Human Physiology Chapters 14 & 15
What is used to measure BP? (Sphygmomanometry)
(a) Cuff pressure exceeds arterial pressure (b) cuff pressure is gradually released - blood flow is reestablished -Korotkoff sound (systolic pressure) (c) cuff pressure no longer is compressing the artery -Korotkoff sound disappears (diastolic pressure) Normal <120/80 mm Hg Prehypertensive! 120/80 - 139/89 mm Hg Hypertensive!! > 139/89 mm Hg
Total blood flow through the entire system is the same as the cardiac output...5 L/min.
...
Contractility
... "the intrinsic ability of a cardiac muscle fiber to contract at any given length" Controlled by 1: nervous 2: endocrine Inotropic agents - affect contractility Positive inotropic effects (i.e. norepinephrine on beta-1 receptors) Will cause an increase in Ca++ Graded Contraction! (Epi/Norepi- adrenergic recep-cAMP 2nd mess.- act on Ca++ channel icreases the time they remain open. )
Arterial resistance is influenced both locally and systemically. How?
1) Local control - usually first level of control to meet the immediate metabolic needs of the tissue (i.e. paracrine control, NO, endothelin) 2) Sympathetic control - regulate blood distribution for homeostasis (i.e. temperature regulation) 3) Hormonal control (i.e. angiotensin II, ANP) - act directly on arterioles or by influencing sympathetic control
Pacemaker potentials
1. At -60mV, If channels are open Permeable to both Na+ and K+ Na+ influx > K+ efflux, which causes a gradual depolarization 2. As the membrane potential becomes more positive, If channels shut, and Ca++ channels open 3. Ca++ enters and causes the action potential 4. Ca++ channels shut at the peak of the AP, while at the same time, slow K+ channels have finally opened 5. K+ efflux leads to repolarization
What affects venous return?
1. Venous contraction/compression: the veins are squeezed by our contracting skeletal muscles which pushes the blood forward causing increase in EDV and SV. 2. Abdominal and thoracic pressure changes (due to breathing): during inspiration the pressure in the thoracic cavity deacreases to create vaccuum to bring blood to heart; Respiratory pump. 3. Sympathetic nervous innervation: causes a vasoconstriction; Catecholamines (epinephrine, norepinephrine, and dopamine) acting on adrenergic receptors This squeezes more blood into the heart EDV increases as will stroke volume
Path of electrical signal in the heart
AP generated in the sinoatrial (SA) node in the right atrium. Wave of depolarization spreads over the internodal pathway and to the atrioventricular (AV) node found at the bottom of the right atrium Depolarization moves into the ventricles to the Purkinje fibers via the atrioventricular (AV) bundle and left/right bundle branches
How do we regulate BP when blood volume changes?
Adjusting for small increase in blood volume is regulated by the kidneys -will not affect long lasting changes in blood pressure Both the renal and cardiovascular system work to restore a loss of blood volume (dehydration, hemorrhage) -Kidneys can only conserve blood volume (not restore it!) -Cardiovascular compensation includes sympathetic nervous stimulation distribution of blood between the arterial and venous sides also helps to maintain arterial blood pressure -If MAP drops, sympathetic stimulation cause venous constriction; this causes more blood to accumulate in the arterial side
Vascular smooth muscle and sympathetic innervation
Although it binds α-receptors to also cause vasoconstriction... ....will have a higher affinity for β2-receptors -Smooth muscle in heart, liver, skeletal muscles -Results in vasodilation -Important in the fight-or-flight response
Where does the apex angle down towards? (Heart)
Angles down towards the left.
What is orthostatic hypotension?
Arterial BP drops; When we get out of bed, our blood will pool in our lower extremities Venous return decreases, and CO falls from 5 to 3 L/min Triggers baroreceptor reflex Heart rate increases Force of contraction increases Vessels constrict Normal BP and CO is returned to normal within 2 heart beats!!!
What is left ventricular hypertrophy?
As the MAP increases (>200 mm Hg), the cardiac muscle must work harder to maintain SV and CO The left ventricle will adapt in size and strength Eventually will lead to left ventricular dysfunction (failure) pulmonary edema, congestive heart failure.
Gimme some info on venules and veins
Blood flow is convergent As venules converge into veins, they become larger in diameter. Veins > arteries; hold more than half of the blood in our bodies. Hence "volume reservoir" Walls are thinner w/ less elastic Readily expand with blood
Pressure
Blood in our vessels exert two pressure components: 1) Dynamic (hydraulic pressure) 2) Lateral (hydrostatic pressure) When a fluid moves through a system (blood moving through the vessels), it will lose pressure This is due to energy lost as friction
What is bulk flow? *know the diagram
Bulk flow : balance between... Filtration - fluid is flowing out of the capillaries Absorption - fluid is flowing into the capillaries Dependent upon (1) hydrostatic pressure (2) osmotic pressure net filtration at the arteriole end net absorption at the venous end.
