Week 13

compliance and age

"Old" artery less compliant/ stiffer than "young" artery At a given MAP, "old" arteries hold less blood than "young" arteries. For an "old" artery to hold the same volume of blood as a "young" artery, the pressure in the "old" artery must be higher. Systolic BP and pulse pressure in elderly > young "Systolic Hypertension of the Elderly" (diastolic can be normal)

starling's hypothesis

"under normal conditions, the amount of fluid filtering outward from the arterial ends of the capillaries *equals almost exactly* the fluid returned to the circulation by absorption".

Skeletal muscle circulation

% of CO: 18% (80% in heavy exercise) local control of blood flow:most important-during exercise Sympathetic control: most important at rest Mechanical effects: compression-temporary decrease in blood flow (especially static exercise) Vasoactive metabolites (vasodilators): lactate,K+,adenosine

coronary circulation

% of CO: 5% a lot of oxygen for its size Local control blood flow: most important Sympathetic control: least important Mechanical effects: compression during systole Vasoactive metabolites: hypoxia, adenosine, NO O2 extraction from blood is high (70%) at rest. To get more O2 to tissue *blood flow must increase*. O2 delivery=flow limited

Pulmonary circulation

%of CO: 100% local control blood flow: most important sympathetic control: least important mechanism effects: lung inflation vasoactive metabolites: hypoxic alveoli>>vasoconstriction differs from other circulations: *Low pressure low resistance 100% cardiac output (CO)*\ purpose:to oxygenate blood: optimize blood flow to alveolar regions rich in oxygen-by reduced flow oxygen-poor alveoli (constricting vessels to this region) hypoxia causes local vasoconstriction of this organ, via O2 sensing K+ channels: (Euler-Likestrand mechanism)

terminal sac period (lung development)

( week 26 to birth) - formed lined by squamous epithelium, capillaries establish close contact

production of surfactant

(Surface active agent, lipoprotein produced by Type Il alveolar cells reduces the surface tension and facilitates expansion of the terminal sacs Production begins around week 20 but only around weeks 22-26 its produced in sufficient amount for survival (with intensive care) By weeks 26-28 — sufficient number of terminal sacs & surfactant (can survive if born prematurely) deficiency is a major cause of Respiratory distress syndrome (RDS) - 1-2% of newborns, (higher in premature babies). Infants develop rapid labored breathing shortly after birth. Prolonged intrauterine asphyxia —irreversible changes in type Il cells rendering them incapable of producing surfactant. Glucocorticoids during pregnancy accelerates fetal lung movements & surfactant production (corticosteroids or exogenous surfactant are indicated in RDS) Signs & Symptoms- underinflated lungs, amorphous deposits in lungs.

pressure in Vena cava

(entering the RA) is called the central venous pressure (CVP) peripheral venous pressure>CVP>RA

muscles of expiration

(superior down to second ribs) quiet breathing expiration, passive recoil of lungs and rib cage principal muscles (rest of cage) external intercostals diaphragm-increases vertical dimension of thoracic cavity, elevates lower ribs

alveolar period (lung development)

(week 32 to 8-10 years) — Primitive alveoli with well developed epithelial — endothelial capillary contacts (blood — air barrier after birth) Mature alveoli are formed after birth as the lungs expand (alveoli formation continues up to 8-10 years)

pump-based hypertension (essential hypertension)

*increase CO* occurs in younger patients, amenable(respond to) to beta blockers (overdeveloped alerting response; excessive sympathetic effect on heart

compensatory mechanism (chronic heart failure)

*increase TRP . increase Blood volume* • Primary abnormality of heart failure is impairment of ventricular function resulting in reduced cardiac output • Counter-regulatory neurohormonal mechanisms are activated to increase afterload and increase preload • Mechanisms try to buffer the fall in CO and help preserve sufficient BP to perfuse vital organs • Renin angiotensin aldosterone system leads to vasoconstriction, NaCI and H20 retention and sympathetic mediation because of Angiotensin I I (potent constrictor) • Aldosterone enhances salt and water retention • Endothelin enhances vasoconstriction especially renal vasculature • ADH — released from atria in response to stretch Sympathetic increase myocardial contractility, heart rate and peripheral vasoconstriction • Prolonged sympathetic lead to hypertrophy and apoptosis • Ventricular hypertrophy is from increased wall tension Hypertrophied ventricles are less compliant; EDP is increased which leads to increase atrial pressure and increase venous pressure

vascular resistance-based hypertension (essential hypertension)

*increase TRP* occurs more in older patients. (smooth muscle abnormally sensitive to vasoconstrictors, endothelial cell dysfunction-abnormal regulation of vascular tone by local factors such as NO)

volume-based hypertension (essential hypertension)

*increase retention of Na and H2O* renal parenchymal disease, renovascular disorders. (failure of the renin angiotensin system to regulate BP)

Mean circulatory filling pressure (MCFP)

+7mmHg is defined as this which is =pressure that would be measured throughout the CVS if the heart stopped beating. There would be no pressure gradient to drive the blood around the circulation.

mean arterial pressure (MAP)

- NOT average of Systolic and diastolic blood pressures, due to shape of aortic pressure pulse - Is actually area under curve (AUC) of arterial pressure tracing - Diastole pressure large contributor - Heart spends longer time in diastole MAP estimated from: DP + 1/3 Pulse Pressure 80 + 1/3(120-80) - — 93 mmHg

endothelin (ET-1)

- Vasoconstrictor Contributes to basal vascular tone. Associated with pathological states. Increased endothelin levels found in: •Hypoxia: partly responsible for pulmonary hypertension seen at high altitudes. •Preeclampsia (acute hypertension of pregnancy). •Cardiac failure: may contribute to the characteristic renal and peripheral vasoconstriction. •Strokes: levels are increased in the CSF following subarachnoid hemorrhages, brain injury. Contributes to cerebral vasospasm.

Pancoast tumor

-limited to the apical lung region. Tends to metastasize to neighbouring structures usually those related to the thoracic outlet-nerves, vessels, bone. Symptoms depend on structures invaded: brachiocephalic vein, phrenic nerve, vagus, stellate( cervicothoracic sympathetic) ganglion Eg.Compression of right recurrent laryngeal nerve presents as hoarseness with right vocal cord paralysis on laryngoscopy Thoracic outlet syndrome-pain and paresthesia and cyanosis in upper limb with compression of the subclavian artery Lung Fields / Parenchyma Costodiaphragmatic reces Horners syndrome***

visceral afferent (lung)

-not to the lung and visceral pleura -bronchi are innervated by these

NO (angina treatment)

-poor blood flow to the heart Nitroglycerin generates this via aldehyde dehydrogenase mode of action: increase cGMP >> vasodilation (venodialation>arteriolar dilation) Venodilation>>>decrease CVP >>> decrease preload (EDV) >>decrease SV decrease CV >>> decrease O2 demand by heart muscles

Static (weightlifting)

-reactive or ischemic hyperemia occurs -sustained tetanic contractions interrupt blood flow>>increased TRP -However, TRP later reduced by build-up of metabolites after contraction (vasodilation later on)

minimum refill time

.13s ventricles get an adequate stroke volume -at high HR atrial systole-becomes important in ventricular filling (contributes up to 40%

Cutaneous circulation

0/0 of CO: 4% (< 1% to 60% with extreme cold or heat) Local control of blood flow: least important Sympathetic Control: most important- temp regulation SKIN: Has a relatively constant metabolic rate (low metabolism). 02 needs are met by low blood flow. Sympathetic Control (most important): - Arteriovenous (AV) anastomoses are innervated by (adrenergic) sympathetics. - Shunting of blood via vasoconstriction of AV shunts (resistance vessels) to direct blood into venous plexuses Note - venous plexus contains most cutaneous blood volume Local Control (weak). Epidermis - Local changes due to temperature - Local changes due to axons and Dermis nitric oxide (NO) - Weak reactive hyperemia - Weak autoregulation

Angina Pectoris (can be predictor of Ml)

02 demand (during exercise) > 02 supply 02 supply restricted - narrowed coronary arteries Cardiac muscle becomes ischemic Algogenic (pain generating) substances released e.g. substance P) Pain (radiates down Left arm) (cardiac chemosensitive afferents converge with somatic afferents) Cold and Stress can trigger Angina (due to t Sympathetic) Coronary occlusion: triggered with exercise Coronary vasospasm: triggered at rest e.g. watching TV.

factors affecting central venous pressure (CVP)

1. Blood volume increase BV>increase CVP>increase VR>increase SV>increased CO>increase MAP Hemorrhage>decrease CVP>decrease VR>decrease SV>decrease CO>decreaseMAP 2. Venomotor tone venoconstriction>increase CVP blood is displaced from peripheral to central veins increase sympathetic tone to veins: increased CVP>increase VR>increased SV

EDEMA causes (physical factors)

1. Hydrostatic pressure: Capillary pressures drive fluid out of capillaries into interstitial space pulmonarv edema: slight increases in hydrostatic pressures in lung capillaries. peripheral edema: Inc in systemic capillary pressures result in inc filtration in lower extremities and intestine. 2. Oncotic pressure: Capillary oncotic pressures keep fluid in capillaries and drive reabsorption. Edema *reduction of plasma proteins: (protein lost in urine, pregnancy, malnutrition, or reduced albumin production by liver). 3. Capillary walls: more permeable e.g. inflammation, ischemia, burns. 4. Lymphatic drainage: Impaired e.g. parasites, surgical lymph node removal. Local edema before blocked nodes.

