midterm study notes

Midterm Study Notes

Mechanics of VentilationMuscles of inspiration Increase vertical dimensions: Diaphragm The major muscle of inspiration (phrenic nerve C3, 4, 5) Resting inspiration descends ~1 cm; can move up to 10 cm Also increases A-P & M-L dimensions (with the assistance of the external intercostals) Resting expiration passive, diaphragm relaxes and elastic recoil of lungs forces air out Abdominal muscles are accessory for expiration Movements of the rib cage Increase A-P dimensions Ribs move forward & upward pump handle motion Primarily ribs 3-6 Extension of thoracic spine (t-spine problems can limit excursion) Increase transverse dimensions Ribs move up & out bucket handle motion Primarily lower ribs Costochondral junction increases, elongating ribs & further increasing volume cavity Lowest 2 ribs (floating ribs not attached to sternum) can only open outwards caliper motionCostovertebral joints 2-9 articulate with vertebral body of same level and the level above (demi-facets) and the corresponding IVD 1, 10-12 articulate only with vertebral body of same level Costotransverse joints Articulation changes shape as you move inferiorly Higher in thorax roll Joint centres lie more in coronal (frontal) place Pump handle motion Lower in thorax glide Joint centres lie more in sagittal plane Bucket handle motionRelationship of lungs to chest wall Pleural membranes cover the lungs and inner surface of the chest wall These membranes glide over one another Remember we have muscular control over the chest wall only, not the lungs Pleura The inside pleural membrane lines the lungs termed the visceral pleura The outside pleural membrane lines the inside of the chest wall termed the parietal pleura The pleural space is a potential space between the two pleura. A very thin film of fluid is found between the two pleura Negative pressure (vacuum) in the pleural space holds lungs to chest wall Pleura is serous membrane Parietal layer Lines cavity (chest wall, diaphragm, mediastinal surface) Sensitive to pain Visceral layer Covers lung (invaginates lobes, reflects off root of lung to become parietal layer) Insensitive to pain Pleural cavity Pleural fluid (lubricant, about 2-5mL) Forms thin film between layers of pleura Allows slightly slimy lungs slither & slide within thorax Constant drainage of serious fluid by lymphatic system creates this negative pressureVentilation Ventilation is not the same as respiration (alveolar-capillary interface respiration and tissue-capillary interface respiration gas exchange) Ventilation is defined as the exchange of air between the atmosphere and alveoli In order to inspire air, our chest cavity volume must increase to create a low pressure environment in the alveoli. Then, since the pressure in the chest is lower than the atmosphere, air flows in from an area of higher pressure to an area of lower pressureRecoil of lung Forces pulling lung inwards 2/3 due to surface tension 1/3 due to elastin Pathology due to loss of elastin E.g., emphysema (causes difficulties with respiration), alpha1-antitrypsin deficiency (predisposed to destruction of connective tissues)Pressures All pressures described in the respiratory system are relative to atmospheric pressure. The pressure within the lungs (alveolar pressure) between breaths is described as 0 mmHg, that is, the same as atmospheric pressure (~760 mmHg) Intrapleural pressure (IPP) is created by the tendency of Chest wall pulling out (also has recoil properties) Lung recoiling inwards Average IPP between breaths is around -4 mmHg (less than atmosphere) Transpulmonary pressure (TP) Is the difference between pressure in the lung and the pleural cavity TP = Palv IPP [ 0 (-4) = 4 mmHg] It is the pressure required to hold the lungs open Always present; without it, lungs would collapse Due to weight of lung IPP is less negative at base than apex Base is more compressed Note: Base expands more on inspiration in an UPRIGHT lung (therefore dimensions increase more in lower thorax than upper) More increase in capacity in the base of the lung than at the apex at rest Tendency to have air trapping in apices of lungs due to higher IPP

Volumes, Capacities, and Blood Flow of the LungsNormal breathing Inspiration happens actively because of muscle contraction Quiet expiration happens passively because of the recoil forces on the lung Elastic tissue Surface tension 3-5% of total energy expended by body goes to breathing Heavy exercise can increase 50-fold In obstructive lung disease, up to 30% of bodys energy expenditure is for breathing even at restLung volumes and capacities Lung volumes Refer to the volume of air associated with different phases of the respiratory cycle Can be measured directly Lung capacities Based on the addition of two or more lung volumes Unlike volumes, which are directly measured, capacities are inferred from the sum of certain lung volumes Lung volumes 4 in total Non-overlapping Subdivisions of the total lung volume Measured by a spirometerTidal and residual volume The average total lung capacity of an adult human male is about 6 L of air (4.2 L in females) Only a small amount of this capacity is used during normal breathing Tidal volume Tidal breathing is normal, resting breathing The tidal volume is the volume of air that is inhaled or exhaled in only a single such breath (normal, healthy individual) Normally 500 mL Residual volume The volume of gas in the lungs at the end of a full forced expiration The stiffness of the chest wall limits further decrease in volume by expiratory muscle force Prevents lungs from collapsing (cant collapse chest wall) Hard to measure involves helium Normally 1200 mLReserve volumes Reserve volumes represent the maximum amounts of air you can inhale or exhale beyond normal, passive tidal respiration Must be inhaled or exhaled actively/full-forced Two types Expiratory reserve volume: The maximal volume of air that can be exhaled from the end-expiratory position I.e., emptying out your lungs as much as you can Whatever remains in your lungs is your residual volume Normally 1200 mL Inspiratory reserve volume: The maximal volume that can be inhaled from the end-inspiratory level I.e., breathing in as much air as you can hold Normally 3100 mLLung capacities Total capacity The total capacity of air in your lungs (add up all 4 volumes) The total volume of gas your lungs can possible hold (i.e., the sum of gas in your lungs following a full forced inspiration) Inspiratory muscle force stretches the chest wall and the lungs beyond their resting positions The stiffness of the lungs limit further expansion by inspiratory muscle force Total lung capacity is around 6000 mL Tidal volume + residual volume + expiratory reserve volume + inspiratory reserve volume Functional residual capacity Volume of lungs after normal passive expiration (during tidal expiration) At FRC, the elastic recoil forces of the lungs and chest wall are equal but opposite and there is no exertion by the diaphragm or other respiratory muscles The tendency of the chest to expand is balanced by the tendency of the lungs to collapse Calculated as FRC = expiratory reserve volume + residual volume 2400 mL = 1200 + 1200 A lowered or elevated FRC is often an indication of some form of respiratory disease Inspiratory capacity The total amount of air that can be actively inspired IC = tidal volume + inspiratory reserve volume 3600 mL = 500 + 3100 Vital capacity The total amount of air that can be expired after fully inhaling Approximately 80% of TLC VC = tidal volume + inspiratory reserve volume + expiratory reserve volume About 4800 mL Variations in VC occur with Height/weight/surface area VC is proportional to height (reason for variation between genders) Age decreased VC with age Posture VC decreases when supine Changes in lung volumes or capacities can be used to diagnose pathological conditions In restrictive diseases (pulmonary fibrosis, weak respiratory muscles), flow is normal, but volumes are decreased In obstructive diseases (asthma, COPD, emphysema), flow rates are impeded Increased residual volume, air trappingFVC and FEV1 FVC = forced vital capacity, the maximum amount of air forcibly expired after maximum inspiration FEV1 = forced expiratory volume in the first second of forced vital capacity maneuver FEV1 and FVC help differentiate obstructive and restrictive lung disorders

Lung volumes/capacities of restricted diseases Compliance of the lung is reduced Increased stiffness of the lung and limited expansion (difficulty inhaling to full capacity) A greater pressure than normal is required to give the same increase in volume Causes of restrictive disorder: pulmonary fibrosis (reduced space in alveoli due to thickening, as well as overall stiffness), pneumonia and pulmonary edema, stiffness of the chest wall, weak muscles (e.g., Duchennes muscular dystrophy) IRV and ERV are decreased (TLC is decreased)

Lung volumes/capacities of obstructive diseases Obstructive difficulty exhaling normal amount Airway obstruction causes an increase in resistance. During normal breathing, the pressure volume relationship is no different from in a normal lung. However, when breathing rapidly, greater pressure is needed to overcome the resistance to flow, and the volume of each breath gets smaller Common obstructive diseases include asthma, bronchitis, emphysema, cystic fibrosis Overall TLC is increased and RV is increased

Not always limited to one type! Combination of obstructive and restrictive disorders E.g., smoker with emphysema that later in life develops a neuromuscular disorder Reduced TLC with reduction in flow

Blood in the lungs Pulmonary blood supply Blood through the lungs for gas exchange Systemic blood supply Blood to the lung tissue/cells

Blood flow through the lungs from the pulmonary artery High flow (5 L/min), low pressure (15 mmHg), low resistance (1-2 mmHg/L/min) circuit Initially arteries, veins, and bronchi run together Toward the periphery: Veins outside of lobe segments Arteries centre of lobe segments Capillaries between arteries and veins ~ 7 micrometers diameter and are short large surface area 50-100 m2 RBCs travel the capillary bed in ~0.75 seconds, lung in 4-5 seconds Small capillary diameter squishes RBCs increases contact between RBCs and capillary wall and therefore increases gas exchange

Blood supply to lung tissue: Bronchial arteries In addition to pulmonary circulation, there are also branches from the systemic circulation Bronchial arteries Arise from the thoracic aorta Supply blood to the bronchi and connective tissue of the lungs Travel with and branch with the bronchi, end at the level of the respiratory bronchioles There are also bronchial veins, but the majority of bronchial arteries are drained by pulmonary veins

Blood volume of lungs Normal blood volume of lungs is 450 mL (70 mL in capillaries) Pulmonary vessels act as reservoir, accommodate up to twice as much blood volume Volume of blood in lungs varies with intrathoracic pressure High intrathoracic pressure (expiration) expels blood from lungs Low intrathoracic pressure (inspiration) increases blood volume Left ventricular failure can cause pooling of blood in lungs and rise in pulmonary pressure

