PhysiologyTest5StudyGuide

DuctlessSecrete hormones (chemical signals) into the blood. Target organs have SPECIFIC hormone receptors

Hypothalamus, pituitary, adrenal gland, thyroid gland, parathyroid gland, pancreatic islets, etc

• Nonpolar hormones must be transported by carrier proteins in plasma, but can diffuse directly through the plasma membrane. Receptors for nonpolar hormones are located inside cells.
• Examples include: steroids (cortisol, testosterone, estrogen, progresterone) produced by adrenal cortex/gonads and thyroid hormones produced by the thyroid gland.

• Polar hormones dissolve in plasma, but cannot diffuse through the plasma membrane. Receptors for polar hormones are located in the plasma membrane of cells, and they act through second messengers.
• Examples include epinephrine (adrenaline) produced by the adrenal medulla and polypeptides, proteins, and glycoproteins (most hormones) produced by the hypothalamus, pituitary, pancreas, and parathyroid.

Hypothalamus secretes releasing hormones (RH) and inhibiting hormones (IH) to the hypothalamo-hypophyseal portal system. This controls anterior pituitary hormone secretion/inhibition.

• Corticotropin-releasing hormone (CRH) stimulates ACTH (adrenal corticotrophic hormone)
• Thyrotropin-releasing hormone (TRH) stimulates TSH (thyroid stimulating hormone) secretion
• Gonadotropic-releasing hormone (GnRH) stimulates FSH (follicle stimulating hormone) and LH (luteinizing hormone)

Neurosecretory neurons in the hypothalamus produce two different peptide hormones (ADH and Oxytocin) which then transported and stored in the posterior pituitary. They are released from the posterior pituitary when the neurons undergo an AP.

(AKA Vasopressin) increases water retention by the kidneys, decreases urine volume (opposite of diuresis), constricts blood vessles

Uterine contraction during childbirth (labor) and milk letdown during breastfeeding

• Hypophysis – extends from the inferior surface of the hypothalamus, linked to hypothalamus by infundibulum
• Posterior lobe (neurohypophysis) is a downgrowth from the brain
• Anterior lobe (adenohypophysis) is derived from oral epithelium

Different cell types secrete 6 peptide (polar) hormones

• TSH (Thyroid stimulating hormone) – activates thyroid gland, increases thyroid hormones, increases size of thyroid gland, stimulated by TRH
• ACTH (Adrenocorticotrophic hormone) – activates adrenal cortex to release cortisol, stimulated by CRH [usually in times of stress]
• GH (Growth hormone) – stimulates growth, protein synthesis, fat breakdown, increases blood glucose levels [works at epiphysial plate]
• Prolactin – breast development and milk production during pregnancy
• LH (Lutenizing hormone)
• FSH (Follicle stimulating hormone) – females: regulates ovaries (egg) and female sex hormones (estrogen and progesterone), males: regulates testes (sperm) and male sex hormones (testosterone), stimulated by GnRH

LH and FSH

• Hormone receptors are located in the hypothalamus and pituitary (in addition to target organs)
• These receptors allow homeostasis of hormone levels (thereby hormone effects) through alteration of RH/IH concentration, sensitivity, etc

• GnRH (hypothalamus) stimulates FSH and LH secretion (anterior pituitary)
• FSH and LH stimulate sex steroid secretion (gonads)
• Sex steroids act on hypothalamus (inhibit GnRH secretion) and anterior pituitary (inhibit sensitivity to GnRH)
• Less stimulation of the gonads causes decreased secretion of sex steroids

• Located above each Kidney
• Contains two distinct tissues; medulla (inner) and cortex (outer)
• Releases hormones in response to stress

• Epinephrine (adrenaline) release is stimulated by pre-ganglionic sympathetic nerve fibers which innervate the adrenal medulla
• It is sympathomimetic to norepinephrine (activates the same receptors in the same manner).
• Increases the effects of the sympathetic system (fight/flight) and increases glucose levels in blood

• Polar hormone (cannot diffuse into cell) requires receptors in the membrane.
• Binds to G-Protein-linked receptor in cell membrane
• G-Protein sub-unit activates Adenalate Cyclase which produces the second messenger cAMP
• cAMP activates various protein kinases which activate/deactivate various enzymes, producing varied effects between cells

• Aldosterone and Cortisol (hydrocortisone) are secreted in response to stress (CRH and ACTH)
• Aldosterone [mineralocorticoids] - increases K+ exretion and Na+ retention by kidneys (regulation of blood pressure/K+ homeostasis)
• Cortisol [glucocorticoids] - elevates blood glucose, amino acids, and fatty acid levels. Also suppresses inflammation and the immune system