Capillary exchange
Capillaries and tissue cells are located within 0.1mm of one another Density is directly proportional to metabolic activity Capillary diameter is only large enough for passage of 1 RBC at a time
Gimme some info on arteries and arterioles.
Carry blood away from the heart Thick smooth muscle layer with a lot of connective tissue (fibrous and elastic) Makes these vessels very stiff. Flow is described as divergent -into smaller vessels As the size of the vessel shrinks, the walls become more muscular and less elastic.
Resistance
Changing pressure in a liquid without changing the volume occurs when the walls of the container contract i.e. ventricular walls during systole increases pressure until the liquid has a place to go ...semilunar valves open and blood flows into the arteries "driving pressure"
Continuous vs. Fenestrated capillaries
Continuous: -endothelial cells are connected to one another via "leaky" junctions -Most common; found in muscle, connective tissue, neural tissue (i.e. blood brain barrier) Fenestrated: -contain large pores, allowing passage of large volumes of fluid -Kidneys and intestines
Hypertension
Described as chronically elevated blood pressure >130-140/80-90 mm Hg 90% is hereditary (primary hypertension) CO is normal, but peripheral resistance is high 10% is usually the secondary result of another underlying problem i.e. fluid retention due to an endocrine disorder. Hypertension is a risk factor for atherosclerosis! High BPdamage the vascular endothelium promotes plaque formation High BP will also put excess strain on the heart !!!!
ECG info
Displays the heart's electrical activity. Late 1800s by Walter Einthoven "Einthoven's Triangle": electrodes placed on both arms and the left leg (creates a triangle around the heart) Lead: pair of electrodes
Things from ECG pt.2
ECG abnormalities: ST-segment depression can indicate myocardial ischemia
Blood flow? (returning to heart)
Enters through the Inferior and Superior Vena Cava. The oxygen poor blood goes into the right atrium and when it contracts, blood flows into the right ventricle through the tricuspid valve. When the right ventricle contracts, blood is pumped into the pulmonary semilunar valve and then it goes to the pulmonary artery where it travels to the lung to get oxygen.
T/F Velocity is not dependent on the flow rate and cross sectional area.
F; Flow rate - this is the volume of blood that passes a given point per unit time (L/min) "How much" Velocity - This is how far a fixed amount of blood travels per unit time "How fast" Relationship between the two is described as: v=Q/A (v is velocity, Q is flow rate, A is cross-sectional area of the vessel)
T/F All vessels contain smooth muscle.
F; Only the endothelium; Circular layer of vascular smooth muscle for vasoconstriction and vasodilation Maintain muscle tone (partial contraction at all times) Depends on Ca++ entry from extracellular fluid.
T/F Valves allow blood to move in both directions.
F; Valves keep blood moving in ONE DIRECTION.
T/F Ventricles contract from the top to the bottom.
F; Ventricles contract from the bottom and upward to push the blood out.
T/F Increase in capillary hydrostatic pressure increases filtration.
F; decreases filtration and increases absorption.
What are varicose veins?
Faulty valves blood pools May be hereditary Other common risk factors include: female, pregnancy, obesity, menopause
Is cardiac muscle contraction graded?
It can be graded meaning that it is dependent on the amount of Ca++ present. More Ca++, more troponin bound and more actin/myosin cross bridges.
Factors that influence SV?
Length of the muscle fiber prior to contraction. -This is dependent on the amount of blood in the ventricle (EDV). Contractility - intrinsic ability for the cardiac muscle to contract at any given length
What happens in most cases of hypertension?
MAP increases! (increased arterial pressure due to increased peripheral resistance and an unchanged cardiac output)
What factors influence MAP?
MAP is a balance between flow into the arteries and out of the arteries. -Flow into the aorta is the same as cardiac output -Flow out of the arteries is influenced by peripheral resistance of the arterioles Therefore: MAP is proportional to CO x R arterioles
What is the MAP and pulse pressure of someone whose blood pressure is 119mmHg/75mmHg
MAP= 75 + (1/3)(44) MAP= 90
Myogenic autoregulation and blood flow
Myogenic autoregulation- Vascular smooth muscle can respond to increased stretch in the vessel wall Will cause constriction Resistance increases /flow decreases How this works: Mechanically gated Ca++ channels open, allowing for Ca++ to enter the cell
A majority of vascular smooth muscle is controlled by sympathetic innervation
Myogenic tone of the arterioles is maintained by tonic release of norepinephrine -Binds to α-adrenergic receptors to cause vasoconstriction
How does ANS affect heart rate?
