+ enters the cell membrane, and the cycling of force generated cross-bridges begins
- ~1% of heart cells do not function in contraction but have a specialized feature for heart excitation; these cells constitute the CONDUCTING SYSTEM and are in electrical contact with the cardiac muscle cells via gap junctions; THE CONDUCTING SYSTEM HELPS INITIATE THE HEARTBEAT AND SPREAD AN ACTION POTENTIAL RAPIDLY THROUGH THE HEART

*INNERVATION
- the heart receives a large supply of sympathetic and parasympathetic nerve fibers
- sympathetic post ganglionic nerve fibers innervate the entire heart and release norepinephrine
- parasympathetic fibers terminate mainly in special cells in the atria and mainly release ACh
- there are subtypes of beta-adrenergic receptors in target tissue
- epinephrine from the adrenal medically also exerts actions on the heart because it binds to the same receptors are norepinephrine
- receptors for ACh are MUSCARINIC RECEPTORS for the heart
*BLOOD SUPPLY
- blood being pumped through the heart chambers does not exchange nutrients and metabolic end products with myocardial tissue
- they receive their blood supply from arteries that branch from the aortas
- arteries supplying the myocardium are CORONARY ARTERIES and the blood flowing through them is the CORONARY BLOOD FLOW
- HEART VALVES
PREVENTS BACKFLOW- ATRIOVENTRICULAR (AV) VALVES- prevent backflow from the ventricles into atria
- PULMONARY VALVE- prevents backflow from pulmonary trunk into right ventricle
- AORTIC VALVE- prevents backflow from aorta into left ventricle
- HEART MUSCLE (MYOCARDIUM)
- CARDIAC MUSCLE CELLS- joined by gap junctions that permit conductions of action potentials from cell to cell
- CONDUCTION SYSTEM- specialized noncontractile cells that initiate cardiac action potentials and regulate their spread through the heart
- CORONARY ARTERIES- perfused by coronary arteries
- INNERVATION- autonomic nervous system (sympathetic and parasympathetic division)
12.4 Heartbeat Coordination
*HEARTBEAT COORDINATION
- the heart is a dual pump in that the left and right sides pump blood separately but simultaneously
- contraction of cardiac muscle is initiated by the depolarization of the plasma membrane
- gap junctions interconnect myocardial cells and allow action potentials to spread from one cell to another
- the initial excitation of one cell results in the excitation of all cardiac muscle cells
- this initial depolarization will normally arise in a small-group of conducting-system cells called the SINOATRIAL (SA) NODE, located in the right atrium near the entrance of the superior vena cava
- the SA node is the pacemaker of the entire heart; its depolarization generates the action potentials that leads to the depolarization of the entirety of the cardiac muscle cells; the discharge of the SA node determines the HEART RATE
- the AP is initiated in the SA node, spreads throughout the myocardium via gap junctions, CONDUCTION IS RAPID ENOUGH TO CONTRACT THE LEFT AND RIGHT ATRIA ESSENTIALLY AT THE SAME TIME, the AP spreads to the ventricles through a conducting system of cardiac cells with reduced contractile capability and conduct APs at a low electrical resistance, the AV node (at base of right atrium) links the atrial depolarization and the ventricular depolarization, INTERNODAL PATHWAYS conduct the AP from the SA to AV node, THE PROPAGATION OF APS THROUGH THE AV NODE IS RELATIVELY SLOW so the delay allows atrial contraction to be completed before ventricular excitation occurs, once the AV node is excited the AP propagates down the interventricular septum which is a pathway of conducting-system fibers called the BUNDLE OF HIS which constitutes the only electrical connection between the atria and ventricles, the bundle of His then divide into left and right BUNDLE BRANCHES which separate at the bottom of the heart and enter the walls of the ventricles, these pathways are called PURKINJIE FIBERS that conduct the AP to monocytes in the ventricles, this rapid conduction allows for the depolarization of the left and right ventricular cells to occur almost simultaneously, RESULTS IN AN EFFICIENT CONTRACTION THAT MOVES BLOOD TO THE EXIT VALVES LIKE SQUEEZING A BOTTLE OF TOOTHPASTE FROM THE BOTTOM UP
- ACTION POTENTIALS:
OCCUR IN ALL CARDIAC CELLS- rapid DEPOLARIZATION in atrial and ventricular muscle cells; positive feedback by increased Na+ permeability
- cells remain depolarized (the plateau phase) for duration of contraction because of prolonged entry of Ca2+ into the cells through plasma membrane L-TYPE CA2+ CHANNELS
- SINOATRIAL (SA) NODE:
SPONTANEOUSLY GENERATES ACTION POTENTIALS THAT LEAD TO DEPOLARIZATION OF CARDIAC CELLS- PACEMAKER POTENTIAL- F-TYPE CATION CHANNELS and T-TYPE CA2+ CHANNELS → membrane potentials depolarizes to threshold → initiates an action potential
- pathways of electrical conduction: SA node → atria → AC node (small delay) → BUNDLE OF HIS → right and left BUNDLE BRANCHES → PURKINJIE FIBERS → ventricular muscle fibers
- CA2+ from the sarcoplasmic reticulum (SR) → cardiac contraction (combining with TROPONIN)
- major signal for Ca2+ release from the SR is extracellular Ca2+ → voltage-gated L-type Ca2+ channels → increase intracellular Ca2+