• Nonpolar hormone (can diffuse into cell)
• Binds directly to protein receptors in cytoplasm or nucleus
• Receptor binds to gene regulatory proteins in the nucleus, stimulates transcription of that gene (protein expression)

• (cortisol) – CRH (hypothalamus) stimulates ACTH secretion (anterior pituitary)
• ACTH stimulates cortisol secretion (adrenal cortex)
• Cortisol inhibits CRH and ACTH secretion (hypothalamus and anterior pituitary)

• Located in the thyroid cartilage, and consisting mainly of thyroid follicles (“water balloons” that trap Iodine)
• Follicular cells (surround the colloid) and colloid (fluid within the follicles)

• Iodine accumulates in colloid (fluid) in follicles and combines with protein resulting in thyroglobulin
• Thyroglobulin is converted to thyroid hormone in the follicular cells

• Thyroid hormone targets general body tissues and increases BMR and body heat production
• It is required for the growth and maturation of the CNS

• (nonpolar) – transported by carrier protein in blood
• Passes directly through cell membrane
• Binds to nuclear receptor (in nucleus)
• Stimulates expression of gene (protein production)

• TRH (hypothalamus) stimulates TSH secretion (anterior pituitary)
• TSH stimulates thyroid hormone AND growth of thyroid
• Thyroid hormone inhibits TSH secretion (anterior pituitary)

• Inadequate Iodine in diet leads to insufficient thyroid hormone (hypothyroidism), hypothalamic pituitary axis responds by increasing TSH secretion, stimulates excessive growth the of the thyroid
• Grave’s disease (autoimmune disease) antibodies mimic effects of TSH, stimulate growth of the thyroid and overproduction of thyroid hormone (hyperthyroidism)

• 4 small organs located on the posterior surface of the thyroid cartilage.
• Detect low Ca2+ levels, secrete parathyroid hormone (PTH)
• PTH increases blood Ca2+ level by increasing osteoclast activity, inhibiting Ca2+ secretion by kidneys, and increasing Ca2+ uptake by intestines

Parathyroid detects blood Ca2+, so there is no brain involvement. When Ca2+ levels reach the set point PTH is secreted in smaller amounts (parathyroid)

• Both endocrine (blood glucose levels) and exocrine (digestive) functions
• Endocrine cells located in islets of Langerhans
• Alpha cells – secrete glucagon
• Beta cells – secrete insulin

• Beta cells detect high blood glucose and secrete insulin
• Insulin increases glucose uptake by muscle, liver, and fat
• increases glucose transporters in plasma membrane (via exoctyosis), promotes removal of glucose from blood (facilitated diffusion), and lowers blood glucose levels
• Promotes conversion of glucose into triglyceride storage in adipose tissue, conversion of glucose to glycogen in skeletal muscle and the liver.

• Blood glucose level is the major factor controlling insulin/glucagon secretion.
• Maintenance of blood glucose at homeostatic levels via negative feedback (islets of Langerhans)

• Alpha cells detect low blood glucose and secrete glucagon
• Increases blood glucose (promotes breakdown of glycogen to glucose, production of glucose from amino acids, promotes breakdown of fat/production of ketone bodies)
• ketone bodies are a byproduct of fatty acid breakdown. Ketone bodies can be used for fuel by heart and brain when glucose is low, but can also lower pH, be secreted in urine, etc

• Insulin deficiency or reduced insulin sensitivity.
• Cells do not take up glucose which results in hyperglycemia (high blood glucose)
• This can lead to dehydration from loss of excess water from urination, which can result in blood volume and pressure problems
• Can lead to starvation when the body can’t use the glucose and glucose is lost in the urine, resulting in the breakdown of fats and formation of ketone bodies

• (juvenile onset) – degeneration of beta cells in pancreas (autoimmune disease)
• No insulin made by body
• Must receive insulin shots

• (adult onset) – cells resistant to the effects of insulin
• Often associated with obesity
• May be controlled by diet and exercise

• Specifically designed to contract and generate mechanical force.
• Functions include locomotion and external movements, internal movements (digestion, circulation, etc), and heat generation (side product)

Skeletal (attached to skeleton), smooth (found in walls of hollow visceral organs), cardiac (heart)

• Connected to skeleton via tendons
• Bends the skeleton at joints
• Arranged in antagonistic pairs (contraction of agonist causes stretching of antagonist)

• Muscle cells/fibers – elongated, multinucleated cells arranged parallel to one another and grouped in fascicles (bundles) by CT.
• Sarcolemma = cell membrane of a myofiber

• A band – (dark band) – runs the length of the thick filaments, includes thin overlap
• H zone – (light area at the center of the A band) – thick filaments with no thin overlap
• I band – (light band) – thin filaments with no thick overlap (across 2 sarcomeres)
• Z disc – (thin dark lines at center of I band) – point of attachment for thin filaments, separates sarcomeres

• Long bundles of myofilaments (actin [thin] and myosin [thick]) within muscle fibers.
• Myofilaments arranged in sarcomeres.