Blood pressures in the lung Mean pulmonary arterial pressure is 15 mmHg Only need enough pressure maintained to lift blood above the heart to the top of lung Therefore, work required of right ventricle is much less than left RV is less muscular than LV

Pressures in the pulmonary circulation Larger pulmonary arteries and veins Subjected to much lower pressures than alveolar vessels Pulled open as lung expands on inspiration Pulmonary capillaries Small and surrounded by gas Subjected to pressure shifts occurring within the thorax during ventilation If alveolar pressure is higher than pressure in capillary, it will cause the capillary to collapse stops perfusion, and leads to the creation of alveolar dead space Tends to occur in upper regions of lung because of increased alveolar pressure combined with lower intracapillary pressure

Regional differences Lower regions of lung are better perfused than upper zones when an individual is upright Gravity is primary determinant, as it creates a hydrostatic pressure gradient Lowest point in lung is 30 cm below highest point Regional arterial blood pressure is typically in the range 5 mmHg near the apex of the lung to 25 mmHg at the base It takes less energy to pump blood to the bottom of the lung than to the top

Ventilation-Perfusion Matching (VA/Q)Perfusion Does not consider systemic circulation that supplies the lungs

Tracheobronchal tree Conducting zone not available for gas exchange Transit and respiratory zone areas where gas exchange takes place

Useful information At rest a normal healthy person breathes ~500 mL of air at a frequency of 12-16 breaths/min. Therefore minute ventilation (VE) = 6-8 L/min Tidal volume or VT is composed of VD (dead space) + VA (alveolar NEW air ~1/7) We replace about 1/7 of alveolar air with each breath Dead space: Proportions of the tidal volume that are not used for gas exchange Anatomical dead space is that area of the tracheobronchal tree not involved in gas exchange. This includes all the conducting airways including the larynx, pharynx, and so on This represents ~ 150 mL in a normal person so that 30% of a tidal volume of 500 mL is wasted In disease states there are areas of the lung which receive adequate ventilation but are under (or not) perfused. Therefore it is more accurate to term all of this as physiological dead space Alveolar volume It is that volume of air participating in gas exchange (only 1/5-1/7 of air in alveoli is fresh air from last breath)

Bohr equation The Bohr equation is used for calculating physiologic dead space and uses the principle that increasing amounts of dead space ventilation augment the difference between PCO2 in arterial blood and expired gas The equation is written as VD/VT = [PaCO2 PECO2]/PaCO2

Introduction to gas exchange Oxygen enters the pulmonary capillaries to be utilized at the cellular level CO2 entering at the cellular level will move into the capillaries and then into the alveoli

Compliance Recoil of lungs is 2/3 due to surface tension and 1/3 due to elastin Chest wall has recoil forces pulling in the opposite direction

Surface tension Surface tension is the force acting across an imaginary line 1 cm long in the surface of a liquid. It is there because the attractive forces between adjacent molecules of the liquid are much stronger than those between the liquid and gas with the result that the liquid surface becomes as small as possible Fluid molecules lining alveoli want to pull the alveoli in on itself due to surface tension Drop of water on non-wetable surface At air-water interface, water molecules are strongly attracted to each other so they act like an elastic membrane, drawing water into a sphere (minimizing surface area) Add detergent (or surfactant) Molecules at surface are no longer as strongly attracted to each other and water flows across surface Reduces surface tension so that water flows

Surfactant Function: Decreases surface tension, decreases recoil & decreases work required for inhalation Consequences of low surfactant: Stiff lungs (low compliance therefore hard to inhale) Areas at atelectasis (decreased or absent air in the entire or part of a lung resulting in loss of lung volume) Alveoli fill with transudate (fluid moving from capillary to alveoli; likely plasma) Without surfactant Surface tension collapse alveoli Fluid drawn into alveoli With surfactant Surface tension decreased (NOT eliminated) Surface tension still responsible for 2/3 of recoil during exhalation Surfactant is a phospholipid, a constituent of which is DPPC (dipalmitoyl phosphatidyl choline), and is produced by type II alveolar epithelial cells Without surfactant, small alveoli tend to empty into large alveoli, because the smaller alveolus generates a larger pressure Surfactant stabilizes alveoli by reducing surface tension This helps to maintain surface area

Compliance Is the change in lung volume produced by change in transpulmonary pressure Compliance = change volume/change pressure The larger the ratio, the greater the compliance (distensibility/stretchability) Compliance of both lungs averages 200 mL/cm of water (normal) Compliance is not elasticity!

Pressure-volume curve (compliance curve) Note that the curve is non-linear is that it is stiffer at higher volumes Hysteresis the inflation curve is not the same as the deflation curve (due to air trapping) Compliance is the slope (change in volume/change in pressure) The compliant behaviour of the lung depends on collagen, elastin, and surface tension Saline-filled lung is more stretchable than air-filled lung

Low lung volumes Note that the normal distribution of ventilation is inverted in very low lung volumes (transient situation)

Compliance Curve Compliance of the respiratory system depends on the combination of lung compliance and chest wall compliance Compliance of chest wall includes costal cartilage, movement in thoracic spine, musculature, etc. Compliance decreases with age due to a variety of factors Patients with restrictive lung disease (fibrosis) have lower than normal compliance Patients with obstructive lung disease (emphysema) have higher than normal compliance

FEV1/FVC ratios in disease Normal ratio is 80% Lower ratios indicate obstructive disease Higher ratios indicate restrictive disease

Regional differences in perfusion (in the upright lung) Note that blood flow per unit volume is better at the bottom of the lung than the top It decreases quite steeply as we move past the middle of the lung and towards the top Blood is heavy/air is light

Pressure gradients PA is alveolar pressure Pa is the pressure at the arterial end of the capillary bed Pv is pressure at the venous end of the capillary bed Top of lung: PA > Pa > Pv Middle of lung: Pa > PA > Pv Bottom of lung: Pa > Pv > PA Note how the pressures preferentially allow for better perfusion at the bases in this upright lung

Graphical VA/Q relationship Note that both ventilation and perfusion are better at the bottom than at the top This holds true for resting lungs or when the demand is not high This changes with activity Note that the decline is steeper for perfusion (blood flow) than it is for ventilation when moving towards the top of the lungs

Regional differences in VA/Q matching Note that VA/Q approaches infinity at the top of the lung (higher ventilation but no perfusion) Best VA/Q matching is middle and base of lung

Shunt and dead space Shunt is defined as an area of adequate perfusion but no ventilation (low VA/Q) Dead space is defined as an area of adequate ventilation but no perfusion (high VA/Q)

Adjustment of airflow to blood flow via CO2 induced change in the airway Initial state left alveolus is receiving too much air for its blood supply Right alveolus is receiving too little air for its blood supply Therefore low alveolar CO2exposure of left bronchiole and high alveolar CO2exposure of right bronchiole Local compensation low alveolar CO2 causes airway constriction, and high alveolar CO2causes airway dilation. Thus airflow is now matched to blood flow Note: Airways are constricted by parasympathetic nerves and dilated by sympathetic nerves as well as by local CO2 concentrations

Adjustment of blood flow to airflow via H+ and O2 induced changes in the arteries Initial state left alveolus is receiving too little blood supply for its airflow and therefore arterial H+ is low and arterial O2 is high. Right alveolus is receiving too much blood supply for its airflow and therefore arterial H+ is high and arterial O2 is low Local compensation low arterial H+ and high arterial O2 causes arterial dilation. High arterial H+ and low arterial O2 causes arterial constriction. This acts to shift the blood away from the poorly ventilated alveolus and to the well-ventilated alveolus Note: This is exactly the opposite of the local control events occurring in the systemic circulation

