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Ot6 Cardac and Pulmonary Dses

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OT 6: CARDIAC AND PULMONARY DISEASES MEMBERS: LABASTIDA, JOY LAVIDES, JULIA LEE, MAISIE MAKILING, RYAN PATI-AN, GAYLE PERENA, KAY POLANCOS, RUCHIN
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Page 1: Ot6 Cardac and Pulmonary Dses

OT 6: CARDIAC AND PULMONARY

DISEASES

MEMBERS:

LABASTIDA, JOY

LAVIDES, JULIA

LEE, MAISIE

MAKILING, RYAN

PATI-AN, GAYLE

PERENA, KAY

POLANCOS, RUCHIN

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CARDIAC AND PULMONARY DISEASES

ANATOMY AND CIRCULATION

The heart and blood vessels work together to maintain a constant flow of blood throughout the body.

The heart, located between the lungs, is pear shaped and about the size of a fist. It functions as a two-sided pump. The right side pumps blood from the body to the lungs; the left side simultaneously pumps blood from the lungs to the body. Each side has two chambers, the upper atrium, and the lower ventricles.

Blood flows to the heart through the venous system. Blood enters the right atrium, which contracts the blood into the right ventricle. Next, the right ventricle contracts and ejects the blood into the lungs, where CO2 is exchanged for O2. The blood then goes to the left atrium. When the left atrium contracts, it send the blood to the right ventricle which then contract and sends the blood in the aorta where it goes to all the parts of the body.

Each ventricle has two valves. These open and close as the heart contracts and relaxes. The input valves are the mitral, between the left atrium and ventricle, and the tricuspid valve between the right atrium and ventricle. The output valves consist of the aortic and pulmonary valves.

Coronary arteries cross over the myocardium to supply it with blood. The arteries are named after their location on the myocardium. The left anterior descending artery is in the left anterior portion and runs a downward direction, it supplies part of the left ventricle. Blockage to this artery will interrupt supply to the left ventricle, and thus lead to serious consequences.

WHAT CAUSES THE HEART TO CONTRACT?

In addition to ordinary muscle tissue the heart also contains nodal and pukinje tissue. These are part of a specialized electrical conduction system that cause the heart to contract and relax. An impulse usually originates in the sinoatrial (SA) node then travels to the atrioventricular (AV) node through the bundle of His then to the purkinje fibers. Nerve impulses travel this pathway 60-100 times per minute, first causing the atria to contract, then the ventricles. Studying these impulses are done with an electrocardiogram (ECG).

The SA node responds to vagal and sympathetic nervous system input. This way, the heart rate increases with anxiety and exercise and decreases

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through relaxation techniques. Electrical impulses causing the heart to contract can be generated from anywhere along the system. This is desirable when the conduction system has been damaged, but is undesirable when life-threatening conduction irregularities develop.

CARDIAC CYCLE

The cardiac cycle occurs in two phases input (diastole), and output (systole).

During the input phase, blood flows through the atria and into the ventricles. The atria contracts and pushes more blood into the ventricles. Once pressure is even in the atria and ventricles, the input valves (bicuspid, and tricuspid) close. The ventricles then contract which results in increases ventricular pressure. When the pressure inside the ventricles exceed that of the blood vessels, the output valves (aortic and pulmonary) open and diastolic BP is attained.

Systolic BP is attained when pressure in the emptying ventricles falls below that of the blood vessels, which causes the output valves to close.

ISCHEMIC HEART DISEASE

Ischemic heart disease or ischemia occurs when a part of the heart is temporarily deprived of sufficient oxygen to meet its demand. The most common cause of cardiac ischemia is coronary artery disease (CAD). CAD is the most common type of heart disease and the leading cause of death in the United States in both men and women. CAD usually develops over time a period of many years without causing symptoms. The internal wall of an artery can become injured. Once the wall is damaged it becomes irregular in shape and more prone to collect plaque (fatty deposits such as cholesterol). Platelets also gather along the arterial wall and clog the artery, thereby creating a lesion in the same manner in which rust can clog a pipe. The artery gradually narrows and thus allows a smaller volume of blood to pass through it. This disease process is called atherosclerosis.