Repeating units of myofilaments along myofibrils

• Length of a sarcomere is from Z disc to Z disc
• Thick filaments at the center, with thin filaments on both ends ( attached to the Z line)
• ½ I band at either end (only thin myofilaments)
• A band at midsection (thick and thin filaments)
• H zone at center (only thick filaments, no thin overlap)

• The contraction and relaxation of a motor fiber in response to an action potential
• An AP always elicits a twitch in a motor unit (no threshold)

• Arrival of a 2nd AP before a muscle fiber relaxes causes more cross bridges to form and more tension to be generated
• When a muscle is stimulated multiple times in rapid succession the strength of contraction increases

The strength of a whole-muscle contraction can be modified by altering the number of motor units involved. (motor unit recruitment)

• Incomplete tetanus – muscle stimulation at high enough rate so that the muscle does not fully relax between contractions
• Complete tetanus – muscle stimulation at high enough rate so that no muscle relaxation occurs (steady state of tension, maximum tension)
• In the body complete tetanus is avoided by activating different motor units in rapid succession to generate a sustained contraction

• Isometric contraction – muscle does not shorten (force generated by the contraction is equal to or less than the load applied)
• Isotonic contraction – muscle shortens (force generated by the contraction exceeds the load applied)

• Thick filaments are stationary, thin filaments slide past the thick filaments and increase overlap (length of filaments do not change, sarcomere shortens)
• A band is unchanged, I band shortens, H band shortens

• Bundles of myosin proteins (intertwining tails and globular heads that project outward towards thin filaments)
• Myosin heads (cross-bridges) contain actin binding sites and an ATPase

• Two twisted strands of actin molecules
• Actin – molecules in polymer chain, contains myosin binding site
• Tropomyosin – wraps around actin, covers myosin binding sites on the actin filaments
• Troponin – Ca2+ binding protein, holds tropomyosin in place until Ca2+ is present

• The myosin head binds to actin (ATP required)
• Power stroke – globular head bends toward center of sarcomere, thin filaments pulled inward
• Cross bridge link broken, head “unbends” (ATP required to unbind crossbridge)
• Myosin binds to next actin molecule on thin filament and repeats process
• sarcomere shortens

• Normal resting length (sarcomere length ~2.0 μm) generates the maximum amount of tension (maximum cross-bridges formed)
• If muscle length increases (sarcomere length >2.2 μm) tension is reduced as overlap between thick and thin filaments decreases
• If muscle length decreases (sarcomere length <2.0 μm) tension is reduces as thin filaments from opposite ends of the sarcomere collide

• APs induce the release of Ca2+ into the sarcoplasm
• Ca2+ binds to troponin on the thin filament, causing a conformational change
• Tropomyosin shift away from the myosin bind sites (conformational change)
• Myosin can now bind to actin

• Network of smooth endoplasmic reticulum around each myofibril (bundles of myofilaments)
• At rest Ca2+ pumps (Ca2+ATPase) move Ca2+ from the sarcoplasm to the sarcoplasmic reticulum, keeping sarcoplasmic Ca2+ levels low
• The Sarcoplasmic reticulum contains voltage-gated Ca2+ ion channels
• Basic function of SR – to store Ca2+ during resting periods and release Ca2+ to stimulate contraction

• Extensions of the sarcolemma that continue to the interior of the muscle fiber and extend around each myofibril. (appear as dimples on the surface of the sarcolemma)
• Carries an AP into the muscle fiber, opening voltage-gated Ca2+ channels in SR

• AP travels down SMN axon to axon terminal (NMJ) inducing the exocytosis of ACh
• ACh binds to nicotinic AChR at the motor end plate and opens ion channels
• Na+ diffuses into cell (via nicotinic AChR) and induces an AP in the sarcolemma of muscle fibers

• Botox blocks the exocytosis of ACh at the SMN
• Curare blocks the Nicotinic AChR on the motor end plate