Gas Exchange and Physiology of Blood GasesDefinitions: Diffusion is the net movement of a molecule from an area of high concentration to an area of low concentration Pressure is the total exerted force of molecules against a surfacePartial Pressures Mixtures of gases in atmospheric air, oxygen, nitrogen, carbon dioxide The pressure created by an individual gas is directly proportional to the concentration of the gas molecule Sum of partial pressures = total pressurePartial Pressures of Inspired Air H2O variable CO2 0.003 mmHg O2 159 mmHg N2 601 mmHg Total pressure 760 mmHgAir Humidification As soon as respiratory air enters the respiratory passages, it is humidified by the fluids on the surfaces of the respiratory passages Humidification causes dilution Partial Pressures of Alveolar Air (after Humidification) H2O 47 mmHg CO2 40 mmHg (CO goes up as it exiting the bloodstream, higher concentration than in atmospheric air) O2 105 mmHg N2 568 mmHg Total pressure 760 mmHgReplacing Alveolar Air The volume of alveolar air replaced by atmospheric air is only about 1/7th of the total residual volume It takes about 16-17 breaths to replace most of the original alveolar air with atmospheric air O2 and CO2 in the Alveoli The concentration of O2 and CO2 is controlled by The amount of alveolar ventilation The rate of absorption or excretion of each gas into the bloodDiffusion of Gases: Respiratory Membrane1. Fluid + surfactant in the alveolus2. Alveolar epithelium3. Epithelial basement membrane4. Thin interstitial space5. Capillary basement membrane often fused with alveolar basement membrane6. Capillary endothelial membrane Thin membrane allows easier/faster diffusion Respiratory Membrane Total surface area = 70 square metres Total quantity of blood in the lung at a given instant is 60-140 mL Average diameter of a capillary is about 5 micrometers which is smaller than a red blood cell Red blood cell must squeeze through the capillary causing the red blood cell wall to contact the capillary wall further facilitating gas exchangeFactors Affecting Diffusion1. Thickness of the membranea. Occasionally increases edema, fibrotic lungs increased thickness in parts of membrane2. Surface area of the membranea. Decreased surface area: Removal of lung or parts of lung, emphysema loss of alveolar walls3. Diffusion coefficient of the gasa. CO2 diffuses 20x more rapidly than O24. Pressure difference of the gas between the two sides of the membrane a. Net diffusion of oxygen into the bloodb. Net diffusion of oxygen into the tissuesc. Net diffusion of CO2 into the alveolusBlood Gases & Acid-Base BalanceOxygen Transport Small amount is dissolved in blood ~0.3 mL/100 mL of blood The remainder is transported by hemoglobin (iron-containing oxygen-transporter in RBC) ~15g/100 mL Oxygen Dissociation Curve Oxygen combines with hemoglobin to form a reversible combination oxyhemoglobin O2 + Hb HbO2 4 O2 can bind to 1 Hb (to each heme/iron group) Primary factor that determines how much O2 is bound to hemoglobin is the PO2Oxygen Dissociation Curve Definitions Oxygen capacity the maximum amount of oxygen that can be combined with Hb (~20.8 mL oxygen/100 mL blood) Oxygen saturation the percentage of oxygen actually bound to Hb compared to the total oxygen capacity E.g., in arteries - O2 saturation ~97.5% at a PO2 of 100 mmHg The actual amount of circulation oxygen is dependent on the amount bound to the Hb and the amount of Hb in the bloodstream Under normal conditions, about 5 mL of oxygen is transported from Hb to the peripheral tissues, leaving about 15 mL still bound to Hb in reserve O2 saturation ~75% in veins Oxygen Dissociation Curve The flat upper portion changes in PO2 lead to minimal changes in loading of oxygen onto hemoglobin The steep lower part represents the ability of the tissues to remove large amounts of oxygen for small changes in capillary PO2 maximizes the exchange Arteries PO2 = 100 mmHg, which gives a 97.5% saturation Veins PO2 = 40 mmHg, which gives a 40% saturation Tissues PO2 = 20 mmHgInfluences on the Curve Factors shifting to the right (e.g., exercise)1. Decrease pH (increase H+)2. Increase temperature3. Increase CO24. Increase DPG (diphosphoglycerate) A shift to the right causes greater O2 removal from Hb for a given PO2 This increases unloading of oxygen at tissues due to the rightward shift (reflects increased demand for oxygen)CO2 CO2 is constantly formed in the body by intracellular metabolic process Increasing metabolic rate increase PCO2 in blood Decreasing metabolic rate decrease PCO2 in blood CO2 Transport Transported three ways Dissolved in solution ~7% Bound to proteins ~23% Bicarbonate ion ~70%Bicarbonate Buffering System Maintains blood pH CO2 in the red blood cell is quickly converted to carbonic acid by the enzyme carbonic anhydrase CO2 + H2O H2CO3 H+ + HCO3- Carbonic acid dissociates into hydrogen ions and bicarbonate ions H+ binds to the Hb molecule (which can induce a conformational change in Hb) and HCO3- diffuses into the blood stream Acid/Base Balance Acid molecules containing hydrogen atoms that can freely release H+ into solution, e.g., HCl, H2CO3 Base an ion or molecule that can readily accept H+ e.g., HCO3- or some proteins like Hb Regulation of H+ in the body is important because almost all enzyme activity in the body is influenced by H+ Buffer System A buffer is any substance that can reversibly bind H+ Buffer + H+ HBuffer Increased H+ forces the reaction to the right (provided the buffer is in excess) Decreased H+ forces the reaction to the leftRegulation of pH, e.g., Acidosis CO2 + H2O H2CO3 H+ + HCO3- Acidosis forces the reaction to shift towards the left, increasing carbon dioxide Respiratory rate increases to blow off excess carbon dioxide, decreasing blood pH

Regulation of Blood Pressure via Kidney Heart AxisPurpose of Lecture You are likely to come across patients with hypertension The kidney plays a significant role in BP regulation There are many drugs which work by altering kidney function to lower BP Common side effect = orthostatic hypotension The Urinary System Two kidneys, two ureters, a bladder, and a urethra Ureters are high in sensory nerve endings (think kidney stones) Filter system for the blood that produces about 180 L of filtrate/day, but only excretes 1.5 L urine/day Regulates blood volume Eliminates metabolic waste produces Excretes excess ions E.g., acid-base balance (homeostasis), when potassium levels get too high (hyperkalemia) cardiac arrest occurs Other functions Regulates blood pressure renin Secretes vitamin D RBC production (erythropoietin) So What? If the kidneys fail then salts and waste products like urea build up and pH of the blood goes down Massive pitting edema results from the salt retention Academia results from the inability to excrete acids Therefore, we cannot stop blood flow to the kidneys EVER (even though with activity, some blood flow to kidney and GI tract is shunted to muscles) Renal artery stenosis leads to increased BP at all costs because we MUST maintain blood flow to kidneyGross Anatomical Features Cortex (more pathology will result in a thinner cortex) Medulla (all the renal pyramids) Renal pelvis Minor calyx Major calyx Nephron collecting duct Renal pyramid Renal column Renal papilla Renal hilumPolycystic Kidney Most healthy people have some renal cysts after age 30-50, but many cysts is pathologic Kidney can become 80-90% damaged before acute renal failure Other problems include hydroureter and hydronephrosis, as well as horseshoe kidneys and supernumary renal arteries Problem with multiple renal arteries is that one may grow over ureter and constrict it The Big Picture of Renal Function The Nephron Afferent arteriole glomerulus efferent arteriole peritubular capillaries Glomerulus contained within Bowmans capsule is the renal corpuscle (filtrate making machine) Filtrate drains into the proximal convoluted tubule, travels through the loop of Henle, and into the distal convoluted tubule Along the way, filtrate is made into urine by reabsorption of material from the filtrate in the tubule to the blood, and secretion of material from the blood to the tubule Collecting duct concentrates the urine Urine goes to the renal calyces then ureters and then the bladder Blood goes back to the venous circulation Filtration and Podocytes Capillary fenestrations and pedicels of a foot process in a podocyte form filtration slits All small molecules can pass into the capsular space and form filtrate, but large molecules (> albumin size) cannot and stay in the blood How Does the Kidney Regulate BP?1. Renin-Angiotensin-Aldosterone System (RAAS)2. Natriuretic Peptide (ANP & BNP)The RAAS1. Sensing of low BP/low volume in afferent arteriole/systematic circulation 2. Sympathetic nerve stimulation3. Low sodium levels and low flow in macula densa of the distal convoluted tubule All of these things cause an increase in release of renin by the juxtaglomerular apparatus Angiotensin II and Blood Pressure Renin converts angiotensinogen into angiotensin I ACE converts angiotensin I into angiotensin II Angiotensin II acts to cause constriction of systemic and glomerular afferent arterioles, causing blood pressure to increase Angiotensin II also causes the release of aldosterone from the adrenal cortex (causes fluid retention) and the release of anti-diuretic hormone (ADH, also called vasopressin) from the posterior pituitary (causes fluid retention) Diabetes inspidus caused by a lack of ADH or a lack of sensitivity to ADH ACE inhibitors, the most common medication for high blood pressure, prevent angiotensin I from becoming angiotensin II and shut down these effects Natriuretic Peptides High blood pressure in the atrium causes distension of the atrium and release of atrial natriuretic peptide (ANP) by atrial myocytes Similarly, distension of the ventricles causes release of brain natriuretic peptide (BNP) These cause increased urine excretion ANP Distension of the atrium of the heart leads to the release of ANP The ANP causes relaxation of the mesangial cells between the glomerular capillaries Once the mesangial cells relax, the glomerular capillaries are more spread out and relaxed so more filtration can occur ANP also relaxes the afferent arteriole of the glomerulus and increases sodium loss Total effect is a decrease in blood volume and therefore a decrease in blood pressureOther Types of Medication for HBP After ACE inhibitors, diuretics are most common (especially thiazides) Osmotic agents (mannitol) Loop agents (e.g., furosemide) Thiazides Aldosterone antagonists ADH antagonists Summary The kidney plays a fundamental role in regulating blood pressure The RAAS acts to raise BP via the heart/kidney axis NP acts to lower pressure via the heart/kidney axis Many drugs will attempt to alter BP by altering kidney function

Control of Breathing (Ventilation)Respiratory Centre Consists of a series of bilateral paired nuclei in the reticular formation of the brain stem Paired nuclei indicates they have a reciprocal connection (they cycle) Dorsal Respiratory Group (DRG) major driving input to rate of breathing Rhythmic activity via pacemaker neurons but has many inputs (limbic system, cortical areas) It is a ramp signal therefore a series of impulses which increase the contraction of respiratory muscles then stops Input to diaphragm via phrenic nerve Ventral Respiratory Group (VRG) Interacts with DRG when demand goes up. Note powerful drive to both inspiration and expiration Note: The output of the DRG and VRG would be delivered to the muscles via their respective peripheral nerves through increased activation of respective motor neuron pools e.g., phrenic motor neurons supplying diaphragm

Input to DRG and VRG Peripheral chemoreceptors Sensitive to partial pressures (e.g., of CO2 and O2) Aortic bodies via the vagus nerve Afferent and efferent connections to DRG and VRG Carotid body via the glosspharyngeal nerve Located at the bifurcation of external and internal carotid arteries Chemosensitive centre Baroreceptors (pressure) and other lung receptors (stretch receptors)

Respiratory Center Pneumotaxic centre (P Centre) Limits inspiration by inhibiting apneustic centre This then increases rate Apneustic centre In balance with P Centre to fine tune the rate during activities such as exercising Potential mechanism is to modulate ramp signal of inspiration Communicates mostly with the DRG but also with the VRG Hering Breuer Inflation Reflex Mediated via stretch receptors in the lung afferents input via vagus nerve Prevents over-inflation of the lung The P Centre and the apneustic centre are actually paired nuclei which cycle. They contribute to the function of the DRG in the medulla The apneustic center has an excitatory effect on inspiration and will tend to prolong inspiration (decreasing RR) The P centre is inhibitory and switches inspiration off (increasing RR). This will then assist in the control of respiratory rate and inspiratory volume Damage to the connections between these centres as a result of brain injury will result in an irregular breathing pattern consisting of prolonged inspiratory gasps interrupted by expiratory efforts

Chemical Control of Ventilation Driven by H+ (pH), CO2, and O2 Hypercapnia (CO2 and H+) contributes the most to drive to breathe Oxygen has a smaller effect

Central Chemosensitive Area Central chemoreceptor thought to be located in the ventrolateral medullary surface Sensitive to H+ only H+ does not cross the blood-brain barrier into the ESF or CSF CO2 on the other hand crosses readily Hence the reaction where carbonic acid very rapidly dissociates into bicarbonate and H+ Therefore, blood CO2 has a greater effect than blood H+ (pH) Effect of CO2 decreases after 1-2 days This is due to the buffering capacity in the blood via the increase in blood bicarbonate Oxygen has NO EFFECT in this area!