- “trigger” Ca2+ opens RYANODINE RECEPTOR CA2+ CHANNELS in SR membrane
- Ca2+ → troponin binding sites that are not saturated → the number of active cross bridges can increase if cytosolic Ca2+ increases still further
- cardiac muscle cannot undergo TETANIC CONTRACTION because of long refractory period
- ELECTROCARDIOGRAM (ECG):
DETECTION OF THE SPREAD OF CARDIAC CELL DEPOLARIZATION AND REPOLARIZATION FROM THE SURFACE OF THE BODY- action potentials create electrical currents that are transmitted through body fluid; the measurement is the summation of many cardiac cell potentials detected by electrodes placed on limbs and thorax
- P WAVE- atrial depolarization
- QRS COMPLEX- ventricular depolarization
- T WAVE- ventricular repolarization
- EXCITATION-CONTRACTION COUPLING:
LINKS ACTION POTENTIALS TO MUSCLE CONTRACTION (SIMILAR TO SKELETAL MUSCLE)- Ca2+-induced Ca2+ release: Ca2+ entry into cytosol through L-type Ca2+ channels releases Ca2+ from SR through ryanodine receptors, with initiates cross-bridge formation
- REFRACTORY PERIOD:
PREVENTS TETANY- due to inactivation of Na+ channels and prolonged depolarized plateau
12.5 Mechanical Events of the Cardiac Cycle
- CARDIAC CYCLE:
SYSTOLE (ventricular contraction) AND DIASTOLE (ventricular relaxation)- ISOVOLUMETRIC VENTRICULAR CONTRACTION (onset of systole)- ventricular pressure rapidly exceeds atrial pressure → AV valves close (the aortic and pulmonary valves not yet open, so no ejection of blood)
- EJECTION PHASE OF SYSTOLE- ventricular pressure exceed aortic and pulmonary trunk pressures → the aortic and pulmonary valves open → ventricles eject blood
- ISOVOLUMETRIC VENTRICULAR RELAXATION (beginning of diastole)- ventricles relax → ventricular pressures decrease below aorta and pulmonary trunk → aortic and pulmonary close; the AV valves also closed, so no change in ventricular volume
- FILLING PHASE OF DIASTOLE- ventricular pressures decrease below atrial pressure → AV valves open → ventricles fill with blood
- filling occurs rapidly; atrial contraction (at end of diastole) adds a little additional blood to the ventricles
- VENTRICULAR VOLUMES AND PRESSURES:
- END-DIASTOLIC VOLUME- amount of blood just before systole
- END-SYSTOLIC VOLUME- amount of blood after ejection
- STROKE VOLUME: amount of blood ejected from the heart with a single contraction
- the patterns of pressure changes in the systemic and pulmonary circulations are similar, but the pulmonary pressures are lower (lower vascular resistance)
- HEAR SOUNDS
- first heart sound: closing of the AV valves; second heart sound: closing of the aortic and pulmonary valves
- MURMURS: due to narrowed or leaky valves; holes in the interventricular septum; create turbulent flow (rather than normal LAMINAR FLOW)
12.6 The Cardiac Output
- CARDIAC OUTPUT (CO): volume of blood each ventricle pumps per units time (e.g., L/min)
- CO = heart rate (HR) × stroke volume (SV)
- HEART RATE CONTROL
- increased by sympathetic input to SA node and plasma epinephrine (CHRONOTROPIC action)
- decreased by parasympathetic input to SA node
- STROKE VOLUME:
VOLUME OF BLOOD EJECTED PER CARDIAC CYCLE- increased by increased end-diastolic volume (PRELOAD) via the FRANK-STARLING MECHANISM
- increased by increase in CONTRACTILITY: force of contraction for a given end-diastolic volume (increased sympathetic stimulation or epinephrine)
- quantified by EJECTION FRACTION, which is the ratio of stroke volume to end-diastolic volume
- contractility increased by sympathetic/catecholaminergic input via increased myocardial cytosolic Ca2+
- AFTERLOAD: ventricular force required to open the semilunar valves during systole; proportional to the aortic pressure for the left ventricle and pulmonary artery pressure for the right ventricle; increased afterload can reduce stroke volume (in certain situations)
12.7 Measurement of Cardiac Function
- ECHOCARDIOGRAPHY:
ASSESSES WALL AND VALVE FUNCTION - CARDIAC ANGIOGRAPHY:
ASSESSES CORONARY ARTERY PATENCY AND BLOOD FLOW
12.6-12.7
- The Cardiac Cycle
A. Overview – Video
B. Mechanical events
C. Volume and pressure
D. Electrical events & heart sounds
E. Clinical Issues - Abnormal heart sounds - Cardiac Output
A. Control of heart rateB. Stroke volume
C. Frank-Starling Mechanism
D. Sympathetic effects on cardiac muscle
* in a healthy system, SV is fairly constant
* if the blood volume drops or if the heart weakens, then SV declines and CO is maintained by increasing
E. Effects of autonomic nervous systemF. Ejection fraction
*ratio of SV to EDV:
EF = SV/EDV
*normal (resting) - 50-75%
*increased contractility causes an increased ejection fraction
- bigger SV per given EDV
G. Afterload
* Pressure that the ventricles must overcome to
force open the aortic and pulmonary valves
*Anything that increases systemic or pulmonary
arterial pressure can increase afterload
- hypertension - Blood
- Blood
- Cells
- Cell fragments
- Plasma (mostly water)
- Plasma carries blood cells, proteins, nutrients,
metabolic wastes, and other molecules being
transported around the body
- Blood
- Blood vessels
all arteries carry blood from the heart all veins carry blood to te heart
are the veins or arteries bkue????