• The events that link muscle excitation (AP) to contraction (crossbridge cycling)
• AP from NMJ propagates down the sarcolemma
• Transverse tubules conduct AP into the cell’s interior
• Voltage gated Ca2+ channels open in the sarcoplasmic reticulum
• Ca2+ is released into the sarcoplasm
• Ca2+ binds to troponin
• Troponin moves tropomyosin away from myosin binding sites
• Crossbridge cycling occurs (muscle contracts)

• NMJ stops firing, muscle APs stop, voltage-gated Ca2+ channels in SR close.
• Ca2+ is pumped back in to the SR via active transport (ATP required)
• Troponin releases Ca2+, tropomyosin re-covers myosin binding site of the actin molecules and cross-bridge cycling is halted
• The cell elastically recoils to its resting length

• Muscle contraction (cross-bridge cycling), muscle relaxation (Ca2+ pump), and the SMN’s Na+/K+ ATPase
• Muscles can use cytosolic ATP [small amount], phosphocreatine (creatine phosphate), aerobic respiration, or anaerobic respiration (fermentation).

• ATP in the muscle is limited, and used up after only a few contractions
• Phosphocreatine is the muscle’s way of storing high-energy phosphate bonds, which it can use to quickly regenerate ATP from ADP
• There is a limited storage of phosphocreatine in the cells

• Aerobic respiration occurs in mitochondria, and requires O2 to form ATP
• Fatty acids contain a large amount of energy, but require O2 for release.
• Fatty acids are the primary nutrient source during light/moderate exercise
• The body’s maximum O2 uptake (thereby delivery to muscles) determines a person’s maximum level of aerobic activity

• Anaerobic respiration is the result of glycolysis and lactate fermentation and does not require O2 to form ATP
• It is a breakdown of glucose (which is stored as glycogen in muscle cells)
• It generates ATP quickly (faster than aerobic respiration) but is less effective than aerobic respiration (only 2ATP/glucose)
• It is used during intense exercise (when the O2 supply cannot keep up with demand)
• Lactate (lactic acid) is produced resulting in muscle soreness and fatigue

Ketone bodies are a byproduct of fatty acid breakdown. Ketone bodies can be used for fuel by heart and brain when glucose is low, but can also lower pH, be secreted in urine, etc

• Elastic elements connect myofilaments to sarcomere (resulting in recoil)
• When muscles are stretched a tension is generated (regardless of muscle activity) due to this property.

Directly related to length of sarcomere (optimal range) and being activated.

• The inability to maintain tension due to previous contractive activity
• ATP stores are used up, glycogen is used up, ion concentrations are disrupted, and there are high lactic acid levels

• Increased O2 consumption (breathing) after excersize
• Restores myoglobin and hemoglobin O2 content, metabolizes lacate

• An increase in the number and size of mitochondira
• An increase in the number of blood capillaries supplying muscles (resulting in an increase of O2, nutrients, and more effective waste removal)
• An increase in the amount of myoglobin in muscle tissue
• An increase in the size of muscle fibers (results from weight training, not aerobic exercise) [size increase is a result of more myofibrils (actin/myosin) not a change in the number of myofibers

• Branched, striated cells connected end to end (contain sarcomeres)
• The basic mechanisms of contraction are similar to skeletal muscle

• Myocardial cells are linked end to end by intercalated disks which contain gap junctions
• This enables APs to travel from one cell directly to the next, causing the myocardium to contract as a single unit
• Specialized myocardial cells (pacemaker cells) generate spontaneous APs that cause the heart to contract a certain frequency (no NMJs)
• Autonomic input does not cause contraction, but does influence rate/force of contraction

• Found in the walls of hollow visceral organs
• Contains small tapered fibers
• Lacks striations (contractile proteins not arranged within myofibrils)
• Has poorly developed SR

• Contractile proteins are arranged in a fish-net network with long, thin filaments attatched to the plasma membrane of dense bodies. (dense bodies ~ Z disks)
• This allows the muscle to contract even when greatly stretched (bladder)

• Depolarization of the sarcolemma opens V-gated Ca2+ channels
• Ca2+ enters the cell from the extracellular fluid (NOT the SR)

• Smooth muscle generates slow, sustained contractions
• Skeletal muscle generates fast, easily fatigued contractions

• Accumulation of liquid in the peritoneal cavity (result of liver failure)
• Lack of albumin from the liver causes a change in the blood’s tonicity and water diffuses out of blood, into peritoneal cavity

• Blood (transport medium) – consists of cells and fluid
• Heart (pump) – drives the circulation of blood
• Blood vessels – tubing that conducts blood to its destination

• Transport medium for gases, nutrients, wastes, hormones, ions, cells, etc
• Volume of ~5L
• Tonicity of ~300 mOsm (.3 Osm)
• pH of ~7.35-7.45

• Plasma (~55% of blood volume) – the fluid portion of blood
• Formed elements (~45% of blood volume) – cells and fragments

Plasma fluid lacking clotting proteins (typical source of antibodies)

A layer of WBCs and platelets that appears after a centrifuge of blood.