(factors influencing normal) lung development

1. Thoracic space for growth 2. Fetal breathing movements 3. Amniotic fluid volume In infants with congenital diaphragmatic hernia the lung is unable to develop normally as the thoracic space is reduced Fetal breathing movements stimulate lung development (cause aspiration of amniotic fluid). At birth lungs are partially filled by amniotic fluid, which is later absorbed by the capillaries & lymphatics [still born infant lung is firm / sinks in water as it has no air but fluid] Oligohydramnios (insufficient amount of amniotic fluid) may lead to retarded development of lungs (hypoplasia)

age effects on CVS

1. arteriosclerotic changes in blood vessel walls 2. decreased baroreceptor sensitivity 3. decrease cardiac performance in exercise

factors affecting pulse pressure

1.Stroke Volume: (short time scale) pulse pressure a SV 2.Arterial compliance: pulse pressure I/ a compliance (longer time scale) Aorta accepts —70ml blood each beat. Expands to accommodate the stroke vol. Recoil creates diastolic pressure. If not compliant (stiff), same volume in smaller space (aorta not expand as much) >>>>inc pressure

hypertension (classification)

90% of cases-ause unknown-primary/essential (benign and malignant) only 10% of cases-specific disease or abnormality-secondary risk factors: age, obesity, diabetes, physical inactivity, excess salt intake, excess alcohol intake, family history; african american>caucasian>asian

regulation of CO

: 1 .Pumping ability of the Heart: Represented by the Cardiac Performance Curves 2. Venous Return (CVP) Represented by the Vascular Function Curves (Venous Return Curves)

MAP

=COxTRP CO=MAP/TRP Darcy's law: applied to cardiovasc. Flow = AP/R AP = Flow (Q) * R AP = MAP- RAP Since RAP = O AP = MAP RAP= right atrial pressure, MAP = mean arterial pressure R= resistance of systemic circulation = total peripheral resistance (T PR) AP = MAP = Flow x Resistance MAP CO x TPR -1 Change one parameter and see effect on 2 others. E.g. what happens to MAP if inc CO and dec TPR? co MAP / TPR

SV

=EDV-ESV

ejection fraction

=EDV-ESV/EDV*100=58%

Negative sign (starling equation)

=absorption taking place : the fall in capillary hydrostatic pressure and rise in IF oncotic pressure

NFP and flux

=delta hydrostatic pressure-delta oncotic pressure Capillary pressures placed first in the equation as the are normally higher

mean arterial pressure (exercise)

=diastolic pressure-1/3 pulse pressure exercise

myocardial muscle fiber length

=filling pressure right atrial pressure end diastolic volume end diastolic pressure

positive sign (of starling equation)

=filtration has taken place examples: high filtration:glomerulus, retinal capillaries increased Pc lower filtration: lung decrease Pc to reduce edema

velocity (capillaires)

=flow/cross sectional area in capillaries is very low vs aorta; allowing adequate time for diffusion and transfer of nutrients -pressures lowest in capillaries-reduce edema same flow (5L/minute) or CO through all vessels capillaries have the slowest velocity. due to having the largest cross sectional area

force of contraction

=ventricular pressure stroke volume cardiac output stroke work

work done by the heart

=work done in ejecting a volume of blood (SV) into the aorta

congestive cardiac failure

A pathophysiological state in which an abnormality of cardiac function is responsible for the failure of the heart to pump blood at a rate commensurate with the requirements of the metabolising tissue. Braunwald 1980 Clinical Features • Exercise Intolerance Breathlessness (Dyspnea) Fatigue Peripheral edema 400,000 new cases each year in US Prevalence: 1% at age 50; 9% at age 80 Mortality: 50% die within 5 years of diagnosis (untreated) Death is due to pump failure or arrhythmias Most common diagnosis of hospitalized patients >65 years Predisposing conditions: Chronic hypertension Coronary artery disease Valvular heart disease

Cardiac phase

A wave Atrial systole augments pressure C wave Ventricular wall tension develops rapidly, causing mitra leaflets to bulge into atrium and increase atrial pressure X' descent Ventricular ejection propels heart towards its apex, pulling away from atria and pulling them open causing a drop in atrial pressure V wave During ventricular ejection blood keeps returning to the atria and fills them up increasing atrial pressure Y descent Opening of mitral valves allows blood to leave atria into ventricel causing drop in atrial pressure

pressure change (on standing)

Add weight of blood column (hydrostatic p.) to BOTH arterial supply to feet AND veins draining feet. 130 cm (in a 1.8m individual) of blood is equivalent to an extra pressure of 95 mm Hg. (hydrostatic pressure) Demonstrated in collapse and distention of veins on back of hand when raised above and below level of heart. Arterial pr (in foot) = 90 + 95 = 185 mmHg Venous pr (foot) = 5 + 95 = 100 Driving pressure = 185 — 100 = 85 (same as in feet of a supine person) AP = Driving Pressure 85!! As long as there is a pressure difference between arteries and veins- blood will flow.

aortic regurgitation

After ejection the SV should remain in the aorta and sustain forward flow. When aortic valve is incompetent backflow from aorta into left ventricle during diastole. Causes the aortic pressure to drop quickly in diastole — water hammer pulse (Corrigan's pulse, collapsing pulse) and increases the pulse pressure by allowing the end diastolic pressure of the aorta to fall to a very low level. No iso-volumetric relaxation of LV.

Hypoalbuminemia

Albumin is major protein in plasma contributing to oncotic pressure, and is produced by the liver. occurs with/in: •Decreased albumin production: cirrhosis, hepatitis •Increased albumin clearance: kidneys. Albumin in urine- marker for kidney disease. •Pregnancy Results in: •Reduced oncotic pressure in capillaries •Less fluid reabsorbed into capillaries •More fluid in interstitial fluid Edema: when interstitial fluid volume accumulation > lymph clearance

laplace law (medical example

Aneurysm - Frequent in large arteries (aorta) due to this law - Aortic distension -Aorta radius large — requires more tension to offset given blood pressure Reaches a point where vessel cannot generate more wall tension Eventually aneurysm can rupture deltaP =2T/r if the pressure inside the vessel is constant, the larger the radius (diameter) of the vessel, the greater the wall tension needed

regulation of capillary exchange

Arteriolar resistance: One arteriole supplies a cluster of capillaries. - Degree of arteriolar tone determines how many capillaries are open Velocity of flow: Transit time through capillary = 0.5 — 2.0 s (low velocity as parallel arrangement, large CSA) Capillary density: lungs > skeletal muscle and skin Capillary permeability: histology

atelectasis

Aspiration Of Foreign Objects • Obstructed airway preventing free passage of air resulting in lung collapse. • Collapse is distal to obstruction • Symptoms: -Difficulty breathing (dyspnea) -coughing

cerebral circulation (autoregulation)

Blood Flow constant, pressures kept between 60 — 180 mm Hg -Autoregulation (myogenic response) for steady supply of oxygen. Less than 60 mm Hg —+ decreased perfusion: confusion, unconsciousness. Chronic high blood pressure shifts autoregulatory curve to right- maintain blood flow at higher pressures.

factors altering VR curve

Blood Volume Venomotor tone Arteriolar resistance (T PR) ALL are factors which affect VR increased Blood volume: increased Venomotor tone: increased T PR (arteriolar vasoconstriction reduces VR because blood is "held" in the arterial side.

blood supply to lungs

Blood supply to lung Bronchial vessels supply the bronchial tree and visceral pleura • Left bronchial arteries — direct branches of aorta Right bronchial artery from posterior intercostal • Bronchial veins drain into the hemiazygos (left bronchial) and azygos veins (right bronchial)

pleural cavity formation

Bronchial buds grow into the pericardioperitoneal canal. Membranous ridges develop from lateral wall. Cranial ridge-pleuropericardial folds Caudal ridge- Pleuroperitoneal folds- Pleuropericardial membrane separate pleural cavity from pericardial cavity. will fuse to form the fibrous pericardium. derived from the intra-embryonic coelom (IEC) -parietal and visceral pleura line the cavity -lung buds will grow out from the primitive gut tube -the primordial pleural cavities expand around the heart

broncus development

By the 24th week about 17 orders of branches are formed with respiratory bronch ioles 7 more generations of branches are formed after birth — 8 years As the lung bud develops it divides into primary buds. The secondary and tertiary buds grow laterally into the pleuroperitoneal canals. Bronchial buds meets trachea— main bronchi Secondary bronchi -lobar, segmental and intrasegmental branches. Segmental bronchus with surrounding mesenchyme- bronchopulmonary segments

increasing EDV

C-D is shifted to the right leads to increase stroke volume prolonged increase in this =cardiac failure

stroke volume (influence on HF)

CO=SV*HR - influenced by: Contractility (decreased calcium uptake in the sarcoplasmic reticulum, low affinity of troponin for calcium, altered substrate metabolism from fatty acid to glucose oxidation, impaired energy production) Preload events (volume and pressure of blood in ventricles at end diastole) Afterload events (volume and pressure of blood in the ventricles during systole, resistance to blood leaving the heart)

cardiac failure

Cardiac contractility is reduced Fluid retention >increase Blood volume Venoconstriction Vascular Function curve is shifted upwards and MSFP increases Overall Effect: Slight decrease, in CO but an increase in RAP Such CV changes are observed moderate cardiac failure.

eventration of diaphragm

Caused by a defective musculature in one half of diaphragm due to failure of the muscle tissue from body wall to extend into the pleuroperitoneal membrane. That half goes up with contraction of diaphragm during respiration- paradoxical respiration.

pleural cavity

Closed cavities containing the lungs Lined by serous membranes- Parietal pleura and visceral pleura Parietal pleura

peritoneal cavity formation

Closure of the pleuroperitoneal opemngs • Septum transversum - partially separates the pericardial and peritoneal cavities. •Pleuroperitoneal folds projecting into pleuroperitoneal canal. •Dorsal mesentery of esophagus •Migration of myoblasts into the peritoneal membrane - results in final closure of the pleuroperitoneal canal

vessel diameter (increase turbulence)

Contact with the vessel wall (surface area contact) slows velocity (v) because of resistance. There is less surface area with increased diameter, thus velocity increases. Decreased SA/volume ratio occurs with t diameter (D) - Reduced blood in contact with a surface area - Increased turbulence. -Think a bigger tube- more area in the middle for turbulence to occur. Re = v Dp/n

HR (Influence on HF)

Ejection Fraction (EF) is the fraction of blood ejected by the ventricle relative to its end-diastolic volume. EF = (SV / ED\/) • 100

water (after hemorrhage, resuscitation with each solution would)

Electrolytes: decrease concentration Plasma proteins: decrease concentration Oncotic pressure: decrease Haematocrit: decrease

0.9% saline (after hemorrhage, resuscitation with each of the solutions would)

Electrolytes: no change Plasma proteins: decrease concentration Oncotic pressure: decrease Haematocrit: decrease

plasma (after hemorrhage, resuscitation with each of the solutions would)

Electrolytes: no change Plasma proteins: no change Oncotic pressure: no change Haematocrit: decrease

whole blood (after hemorrhage, resuscitation with each of the solutions would)

Electrolytes: no change Plasma proteins: no change Oncotic pressure: no change Haematocrit: no change

Vasodilation in imb

Elevated pressures at capillaries, increased filtration. Increase fluid in If increased If hydrostatic pressures Increased increased lymph flow Note: reason why edema not occur when lymphatics functional http:j/faculty_pasadena

reynolds equation

Factors which increase Turbulence High flow velocity Large vessel diameter High blood density Factors which decrease Turbulence increase Viscosity n p (Re) = pro-turbulence factors : anti — turbulence factors Critical value for Re = 2000 When Re > 2000 laminar flow becomes turbulent Velocity most important as: viscosity, density usually constant

contractility (inotropism)