Peripheral Chemoreceptors Very sensitive to decreases in O2 Also sensitive to H+ and CO2

What is Important to Know as PTs Know that there exists neural oscillators in the medulla that support inspiration and expiration Have to be under some automatic control because, for example, we dont stop breathing when we are asleep! So these areas have to have pacemaker cells However these areas are finely modulated (tuned) to generate respiratory-related motor activities like talking, singing, eating, etc.

Control of the HeartSkeletal Muscle and Cardiac Muscle Compare and contrast Both have contractile elements Cardiac muscle has elements of both smooth and striated muscle Can generate action potentials that spread to adjacent cells. Note intercalated discs Can observe gap junctions Can contract to produce force Cardiac muscle, unlike skeletal muscle has automaticity The heart is a functional syncytium a syncytium is a multinucleated protoplasmic mass formed by the secondary union of originally separate cells funny way to describe a heart but note functional Basically, a mass of cells that functionally behave all together

Histology Purkinje cells part of the conducting system of the heart (they conduct rather than contract). Are in fact modified cardiac muscle Note no T-tubules Note no gap junctions and no intercalated discs SA node Intrinsic pacemaker of the heart (because it has the fastest rate of firing) Has both sympathetic and parasympathetic drive/input

Cardiac Action Potential Partial repolarization is due to closing of fast sodium channels Plateau is due to slow sodium and calcium channels Repolarization due to increased activation of potassium channels and closing of slow sodium and calcium channels

Relationship of AP to Twitch There is an overlap between the action potential and muscle twitch in cardiac muscle (unlike in skeletal muscle)

Ion Currents Notice differences in ionic flow in different cardiac cells Note pacemaker potential in SA nodal cell Slow leaking potassium = automaticity Pacemaker current depends on extra ionic current Provides nodal cell with automaticity

Conducting System Notice the presence of the SA node and AV node Notice the intemodal pathways The significant of the AV delay = allows time for ventricular filling

The ECG Signal Is a cumulative sum of APs (not a single AP) P wave = depolarization of atria QRS = depolarization of ventricles T wave = rapid depolarization of ventricles U wave = usually very small but reflects the final phase of the Purkinje fiber repolarization P-R interval ~ 0.12-0.20 seconds Delay between SA and AV node Problems indicate alterations in ventricular filling S-T segment is the plateau initial phase of ventricular repolarization Pathology if above or below the isoelectric line The time when the entire ventricular muscle is depolarized The T wave is the rapid phase of ventricular repolarization Q-T interval is the period of electrical systole of ventricles

Myocardial Infarction Triad1. Ischemia Characteristic sign of ischemia is an inverted T wave (caused by reduced supply from the coronary arteries) May see these transiently (e.g., during a stress test or in angina patients)2. Injury Elevation of S-T segment signifies acute injury (MI is new/acute)3. Infarction a. Necrosis Abnormal Q wave indicates necrosis cell death in left ventricle Significant Q wave 1 mm or greater wide (40 msec duration) Abnormal Q wave = electrical void of necrotic infarct

S-T Segment Depression Can be caused by Subendocardial (partial thickness) MI Positive stress test Digitalis medication

Ventricular Fibrillation Normally, ventricular contraction starts with the inner lining of the muscle and progresses to the outer layer Ventricular fibrillation disturbs this mechanism and causes random firing (outside muscle contracts before inside, and is ineffective)

Autonomic Control of the Heart Sympathetic drive increases both HR and force of contraction (efferents to SA and AV node, and cardiac muscle) Parasympathetic drive decreases HR (efferents to SA and AV node only) Notice that the vagus nerve delivers parasympathetic impulses Resting HR is a reflection of the balance between these two systems

Mechanics and Physiology of Breathing Respiratory tract Nasal cavity mouth pharynx larynx trachea main bronchus lobar bronchus segmental bronchus conducting bronchiole terminal bronchiole respiratory bronchiole alveolar duct alveolar sac alveolus Lungs can be expanded and contracted in two ways By downward and upward movement of the diaphragm to lengthen or shorten the chest cavity By elevation and depression of the ribs to increase and decrease the anteroposterior diameter of the chest cavity Normal quiet breathing is accomplished almost entirely by movement of the diaphragm During inspiration, contraction of the diaphragm pulls the lower surfaces of the lungs downward During expiration, the diaphragm relaxes, and the elastic recoil of the lungs, chest wall, and abdominal structures compresses the lungs and expels the air During heavy breathing, the elastic forces are not powerful enough to cause rapid expiration Extra force is achieved by contraction of the abdominal muscles, which pushes the abdominal contents upward against the bottom of the diaphragm, thereby compressing the lungs All the muscles that elevate the chest cage are classified as muscles of inspiration When the rib cage is elevated, the ribs project almost directly forward, so that the sternum also moves forward, away from the spine, increasing the anteroposterior diameter of the chest cavity Most important = external intercostals Others include sternocleiomastoid (which lift upward on the sternum), serratus anterior (which lift many of the ribs), and scalenes( which lift the first two ribs) All the muscles that depress the chest cage are classified as muscles of expiration Most important = rectus abdominus (pulling down on lower ribs at same time as pressing abdominal contents upward against the diaphragm) and internal intercostals Lung is an elastic structure that collapses whenever there is no force to keep it inflated Lung is attached to the walls of the chest cage only at the hilum Lung floats in the thoracic cavity, surrounded by a thin layer of pleural fluid that lubricates movement of the lungs within the cavity Continual suction of excess fluid into lymphatic channels maintains a slight suction between the visceral pleural surface and the parietal pleural surface Slightly negative pleural pressure Therefore, the lungs are held to the thoracic wall as if glued there, expect that they are well lubricated and can slide freely as the chest expands and contracts During inspiration, expansion of the chest cage pulls outward on the lungs with greater force and creates more negative pressure = increase in lung volume Alveolar pressure is the pressure inside the lung alveoli To cause inward flow of air during inspiration, the pressure in the alveoli must fall to a value slightly below atmospheric pressure to pull air into the lungs During expiration, the alveolar pressure must rise to slightly above atmospheric pressure to force the inspired air out of the lungs Transpulmonary pressure = pressure difference between alveolar pressure and plural pressure A measure of the elastic forces in the lungs; recoil pressure Airways are lined with goblet cells that produce mucous, as well as cilia, that continually beat upwards This creates a mucous elevator that is very effective at trapping and removing inspired particles

Role of CV System in Gas Transport Heart is two separate pumps (divided by septum) A right heart that pumps blood through the lungs (right AV valve = tricuspid) A left heart that pumps blood through the peripheral organs (left AV valve = mitral/bicuspid) Each of these hearts is a pulsatile two-chamber pump composed of an atrium and a ventricle Each atrium is a weak primer pump for the ventricle, helping to move blood into the ventricle Ventricles then supply the main pumping force that propels the blood either through the pulmonary circulation by the right ventricle, or through the peripheral/systemic circulation by the left ventricle Function of the arteries (more elastic, more muscular) is to transport blood under high pressure to the tissues Function of the capillaries is to exchange fluid, nutrients, electrolytes, hormones, and other substances between the blood and the interstitial fluid The veins function as conduits for transport of blood from venules back to the heart Pulmonary circulation contains approximately 9% of total blood volume at any given time