• 90% water – dissolved materials (ions, gases, nutrients, etc) the fluid medium for transport of blood cells and plasma proteins
• 7-9% proteins
• albumin - maintains osmotic pressure of blood
• α & β globulins – carrier proteins for lipids (amphipathic molecules)
• gamma globulins – antibodies
• other proteins – hormones, fibrinogen, etc

• Erythrocytes – red blood cells
• Leukocytes – white blood cells
• Thrombocytes – blood platelets

• Thin, biconcave disc-shaped cells (7.5 μm diameter) that lack nuclei and mitochondria and contain many molecules of hemoglobin
• Transport respiratory gases (mainly O2) on hemoglobin

• Erythrocyte production occurs in myeloid tissue (bone marrow) and creates ~200 billion RBCs per day
• Stimulated by Erythropoetin (a hormone) secreted by the kidneys in response to decreasing O2 concentration in blood

• RBCs last only 120 days after release into the blood stream due to their lack of nuclei and mitochondria
• Old cells are engulfed by phagocytic cells in the spleen, liver, and bone marrow

• A protein made of 4 heme subunits (quaternary structure), it contains iron and reversibly binds O2 and CO2
• Hemoglobin changes color when bound to O2 (bound = bright red, unbound = dark maroon)
• Cyanosis (light blue/grey lips and finger nails) is a result of inadequate O2 levels
• Anemia is an inadequate RBC count in the blood (or amount of hemoglobin)

• Immunity: defense against harmful foreign invaders or abnormal cells
• Functions: destroy pathogens (bacteria, viruses, protozoans, and worms), destroy cancer cells, remove dead/injured cells (wound healing)
• Granular: neutrophils, eosinophils, basophils
• Agranular: lymphocytes, monocytes

• Neutrophils: Show very little stain. Phagoctyes (devour pathogens and dead cells), are able to leave blood vessels and enter CT
• Eosinophils: Show pink/orange under stain. Attacks parasites
• Basophils: Show dark stains that obscure nucleus. Produce histamine, promoting allergic reactions
• Lymphoctyes: part of the lymphatic system, functions in immune responses
• Monocytes: Circulating phagocytes, differentiate into “wandering macrophages” in tissues outside of blood

• Platelets are cell fragments from megakaryocytes in bone marrow
• Last 5-9 days in circulation
• Important in forming clots to stop bleeding when blood vessels are damaged (platelets attach to collagen and form a platelet plug, fibrin is formed (from fibrinogen) to reinforce the clot)

• Cells have markers on their surfaces that identify them as part of your body, foreign markers act as antigens and evoke an immunological defense mechanism)
• Erythrocytes have relatively few markers (ABO blood types and Rh factor (antigen))

A hollow, muscular organ located in the center of the thoracic cavity (mediastinum) which pumps constantly (at variable rates).

• Pulmonary circuit: heart (right) -> lungs -> heart (left). Exchanges gas with the atmosphere (releases CO2, picks up O2)
• Systemic circuit: heart (left) -> organs -> heart (right). Exchanges gas with body tissues (releases O2, picks up CO2)

4 chambers: L/R atria receive blood from veins, L/R ventricles pump blood into arteries

• The interventricular septum divides the heart into 2 parallel pumps with different chemistries and different pressures
• The right side pumps deoxygenated blood at low pressure (low resistance)
• The left side pumps oxygenated blood at high pressure (high resistance)
• The flow between sides remains equal (flow = pressure / resistance)

• Atrioventricular valves [right (tricuspid) and left (bicuspid / mitral)] allow blood to flow from the atrium to the ventricle ONLY (1 way valve). Chordae tendinae attached to papillary muscles prevents valves from everting during ventricular contraction.
• Semilunar valves [pulmonary (left) and aortic (right)] are located at the openings of the arteries that leave the ventricles and prevent blackflow of blood during ventricular relaxations.