Force of contraction achieved from a given fiber length. OR A change in the contractile force of the heart that is NOT due to changes in fiber length. A POSITIVE INOTROPE: increase in this e.g. Sympathetic activity (release of NE and EPI)

intercostal nerves

Formed by ventral primary rami Give two branches Lateral cutaneous branch Anterior cutaneous branch Function sensory and motor innervation of the thoracic wall and upper abdomen Sensory innervation parietal pleura and to periphery of diaphragm Dermatome (skin) and myotome (muscles) — innervated by a single pair of spinal nerves. Intercostal nerve block — Provides anesthesia for surgical procedures or rib trauma T12 intercostal nerve = Subcostal

cardiovascular responses to exercise

Heart rate: greatly increased stroke volume: increased pulse pressure: increased (increased stroke volume) cardiac output: greatly increased venous return: increased Mean arterial pressure: slight increase total peripheral resistance (TRP): greatly decreased (vasodilation in skeletal muscle) Arteriovenous O2 difference:greatly increased (increased O2 consumption in tissue)

mitral stenosis

High resistance between the L atrium and L ventricle, reduces flow into ventricle but increases flow velocity. Atrial pressures are always elevated above normal, but in diastole the high atrial pressure and low ventricular pressure gives rise to a large pressure gradient to fill the heart and cause turbulent inflow. Pre-systolic kick due to atrial contraction. Ventricular filling is reduced.

pleura (meet)

Hilum the two layers come together at the root of the lung-mediastinal pleura meets visceral pleura

Movement of lymph

Hydrostatic pressures • Interstitial volume relatively constant. Interstitial press normally low (Pif). •Pumping action of open terminal ends of lymphatics draw fluid into lymphatics. •Transient increases in Pif (more fluid) drive fluid into lymphatics, & inc lymphatic pumping. •After the valves: Lymphatic (P ) <Interstitium (Pif) . Because of lymph after valves vessels pumping. Movement • Valves in lymphatics -5 one way movement of lymph. • Contraction/Pumping: Movement of lymphatic fluids. Pressures in larger lymphatics can be 100 mm Hg. • Compression: by skeletal muscles, respiratory movements and intestinal contractions.

Reactive (post-ischemic) hyperemia

Hypoxia Hypoxia -5 Vasodilation • Activation of different K + channels (KAT? and Kir) — hyperpolarization and L-type Ca2+ channel closure • Vascular myocytes (smooth muscle) relax in hypoxia

Systolic heart failure

Impaired transduction or excitation- contraction = less force and lower inotropy Compensatory increases in preload (volume status) help to normalize stroke volume but reduce ejection fraction Increased volume increases passive wall stress which causes adaptive increase of sarcomeres in series to increase chamber sue, eccentric hypertrophy Dilated ventricle with increased compliance, allows accommodation of large volumes with little increase in diastolic pressures

EDEMA (consequences)

Impairs cell nutrition Tissue Edema: Causes discomfort and Imobility (seen when fluid vol doubles in limb - limb vol. u failure) Skin ulcerates and blisters Pulmonary Edema: (LV failure, backup lungs) Prone to infection — cellulitis (bacterial infection) Difficult to inflate lung -+ dyspnea (difficult/laboured breathing) Fluid enters alveoli. 02 and C02 exchange impaired.

shock

Inadequate organ perfusion and delivery of nutrients necessary for normal tissue and cellular function. Initially it may be reversible but life-threatening if not treated properly. General Features: (many due to compensatory responses) • Cold, sweaty, clammy skin (due to increase sympathetic) • Rapid and weak Pulse: tachycardia and a small SV • Rapid and shallow respirations •Often altered consciousness (drowsiness), confusion, irritability, weakness and collapse • decrease Pulse Pressure: (MAP may be normal) — systolic BP <100mmHg •decrease Urine Output: (Oliguria<30ml/hr)

mitral regurgitation

Incompetent mitral valve allows backflow from high pressure ventricle to atria during systole. Augmented atrial pressures in ventricular systole lead to highly exacerbated V wave. Leaking ventricle during systole means no iso-volumetric contraction and no iso-volumetric relaxation as ventricular pressure still exceed atrial pressures at this time. Pan systolic murmur.

metabolic (active) hyperemia

Increase in Blood Flow to an organ due to an increase production of vasodilator metabolites and endothelial secretions Explains the increase in blood flow to skeletal and cardiac muscle during exercise

needle decompression

Indication :Tension pneumothorax-when thoracostomy is not possible in prehospital setting. Tube thoracostomy should follow. Site: 2nd intercostal space in midclavicular line in affected hemithorax. Equipment :Large bore needle- 14/16 gauge

tube thoracostomy

Indication:relieve trapped collections of air or fluid in the thorax Site: 4th or 5th intercostal space between the anterior axillary and midaxillary lines

primitive gut

Intra-embryonic part of the yolk sac is divided into foregut, midgut & hindgut. Laryngotracheal groove appears as a median outgrowth in the floor of the primordial pharynx. Endoderm of the laryngotracheal groove — epithelium and glands of the lungs, larynx, trachea, bronchi. Splanchnic mesoderm- connective tissue , cartilage smooth muscle

endotracheal intubation

Introduction into the trachea Epiglottis and vocal cords should be visualized with laryngoscope prior to intubation Ensure correct tube placement after. Look, Listen! Care should be taken to not cause to much trauma to the tract, and mouth structures and laryngeal areas.

guyton cross plot

Is used to predict how changes in the various parameters (Contractility, Blood Volume, Venomotor Tone, TPR) alter CO and RAP. A permanent change in CO, VR or RAP can only induced by changing either the cardiac function curve, or the vascular function curve or both decreased contractility causes red line to shift right (decrease shift left) changing blood volume causes the blue line to shift up (increase blood volume) or down (decrease blood volume) arteriolar constriction (increase TRP) causes a down shift in blue line and right shift of red line decrease TRP (arteriolar vasodilation) causes a left shift in red line and up shift in blue line

aorty stenosis (relevant concepts)

It emphasizes the hemodynamics law Darcy's law Flow AP/ R COz MAP/ TPR MAP = mean arterial pressure TPR = total peripheral resistance Syncope: Cannot increase CO, dec resistance. MAP lowered Angina: reduced pressures in aorta- less blood flow to heart muscle. Reduced coronary flow reserve. Pulse pressure: Systolic- diastolic. Systolic lowered. Stroke vol also decreased. Note- there are other theories such as also vasovagal response that are covered in the next lecture). Note: classic catheterization has been replaced by hemodynamic assessment in the echocardiography

laryngeal development

Laryngeal cartilages and muscles are derived from the 4th & 6th pairs of pharyngeal arches. The Laryngeal cartilages develop from mesenchyme derived from neural crest cells. •Arytenoid swellings-mesenchyme at cranial end of Laryngotracheal tube •caudal part of hypopharyngeal eminence -epiglottal swelling •Laryngeal ventricles-recanalization of the larynx

venous drainage (parietal pleura)

Left posterior intercostal vein- L brachiocephalic, hemi azygos and accessory azygos veins (azygos-superior vena cava (SVC) right posterior intercostal R brachiocephalic vein, azygos-SVC

S3

Low frequency (difficult to hear) Rush of blood into ventricles from atria (recoil vibration) Common in young people. May be pathological Kentucky Gallop

systemic circulation (changes during exercise)

MAP = CO x TPR Several changes to enhance 02 delivery to exercising muscles • Systolic B.P increases via muscle chemoreflex, diastolic remains near resting values (Rise in MAP is normally less than increment in CO, reflecting a decrease in peripheral vascular resistance) • Distribution of blood flow related to skeletal muscle vasodilation due to local decreases in pH and Pa02, and local increases in NO, adenosine, potassium • A rightward shift (decreased oxygen affinity) of oxyhaemoglobin dissociation curve with acidosis increase skeletal muscle oxygen extraction.

osmosis

Mechanism for fluid transport: Driven by osmotic and hydrostatic pressures Important: 3 elements Capillaries & endothelium (permeability) Interstitium: 40% less proteins than plasma Electrolytes are found equally in blood and the interstitial fluid — not contribute to fluid exchange

positional changes of the diaphragm (development)

Musculature for diaphragm derived from 3,4 & 5th cervical somites and descend with the septum transversum Innervation from C3, 4, 5 spinal nerve — keeps the diaphragm alive"

aortic compliance

NOT AS COMPLIANT AS VEINS Aorta (and arteries) develop and withstand high pressures. Stable resistance. Dec compliance in artery (stiffness) comes with an increase in pressure. Thus pressures higher in arteries.

consequences of blood loss

Normal Blood Volume: — 5 L (—65% in veins) 5-10% loss =no change in MAP -15-20%loss=modest decrease MAP:reflexes>>full recovery -20-30% blood loss MAP 60-80mm Hg;rarely fatal -30-40% loss=MAP 50-70mmHg;serious shock responses which could become irreversible >50% blood loss=fatal

Cerebral circulation

O2 consumption: 15% at rest (large for tissue size) local control blood flow: most important Sympathetic control: least important (functional sympatholysis, sparse innervation) Mechanical effects: increase intracranial press>>> decrease blood flow Vasoactive metabolites: CO2, pH+,adenosine relies mainly on blood glucose as energy source disruption of blood flow seconds>>unconsciousness few minutes>> irreversible brain death

treatment (cardiac failure)

Objectives of Treatment • decrease clinical symptoms of edema and dyspnea • To improve CV function to enhance organ perfusion and exercise capacity • decrease mortality

S4

Occurs just before SI Due to atrial systole Usually pathological Stiff ventricle Tennessee

role of CVS (during exercise)

Oxygen delivery to muscles is achieved by: increases in extraction of 02 by exercising muscles Increases in HR. (Max HR 220- age in years) Increases in SV. (SV increases in a hyperbolic fashion vs. V02. Max values can be increased up to 100% with training. (contractility, increase in LV filling enhanced) >Decreases in systemic and pulmonary vascular resistance

Cerebral circulation (CO2, O2 regulation)

PO2: Large decrease in O2 (hypoxemia) before large increase in blood flow PCO2: brain responsive to small changes in PCO2. increased PCO2 (hypercapnia)>> vasodilation, decreased PCO2 (hypocapnia)>>> vasoconstriction. PCO2 alters pH via formation of carbonic acid

radius of curvature

Panel b. and c. have the same wall stress (and same thickness) Acute angle of radius in b. means more of the tension vector is inwardly directed Greater pressures can therefore be formed by smaller radius with an equivalent wall stress Alternatively — less wall stress is required to get to a target pressure e.g. pressure to open aortic valve, in a small radius chamber 6.