Gas Transport by Blood Diffusion of oxygen from the alveoli into the pulmonary blood and diffusion of carbon dioxide in the opposite direction, out of the blood Gases diffuse from areas of high concentration to areas of low concentration Partial pressure of the gas is directly proportional to the concentration of the gas The partial pressure of oxygen is generally greater in the gas phase in the alveoli than in the dissolved state in the pulmonary blood = net diffusion of oxygen into the blood Normal alveolar PO2 is 104 mmHg The partial pressure of carbon dioxide is generally greater in the dissolved state in the pulmonary blood than in the gas phase in the alveoli = net diffusion of carbon dioxide out of the blood Normal alveolar PCO2 is 40 mmHg Carbon dioxide diffuses about 20 times as rapidly as oxygen because it is much more soluble in water Alveolar walls are extremely thin, and between the alveoli is an almost solid network of interconnecting capillaries Flow of blood can be described as a sheet of flowing blood Alveolar gases are in very close proximity to the blood of the pulmonary capillaries Respiratory membrane is very thin (averages 0.6 micrometers), and total surface area of respiratory membrane is 70 square meters Total quantity of blood in the capillaries of the lungs at any given instant is 60-140 mL Looking at these two factors = easy to understand how fast oxygen and carbon dioxide can be exchanged Must consider: some areas of the lungs are well ventilated but have almost no blood flow, whereas other areas may have excellent blood flow but little or no ventilation Normal VA/Q ratio is 0.8 Mismatch occurs to some degree in a healthy lung, but especially in lung diseases This mismatch of ventilation and perfusion seriously impairs gas exchange through the respiratory membrane When ventilation/perfusion ratio is below normal = inadequate ventilation to provide the oxygen needed to fully oxygenate the blood flowing through the alveolar capillaries A certain fraction of the venous blood passing through the pulmonary capillaries does not become oxygenated = shunted blood Total amount of shunted blood per minutes = physiologic shunt The greater the physiologic shunt, the greater the amount of blood that fails to be oxygenated as it passes through the lungs When ventilation/perfusion ratio is greater than normal = far more available oxygen in the alveoli than can be transported away from the alveoli by the flowing blood Ventilation of these alveoli is said to be wasted Ventilation of anatomical dead space areas is also wasted The sum of these two types of wasted ventilation is called the physiologic dead space When the physiologic dead space is great, much of the work of ventilation is wasted effort because so much of the ventilating air never reaches the blood About 97% of oxygen transported from the lungs to the tissues is carried in chemical combination with hemoglobin in the red blood cells Remaining 3% is transported in the dissolved state in the water of the plasma and blood cells Oxygen molecule combines loosely and reversibly with the heme portion of hemoglobin When PO2 is high, as in the pulmonary capillaries, oxygen binds with the hemoglobin When PO2 is low, as in the tissue capillaries, oxygen is released from the hemoglobin Bohr effect: increase in carbon dioxide in the blood causes oxygen to be displaced from hemoglobin Increases in blood carbon dioxide and hydrogen ions has a significant effect by enhancing the release of oxygen from the blood in the tissues As the blood passes through the tissues, carbon dioxide diffuses from the tissue cells into the blood This increases the blood PCO2, which in turn raises the blood carbonic acid and hydrogen ion concentration These effects shift the oxygen-hemoglobin dissociation curve to the right, forcing oxygen away from the hemoglobin and therefore delivering increased amounts of oxygen to the tissues Carbon dioxide diffuses out of the tissue cells in the dissolved molecular carbon dioxide form A small portion (7%) of the carbon dioxide is transported in the dissolved state to the lungs About 70% of the dissolved carbon dioxide in the blood reacts immediately with water to form carbonic acid (catalyzed by enzyme carbonic anhydrase, found in red blood cells) Carbonic acid formed in the red blood cells dissociates into hydrogen and bicarbonate ions Most of the hydrogen ions then combine with the hemoglobin in the red blood cells (hemoglobin is a powerful acid-base buffer) Many of the bicarbonate ions diffuse from the red blood cells into the plasma, while chloride ions diffuse into the red blood cells to take their place (bicarbonate-chloride carrier protein in the red blood cell membrane) Reversible reaction More than 20% of the dissolved carbon dioxide reacts directly with amine radicals of the hemoglobin molecule to form the compound carbaminohemoglobin Reversible reaction with a loose bond, so that the carbon dioxide is easily released into the alveoli, where the PCO2 is lower than in the pulmonary capillaries Haldane Effect: binding of oxygen with hemoglobin tends to displace carbon dioxide from the blood Combination of oxygen with hemoglobin in the lungs causes the hemoglobin to become a stronger acid The more highly acidic hemoglobin has less tendency to combine with carbon dioxide to form carbaminohemoglobin, thus displacing much of the carbon dioxide that is present in the carbamino form in the blood The increased acidity of the hemoglobin also causes it to release an excess of hydrogen ions, and these bind with bicarbonate ions to form carbonic acid; this then dissociates into water and carbon dioxides, and the carbon diode is released from the blood into the alveoli

PPENDERS for Abdominal Aortic Aneurysm Pathophysiology Abnormal dilation of abdominal aorta resulting in diameter > 30 mm (or 1.5 times expected normal diameter) Aortic wall loses elasticity through loss of elastic fibers and degradation of collagen Proteolytic process enzymes that degrade (MMP) increase while inhibitors decrease True aneurysm = dilation involves all 3 layers of artery wall (intima, media, and adventitia) False aneurysm = communication of blood between layers of artery wall and arterial lumen, so not all 3 layers are dilated Most common location is infrarenal Shape can be fusiform (widening all around diameter of aorta) or saccular (bulging on one side of the aorta) Types Atherosclerotic or nonspecific aneurysm Most common type Strongly associated with progressive atherosclerosis and atherosclerotic risk factors Congenital aneurysm AAA may be more frequent in individuals with genetic predisposition to connective tissue disorders (e.g., Marfan syndrome) Inflammatory aneurysm Variant of atherosclerotic aneurysm Wall of aneurysm thickened with dense, shiny, white fibrosis and adherence to surrounding tissues Tends to be more symptomatic than noninflammatory aneurysms Infectious (mycotic) aneurysm Bacterial inflammation of arterial wall, sometimes of existing aneurysm Most commonly Staphylococcus or Salmonella in primary aortic infections AAA rupture is an immediate surgical emergency Should be considered as a possibility until ruled out in any patient with hypotension, abdominal pain, and palpable mass Other concerns of an AAA are compression of neighbouring structures and increased clotting Prognosis AAA > 5-5.5 cm has high rupture rate if untreated 65% of those who have a rupture will die Risk factors for rupture include current smoking, increased blood pressure, larger AAA diameter, and female sex Poor preoperative lung and renal function are associated with postoperative mortality Epidemiology Most affected: Men > 65 years old Caucasians and Native Americans have higher risk of AAA than Blacks, Hispanics, and Asians Natural History Some aneurysms are dormant for months to years then suddenly grow Large aneurysms usually grow more rapidly Growth rate of small AAAs may increase with increasing baseline diameter Growth rate higher in smokers Aneurysm size is a strong predictor of risk of rupture 6-6.9 cm = 10-20% Differential Diagnosis AAA associated with increased incidence of coronary artery disease, peripheral arterial disease, hernia (in surgical patients), COPD, polycystic kidney disease, and obstructive sleep apnea Often asymptomatic and usually discovered incidentally by physical exam, abdominal ultrasound, or other imaging AAA rupture may mimic Nephrolithiasis (kidney stones) Diverticulitis (formation of pouches within the bowel wall) Gastrointestinal hemorrhage (blood loss from the GI tract) Etiology In most cases associated with atherosclerosis Build-up of plaque within arteries from excess fat, cholesterol, calcium, etc. Over time causes hardening and narrowing of arteries Risk Factors Smoking Clinical vascular disease/cardiovascular disease Male Older age Hypertension Hyperlipidemia Atherosclerotic disease Family history of AAA Previous aortic aneurysm Excess weight Signs and Symptoms Usually asymptomatic until rupture If present, symptoms can include Vague, chronic abdominal pain Low back pain Mid-abdominal or flank pain which may radiate to back, groin, or scrotum Potential palpable pulsatile nontender mass But, clinical exam not reliable to rule out AAA, especially in obese patients Rupture can present with acute abdominal or flank pain with fainting or shock

Surgery for an AAA Surgery recommended for AAA > 5.5 cm, or symptomatic AAA of any diameter Indications for AAA repair: Ruptured AAA Symptomatic AAA Rapidly expanding aneurysm (>1 cm/year) Asymptomatic aneurysms > 5.5 cm Thromboembolism Complicated aneurysms Relative contraindications to AAA repair Advanced age Class III or IV angina Heart failure Pre-existing renal impairment COPD Open surgery or endovascular aneurysm repair (EVAR) EVAR entry through femoral artery EVAR has lower perioperative mortality than open repair, but similar all-cause mortality at 2-4 years and increased risk for additional surgical intervention Open surgery is associated with a longer hospital stay ACCF/AHA recommendations: Open or EVAR of infrarenal AAAs indicated in patients who are good surgical candidates Open aneurysm repair reasonable to perform in patients who are good surgical candidates but who cannot comply with periodic long-term surveillance required after endovascular repair

General Anesthesia Anesthesia = condition in which sensations, principally pain and anxiety, are blocked To allow patients to undergo invasive procedures, such as major surgery, without pain or distress Allows health care professionals to perform an indicated procedure without the additional impediments associated with an excited, combative, and mobile patient Patients who undergo general anesthesia cannot control or protect their airway, may require assisted ventilation, and often have depressed cardiovascular function Cause peripheral vasodilation and inhibit sympathetic autonomic regulation Patient can no longer autoregulate the circulation and tissue perfusion Also results in redistribution of blood flow to the skin and loss of thermoregulation with resultant heat loss, a decrease in core temperature, and hypothermia Aggressive monitoring and hemodynamic control are essential to achieve the best outcomes Data does indicate that general anesthesia is associated with relative depression of diaphragmatic function after aortic surgery (potential cause = overactive inhibitory reflexes of phrenic activity arising from the abdominal wall and/or viscera) Anesthesia causes nausea, vomiting Those under general anesthesia will have atelectasis of the lower lobes 90% of the time post-op Anesthesia also increases the VA/Q mismatch as well as depresses the sigh reflex (which leads to atelectasis)

Smoking Smoking is the leading cause of preventable premature morbidity and mortality in the United States and many other countries A lifelong smoker has a one in three chance of dying prematurely from a complication of smoking Current smokers have a life expectancy shortened by 10 years Smoking is the major cause of lung cancer and COPD in developed countries Smoking is also a substantial causative factor in respiratory infections, including pneumococcal pneumonia, influenza, and tuberculosis Tobacco use is a major cause of death from cancer, cardiovascular disease, and pulmonary disease Cardiovascular disease: Sudden death Acute myocardial infarction Unstable angina Stroke Peripheral arterial occlusive disease Aortic aneurysm Pulmonary disease Lung cancer Chronic bronchitis Emphysema Asthma Smoking is also a major risk factor for osteoporosis, reproductive disorders, and fire-related and trauma-related injuries COPD More than 80% of COPD is attributable to cigarette smoking Causes loss of cilia, mucous gland hyperplasia, increased number of goblet cells in the central airways, inflammation, goblet cell metaplasia, squamous metaplasic, mucus plugging of small airways, destruction of alveoli, and a reduced number of small arteries Also consider the carbon monoxide in cigarette smoke reduced capacity of hemoglobin to carry oxygen and impairs oxygen release at the tissues Cardiovascular disease Cigarette smoking accounts for about 20% of CV deaths in the United States Smoking accelerates atherosclerosis and promotes acute ischemic events Mechanics are believe to include Hemodynamic stress (nicotine increases heart rate and transiently increases blood pressure) Endothelial injury and dysfunction (nitric oxide release and resultant vasodilation are impaired) Developed of an atherogenic lipid profile Enhanced coagulability Arrhythmogenesis Relative hypoxemia because of the effects of carbon monoxide Overall increase in inflammatory agents