• Pulmonary circuit: Deoxygenated blood enters the right atrium from the vena cava -> right AV valve -> right ventricle -> pulmonary semilunar valve -> pulmonary trunk and arteries -> lungs -> pulmonary veins
• Systemic circuit: Oxygenated blood enters left atrium through pulmonary veins -> left AV valve -> left ventricle -> aortic semilunar valve -> aorta -> tissues -> veins

• The contraction (systole) and relaxation (diastole) of the heart’s ventricles (simultaneous)
• 1. Isovolumetric contraction [systole]
• 2. Ejection [systole]
• 3. Isovolumetric relaxation [diastole]
• 4. Rapid filling [diastole]
• 5. Atrial contraction [diastole]

• [systole] beginning of ventricle contraction, no blood ejected
• semilunar valves closed for the duration
• when ventricle pressure rises above atrial pressure (~0 mmHg) AV valves shut

• [systole] blood flows out of ventricles into arteries
• Pressure in ventricles exceeds pressure in arteries, semilunar valve opens
• blood flows into arteries, causing ventricular pressure to fall
• AV valve closed for the duration
• pressure forces the semilunar valves open and blood is ejected from the ventricle

• [diastole] beginning of ventricle relaxation, no blood ejected/filled
• Pressure in ventricle drops below arterial pressure, semilunar valve closes (prevents backflow of blood)
• No change in ventricular volume
• AV valve closed for duration

• [diastole] blood flows out of atrium into ventricle
• Pressure in ventricles falls below atrial pressure, AV valve opens
• Blood flows from atrium into ventricles
• Semilunar valve closed for duration

• [diastole] – small atrial contraction before ventricle contraction
• Small atrial contraction pushes final amount of blood into ventricles just prior to ventricle contraction (creates EDV)

• Diastole ~.5s
• Systole ~.3s

End diastolic volume – the amount of blood in the ventricles at the end of diastole (nearly full)

End systolic volume – the amount of blood in the ventricles at the end of systole (nearly empty)

Stroke volume – the amount of blood ejected by the ventricles (EDV – ESV)

• Lub (first sound) – closing of the AV valves at the start of systole
• Dub (second sound) – closing of the semilunar valves at the start of diastole

• Sinoatrial (SA) node (right atrium near superior vena cava) – pacemaker of the heart, site where APs are first generated
• Atrioventricular (AV) node (bottom/middle right atrium to interventricular septum) – delays conduction to ventricles
• Atriolventricular bundle (bundle of His) (interventricular septum, splits into two) – conducts signals through the interventricular septum
• Purkinje fibers (middle apex of heart up sides of heart) – conducts signals up lateral walls of ventricle

• SA node cells undergo spontaneous pacemaker potentials which creates APs
• APs conducted through the atrial network
• Atrial fibers activated (atrial contraction)
• APs excite AV node which delays AP (allows completion of atrial contraction)
• APs of AV node travel down AV bundle to apex of heart
• Signals conducted to Purkinje fibers throughout ventricle (ventricular contraction)
• Contraction from Apex upward to accommodate “pumping” to ateries located at top of heart

• Modified cardiac muscle cells that spontaneously produce pacemaker potentials
• Pacemaker potentials are spontaneous depolarizations during diastole that lead to the APs for contraction. They begin again almost immediately after pacemaker cell repolarization.

• The myocardial AP is triggered when myocardial cells receive the AP originally generated by the SA node
• Myocardial APs have a prolonged duration when compared to the neural “spike” AP, and have involvement of 3 V-gated ion channels rather than just 2.
• Na VG channels are opened to begin AP, Na+ flows in causing depolarization
• The 200-300msec plateu phase is caused by a slow Ca2+ influx which combats the slow K+ output from K+ leak channels
• Repolarization occurs by the delayed opening of VG K+ channels (and closing of Ca2+)
• The prolonged refractory period ensures a pumping action without the possibility of summation (allows relaxation)

Electrocardiogram – recording electrodes on extremities allow a recording of the electrical activity of the heart (not contraction)

• P wave (initial hill) – depolarization in atria just before contraction
• QRS complex (small valley, large spike, deeper valley) – depolarization of ventricles just before contraction (beginning of systole), also includes atrial repolarization (not shown on ECG)
• T wave (final hill followed by nothing until next P wave) – repolarization of ventricles (beginning of diastole)

Waveform shapes, time intervals, segments,etc can be used to diagnose cardiac pathologies

• Bradycardia – abnormally slow heartbeat (<60bpm)
• Tachycardia – abnormally fast heartbeat (>100bpm)
• Flutter – extremely rapid, but coordinate heartbeat (200-300bpm)
• Fibrillation – different cells product APs and contract and different times (uncoordinated pumping). Defibrillator shocks the heart, putting the entire myocardium into a refractory period (“resetting” the heart)