Serotonin 5HT (vasoconstrictor)

Paracrine Control of Blood Flow: Autocoids vasoconstrictors from platelets during clotting - vasoconstriction (stops the bleeding). Coronary circulation: Atheromatous coronary arteries- inappropriate platelet activation release can cause coronary vasospasm. Cerebral circulation: partly responsible cerebral vasospasm (migraine, following a subarachnoid hemorrhage).

thromboxane (vasoconstrictor)

Paracrine Control of Blood Flow: Autocoids vasoconstrictors ::: Platelets from arachidonic acid via COX. Involved in clotting and helps to stop bleeding. Inappropriate platelets activation >> thromboxane release can cause coronary vasospasm. Clinical box- Thrombosis: Clot within in blood vessel. Thromboxane platelet aggregation. Aspirin (in low doses) inhibits thromboxane formation in platelets. Aspirin >> prevent thrombosis in coronary atheroma.

Diastolic heart failure

Pressure overload e.g. hypertension Need to contract more forcefully so wall thickness increases to increase contractile force Concentric hypertrophy (more sarcomeres in parallel) normalizes wall stress and reduces chamber size — good for systolic function Chamber compliance decreases and therefore diastolic pressures increase, inhibiting diastolic filling Ejection fractions tends to be maintained reasonably well

intraembryonic coelom

Primordium of future body cavities. Develops in the lateral mesoderm. Divides the lateral mesoderm into 2 layers Somatopleure - parietal layer of: serous pericardium, pleura and peritoneum Splanchnopleure-visceral pericardium, pleura and peritoneum

Endothelial control of blood flow (intrinsic)

Prostacyclin (PG12) Vasodilator -A prostaglandin - Inhibits platelet aggregation - Produced in response to thrombin. Both NO (or EDHF) and prostacyclin limit spread of platelet aggregation and prevent uncontrolled vascular thrombosis.

metabolic vasodilators

Released by metabolically-active tissues Adenosine: Low Pa02: (Hypoxia) formed from AMP (particularly in skeletal and cardiac muscles). Good correlation between metabolic rate in cardiac muscle, adenosine content and coronary blood flow. (In renal — constrictor) Cerebral blood vessels very sensitive change PC02 and [H+]. Arterial pC02 important regulator of cerebral blood flow. Pa02 normally —100 mm Hg. Pa02 < 40 mm Hg vasodilation increase in blood flow helps to restore the oxygen supply to the tissue. Exception lungs: hypoxia constricts pulmonary vessels. Interstitial K+: Skeletal muscle & brain activity t with t action potentials. Skeletal muscle [K+]o increase from 4 mM 9 mM. t paradoxical relaxation of vascular smooth muscle- (vasodilation) and increased blood flow. Metabolic vasodilators responsible for Active and Reactive Hyperemia.

arterioles (resistance)

Resistance arterioles: region of greatest pressure drop Flow from: High pressure (aorta, arteries) *low pressure (capillaries) Lowest pressure (right atrium) Arteriole: Bigger Drop in pressure gradient (AP). 50-70% drop. Resistance Greater! Capillary: Smaller drop in pressure gradient (AP). Resistance Less! Right only 1 capillary *resistance is greatest in capillaries* but overall low atrium Note: Arterial pressure not — O as in ventricle; recoil leads to diastolic pressure

turbulent flow

Reynolds number exceeds 2000 (alpha square root of delta P) requires an increased pressure to maintain flow (flow is not as efficient) Noisy-heard by auscultation. called bruit. eddies are chaotic Reynolds number is used to predict whether blood flow is laminar or this

myogenic control of blood flow (function)

Safeguards blood flow to individual organs when BP falls. Stabilizes capillary perfusion pressure (prevents edema should BP rise). Resistance arterioles alter resistance. Autoregulation MOST important in resistance arterioles of: • Cerebral circulation • Renal circulation

vasodilation (arterioles resistance)

Short term: Elevated pressures at capillaries, increased edema. Clinical examples: Septic shock, or anaphylaxis* massive vasodilation. However, (longer time than shown) there is eventually pooling of blood in capacitance vessels (venules, veins), hypotension, reduced tissue perfusion, changes in heart rate etc. [medical emergency]. Exercise- massive reduction of resistance- inc blood flow muscles. Redistribution of blood flow to other tissues to maintain MAP

capillaries (resistance)

Smaller drop in pressure gradient (AP). Resistance Less! Right only 1 capillary *resistance is greatest in capillaries* but only due to being in series total resistance in artery to vein=sum of the resistances of the individual components atrium Note: Arterial pressure not — O as in ventricle; recoil leads to diastolic pressure

thoracic cavity

Space found in the upper trunk region. • Separated from the abdominal cavity by the diaphragm. Protected externally by ribs and muscles. • House important organs(heart, lung, esophagus) • Contains the mediastinum and three serous cavities -two pleural cavities -one pericardial cavity

hemodynamics

Study of: Blood Flow in the Cardiovascular System Pressure Resistance and how they are related. Consider: Why does blood flow round the circulation? What factors affect flow? What determines velocity of blood flow? What are the characteristics of blood flow?

EDEMA (locations)

Subcutaneous tissue: >>> peripheral edema Lungs: >>> Pulmonary edema Abdominal cavity: >>>>ascites

salt imbalance or renal

Sustained blood volume = Sustained Blood Pressure • If t renal artery pressure - t GFR and t excretion of Na+ and H20. • In HTN, pressure- naturesis curve is shifted to right • Shift of curve could be due to renal tissue damage or RAS • In HTN- higher arterial pressure required to excrete Na+ and H20; retention resulting in T blood volume • increase blood volume sustains increase blood pressure

neurogenic or stress

Sustained pump activity + sustained vascular resistance = Sustained Blood Pressure • If t renal artery pressure - t GFR and t excretion of Na+ and H20. • In H TN, pressure- naturesis curve is shifted to right • Shift of curve could be due to renal tissue damage or RAS • In H TN- higher arterial pressure required to excrete Na+ and H20; retention resulting in T blood volume • T blood volume sustains T blood pressure

resistance (regulation in organs)

Sympathetic NS: innervates and stimulates arterioles Since, Resistance alpha 1/ r ^4 Small decrease in arteriolar radius causes a large t in resistance. Arterioles are called "resistance vessels"

coronary circulation (physio)

Systole - vascular Diastole - maximal flow Pressure differences less in right ventricle Tachycardia shortens diastole (reducing flow) but is overridden by metabolic (active) hyperemia (vasodilation). Metabolic hyperemia most important mechanism for increasing coronary blood flow. flow reserve- difference between maximum flow via vasodilation and flow at rest. (Dec in disease)

pulse pressure

Systolic press: Aorta fills and expands with stroke volume Pulse Pressure Diastolic press: Elastic recoil of aorta/ resistance this= 120 - 80 = 40 mmHg * gives clues about stroke volume (SV):* - Congestive heart failure, hemorrhage (dec PP and SV) - Aortic regurgitation and athletes (inc PP and SV)

steady state CO

The Cardiac Performance Curve and the Vascular Function Curve intersect at Equilibrium Point. At this point VR and CO are EQUAL, and since VR = CO the equilibrium point represents the steady state CO.

primitive lungs

The lower respiratory organs (larynx, trachea, bronchi, and lungs) begin development during the 4th week as an outgrowth (respiratory bud) from the primitive foregut tube (endoderm) Respiratory bud endoderm gives rise to the epithelial lining of larynx, trachea, bronchi and alveoli of lungs

factors effecting venous return (VR)

Venous Pumps: Valves in peripheral veins prevent backflow of blood. contraction of skeletal muscles Muscle pump: compress veins rhythmically displaces blood forward (no backflow as valves in peripheral veins) Central venous pressure (CVP) is maintained, maintaining VR and EDV. Thus: Venous pressure in feet is l, because blood drains quickly into the veins in muscle (pumping action). Capillary pressure is lin feet and ankles and tendency to form edema is decreased

cardiac performance curve

Venous pressure, mm Hg Right Atrial Pressure Slope off — not likely to be seen in patients as we never get to those filling pressures. Due to leaking AV valves— other reason due to Law of Laplace!! Can be done clinically Easier to measure RAP than EDV A Ventricular Function Curve whose y-axis is STROKE WORK (or Stroke Volume) and x-axis is RIGHT ATRIAL PRESSURE is called a

Tracheo-esophageal fistula (TEF)

abnormal communication between trachea & esophagus due to defective development(incomplete division of the upper foregut) of the tracheo-esophageal septum [1 in 3,000 births; common in males] may be associated with esophageal atresia In about 30% of cases TEF may be associated with other anomalies. TEF may be a component of VACTERL — Vertebral anomalies, Anal atresia, Cardiac defects, TEF, Esophageal atresia, Renal anomalies & Limb defects TEF may be associated with poly-hydramnios [excessive quantity of amniotic fluid] — as esophageal atresia inhibits free passage to the intestines of swallowed amniotic fluid. Signs & Symptoms -coughing and choking during feeding, pneumoia, pneumonitis, poly-hydramnios. Upper esophageal segment ends blindly , inferior end joins the trachea (most common) Swallowed fluid fills the esophageal pouch and regurgitates Infants with this cough & choke when swallowing, due to accumulation of fluid in the mouth / respiratory tract [may pass into the lungs — causes pneumonitis / lung infection]

kinetic work

accelerating the blood through the valves into the aorta (and pulmonary arteries)-usually very minor

muscles of inspiration

accessory sternocleidomastoid scalenes (anterior posterior, middle) active breathing internal intercostals abdominal -depress lower ribs compress abdominal contents -push up diaphragm -rectus abdominis int&ext obliques transversus abdominis

phasic dynamic exercise (running)

active hyperemia is predominant -blood flow not interrupted. capillary recruitment>>reduced resistance (TRP) increased sympathetic discharge increase during exercise. but metabolic hyperemia OVERRIDES sympathetic induced vasoconstriction. thus local control of blood flow overrides sympathetics

timeline (heart failure)

acute and chronic acute-sudden (MI) chronic-gradual impairment, progressive (valvular heart disease)

hydrostatic pressures (on capillary)

all 4 occur along entire length of capillary -capillary hydrostatic pressure predominant at arteriolar end is the "push pressure" *higher favors filtration from capillary*

improve myocardial contractility (therapeutic options to maximise cardiac function)

an inotrope, dobutamine which in most patients acts as a vasodilator

lactate threshold during exercise

around 1.8 VO2 (L/min) denotes the rise in blood lactate

internal transfusion

arterial pressur elower in the upright position than in the lying position. decrease blood voolume>>>decrease capillary hydrostatic pressure>>>increase absorption of fluid from interstitium to blood which restores blood volume however *blood now more dilute-O2 carrying capacity is decreased and viscosity is decreased*

TRP (effect on Vascular Function Curve)

arteriolar tone has little effect on MCFP because most of the blood volume is in the venous system Arteriolar constriction reduces VR, blood is held on the arterial side and consequently less blood flows into the heart.

vena cava compliance

at very high pressures all fibers stretched At low pressures- veins collapse! VERY COMPLIANT Vascular tone (SNS) shifts compliance curve down and to the right. Steep slope at low pressures: - Low press/vol, large veins collapse - Inc press/vol, inc circular shape - Until vessels attain circ shape, walls not stretched much - Small changes in pressure with large changes in volume. Vena cava: capacitance vessels, adjustable reservoirs of blood. Compliant. Thus venous pressure not so high.