Inactivity Inactivity can cause increased work of breathing Decreased chest wall compliance Weaker respiratory muscles

PT Pre-Op Assessment Become aware of other comorbidities/diagnoses as well as past medical history Learn about current symptoms (get baseline to compare) Become aware of medications Risk factors for heart disease: hypertension, smoking, elevated serum cholesterol or dietary cholesterol intake, family history of heart disease, stress, sedentary lifestyle, older age, male gender, obesity, diabetes Relevant social history: long-term smoking Baselines for clinical laboratory data, radiologic studies, oxygen therapy, PFT, vital signs, etc. Gain consent for post-op assessment/intervention Learn about home environment and family situation Able to run through exercises ahead of time If able to do a pre-op intervention Smoking cessation Increase strength of respiratory/coughing msucles

PT Post-Op Because of the invasiveness of this procedure throughout the abdomen, patients undergoing this procedure are at high risk for pulmonary complications Incisional pain and the use of the abdominal musculature in coughing discourage the patients from full inspirations as well as effective forceful coughing or huffing Appropriate bronchial hygiene techniques are essential for decreasing the incidence of pulmonary complications, especially in patients with chronic pulmonary disease Assess for pulmonary symptoms: Shortness of breath Dyspnea on exertion Audible wheezing Cough Increased work of breathing Sputum production Look for rapid breathing rate, shallow depth, associated with accessory muscle activity Inspection General appearance LOC Body type Posture/positioning Skin tone Need for external support equipment Facial characteristics Distress = nasal flaring, sweating, paleness, enlarged pupils Evaluation of the neck Accessory muscle activity Jugular venous distension Evaluation of the chest Breathing patterns Breathing rates Inspiratory to expiratory ratios Symmetry of chest wall motion Phonation Cough Cough production Appearance of extremities Palpation Tracheal position Fremitus Muscle activity of chest wall and diaphragm Chest wall pain or discomfort Pulses Percussion Ausculation Activity evaluation Assess response to situations: rest (supine), sitting, standing, ADL, ambulation of some distance Heart rate Heart rhythm Blood pressure Oxygen saturation

Hb and WBC Normal range of hemoglobin is 12-16 g/100 mL for females and 13-17 g/100 mL for males Many facilities use a cut-off value for Hb of 60 mmHg (72 mmHg) He does have SpO2 of 88% or less (80%) with exertion on room air We would have to assess whether his exercise tolerance improves with O2 If yes, he would qualify for Hypoxemia During Exertion Funding Respirologist/internist with respiratory medicine expertise must agree to sign HOPA Independent facility is responsible for HOP requalification testing at 90 days and 12 months after initial HOP application

Analysis Statement for Ben71-year-old male presenting with acute exacerbation of COPD, c/o dyspnea/orthopnea. On 2L/min O2 delivered by nasal cannulas. Breathing patterns altered (increased accessory muscle use and decreased lateral costal expansion). Reduced FEV1/FVC% consistent with obstructive lung disease. Reduced PO2 consistent with mild hypoxemia. Minimal assistance required with ambulation and transfers from bed to chair.

Pack-Year A way to measure the amount a person has smoked over a long period of time. It is calculated by multiplying the number of packs of cigarettes smoked per day by the number of years the person has smoked. For example, 1 pack year is equal to smoking 1 pack per day for 1 year, or 2 packs per day for half a year, and so on. Odds ratio for COPD with a 40 or greater pack year history is 4.58

MMRC Dyspnea Scale Purpose is to assess the level of physical activity necessary to precipitate breathlessness (NOT level of actual dyspnea) Self-administered scale consisting of five descriptive statements regarding levels of physical activity that precipitate shortness of breath The patient is asked to select the grade (0-4) that best describes their shortness of breath (0 = least severe, 4 = most severe) Has been validated in individuals with COPD MMRC score of 0 in healthy individuals is to be expected Bens MMRC score is 3

6MWT- COPD Normative data from Hill (2011) sets Bens predicted distance at 586 m Ben only walked 175 m MCID of 30 m (ATS/ERS 2014) Data from Solway et al. (2002) indicates that Ben may need a gait aid (subjects who walked 5-6 weeks Prognosis Mortality 4.6% in-hospital and 4.5% at 6 months in patients admitted with STEMI 11% of in-hospital patients developed heart failure or pulmonary edema Epidemiology Most affected are adults with coronary artery disease 70% of patients with STEMI are men Incidence of myocardial infarction appears to be decreasing in United States 70% STEMIs, 30% NSTEMIs Theres a heart attack every 7 minutes in Canada Differential Diagnosis Thoracic aortic aneurysm and dissection Unstable angina Pulmonary embolism Esophageal rupture Tension pneumothorax Perforating ulcer Myocarditis Rib fracture Anxiety disorder Panic attack Diagnosis Chest discomfort (intense pressure) ECG changes Elevated biomarkers Atypical presentation common in older adults, women, and patients with diabetes Etiology/Natural History Atherosclerotic plaque due to CAD may rupture resulting in thrombus occluding the coronary artery (most common cause) Less commonly, plaque erosion characterized by disrupted or absent endothelium on top of plaque with abundant smooth muscle cells and proteoglycans may cause coronary obstructions via thrombi development on dysfunctional intima Nonatherosclerotic causes include Emboli Mechanical obstruction (e.g., chest trauma, dissection of coronary arteries) Increased vasomotor tone (e.g., variant angina pectoris, nitroglycerin withdrawal) Arteritis Aortic stenosis Cocaine abuse Coronary vasospasm Risk Factors Major risk factor is coronary artery disease CAD major risk factors Tobacco exposure Includes cigarette or cigar smoking, or spit or chewing tobacco Passive (second-hand) cigarette smoke also increases risk Dyslipidemia Elevated triglyceride levels; elevated total LDL or non-HDL cholesterol levels; low HDL cholesterol levels Hypertension Diabetes Hyperglycemia in people without diabetes also associated with increased risk Obesity Metabolic syndrome (hypertension, obesity, dyslipidemia, and insulin resistance) Family history of cardiovascular disease in first-degree relative Elevated high-sensitivity C-reactive protein (CRP) levels Atherosclerosis in non-coronary arteries Low ankle-brachial pressure index Carotid bruits Transient ischemia attack or ischemic stroke Potential triggering events Anger Unemployment status and cumulative job loss Exposure to traffic Acute infection (e.g., acute respiratory infection) Episodic physical and/or sexual activity Death of loved one Shift to and from daylight saving time Viewing World Cup soccer (in Germany) Atrial fibrillation Medication/drug use Cocaine NSAIDs Inhaled beta-2 agonists HIV positive Signs and Symptoms Chest pain or pressure frequently in substernal region, which may radiate to neck, jaw, left shoulder, or left arm Dyspnea Nausea and vomiting Diaphoresis (sweating) Fatigue Palpitations Denial Myocardial infarction is a major risk factor for heart failure He should be aware of most common symptoms Dyspnea Fatigue Edema Likely risk factors that he can modify are hypertension, obesity, metabolic syndrome, diet (increase sodium intake results in increased risk for heart failure), smoking

Acute Coronary Syndrome Spectrum of acute myocardial ischemia and/or necrosis usually secondary to reduction in coronary blood flow, including Unstable angina Differentiated from NSTEMI by absence of cardiac biomarkers indicating ischemic myocardial necrosis Non-ST-elevation myocardial infarction Suggested by absence of persistent ST-segment elevation Elevated cardiac biomarkers ST-elevation myocardial infarction

Creatine Kinase Creatine phosphokinase is a marker that is diagnostic of cardiac injury CPK has been used as a cardiac marker for more than 35 years; however, it has been shown to be elevated after cardiac surgery and cardiopulmonary resuscitation (especially if the person was defibrillated), and has been shown to be abnormally elevated in patients undergoing thrombolysis with streptokinase or tissue plasminogen activator False-elevated CPK levels in patients without MI was evidenced in 43.3% of elective hip surgery patients CPK-MB (the isoenzyme which is most conclusive for myocardial injury) > 3% is considered abnormal Normal values for CPK-MB are 0-3% Normal values for CPK are 55-71 Onset of rise is within 3-4 hours, time of peak rise is about 33 hours, and return to normal is within 3 days

Troponin I Troponin is a marker that is diagnostic of cardiac injury Now considered the gold standard Elevated levels of troponin occur earlier and may last for up to 5-7 days in plasma Normal range = 0-0.1 ng/mL (not detectable by normal blood test) Levels > 0.3 ng/L indicate potential risk of MI Onset of rise is within 4-6 hours, time of peak rise is within 12-24 hours, and return to normal is within 4-7 days Three tests are usually done acutely

PTT Partial Thromboplastin Time Looks at how long it takes for blood to clot In general, clotting should occur between 28-38 seconds If a person is taking blood thinners (such as Juusi) clotting takes up to two-and-a-half times longer (1.5-2.5 times longer when therapeutic)

INR International Normalized Ratio, developed to standardize prothrombin time values, so that test results from different thromboplastins and coagulation analyzers become equivalent Post-MI patients have a target INR of 3 (2.5-3.5) Normal values are 0.9 to 1.2 (in the general population) INR values > 4.5 increase the risk of major haemorrhage INR < 2 increases the risk of thromboembolism