• Tubes that conduct blood through the body
• Elastic arteries -> muscular arteries -> arterioles -> capillaries -> venules -> veins

• The force exerted on blood vessel walls by blood, produced by heart contractions.
• Blood pressure is the major driving force for the flow of blood through the blood vessels.
• Blood pressure decreases as blood moves farther from the heart
• Blood pressure is a function of cardiac output and Total Peripheral Resistance
• (Flow = Pressure/Resistance AKA Pressure = Flow x Resistance)

Pressure of blood in the arteries during ventricular systole

Pressure of blood in the arteries during ventricular diastole

The difference between systolic and diastolic pressure

• (MAP) is the average blood pressure throughout the cardiac cycle
• It is not a simple mean, because systole and diastole have different lengths (.3msec vs. .5msec)
• This measurement is the most functionally relevant to blood movement in the body

• Place cuff, pump pressure to ~160 mmHg (higher than BP)
• Gradually release pressure until you hear the first sound [first Kortkoff sound] caused by ventricular systole forcing a small amount of blood under the cuff
• Continue to release, there will be continued sounds during ventricular systole
• Release until no sounds occur [final Korotkoff sound] caused by cuff pressure being equal to ventricular diastole pressure

• BP greater than 140/90 without known cause
• Increased risk of atherosclerosis, heart attack, and stroke
• Stop smoking, lose weight, lower salt intake
• Diuretics (decrease blood volume), α-blockers and β-blockers (adrenergic receptor blockers), Ca2+ blockers (prevent Ca2+ channels in blood vessel smooth muscle from opening, prevent contraction), ACE inhibitors (prevent angiotensin I -> angiotensin II) and ARB (block angiotensin II binding sites)

• Large vessels receiving blood from the heart.
• Rapid transport of blood (large radius, high pressure)
• Pressure reservoirs (walls expand upon systole, recoil during diastole)
• Maintain blood flow during ventricular diastole

• Small arteries
• Provide greatest resistance to blood flow (caused by friction to flow of blood from small radius)

• Resistance is inversely proportional to a change in the radius^4
• Radius is used to control blood flow to different organs by sympathetic control (no parasympathetic control) of the smooth muscle in the arteriole wall.

• [P=FR] – Blood pressure falls dramatically
• An increase in total cross-sectional area decreases the flow which makes up for the increase in resistance caused by the smaller radius

• Very thin vessels which have enormous quantities in the body
• Walls consist of a single endothelial cell layer
• Site of material exchange between blood and interstitial fluid

• Short diffusion distance (thin capillary walls, narrow diameter)
• High surface area (extensive branching – close to ALL cells)
• Slow blood flow (increases time for exchange to occur)

• (SV) amount of blood ejected by ventricles per beat
• Depends on EDV [direct], contractility [direct], and TPR [indirect]
• Frank-Starling Law
• External influences (sympathoadrenal system increases contractility and heart rate)

• Increased EDV causes increased contractility and increased SV
• Volume in must equal volume out, amount of contraction is dependent on how “full” the chamber is (how stretched the sarcomeres are)

• Cardiac output [volume/min] = heart rate [beats/min] x stroke volume [volume/beat]
• [Cardiac rate] parasympathetic nerves (decrease), sympathetic nerves (increase)
• [Stroke volume] TPR (decrease), EDV (increase), contraction strength (increase, contraction strength increased by stretch and sympathetic nerves)

• Total blood flow resistance the left ventricle must overcome
• Direct: Vessel length and blood viscosity
• Indirect: radius^4 <- very powerful in changing resistance

• Dependant on venous return
• Important to stroke volume

• Skeletal muscle pump – skeletal muscle moving blood through the veins, against gravity
• Breathing pump – diaphragm moving blood through the veins, against gravity
• One-way venous valves – prevent blood from flowing backward in veins
• Without these measures blood pooling will occur in veins.