S=PR/2w

athletes develop thicker walled heart, this means the myocardial tissue experiences *less wall stress* for any given pressure (even if wall tension remains constant) -wall stress and oxygen consumption proportionate

root

attaches lung to structures in the mediastinum -formed by structures entering and leaving the lung -bronchi -pulmonary artery (venous blood) -pulmonary vein (arterial blood) -bronchial arteries -lymph vessels -nerves

Myogenic (control of blood flow)

autoregulation Blood flow a MAP (Bulk Flow or Darcy's Law) If MAP rises, blood flow is expected to increase. BUT Between MAP of 60 — 160 mm Hg there is NO appreciable t in Blood Flow! MYOGENIC RESPONSE. It is responsible for autoregulation of blood flow. • Stretch of blood vessel wall (by inc pressure) • Contraction of the smooth muscle of resistance arterioles • Dec radius, inc Resistance. • Keep blood flow constant

oblique fissures

begin at the spinous process of the scapula (T4) and follow rib 6 anteriorly

CPP (cranial perfusion pressure)

blood flow to brain has to be carefully regulated CPP=MAP-ICP intracranial pressure (other tissues MAP-CVP not in the brain) if ICP too igh-veins compressed and poor blood flow head injuries-need to relieve ICP or not get blood flow (cut hole in skull to allow for swelling.

inferior thoracic aperture

boundaries -12th thoracic vertebra -11th and 12th pair of ribs -costal cartilages of ribs 7th-10th (costal margin) -xiphisternal joint -closed by the diaphragm

superior thoracic aperture

boundaries 1st body of thoracic vertebra 1st pair of ribs and their costal cartilages -manubrium of the sternum

COngenital diaphragmatic hernia (causes)

by a defective formation or fusion of pleuroperitoneal folds with the other parts of the diaphragm. More common on the left side Re-entry of viscera into the abdomen may pass into the thorax in large openings.

exercise

can be defined as bodily activity (usually planned, structured, repetitive and purposeful), which enhances or maintains physical fitness and overall health or wellness With exercise require integration of skeletal muscles, energy supply, cardiac, respiratory and circulatory systems.

Epinephrine (hormonal control of blood flow)

can cause BOTH vasodilation and vasoconstriction Differential action of this on a and beta receptors due to concentration At normal plasma concs of e: preferentially binds ß2 receptor -5 vasodilation, inc HR, and dec T PR Drug concentrations (higher than physiological): preferentially binds receptor >> vasoconstriction

lymphatic drainage

capillaries of lymph merge into the thoracic duct, thoracic duct drains lymph into the left subclavian vein -this reduces (protein) in interstitium-controls interstitium colloid pressure

hypovolemic (shock low stroke volume)

cause: decrease blood volume due to: hemorrhage, diarrhea, vomiting Skin: cold clammy PCWP (preload): greatly decreased CO: decreased SVR (afterload): increased Treatment: IV fluids

anaphylactic (vasodilation/distributive shock)

cause: decreased TPR due to: allergic reaction (histamine release) Skin: warm dry PCWP (preload): decreased CO: increased SVR (afterload): greatly decreased Treatment: IV fluids, pressors

septic (vasodilation/distributive shock)

cause: decreased TPR due to: endotoxins Skin: warm dry PCWP (preload): decreased CO: increased SVR (afterload): greatly decreased Treatment: IV fluids, pressors

neurogenic (vasodilation/distributive shock)

cause: disruption of neurogenic vasomotor control due to: major brain or spinal injury Skin: warm dry PCWP (preload): decreased CO: decreased SVR (afterload): greatly decreased Treatment: IV fluids, pressors

obstructive (shock low stroke volume)

cause: obstruction to blood flow due to: major pulmonary embolism, cardiac tamponade, tensions pneumothorax Skin: cold clammy PCWP (preload): increased CO: greatly decreased SVR (afterload): increased Treatment: relieve obstruction

cardiogenic (shock low stroke volume)

cause: pump failure due to: arrhythmias Skin: cold clammy PCWP (preload): increased CO: greatly decreased SVR (afterload): increased Treatment: inotropes, diuresis

End diastolic volume increase (filling pressure)

causing force of contraction increases (stroke volume)

congenital hiatal hernia(common sites of diaphragmatic hernia)

central esophageal hiatus may be abnormally large

H+ (metabolic vasodilators)

cerebral blood vessels very sensitive to change in PCO2 and this. arterial pCO2 important regulator of cerebral blood flow

diastolic pressure (aortic compliance)

changes in this caused by a stiffer aorta, the diastolic phase run off is slower. the diastolic pressures remain higher (pink line) heart rate-diastole longer with slower heart rate. thus pressures go even lower with time (blue line)

Incompetence (valve abnormalities)

closed valve is leaky causing regurgitation/ insufficiency turbulent flow

S1

closure of A-V valves (mitral and tricuspid) Lubb is due to closure of both Tricuspid and Mitral Valves. They close at about the same time.

S2

closure of the aortic and pulmonic valves Dupp is due to closure of aortic valve and pulmonary valve. But the aortic valve closes BEFORE the pulmonary valve during inspiration (inc. thoracic vol.) and causes splitting of (transient drop in blood to LA with inc. in blood to RA).

pleural effusion

collection of excess fluid in the pleural cavity

pulmonary edema

collection of fluid in the alveoli

continuous capillaries

continuous ring of endothelial cells surrounded by a continuous basement membrane found in most tissue (eg. skeletal muscle)

stroke work

contracting and pumping blood into the aorta (and pulmonary artery) External work is area under the curve CD on a pressure volume loop. Curve AB is filling of the heart with blood and therefore the area below curve AB is work done on the heart by blood. The areas within the ABCDA curve is therefore the work done by the heart on the blood for a single heart beat. Smaller loop = less work Stroke volume = difference between lines AD and BC = Area of Pressure — Volume Loop

increase metabolic activity

correlates well with increase blood flow individual organs regulate own blood flow apha metabolic requirements

compliance

dV/dP slope of the line in this plot many cardio plots depict pressure on y axis and volume on x axis reciprocal of this plot= this *decrease in this =stiffer*

thiazide and thiazide-like diuretics (drug therapy for hypertension)

decrease ECF

alpha 1 receptor antagonists(drug therapy for hypertension)

decrease TRP

calcium channel blockers (drug therapy for hypertension)

decrease TRP

angiotensin converting enzyme inhibitors & angiotensin 2 receptor blockers (drug therapy for hypertension)

decrease angiotensin 2 (and aldosterone decrease vascular tone and decrease ECF volume

venous PO2 (exercise)

decreases by half

resistance

determined by 1/radius^4 of vessel decrease radius/constriction>>>> increase resistence used to regulate flow in body

functional (manifestation of heart failure)

diastolic and systolic systolic-impaired myocardial contraction diastolic-poor ventricular filling or abnormal ventricular relaxation

salt imbalance (renal hypothesis in essential hypertension)

discrepancy between Na+ intake and Na+ excretion (intake>excretion)>>increase ECF>>> increase plasma volume>>increase VR>>. increase SV and increase BP>>*vascular smooth muscle hypertrophy*>>vasoconstriction>>>*increase TRP*

flow reserve (coronary circulation)

disease decreases this. diseased arterioles cannot compensate (by further dilation) for shortened diastole and increased demand. increased HR decreases perfusion

pleura

double-layer serous membrane (parietal and visceral) cavities lined by this

Hyperkalemia on smooth muscles

due to increased activity of cardiac/skel muscle- local increases in K + ions. Local control of blood flow via vasodilation of smooth muscle (active hyperemia). Most cells: Hyperkalemia reduces driving force, thus decrease K + efflux and membrane depolarization. Paradoxical effect in smooth muscle: Depolarization NOT occur! Hyperkalemia reduces driving force BUT opens special K+ channels! Increased conductance of K + activated K + channels offsets reduced driving force. Thus membrane not depolarize. activated channels & hyperkalemia • Channel conductance via channel, and Na/K pump activity increased • Increased K+ ion efflux, offsets decreased DF, stabilizes Vm near EK or hyperpolarized cell membrane • Closure of L-type Ca2+ channels. • Smooth muscle relaxation (recall some resting tone exists in vasc SM)

increase preload (therapeutic options to maximise cardiac function)

e.g. giving fluids to increase filling pressures, in a setting with impaired myocardial contractility, will only produce a small increase in SV and CO

recumbent position

entire body at heart level Pressure drop of — 5 mmHg between aorta and dorsalis pedis artery in foot. Pressure in foot = 90 mm Hg deltaP = Driving Pressure 85!! Pressure in veins draining the foot is 5 mm Hg.

laryngotracheal groove

evaginates forming laryngotracheal diverticulum (lung bud) anterior to the foregut. Splanchnic mesoderm surrounding th laryngotracheal develop into the cartilage, connective tissue and muscles of the trachea. Tracheoesophagal septum divides the foregut into: Ventral- laryngotracheal tube Dorsal -oropharynx and esophagus

neurogenic (stressor hypothesis in essential hypertension)

exaggerated alerting responses>> increase sympathetic outflow>>> bouts of reversible hypertension>>>*vascular smooth muscle hypertrophy*>>>vasoconstriction>>>*chronic increase TPR*

capillary (parallel)

flow in this way can occur through paths with least resistance. flow in and out remains the same total resistance across a parallel arrangement is less than the sum of the individual components.