Heparin Heparin is an anticoagulant that acts as a thrombin inhibitor Thereby prevents the influence of thrombin on fibrinogen It is used prophylactically to prevent blood clot formation May also be used when a thrombus is already formed to prevent emboli Prevention of an impending acute myocardial infarction includes the emergency use of anticoagulants and antiplatelet agents as part of acute coronary syndrome management

Nitroglycerin One of the oldest anti-ischemic medications Nitrates are converted in the vessels to nitric oxide, which increases the action of the secondary messenger cGMP This seems to stimulate a kinase enzyme that decreases the sensitivity of the contractile proteins to calcium and relaxes the blood vessels This group of drugs is unusually selective in that it almost exclusively acts on smooth muscle cells, in particular on vascular smooth muscle cells As a venodilator, nitrates decrease venous return (preload) As an arteriodilator, nitrates decrease afterload As a relaxant for coronary artery smooth muscle, nitrates possibly increase coronary artery blood supply These factures decrease myocardial oxygen demand Can be taken in different forms (sublingual, spray, percutaneous ointment, oral, intravenous, transdermal patch) Side effects include headache, hypotension and dizziness, reflex tachycardia, flushing of the skin, nausea and vomiting Contraindications include pregnant women, breast feeding, and consuming alcohol while on nitroglycerin Effect of nitroglycerin may be diminished by heparin

Angiogram Invasive coronary angiography remains the standard for identifying coronary artery narrowing related to coronary artery disease Angiography is performed under local anesthesia with small-diameter catheters introduced through a transarterial sheath In the majority of cases, either the femoral or the radial route is used Through the catheters, iodinated contrast media is injected selectively into the left and right coronary arteries A few angiographic projections are used to enable visualization of the whole coronary tree Used to establish or rule out the presence of coronary stenoses, define therapeutic options, and determine prognosis In patients with STEMI, guidelines recommend coronary angiography in the acute phase No absolute contraindications, but relative contraindications include febrile untreated infection, severe anemia, severe electrolyte imbalance, active bleeding, acute renal failure, and ongoing stroke

Cardiac Rehab Cardiac rehab is a program of exercise, education, and counselling designed to help you recover from a heart attack or other heart conditions Help you to regain your strength, prevent your condition from getting worse, and reduce your risk of having heart problems in the future Open to those who have had a heart attack, heart surgery, or have heart disease Cardiac rehab team may include physicians, exercise physiologists, nurses, occupational therapists, physical educators, dieticians, psychiatrists, physiotherapists, and/or social workers Generally include a medical assessment, physical activity, lifestyle education, and psychosocial support Phases of cardiac rehab Phase I: Acute phase or monitoring phase Beings when patient medically stable following an MI, CABG, PTCA, valve repair, heart transplantation, or CHF Phase II: Subacute phase of rehab or conditioning phase Begins as early as 24 hours after discharge and lasts up to 6 weeks. Frequency of visits depends on the patients clinical needs. Initiate secondary prevention of disease Phase III: Training or intensive rehabilitation Beings at end of Phase III and extends indefinitely. Patients exercise in larger groups and continue to progress in their exercise program. Resistance training often begins in this phase Phase IV: Ongoing conditioning (maintenance) phase or prevention phase Candidates are individuals who are at high risk for infarction because of their risk factor profile, as well as those who want to continue to be followed by supervision of trained personnel Physician referral may be needed Progressive activity for 5-day length of stay (Phase I) Day 1, CCU (MET level 1-2) Bedrest until stable, use of bedside commode, out of bed to chair if stable Day 2, step-down unit (MET level 2-3) Full assessment Sitting warm-ups, walking in room, self-care activities Education: explanation of event, treatment plan Day 3-5 Out of bed as tolerated if stable, walk 5-10 minutes in hall (supervised as needed) (MET level2-3) Shower with seat, walk 5-10 minutes 2-3 times/day, up/down one half flight of stairs (MET level 3-4) Education: Assess readiness to learn Teach signs/symptoms Nitroglycerin use Emergency response to symptoms Safety factors Dos and donts for home activity Introduce Phase II

ECG Interpretation Ischemia is classically demonstrated on the 12-lead ECG with T-wave inversion or ST-segment changes The T wave may vary from a flat configuration to a depressed inverted wave However, T-wave becoming sharp and peaked is the most acute sign The location of the ST segment is another indication of ischemia or injury Elevation of the ST segment above the baseline indicates acute injury In the presence of an acute infarction, the ST segment elevates and then later returns to the level of baseline (within 24-48 hours) Indicates early repolarization of the ventricles During myocardial injury, alterations in the initial portion of the QRS complex occur The presence of a significant Q wave is also diagnostic for infarction Typically due to previous MI absence of electrical activity Occurs hours after MI

Cardiac Output Volume of blood pumped from the right or left ventricle per minute CO = SV x HR Stroke volume is determined by the preload, myocardial distensibility, myocardial contractility, and afterload

Preload The end-diastolic muscle fibre length of the ventricles before systolic ejection On the left side it reflects the left ventricular end-diastolic volume Dependent on venous return, blood volume, and left atrial contraction An increase in ventricular volume stretches the myocardial fibres and increases the force of myocardial contraction (Starling effect) and stroke volume Starling effect is limited by the physiologic limits of distension of the myocardium Excessive stretching (fluid overload) leads to suboptimal overlap of the actin and myosin filaments, impairing rather than enhancing contractility

Afterload The resistance to the ejection of blood during ventricular systole Afterload of the left ventricle is determined primarily by four factors Distensilbity of the aorta Vascular resistance Patency of the aortic valve Viscosity of the blood

Valsalva The normal physiological response consists of four phases. 1. Initial pressure rise On application of expiratory force, pressure rises inside the chest forcing blood out of the pulmonary circulationinto theleft atrium. This causes a mild rise instroke volume.2. Reduced venous return and compensation Return of systemic blood to the heart is impeded by the pressure inside the chest. The output of the heart is reduced and stroke volume falls. This occurs from 5 to about 14 seconds in the illustration. The fall in stroke volume reflexively causes blood vessels to constrict with some rise in pressure (15 to 20 seconds). This compensation can be quite marked with pressure returning to near or even above normal, but thecardiac outputand blood flow to the body remains low. During this time, the pulse rate increases (compensatory tachycardia).3. Pressure release The pressure on the chest is released, allowing the pulmonary vessels and theaortato re-expand causing a further initial slight fall in stroke volume (20 to 23 seconds) due to decreasedleft atrialreturn and increased aortic volume, respectively. Venous blood can once more enter the chest and the heart, cardiac output begins to increase.4. Return of cardiac output Blood return to the heart is enhanced by the effect of entry of blood, which had been dammed back, causing a rapid increase in cardiac output (24 seconds on). The stroke volume usually rises above normal before returning to a normal level. With return of blood pressure, the pulse rate returns towards normal.

Activity Restrictions Prior to Starting Cardiac Rehab Activities during weeks 1-3 at home Sit outside Do light housework Engage in hobbies or activities you can do sitting down (reading, crafts) Climb one flight of stairs slowly Walk around your house or yard (or as instructed by your doctor or cardiac rehab team) Ride in a car as a passenger (short trips of about half an hour) Lift up to 5 lbs. Make a few social visits Weeks 3-6 Continue walking as instructed by your doctor or cardiac rehab team Climb two flights of stairs Resume sexual relations once you can climb two flights (but avoid if you have had a large meal or alcohol in the past two hours or are feeling tired) Make more social visits Garden, grocery shop, or housework (lightly) Lift up to 10 lbs. Ride in a car for up to one hour, or, if approved by your doctor, driving Dance (slowly), fish, sail a small boat, cycle at medium speed, play table tennis or 5-pin bowling Weeks 6+ Resume all normal levels of activity for you such as walking at a brisk pace, swimming, cycling, skating (go at your own pace and rest when necessary) Lift or carry up to 20 lb Return to work, with your doctors approval (usually 8-16 weeks) Golf Start with 9 holes and play during the cooler parts of the day in the summer months Use a cart to carry your clubs Be careful of Very hot or very cold water Lifting heavy weights Pushing or pulling actions that cause you to hold your breath Working for long periods with you arms above your head Repetitive arm work such as raking, digging, grass cutting or vacuuming Snow shovelling Activity after meal Driving (for at least 4-6 weeks) Sexual relations (for usually around 2-3 weeks) Air travel

Criteria for Discharge from PT Services Able to perform ADLs Able to ambulate independently Able to climb stairs independently Independent with transfer Safety all of this with no symptoms