blood viscotiy- weeks or days
total blood vessel length- months
diameter- minute to minute - Pressure, flow, and resistance
KNOW SYMPATHETIC AFFECTS ON HEART PATHWAY
12.18-19
- Arteries
A. Elastic
B. Muscular
C. Pressures - Arterioles
* smallest arteries
* surrounded by smooth muscle
* controlled by neural, hormonal, local signals
A. Systemic controls
* SNS activation affects blood vessel diameter
* arteriolar response depends on receptors encountered (α1 & α2)
* **alpha-adrenergic receptors- binding of NE & E cause vasoconstriction
* **beta-adrenergic receptor (β2)- binding of E causes vasodilation
* no significant PNS effects
* vasomotor tone
- primarily by α-receptors
a. more APs → vasoconstriction
b. fewer APs → vasodilation via blood pushing open vessels
B. Local regulation
* endothelial cells secrete autocrine and paracrine agents
- induce relaxation or contraction of adjacent smooth muscle
* ACTIVE HYPEREMIA
- increased blood flow due to increased metabolic activity
- metabolites cause vasodilation
- O2-demand matches O2-supply
- most developed in
a. skeletal muscle → exercise
b. cardiac muscle
c. glands
* flow autoregulation
- change in blood pressure results in change in blood vessel diameter
- myogenic response
- stretch → ion influx → AP → contractions of vessel smooth muscle
* blood flow stays constant over a wide range of blood pressures
C. Systemic & Local Regulation
* NITRIC OXIDE (NO) ANS NEURONS
- nitric oxide causes vasodilation
- major sites of action
a. penis
b. clitoris
c. GI tract (enteric nervous system)
- viagra (sildenafil) inhibits PDE-5
a. cGMP accumulates to increase effects of nitric oxide - Capillaries
* smallest blood vessels
* site of gas and nutrient exchange- diffusion of “good stuff” out of the blood into the tissues
- diffusion of “bad stuff” back into the blood
* anatomy of capillary network - velocity is slowest in the capillary
- greater total cross-sectional area
- Veins
* less smooth muscle, more elastin and thinner walls than arteries
* highly distensible- called capacitance vessels
- act as blood reservoirs
* blood pressure in veins is ~15 mmHg - not sufficient to move blood back to the heart
A. Venous pressure- SNS Activity
- APs in SNS neurons → release NE onto α1 & α2 receptors
- cause smooth muscle contraction and a narrowing of the lumen of veins → ↑ pressure
- blood volume
- more blood in the system → more pressure on the walls of the vessels
- respiratory pump
- pressure changes in the central cavity due to breathing
- helps to propel blood back to heart
- muscular pump
- skeletal muscles squeeze blood in veins
- semilunar valves enforce the one-way flow
B. Varicose Veins
* valves prevent the backflow of venous blood
* varicose veins- veins that have become dilated
- due to an incompetent (leaky) valve
* about 15% of adults
- mainly in the lower limbs
- SNS Activity
- Integrated Regulation of Systemic Arterial Pressure
- Baroreceptors
- Hypotension
- Cardiogenic Shock
- Hypertension
more pressure more stretch more contraction (more sodium and calcium coming through so smooth muscle contracts) more response
**TO LEARN INTEGRATED SYSTEMIC AND LOCAL CONTROLS GRAPH, MAKE SURE TO LEARN FACTORS THEN THINGS THAT INHIBIT AFTER KNOW IT ALL **
know how hemorrhage works