horizontal fissure

follows 4th intercostal space laterally to meet oblique fissure (only in right lung)

adenosine (metabolic vasodilators)

formed from AMP (particularly in skeletal and cardiac muscles). Good correlation between metabolic rate in cardiac muscle, adenosine content and coronary blood flow (in renal-constrictor)

Histamine (vasodilator)

from mast cells>> inflammatory response. Dilates arterioles and constricts veins and increases venular permeability. redness and edema of inflammation

sympathetics (lung)

from the trunk via the *cardiopulmonary nerves* bronchodilation (beta receptors),vasoconstriction nerves are distributed long bronchial tree and pulmonary vessels

parasympathetic (innervation of lung)

from vagus n. bronchoconstriction, vasodilation and increased mucus secretion by glands

exercise vasodilation (skeletal muscle circulation)

functional sympatholysis: local control/increased vasoactive metabolite concentrations override sympathetics!! -massive increase in blood flow to muscle (capillary recruitment) -TRP and MAP changes depending on static vs. dynamic exercise

pericardial coelom

future pericardial cavity

peritoneal coelom

future peritoneal cavity continuous with the extraembryonic coelom at the umbilicus

pericardioperitoneal canal

future pleural cavities

medial surface left lung

heart aortic arch thoracic aorta esophagus

medial surface right lung

heart IVC SVC azygos vein esophagus

Fenestrated capillaries

highly permeable to water and solutes -tissues that specialize in fluid exchange (eg. pancreas, endocrine glands, glomeruili)

Oncotic pressure (capillaries)

if higher favors reabsorption into capillary is the "pull pressure" predominates in venular end

heart radius

if this doubles-wall tension required to get same pressure doubles, and therefore wall thickness with have to double, in other words there is increased demand on the heart

class 4 (heart failure)

inability to carry on any physical activity without discomfort but also symptoms of this or anginal syndrome even at rest, with increased discomfort if any physical activity is undertaken (classification based on symptom severity and the amount of exertion needed to provoke symptoms)

Dynamic exercise (MAP=COxTRP)

increase COx decrease TRP (inc blood flow in muscles)=no large increase in MAP

Static exercise (MAP=COxTRP)

increase COx increase TRP (dec blood flow in muscles due to flow occlusion)=MAP increases

hypertension

increase TRP (vasoconstriction or atherosclerotic changes) increased CO (cardiac remodeling/hypertrophy) increase blood volume (retention or renal disease)

initial compensatory mechanism

increase blood volume increase TRP increase HR continuous sympathetic activity increase angiotensin 2

Elastance

increase in this =stiffer

hyperemia

increased blood flow in a tissue or organ. Usually due to local control of blood flow

velocity relationship

increased inotropy changes available myosin-actin interaction and Fmax as well as Vmax

Metabolic Hyperemia

increased metabolic activity results in local increases in metabolite concentrations. Metabolites override sympathetic activity (functional sympatholysis) eg. inhibits sympathetic-mediated vasoconstriction that occurs during exercise.

VFC (on VR curve)

increased venoconstriction > increase CVP> increased VR the larger the blood volume the easier it is for blood to flow back to the heart, when veins are constricted, blood is displaced towards the heart and VR is increased

consequences of hypertension

increased work load of the LV-cardiac failure (congestive) increased risk of vascular disorders- cerebral hemorrhage aortic aneurysms deposition of proteins>>loss of nephrons-renal damage and chronic renal failure increased risk of developing atheroma-coronary artery disease (60% of CVAs and 50% of Ischemic Heart Disease is due to inadequately treated hypertension).

paravertebral (at rest exhaled)

inferior border of lung TV 10 inferior edge of parietal pleura TV 12

mid clavicular line(at rest exhaled pleura)

inferior border of lung rib 6 inferior edge of parietal pleura rib 8

mid-axillary line (at rest exhaled)

inferior border of lung rib 8 inferior edge of parietal pleura rib 10

lung lymphatic drainage (series)

intrapulmonary vessels and nodes>>>bronchopulmonary (hilar) nodes>>>tracheobronchial (carinal) nodes>>>> paratracheal nodes>>>>>bronchomediastinal lymph trunk>>>>right thoracic trunk/thoracic duct>>>>systemic venous system

aorty stenosis

is a 60-year-old man who was brought to the clinic for his annual physical. He has a history of chest pains (angina), exertional syncope (fainting) and periods of confusion. He has a past medical history of aortic stenosis due to rheumatic heart disease. He was given a stress test (exercise on treadmill) to increase his heart rate, but he subsequently passed out (syncope). We will use this case to connect some concepts from the lecture

physical activity

is defined as bodily movement produced by the contraction of skeletal muscle that increases energy expenditure above the basal level. Categories of physical activity include - household, work, leisure activity, and transportation.

minute ventilation

is dependent on the intensity of dynamic exercise overall this can increase approx 10 fold with intense exertion respiratory muscles accomplish increase in ventilation primarily by increasing tidal volume

resistance in arterioles

is greater than capillaries (plural) due to parallel arrangement of capillaries pressure drop greatest across resistance arterioles

resistance in one capillary

is greater than one arteriole in series

blood flow to organ (exercise)

is increased. I. Increase total blood flow — increase cardiac output 2. Redistribution of blood to some organs at the expense of other organs increase O2 delivery to both skeletal and cardiac muscle

tension (pneumothorax)

is the condition in which the air filling the pleural cavity can not escape (forming one-way valve). In this condition the visceral pleura are ruptured. The pressure in the pleural cavity builds up with every breath causing mediastinal shift. This condition leads to severe shortness of breath, as well as circulatory collape and requires urgent intervention.

mean pressure in major artery (supplying organ)

is the same there is very little drop in pressure between the aorta and the large arteries supplying the various organs blood distribution in Parallel

Discontinuous capillaries

large junctions and discontinuities. highly permeable to plasma (eg. spleen, bone marrow (WBC,RBC synthesis) Liver (albumin production))

increased afterload

leads to decrease stroke volume and decreased ejection fraction prolonging of this (hypertension) leads to cardiac failure

increasing contractility

leads to increase stroke volume (stroke work) and ejection fraction changes in this change the slope of the active tension curve

Cerebral ischemia (positive feedback in decompensated shock)

leads to initially strong sump activation>>>VMC become hypoxic>>>>decrease sympathetic drive

Parasympathetic activity (control of blood flow)

leads to vasodilation limited distribution to blood vessels. release Ach which binds to muscarinic receptors activation of M receptors>>> increase NO>> vasodilation

Lungs

left has 2 lobes (superior and inferior) and only oblique fissure right has 3 superior, middle, inferior has an oblique fissure, and a horizontal fissure along the costal surface

anatomical (heart failure)

left, right and biventricular left-reduced left ventricular output,and or increased left atrial or pulmonary venous pressure-mitral stenosis leading to pulmonary congestion right-reduced right ventricular output for any given right atrial pressure-lung disease-peripheral edema biventricular-failure of both ventricles either due to ischemia or progression of disease

deriving cardiac performance from length tension graph

left; pressure volume relationship ( like length tension curve) On the ascending part of the length tension relationship, increasing preload increased the stroke volume (SV) when the afterload is maintained at a constant

nondrug therapy (hypertension)

lifestyle modification reduce BMI -regular physical exercise -increase consumption of fruits and vegetables -restrict salt intake -quit smoking -low saturated fat diet

paracrine activity of NO

ligands act on endothelial cells NO generated NO diffuses to vascular SM cell NO-Vasodialation

activation of the renin angiotensin system

long term response to hemorrhage -to replace fluid loss

autoregulation

maintain organ blood flow via vascular smooth muscle contraction/relaxation. specific to brain, kidney, heart. also called bayless myogenic response/myogenic response

maintenance of cerebral perfusion

maintained at any cost to the remaining circulation. circle of willis: interconnecting arterial vessels safety mechanism for this. especially if an artery occluded

class 3 (heart failure)

marked limitation of physical activity in which less-than- ordinary activity results in fatigue, palpitation, dyspnea, or anginal pain; the person is comfortable at rest (classification based on symptom severity and the amount of exertion needed to provoke symptoms)

Cerebral sympathetic control

minimal effect on cerebral blood flow. sparsely innervates cerebral arterioles and arteries (a1 receptors)

baroreceptors (role in HTN)

modulate moment to moment changes in BP — not involved in long term regulation Reflex does not prevent development of chronic HTN because baroreceptors constantly reset themselves. — 1 -2 days of high BP — baroreceptor firing (initially increased) goes back to normal (rapidly adapting receptors!)

therapeutic targets (HF)

modulate the neurohumoral systems that are activated by compromised cardiac function. The renin-angiotensin—aldosterone system can be inhibited by (I) S•adrenergic antagonists, which inhibit renin release by the juxtaglomerular cells of the kidney; (2) ACE inhibitors, which prevent the conversion of angiotensin I to the active hormone angiotensin Il; and (3) spironolactone, which competitively antagonizes aldosterone binding to the mineralocorticoid receptor. Diuretics promote Na' excretion, and thereby counteract the Na' retention stimulated by activation of the system. Venodilators counteract the effect of intravascular WIume expansion by increasing peripheral venous capacitance and thereby decreasing preload. Direct arterial vasodilators alleviate the a-adrenergic receptor•mediated and angiotensin Il receptor• mediated vasoconstriction induced by increased sympathetic outflow. Cardiac glp:osides, ß•adrenergic agonists, and cardiac phosphodiesterase inhibitors are also used in BF to increase myocardial contractility (not shown).

preload (heart)

myocardial end diastolic wall stress. Which means heart geometry is important! Increased wall thickness spreads the force over a larger cross section. The law of LaPIace (next slides) tells us that the radius of curvature is also very important. This also means afterload has to be redefined! New definition; systolic ventricular wall stress. During ejection its gets complicated! Limit ourselves to thinking about the ventricular wall stress required to get the ventricular pressure above aortic pressure for ejection to begin. . Terms associated; end diastolic volume, end diastolic pressure, end diastolic radius F=mg New definition; myocardial end diastolic wall stress

tracheal stenosis

narrowing and obstruction of the trachea secondary to unequal partitioning of the foregut into esophagus and trachea

reduce afterload (therapeutic options to maximise cardiac function)

nitrates (arteriolar dilator), counterpulsation intra-aortic balloon

class 1 (heart failure)

no limitation of physical activity (classification based on symptom severity and the amount of exertion needed to provoke symptoms)

essential hypertension (pathogenesis)

no unifying hypothesis -multiple defects of blood pressure regulation interacting with enviromental stressors (multifactorial) *MAP=COxTRP* 1degree pathology: increase TRP or increase CO and/or increase blood volume note: no matter how high the CO or TRP, renal excretion has the capacity to return BP to normal by decreasing blood volume