Cardiorespiratory Examination and AssessmentAssessing Respiratory Function IPPA system Inspection (observation) Lung location reflected onto chest wall (surface anatomy) Chest expansion/Thoracic excursion Position Posture Body structure Height, shape of chest , adipose tissue Scars Skin color Cyanosis, pallor Digital clubbing Breathing pattern At tidal volume or at maximal inspiratory effort; apical/diaphragmatic Shortness of breath- dyspnea, orthopnea (SOB in supine) Effort of breathing Nasal flaring, accessory muscle use Jugular vein distension (if the vein is distended above the level of the clavicle) Peripheral vascular changes Palpation Temperature of skin Symmetry of chest movement Chest excursions/diaphragmatic excursions Trachea (position/movement) Pulses: carotid, brachial, radial, femoral, popliteal, tibialis posterior, dorsalis pedis Peripheral edema Capillary refill (press nail beds) Percussion (Mediate Percussion) When might you not want to percuss? Open wounds Fractures Implanted devices Subcutaneous ports Consolidation = dull Pleural effusion = dull Pneumothorax = hyperresonant Atelectasis = dull Procedure for mediate percussion Seek a quiet place Client sitting or supine Identify any areas to avoid percussing at this time Middle finger on non-dominant hand is placed firmly on the chest wall in intercostal space and parallel to ribs (keep rest of hand off chest) Middle finger of dominant hand strikes the middle or distal phalanx of the other had with quick, sharp motion Feel and listen to all aspects of chest in systematic way Compare left and right, upper and lower Note quality of the sound is it normal, dull, or tympanic (hyperresonant)? May need to have client take a deep breath to listen to the lower lobes Auscultation Basics Quiet environment, warm room, warm stethoscope Proper position If possible, client should be sitting Position yourself so you can monitor your clients face Bare skin Systematic method (R/L, upper/lower) Compare side to side before upper/lower Patient comfort (draping, position, time) Patient safety Watch sitting balance if patient is weak prevent from falling Avoid hyperventilation patient can become dizzy allow patient to rest every few breaths Use diaphragm of stethoscope, press firmly Listen to one complete respiratory cycle at each site Client breaths in and out through their mouth, taking deep breaths as consistently as possible Note the intensity and length of breath sounds Note the presence or absence of adventitious sounds Always clean your stethoscope after each use! Common errors in auscultating lung sounds Listening through the patients gown Allowing the stethoscope tubing to rub against sheets, bed rail, gown Interpreting chest hair sounds as adventitious lung sounds Auscultating only the convenient areas What are we looking for? Is the intensity of breath sounds increased, normal, or decreased? Is the character of breath sounds normal or abnormal? Are there any abnormal or adventitious sounds? Need to document these sounds and specify lobe/segment Normal breath sounds Vesicular Soft Low-pitched Primarily heard during inspiration and minimally heard in the first 1/3 of expiration Flow from inspiration to expiration, no break Heard over most of the lung/thorax areas Bronchial Loud (tubular, hollow) High-pitched Equal inspiratory/expiratory duration Pause between inspiratory and expiratory components Heard normally over the manubrium (trachea) not a standard area for auscultation If present in other lung areas = abnormal (consolidation) Abnormal breath sounds Absent or diminished vesicular breath sounds Shallow breaths, frail/elderly Decrease in lung tissue density Emphysema Fibrosis Pleural effusion Pneumothorax Atelectasis (collapse) absent unless its in the upper lobes Adventitious sounds Crackles Fine (high pitched, very brief) Coarse (low pitched, brief) Mechanism Sudden opening of small, previously closed airways Air bubbling through secretions Causes Pulmonary edema, consolidation, atelectasis, COPD, etc. Wheezes Continuous, high-pitched, musical, expiratory Monophonic (suggestive of one airway obstruction) Polyphonic (if inspiratory static bronchoconstriction tumours, foreign bodies) Mechanism Air flowing through narrowed airways Causes Asthma Acute or chronic bronchitis Other considerations Paroxysmal nocturnal dyspnea (PND) sudden onset of SOB at night in supine Fluid balance sudden weight gain may be related to fluid retention (they measure fluid in and out in the ICU) Intermittent claudication Disabling pain during walking Caused by Systemic complication of artherosclerosis With or without overt ischemic heart disease Intercostal indrawing = skin pulling in between ribs on inspiration (sign of respiratory distress) Assessment/diagnostic tests and procedures Spirometry (FVC, FEV6, FEV1) Oxygen saturation of the blood (SpO2) Walking tests (self-paced walking test) Blood pressure measurement

Pulses Use tips of middle and index fingers (not thumb) Press firmly and gently Assess Rate Strength Regularity Carotid either side of trachea Brachial medial aspect of antecubital fossa Radial anterolateral wrist Femoral between iliac crest and groin Popliteal behind knee Tibialis posterior behind medial malleolus Dorsalis pedis dorsal aspect of foot

Anatomy of the Bronchopulmonary Segments Left Upper Apicoposterior Posterior parallel with T2 Anterior Anterior above 2nd rib AND below 2nd rib Superior lingula Anterior under 4th rib, lateral to nipple Inferior lingula Cannot be ausculatated Lower Superior Posterior parallel with T4/T5 Lateral basal Posterior/lateral just anterior to mid-axillary line parallel with xiphoid process (below 6th rib) Anteromedial basal Cannot be auscultated Posterior basal Posterior parallel with T7/8 Right Upper Apical Posterior parallel with T1/2 Anterior Anterior above 2nd rib AND below 2nd rib Posterior Posterior parallel with T2/T3 and more lateral Middle Lateral Anterior under 4th rib, lateral to nipple Medial Cannot be auscultated Lower Superior Posterior parallel with T4/5 Lateral basal Lateral just anterior to mid-axillary line parallel with xiphoid process (below 6th rib) Medial basal Cannot be auscultated Posterior basal Posterior parallel with T7/8 Anterior basal Anterior lateral under 6th rib

Basic Principles of Chest X-Ray Interpretation Metal or contract material very white Bone/calcium white Soft tissues whitish Fat slightly black Air black A Structured Approach to CXR Interpretation1. Trachea and bronchi2. Heart3. Mediastinum4. Hila5. Lungs6. Pleura7. Chest wall Additional Key Anatomical Structures Clavicles Ribs DiaphragmAtelectasis incomplete expansion or volume loss in lungConsolidation blood, pus, water, and sometimes tumor in airspaces On x-ray, can still see border of diaphragm (cannot in atelectasis)Pleural effusion fluid in pleural space No sharp lines on x-ray Pneumothorax lung collapse. Air between outside surface of lung and inside surface of chest wall

30 Second Sit to Stand Number of times sit to stand completed in 30 seconds Predictive equations available for specific ages

Respiratory Adjuncts and Supplemental Oxygen Respiratory Therapy Adjuncts Therapies used to correct pulmonary problems Aerosol and humidity therapy Bronchodilator therapy Oxygen therapy Bronchial hygiene therapy Lung expansion therapy Airway management NIPPV Mechanical ventilation Lung Volume Recruitment Also referred to as breath stacking Used when patients have difficulty with deep breathing, or have persistent atelectasis Patient is bed-ridden, weak diaphragm Sometimes used in combination with in-exsufflation in patients with neuromuscular diseases Uses a one-way valve to prevent exhalation Subsequent breaths are delivered and stacked onto each other Device is removed and patient exhales In-Exsufflation Used to facilitate secretion removal in patients with ineffective cough/clearance of secretions Objective measurements: Recommended when patients have peak cough flow < 270 L/min Provides positive pressure during inspiration Applies negative pressure during exhalation to facilitate secretion clearance Timing is key: In-2-3, Out-2-3Peak Cough Flow Measures peak flow during a cough maneuver Important monitor in patients with muscle weakness Guidelines: PCF > 270 L/min Oscillating Positive Expiratory Pressure Designed to aid in the loosening and removal of mucus build-up in the lungs Valves cause oscillating pressure in the airways which helps to loosen secretions Patients usually instructed to perform various breathing/coughing exercises with use Has started to replace manual chest physiotherapy Oxygen TherapyNormal Healthy Range for SpO2 Normal range for healthy young adults 96-98% Slight fall with advanced age Mean SpO2 of 96.7% in patients > 70 years of age Effects of Sudden Hypoxia Impaired mental function begins at 84% Loss of consciousness occurs at 80% oxygen Unreliable Total flow depends on the flow meter or oxygen tank Humidity TherapyThe Effect of Dry Gas The medical gas in a hospital has not water content To protect medical equipment When the air we breathe is extremely dry, the mucus layer of the airways may become thick and tenacious Coughing is less productive Cold Humidity Therapy Uses air-entrainment device Provides large nebulized humidity Particles are larger than bacteria and viruses Can transmit infection Equipment needs regular changing Heated Humidity Therapy Devices provide heated pass-over humidity Particles are smaller than bacteria and virus Equipment changed as needed or at planned intervals Different temperature options for optimizing humidification 31 degrees C for non-invasive application (face) 37 degrees C for invasive application (endotracheal)High-Flow Nasal Cannula Designed to deliver high flow oxygen Large cannula fill approximately 50% of the nares Flow rates (depends on device): Adult 35-55 L/minBenefits to HFNC Improved comfort Can meet inspiratory flow demand Deliver up to 100% oxygen accurately Washout of anatomical deadspace Optimized mucocillary clearance Constant flow rate at all oxygen levels Airway Clearance and OxygenationChest Physiotherapy as Airway Clearance: Oxygenation CPT: Postural drainage, percussion, and vibration Evidence regarding benefit in oxygenation and gas exchange is lacking Devices such as a Flutter and Intrapulmonary Percussive Ventilation (IPV) have proven beneficial Physical and Respiratory Therapy Traditionally the link between respiratory and physical therapy practice was surrounding airway clearance techniques Over the years, airway clearance techniques with various devices have outperformed chest physiotherapy in certain areas of patient care Currently the strongest benefit for what the physiotherapist and respiratory therapist provides occurs in the critical care an d rehabilitation settings Evidence of CPT reduce risk of ventilator associated pneumonia Mobilization of ICU patients Strength training with COPD patients Room for improvement: Recognizing patients whom which humidity therapy would be beneficial and discussing the options available

Managing, Monitoring, and Mobilizing the Post-Op PatientThe Nurse-Physiotherapist Relationship Both focused on a common goal: Assisting the patient in their recovery to return to previous or optimal level of functioning Knowledge and expertise is mutually beneficial Should be a mutually respectful relationship Approach to Communication with Nursing Staff Perceived barriers Do your homework Have you formulated a plan based on information gathered?Questions to ask the Nurse How is the patient this morning? How was his/her night? Has their pain been well controlled? Do you think he/she needs anything for pain before we get them up? Is there anything I need to know before I go in to see him/her?After mobilizing... Report back to the RN with pertinent info when you are finished Leaving the patients as you found them is really helpful and considerate High fives all around if they still have all the tubes/lines they started with Pain Management for the Post-Op Patient Understanding Pain Management in the Post-Op Patient Patients report that some of the most painful surgeries are intrathoracic surgeries, gastric surgeries, and abdominal surgeries, with pain lasting from 2 to 8 days Analgesics treat pain by either reducing the capacity of the nerve fibers to sense pain or by reducing pain recognition by higher centres in the brain Opioids- most commonly used analges