• (Short term blood pressure regulation)
• The baroreceptor reflex regulates heart rate and blood pressure [negative feedback loop]
• Baroreceptors detect blood pressure (located in the aortic arch and carotid sinuses)
• Baroreceptors send signals to the reticular formation in the medulla
• In response: the sympathetic system causes increased heart rate and blood pressure or the parasympathetic system causes decreased heart rate and blood pressure

• Feeling faint upon standing up as a result of the baroreceptor reflex latent period (a few seconds)
• Caused by lowered blood pressure when standing after laying down (increased gravity requires increased contraction of the heart) which results in decreased blood flow to the brain

• (Long term blood pressure regulation)
• Increased blood volume causes increased stroke volume
• Increased stroke volume causes increased cardiac output
• Mean Arterial Pressure = cardiac output x total peripheral resistance
• Therefore: increased blood volume causes increased MAP [BP]
• Excretion of urine by the kidneys is the major way the body regulates blood volume (ADH, aldosterone)

• Filtration: movement of fluid and solutes from capillary to interstitial fluid (driven by hydrostatic pressure AKA BP)
• Absorption: diffusion of fluid and solutes from interstitial fluid to capillary (driven by osmotic pressure)
• Proteins do not leave the capillaries (think albumin) and create the osmotic pressure that drives reabsorption of fluid.

The volume of fluid that is filtered out by capillaries but not reabsorbed (~4L/day) which needs to be returned to blood.

• Lymph capillaries take up interstitial fluid (lymph)
• One way flow (unlike circular blood flow)
• Cells, bacteria, and debri are also taken up (these may be too large for blood capillaries)
• Lymph flows through lymph nodes (immune defense cleans/filters the lymph)
• Clean lymph flows back into bloodstream at the subclavian veins
• The lymph system prevents edema

• Excessive fluid accumulation caused by failure of lymph drainage (eg. Removal of lymph nodes)
• Elephantiasis is caused by parasites that block lymph flow

• Filtration of blood by glomeruli (180L/day)
• Reabsorption of useful solutes (99% of water reabsorbed, ~1.5 L excreted in urine/day)

• ADH from posterior pituitary increased water reabsorption
• Aldosterone from adrenal cortex increases reabsorption of Na+, Cl-, water / increases K+ excretion
• Increased absorption of water increases blood volume, raising BP.

Increased blood volume results in increased blood pressure

• Secreted by posterior pituitary in response to increased blood osmolarity (low blood volume and/or increased solute concentration) (eg dehydration or salt ingestion)
• Increases water retention by the kidneys (increases blood volume)
• Acts by “telling” cells in the kidney to insert additional aquaporins (for water retention)

• Secreted by adrenal cortex in response to low blood pressure and low blood flow to kidneys
• Increases reabsorption of both salt (and water) by the kidneys (prevents reduction of blood volume even if salt levels are low)
• Low NaCl -> Low OsM -> increased urine -> decreased blood volume -> decreased blood pressure [it prevents this from happening]

• Through the renin –angiotensin-aldosterone system
• 1 – Kidney cells detect low blood pressure
• 2 – cells in the juxtaglomerular apparatus of kidney tubules secrete renin (an enzyme) into the blood
• 3 – Renin converts angiotensinogen (already in the blood) to angiotensin I
• 4 – ACE (angiotensin converting enzyme) converts angiotensin I into angiotensin II as it circulates in the blood
• 5 – angiotensin II stimulates aldosterone secretion and vasoconstriction of arterioles

• Intrinsic control: increased blood flow to areas with an increased metabolism (eg skel muscle). Blood vessels dilate, and hyperemia (localized increase in blood flow) occurs
• Extrinsic control: sympathetic activation and adrenaline (increase in HR and SV). Parasympathetic activation (decrease in HR and SV).

• Blood flow increases dramatically to the heart and skeletal muscles, yielding an increased cardiac output [due increased heart rate, stroke volume, sympathetic input, and Frank-Starling law]
• Intrinsic metabolic vasodilation in skeletal muscles and heart (increased blood delivery to muscles, active hyperemia)
• Sympathetic nerve-induced vasoconstriction in the viscera and skin

• % changes: GI – decreased, heart – equal, kidneys – decreased, bone – decreased, brain – decreased, skin – decreased, skeletal muscle – dramatic increase
• L/min: GI – equal, heart – increased, kidneys – decreased, bone – decreased, brain – equal, skin – decreased, skeletal muscle – dramatically increased
• Total cardiac output from 5L/min resting to 25L/min active

• Vasodilation in response to high body temperature
• vasoconstriction in response to low body temperature
• Sympathetic control of vascular smooth muscle [no parasympathetic], hypothalamic control of autonomic nervous system

• Autoregulation maintains constant blood FLOW to the brain (F = P/R)
• Brain needs constant flow due to enclosure in skull (can’t expand)
• increased blood pressure (increased flow) causes vasoconstriction (decreased flow)
• Decreased blood pressure (decreased flow) causes vasodilation (increased flow)
• Active hyperemia causes increased blood flow to brain regions with increased activity (eg. Visual stimulation will direct flow to occipital lobe) (seen with fMRI and PET scans)