Low PaO2 hypoxia (metabolic vasodilators)

normally-100mm Hg. when this is less than 40mm Hg>>> vasodilation increase in blood flow helps to restore the oxygen supply to the tissue. *Exception lungs: hypoxia constricts pulmonary vessels*

laryngeal atresia

obstruction of upper airway in the fetus (*congenital high airway obstruction syndrome*) signs and symptoms-dialted distal airway, hyperplastic lungs, flattened or inverted diaphragm, fetal hydops, ascites.

stenosis (valve abnormality)

opened valve is narrowed form of resistance that increases pressure upstream of affected valve turbulent flow

laminar flow

parabolic profile: concentric rings of equal flow rates;slowest at the edges (friction with the walls) highest at the centre flow is silent

s1 splitting

pathological occurs in conduction defects on one side of the heart

s2 splitting

physiological accentuated during inspiration (drop in intrathoracic pressure-increases venous return to RA and RV-delays valve closure. increased cross sectional area in pulmonary system=drop in blood to LA and LV pathological-conduction defects

congenital diaphragmatic hernia (common sites of diaphragmatic hernia)

posterolateral defects defect of pleuroperitoneal membrane -abdominal contents herniate into the thorax -more common on the left side

pneumothorax

presence of air in the pleural cavity Spontaneous- Absence of lung disease, no prior provoking event, ruptured bleb or bullae Traumatic- introduction of air in the pleural cavity secondary injury to the pleura Blunt or penetrating trauma Other causes Inflammation Smoking Underlying pulmonary disease.

gravity on blood pressure

pressure in foot greater than heart due to blood flow against pressure gradient

clamped aorta

pressure- volume changes that actually occur in the LV during cardiac cycle so if the aorta was clamped shut the maximum tension that could be developed by the ventricle would be at point G A repeat series of iso-volumetric contractions (clamped aorta) from different start volumes (a, b and c) represent the maximum iso-volumetric tension developed at each different preload — forms line of total tension (line on a', b' and a to a', b to b' and c to c' is active tension. The same data on a pressure-volume curve is called the End Systolic Pressure volume Relationship (ESPVR), whilst the passive tension line is called End Diastolic Pressure Volume Relationship (EDPVR).

bronchial tree

primary main bronchus-to lung secondary (lobar) bronchus-to lobe tertiary (segmental) bronchus-to lobe segment each lobe segment has own arterial supply, segmental bronchus

long term consequences (compensatory mechanism)

pulmonary edema increased afterload; decreased SV and CO increased metabolic demand down regulation of B receptors increase cytokines and fibroblasts adverse remodelling of the heart heart now goes into decompensated state

anteromedial defects (common sites of diaphragmatic hernia)

rare 2-5% defect between costal and sternal musculature

beta adrenergic blockers (drug therapy for hypertension)

reduce contractility, reduce rat- decrease CO

dysfunction of blood flow (coronary circulation)

reduction (eg. coronary atherosclerosis) dec myocardial O2 supply. result>>myocardial ischemia, angina pectoris (chest pain). Switch to anaerobic glycolysis, FFA oxidation. Complete block: rapid nutrient depletion>>>infarc, necrosis

hilum

region where the mediastinal pleura meets the visceral pleura -several structures enter and leave the lung at this point

Metabolic hyperemia (cerebral circulation)

regional increase in neuronal activity>> increased O2 demand increased blood flow due to this astrocytes play a role: neurovascular coupling of neurons and vasculature Regional changes cerebral perfusion (whole brain): autoregulation

decompensated shock

severe prolonged shock: occurs: loss of >30% blood volume no fluid replacement for 3-4 hours initially: increase sympathetic activity (BP may be maintained) later: decrease sympathetic activity (overridden by metabolic vasodilators) *massive tissue vasodilation overrides the increased sympathetic vasoconstriction (sympathetic escape)*

braroreceptor reflex

short term response to hemorrhage this helps to preserve perfusion of heart and brain

Vasoconstriction

short term: reduced pressure at capillaries clinical examples: Preeclampsia >>massive _____________ (endothelin) reduced pressure in capillaries, reduced tissue perfusion

interstitial K+ (metabolic vasodilators)

skeletal muscle and brain activity>> increase this with increase action potentials. skeletal muscle this increases from 4mM>>9mM *increase in this>> paradoxical relaxation of vascular smooth muscle-(vasodilation ) and increased blood flow*

class 2 (heart failure)

slight limitation of physical activity in which ordinary physical activity leads to fatigue, palpitation, dyspnea, or anginal pain; the person is comfortable at rest (classification based on symptom severity and the amount of exertion needed to provoke symptoms)

bronchopulmonary segments

smallest functional unit of lung conical in shape surgically resectable without affecting neighboring regions. tertiary bronchi supply bronchopulmonary segments a branch of pulmonary artery accompany the tertiary bronchi Drained by pulmonary veins The segmental bronchi are followed by branches of th pulmonary artery. Pulmonary artery and veins provide blood supply to the visceral pleura as well. Pulmonary vein leave the lung in the intersegmental septa.

Bacterial endotoxins

stimulate monocytes and macrophages release of interferon-gamma- a potent stimulator of iNOS. (Inc NO) — Can result in severe hypotension — endotoxin shock. results from specific activation of inducible NOS (iNOS), which has higher activity than endothelial NOS (eNOS)

Bradykinin (vasodilator)

stimulates nociceptors and is a potent algogen (pain producer)

cough reflex

stretch receptors on the alveoli and irritant receptors on the secondary bronchus along the pulmonary plexus following the vagus nerve wrap around the aortic arch and synapse in the DRG, cough receptors in the trachea

cardiac output (exercise)

stroke volume * heart rate exercise

arterial supply (to parietal pleura)

subclavian-internal thoracic artery (ITA)-1st-6th anterior intercostal arteries 9th anterior intercostal arteries and superior epigastric artery subclavian-costocervical trunk-1st and 2nd posterior intercostal artery aorta-3rd-11th posterior intercostal arteries

superior laryngeal nerve

supplies sensory fibers above the vocal cords

lungs

surrounded by the pleural cavity

at rest vasoconstriction (skeletal muscle circulation)

sympathetics dominate even at this state -rich sympathetic innervation (NE>>a1/2 receptors>cause this) -normal total peripheral resistance (TPR) and MAP -low concentrations of vasoactive metabolites (lactate, K+, adenosine at rest) and thus, do not override sympathetics

pulse pressure (exercise)

systolic pressure-diastolic pressure exercise

reactive (post-ischemic) hyperemia

temporary occlusion of a blood vessel>>build up of metabolites downstream of the occlusion>>>vasodilation downstream>>> increase blood flow the longer the period of occlusion the longer the subsequent hyperemia

hypertension

that level of BP above which investigation and treatment do more good than harm

pneumonia

the normal air-filled spaces of the alveoli become filled with denser material like fluid, pus

control heart rate (therapeutic options to maximise cardiac function)

the optimum heart rate 90-110 beats/min. correction of low K and Mg first step in treating tachyarrhythmias

pericardial cavity formation

the pericardial coeloms fuse forming the pericardial cavity. Head fold brings the heart and pericardial cavity anterior to the foregut. The pericardial cavity is lined by a visceral and parietal layer. The pericardial cavity is continuous with the pericardioperitoneal canals. Closing of the ventral wall separates the IEC from the EEC. per eudium)

non tension pneumothorax

there is no valve mechanism (unsealed opening) as a result there is no build up pressure.

sympathetic activity (control of blood flow)

this causes vasoconstriction tonic activity on blood vessels>> partially constricted decrease tone>>vasodilation increase tone>>> vasoconstriction tone in one organ can be regulated independently of other tissues

exercise (effects on pressure volume loop)

this increases sympathetic tone, (also increase contractility) increasing venomotor tone, increasing venous return increased EDV increasing preload leading to an *increased stroke volume* very large increase in SV

tissue hypoxia due to decreased perfusion (positive feedback in decompensated shock)

tissue hypoxia due to decreased perfusion>>>metabolic acidosis>>>decreased contractility>> decreased CO and TPR>>>> decreased MAP even more

blood flow

to organs due to 1. symathetic and 2. local control of blood flow. depends on specific organ and metabolism

graves disease

vasodilation of resistance arterioles • Immune disorder -5 over production of thyroid hormones Hyperthyroidism, basal metabolism elevated • Inc metabolism associated with arteriolar vasodilation • Reduced arteriolar resistance reduced dampening of pulsatile arterial pressure in capillaries • pulsatile flow in capillaries- observed in fingernail beds of patients

Nitric oxide

vasodilator (formerly endothelium-derived hyperpolarizing factor (EDHF) or EDRF, R -relaxing Main stimulus for production = shear stress at endothelial cell (detected by glycocalyx on endothelial lumen) Stimulates guanylyl cyclase increase cGMP —Y Vasodilation Continually modulates basal vascular tone. Responsible for: •Flow-induced vasodilation of exercise • Vasodilation of erection • Vasodilation of inflammation

Extrinsic mechanism (of vascular tone)

vasomotor nerves (primarily sympathetic adrenergic, some specialized vascular beds exception) Vasoactive hormones (epinephrine, norepinephrine, angiotensin 2, vasopressin) autonomic nervous system circulating hormones (eg. EPI, angiotensin 2) More involved in overall control of blood flow and BP (MAP)

incomplete tracheal atresia

web fo tissue obstructing airflow

canalicular period (lung development)

week 16-26 terminal bronchiole divides into 2 or more respiratory bronchioles, which in turn divide into 3-6 alveolar ducts. Type Il Alveolar cells appear which produce surfactant Surfactant secretion starts during the 20th week, increases gradually with a sharp increase during last 2 weeks of pregnancy

pseudo-glandular stage (lung development)

week 6-16-major elements of the lung are formed but no respiratory bronchioles

Vascular function (VR) curve

when RAP is <0 veins collapse and blood flow back to the heart is impeded. curve is flat VFC is very steep: veins are very distensible When RAP is +7mmHg, there is no pressure gradient between the veins and the RA and the VR is zero It is the relationship between VR and RAP Amount of blood flowing into the heart (i.e. VR) depends on the pressure gradient between the veins and the RA (i.e. the RAP). Venous pressure, mm Hg Right Atrial Pressure The faster the heart pumps the lower the right atrial pressure falls. Increasing the pressure difference between the RA and the peripheral veins and increasing VR.