Normal tonic control comes from the parasympathetic branch. To speed up rate Decrease parasympathetic Increase sympathetic (catecholamines acting on β1 adrenergic receptors) (Increases permeability of Na in IF channel & decreases the permeability of K) To slow the heart Increase parasympathetic pathway ACh acting on muscarinic receptors
Pressure pt. 2
Occurs when the walls of the container contract i.e. ventricular walls during systole increases pressure until the liquid has a place to go ...semilunar valves open and blood flows into the arteries "driving pressure"
Blood Flow? (Leaving heart)
Oxygenated blood leaves the lungs through the pulmonary vein and goes into the left atrium. When it contracts, the blood travels through the bicuspid valve and into the left ventricle. When that contracts, the blood is pumped into the aortic semilunar valve and then into the aorta before going through the rest of the body.
How are myocardial autorhythmic cells able to generate AP?
PACEMAKER POTENTIAL; Starts at -60mV and slowly moves towards threshold
Things from ECG
PQ segment - atrial contraction. ST segment- ventricular contraction P wave to P wave or R wave to R wave ? -Tells us heart rate QRS complex follow the P wave, and the P-R segment the same length. -Problem in the AV node
Myocardial Action Potentials
Phase 4: -resting potential (-90mV) Phase 0: depolarization voltage-gated Na+ channels open and Na+ enters (channels close at +20mV) Phase 1: initial repolarization K+ begins to leave via K+ channels (L-type Ca channels on surface open up) Phase 2: plateau slow voltage-gated Ca++ channels finally open after initial depolarization; some "fast" K+ will shut (prevents tetanus of heart) Phase 3: rapid repolarization slow voltage-gated K+ channels are open; resting potential is reestablished *The longer the AP in cardiac muscle prevents tetanus.
Cardiac Cycle (cont'd)
Point C: Ventricular pressure will exceed aortic pressure, aortic valves open Pressure continues to rise Volume in the ventricle decreases as blood is ejected into the aorta (C→D). Point D: - ventricular contraction is complete; the amount of blood remaining in the ventricle at this point is referred to End Systolic Volume (ESV) ≈65mL The ventricle relaxes (D→A); the aortic valve is shut, and therefore volume does not change Isovolumic relaxation
Functions of the Cardiovascular System?
Primary responsibility is to transport materials such as: nutrients, water, and gases to body tissues; Materials from cell to cell within the body; Waste products/metabolites that cells eliminate. Also transports to the lungs and kidneys for excretions.
Resistance in Arterioles
R is proportional to 8Lη/πr4 Length and viscosity are constant... Therefore, R is proportional to 1/r4
Pressure pt. 3
Remember, blood flows from areas of higher to lower pressure! The larger the pressure gradient, flow will increase: Flow is proportional to ΔP (gradient) Not dependent on the total pressure Flow depends on ΔP!! (Not absolute pressure...) decreasing flow= 1/increasing resistance Flow= gradient/resistance Flow= gradient/ radius to the 4th power.
Parts of an ECG
Series of waves and segments P wave: atrial depolarization QRS complex: ventricular depolarization T wave: ventricular repolarization
Cardiac cell relaxation.
Similar to skeletal muscle cell in that Ca is pumped back into the SR via action of the Ca ATPase. Ca++ is also pumped out of the cell via Na+ Ca++ exchanger.
Gimme some info on capillaries
Site of exchange between the blood and the interstitial fluid Lack smooth muscle and fibrous/elastic connective tissue facilitates exchange Single endothelial layer supported by a basement membrane Pericytes: cells surrounding the capillaries Contribute to "tightness" characteristic of capillaries i.e. blood brain barrier.
T/F Ca2+ binds to troponin and follows the same contractile mechanism as skeletal muscle.
T; Action potential moves across the sarcolemma and into the t-tubule (depolarization) which opens the voltage gated L-type Calcium on the cell membrane (surface of cardiac cell). When the Ca++ enters the cell it causes RyR on the SR to open for a Ca++ induced Ca++ release that results in a Ca++ "spark". Several sparks lead to a Calcium signal that binds to troponin causing tropomyosin to move and allows for actin and myosin to bind...
T/F A decreased plasma protein concentration favors absorption.
T; Filtration is decreased and absorption is increased.
T/F Blood flows down a pressure gradient.
T; The highest pressure occurs in aorta due to LV contraction Pressure will continually decrease throughout the circulation lowest in the vena cava
T/F Cardiac muscle cells do not need nerve innervation to contract.
T; The signal is myogenic therefore it comes from within but can be influenced by ANS innervation.
T/F Edema is the accumulation of fluid in the interstitial space due to high absorption.