functional sympatholysis

where local control of blood flow overrides sympathetic activity. Transient vasoconstriction due to increased sympathetics (a-recept), BUT followed by vasodilation due to increase local released metabolites. *important in: skeletal, heart brain*

right main bronchus

wider, shorter and more verticle inhaled foreign objects tend to get lodge in the wider and more vertical bronchus

local response (to exercise induced blood flow increase)

— As work rate increases, lactic acid is formed, this stimulates muscle afferent nerves (muscle chemoreflex), information to CVS centre increases sympathetic activity to heart and systemic resistance vessels Within same muscles low P02 increased NO, vasodilator prostanoids and åssociated local vasoactive factors dilate arterioles • Vasodilation in skeletal muscle • Decreased total peripheral resistance (T PR) • Adenosine and decreased P02 results in coronary vasodilation and increased blood flow.

measuring blood flow (oxygen extraction)

— Fick principle Oxygen extraction - Rate of 02 loss/min - Amt of 02 loss/vol - Can calc blood flow*>>ml/min 100 ml blood = 19 mls 02 arterial (0.19 per ml) 100 ml blood = 14 mls 02 venous (0.14 per ml) i.e. amt of 02 loss per ml blood gave 0.05 mls 02. Know 02 extraction/time 250 What vol of blood holds 250 mls 02 every min = 5000 ml Law of conservation of mass: Rate 02 removal = [02] pulmonary flow in (artery) - [02] pulmonary flow out (veins) Rate 02 removal (over time) Flow * conc in —w Flow * conc out

tension pheumothorax

— accumulation of gas or air in the pleural cavity •Life threatening-displacement of structures of the mediastinum interrupting cardiopulmonary function. •Involves visceral and parietal pleura and tracheobronchial tree. •Mechanism -Flap valve present -displacement of mediastinum to opposite side -Compression of heart and great vessel: Signs & Symptoms Dyspnea Chest pain Tracheal deviation Hypotension Neck vein distension Hyperresonance

lymphatic drainage (thoracic wall)

— anteriorly to parasternal nodes — Posteriorly to intercostal nodes — Inferiorly to diaphragmatic nodes • Most lymph nodes from thorax eventually drain into thoracic duct — Upper part of right thorax into right lymphatic duct

aortic stenosis

—Highresistanceto outflow from ventricle to aorta. Therefore ventricular pressure much higher than aortic pressure due to reduced outflow from ventricle. Increased pressure gradient with reduced flow but increased flow velocity — therefore turbulence in systole across aortic valve (Flow Velocity = Flow/CSA). Crescendo-decrescendo murmur.

Resuscitation

• At least one approx. 16 gauge IV. Catheter • Normal saline (NaCl) at a rate that will keep systolic B.P. >100 m.m. Hg. and pulse < 100/ min • Supplemental oxygen • Monitor airway, clinical status, vital signs, urine output, N/G tube output if one in place • Transfuse: — i) for haemodynamic instability despite N.Nacl infusion — ii) Hb < 7g/dl in low risk patients — iii) Hb < 9g\dl in high risk patients (elderly, coronary artery disease ) • Give fresh frozen plasma for coagulopathy • Platelets for platelet count < 50,000 or platelet dysfunction

bayliss myogenic response

• Contributes to basal tone • Stabilizes blood flow and capillary filtration pressure if arterial pressure changes (autoregulation) 1. Experimental increase in arterial pressure 2. Stretch of blood vessels -5 SM contraction -5 inc in wall tension 3. Transient increase in vessel diameter, and then autoregulation 4. Reduced vessel diameter (radius), increased Resistance and decreased flow. 5. Red lines: Addition of Ca2+ channel blocker abrogates myogenic response (no SM contraction, and vessel diameter and blood flow remain high) Q=AP/R. Inc pressure gradient- increase resistance- flow — normal

response of respiratory system to training (key points)

• Decrease in minute ventilation necessary to achieve a given V02. Lower minute ventilation a function of ventilatory training rather than changes in control of respiration • Lactate levels at \/02 max for a given level of work less in trained subjects than sedentary controls • Lactate threshold at above 40% of the predicted V02 Contrast at a lower % in exercise among patients wifh cardiovascular disease, higher in endurance athletes

respiratory responses to exercise

• Exercise increases oxygen consumption and C02 production — pulmonary responses to maintain haemostasis • Lactate builds up when it is produced faster than it can be metabolised via the T CA cycle —anaerobic threshold or lactate threshold • Acidosis causes further increase in ventilation — lowering arterial PC02 and holding pH normal

Metabolic adaptation to endurance training

• Increase in size and number of muscle mitochodria. Increased TCA intermediates in muscle mitochondria • Increase storage of glycogen in skeletal muscle • Increased fat utilisation, spares glycogen stores

training (response of the respiratory system)

• Lung diffusing capacity, lung mechanics and lung volumes change little with training • Training doesn't improve the vital capacity. Even exercise designed specifically to increase inspiratory muscle strength elevates vital capacity by only 3%. • The primary respiratory changes with training are as a result of lower lactate production which reduces ventilatory demands at heavy work levels

Lymphatic (filtration)

• Majority of fluid filtered at the arterial end is reabsorbed at the venous end. • Filtration arteriolar end of capillaries > reabsorption at venous end: —2-4 L/day. Starling hypothesis a bit off with "'filtration almost exactly = reabsorption" • However fluid does not normally accumulate in interstitium • Fluid not reabsorbed in capillaries is drained by the lymphatic system. -(—5-10% of filtrate transported out of tissues by lymphatics) • Proteins and bacteria removed. • Lymphatics absent in myocardium • Lymphatics were thought to be absent in brain: glymphatics recently discovered

response of CVS (to training)

• Muscle mass of ventricles increases (hypertrophy usually symmetrical) — force of contraction increases •LV size generally normal or increased (even to suggest dilated cardiomyopathy) but normal LV systolic function and no regional wall abnormalities •TPR decreases — increased capillary capacity

CNS/systemic response (exercise)

• Muscle mechanoreceptors and chemoreceptors trigger reflexes that send afferent signals to the cerebral motor cortex. reduces vagal tone, resets arterial baroreceptors to higher level • Increased sympathetic outflow to heart and blood vessels • Increased heart rate and increased contractility • Increased stroke volume • Increased cardiac output • Increased arteriolar constriction • Increased venoconstriction • Increased venous return

risks of exercise

• Musculoskeletal injury most common risk • Increased risk of arrhythmia during exercise in patients with previous rhythm disturbances and heart disease • Sudden cardiac death. In those < 35 years more likely myocarditis, hypertrophic cardiomyopathy, coronary anomalies; >35 years coronary artery disease • Rhabdomylsis - a syndrome caused by injury to skeletal muscle and involves leakage of large quantities of potentially toxic intracellular contents into plasma • Exercise induced bronchoconstriction — asthmatic presentation • Hyper/hypothermia, dehydration • In intense training -amenorrhoea, infertility especially in women with low body weight.

NO (control of Vascular tone)

• NO important in vascular tone (vasodilation) • Inhibit NO synthase (NOS) *Block NO production vasoconstriction • Add back enzyme substrate L-Arg *restore vasodilation and increased blood flow

exercise prescription

• Not one size fits all for all individuals •Activity should be enjoyable, accessible, within financial means, safe for the individual • Moderate intensity exercise for 50 mins x 3 wkly • Stress that even modest increases in physical activity are associated with improved health outcomes •Counsel be provided to promote a healthy diet

correct hypoxaemia (resuscitation)

• Oxygen therapy • Consider ventilation for - Intractable hypoxaemia - Hypercapnia Pa C02 > 50 m.m Hg. - Respiratory distress - Impaired conscious level

management of shock

• Restore blood volume by infusion of fluids and where appropriate blood • Ensure adequate lung ventilation and provide extra oxygen. • Use interventions that improve cardiac performance

Inflammation (NO)

• Results from specific activation of inducible NOS (iNOS), which has higher activity than endothelial NOS (eNOS). this causes NO to : bradykinin, substance P, thrombin activate both endothelial NOS (eNOS) and inducible NOS (iNOS). (Inc NO)

Compensated vs Decompensated HF

• The blood volume increase causes increased CO initially • As cardiac performance declines no further CO is seen with increased blood volume — de- compensated HF

musculoskeletal adaptations to training

• Type of training affects the muscular adaptations e.g. in endurance training — mitochondrial biogenesis, fast to slow fibre transformation, expansion of muscle capillary bed, changes in substrate metabolism and increased cardiac output • Resistance training- increase size protein content of muscle fibres

medical evaluation prior to exercise

•Appropriate history with age, past medical history, focusing especially on cardiac, pulmonary, orthopaedic history. •History of diabetes, hypertension, hyperlipidaemia • General physical condition •Medication use e.g. Sulphonylureas, insulin, betablockers, nitrates •Anticipated type of exercise • Disabilities • Screening not necessary for asymptomatic clients at low risk of coronary artery disease. • Perform periodic exercise stress testing in asymptomatic clients with multiple cardiovascular risk factors e.g. Hypertension, diabetes, hypercholesterolaemia, smoking. • H/O premature myocardial infarct or sudden cardiac death in a first degree relative < 60 yrs old. • Appropriate screening blood tests based on history.

intrinsic mechanism (of vascular tone)

•Myogenic response •Metabolic •Reactive (post-ischemic) hyperemia •Metabolic hyperemia •paradoxical effect of K + •Endothelial (NO, endothelin) •Paracrine/Autocoids local factors found within the organ ensure that each organ has adequate blood flow at all times

single line flow

•Occurs in capillaries •RBC diameter > capillary diameter •RBC flexes as passes through the capillary •RBC actually flows faster than plasma (less friction in axial flow, vs plasma at boundary flow) Sickle cell anemia: Red blood cell (RBC) is rigid, Hemogobin Hb rod-like and RBC sickle shape. Do not pass easily through capillary tissue ischemia and painful "sickling crisis". Low blood flow: RBCs may stick together and to endothelial lining.

head fold

•Septum transversum forms. •Septum transversum partition separates the pericardial and abdominal cavities. •Head fold brings the heart and pericardial cavity anterior to the foregut. •Heart remains suspended by the dorsal mesocardium Pencanlopentoneal caml Esomageal pan ot Tracneal part ot Pericardial cavity

thoracic cage

•Structures between the thorax and upper limb pass over the first rib. •Cervical rib, small scalene triangle, small costoclavicular triangle may result in compression of neurovascular structures. •Cervical interventions can affect lung function or lung tumors can invade neck structures.