T; accumulation of fluid in the interstitial space Results in swelling Results from an alteration in capillary exchange Filtration >Absorption Can also occur as a result of inadequate lymph drainage (obstruction) Elephantiasis (parasite)
T/F Arterioles are arranged in parallel
T; blood flow through all the arterioles at the same time is equal to CO Flow can be shunted and redirected
T/F Both atria contract at the same time, followed by both ventricles.
T; both atria contract at the same time, followed by both ventricles.
What prevents back flow in the heart? Describe them.
The heart valves; Antrioventricular valves between the atria and ventricles (Tricuspid for right atrium and ventricle and Bicuspid for left atrium and ventricle). Semilunar valves between the ventricles and arteries (Pulmonary between right ventricle and artery and Aortic between left ventricle and the aorta).
Tell me about cardiac muscle cells
The signal for contraction comes from within the cell which is the autorythmic cells (pacemakers). These cells are smaller and fewer than other myocardial contractile cells and also lack sarcomeres (no contraction).
Cardiac Cycle: 5 phases (know the diagram)
The starting point is A Ventricle is relaxed Holding the least amount of blood that it will hold during the cycle As ventricles fill, the volume increases without the pressure increasing (expansion) (A→B) at this point - End Diastolic Volume (EDV) ≈135mL Point B: Ventricle contracts with both mitral and aortic valve shut - therefore pressure increases as the volume remains constant (B→C) Isolvolumic Contraction
Preload
The ventricle wall stretches as it fills with more blood, causing a stronger force of contraction. When preload increases, SV increases.
What is blood pressure?
This is the driving force for blood Generated by ventricular contraction During ventricular diastole, the semilunar valves shut and the elastic arteriole walls will recoil -Driving pressure wave
What is the point of AV node delay?
Transmission through the AV node is slower (1/20th the speed) than in the rest of the internodal system. This allows for the atria to complete contraction before ventricular contraction **Note - upstream pacemakers set the rate!
What are referred to as the volume reservoir?
Veins
What is pericarditis?
When there is a friction rub against the surrounding of the heart when the heart pumps; Swelling or irritation of the surrounding connective tissue of the heart, the Pericardium.
What is stroke volume?
amount of blood pumped by one ventricle during a contraction = EDV - ESV = 135 mL - 65 mL = 70 mL During exercise volume increases to 100 mL.
Blood distribution to tissues?
dependent on the metabolic needs of that tissue -Resting muscle receive ≈20% of CO -Working ≈85%
What is angiogenesis?
development of new blood vessels Necessary for normal development Occurs during wound healing and uterine lining growth, and in response to endurance training Controlled by cytokines and growth factors released from the endothelium or surrounding tissues. Stimulate (mitogens): VEGF (vascular endothelial growth factor) and FGF (fibroblast growth factor) Inhibit: angiostatin and endostatin Plays a role in the growth of malignant tumors
Tell me about paracrines
function in local control over vascular smooth muscle contraction i.e. O2, CO2, NO (EDRF) Re-active Hyperemia: -Blood flow is blocked at a certain tissue ↓O2 and ↑CO2 -Local hypoxia produces NO -CO2 and NO act as vasodilators -Blood flow is increased
What is atherosclerosis?
hardening of the arteries; inflammatory process Fatty deposits form inside the arterial blood vessel... Triglycerides and cholesterol in the serum Cause of almost one out of three deaths in the US (35 years and older) Excess LDL leads to the development of atherosclerosis.
Afterload
load that the ventricle has to "overcome" during contraction Determined by: (1) arterial blood pressure (2) EDV associated with many cardiovascular pathologies Loss of aortic compliance Systemic hypertension May result in left ventricular hypertrophy (LVH)
What is cardiac output?
standard measure of cardiac performance. Blood volume pumped by one ventricle in a given period of time. = HR (beats/min.) x stroke volume =72 (beats/min) x 70mL/beat CO ≈5 L/min (at rest) This can increase up to 30-35L/min during exercise Normally the same in both ventricles If it decreases in one, it will result in a pooling of blood in the circulation behind the weaker side of the heart
What is the Frank-Starling Law?
stroke volume is proportional to EDV.
Capillary flow velocity
the smaller vessel area, the higher flow velocity (if rate is constant) capillaries - FLOW RATE IS LOW!...therefore velocity is low... but, consider the total cross-sectional area of the capillary
What is mean arterial pressure?
this is a single value to represent the driving pressure in our vessels MAP = diastolic pressure + (1/3)(systolic - diastolic)
How is exchanges accomplished?
via diffusion and transcytosis; Exchange takes place either by movement between endothelial cells (paracellular) or through the cells (endothelial transport) Small solutes or gases move either directly through or between the cell (depending on lipid solubility) Larger solutes and proteins require vesicles: i.e. - transcytosis
What is hypoxia?
when no/low oxygen is available at a tissue.