If a coronary artery is partially or completely blocked, the part of the heart supplied by that artery may not receive sufficient oxygen to meet its needs. Persons with partial blockage of a coronary artery may be free of symptoms at rest but have angina, a type of chest pain with eating, exercise, exertion or exposure to cold. Angina varies from individual to individual and has been described as squeezing, tightness, fullness, pressure, or a sharp pain in the

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chest. The pain may also radiate to other parts of the body, usually he arm, back, neck or jaw. Angina has also been confused with indigestion. Rest or medication or both will frequently relieve angina. Angina is a warning sign that should not be ignored. It is a sign that CAD is present- that the individual may be a candidate for a heart attack.

Chest pain that is not relieved by rest or nitroglycerin indicates a myocardial infarction (MI), or heart attack. A patient who has this type of pain should seek emergency medical help immediately. Individuals who attribute their symptoms to anxiety and stress are more likely to delay emergency care. MI is significant because part of the heart muscle dies as a result of lack of oxygen. If a substantial section of the heart is damaged, it will stop pumping (cardiac arrest).

Restrictions in activity are prescribed for the first 6 weeks after a heart attack because newly damaged heart muscle, like any injured body tissue is easily reinjured. During a heart attack, metabolic waste products accumulate in the damaged myocardium and make it irritable and prone to electrical irregularities such as premature ventricular contractions. A delicate balance of rest and activity must be maintained to allow the damage area of myocardium to heal while also maintaining the strength of the healthy part of the heart. OT is frequently recommended to guide the patient toward a safe level of activity or participation in occupation, during this acute period of recovery.

At approximately 6 weeks after an MI, scar tissue forms and the risk of extending the MI decrease. The scarred part of the heart muscle is not elastic and does not contract with each heartbeat. Therefore the heart does not pump as well. A graded exercise program will help strengthen the healthy part of the myocardium and improve cardiac output.

CAD can also lead to congestive heart failure (CHF). Similarly, infections can lead to CHF. This disease process develops over time with the heart becoming progressively weaker. CHF occurs when the heart is unable to pump effectively enough to meet the demand and fluid backs up into the lungs or the body. The fluid buildup in the lungs causes shortness of breath. Fluid overload is serious because it puts a greater workload on the heart as the heart strains while attempting to clear the excess fluid, which may result in further congestion. Heart size if often enlarged in persons with CHF to promote fluid loss through the urinary system. Low-sodium diets and fluid restriction reduce the overall amount of fluid in the body, CHF cannot be cure but with diet, medications and rest, people with this condition can live longer and participate more fully in life.

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Once an acute exacerbation of CHF is controlled, gradual resumption of activity will promote improved function. If activity is resumed to quickly, another acute episode may follow. Patients who have difficulty resuming their former level of activity may self limit their recovery. OT can guide clients with acute CHF toward an optimal level of function via graded self-care tasks.

VALVULAR DISEASE

The heart valves, which are responsible for controlling the direction and flow of blood through the heart, may become damaged by disease or infection. Two complications result from valvular disease: volume overload and pressure overload. A fibrous mitral valve will fail to close properly, and blood will be regurgitated back to the atria when the left ventricle contracts. Volume overload results when fluid accumulates in the lungs, thereby causing shortness of breath. Volume overload increases the potential for atrial fibrillation, which results in irregular and ineffective contraction in both atria. Blood flow through the heart slows, and blood clots (emboli) may develop in the ventricles. Many cerberovascular accidents are caused when emboli ejected from the left ventricle enter the circulatory system of the brain.

If the aortic valve fails to close properly (aortic insufficiency), CHF or ischemia may result. Another disorder of the aortic valve is aortic stenosis (narrowing), which results in pressure overload. The left ventricle, which must work harder to open the sticky valve, becomes enlarged and cardiac output decreases. Ventricular arrhythmia (irregular rhythm of heartbeat), cerebral insufficiency, confusion, syncope (fainting) and even sudden death may result from aortic stenosis. Surgery to repair or replace the damaged valves is frequently recommended.

Cardiac Risk Factors

Many scientific studies have been conducted to determine the causes of heart disease. The most famous of these, the Framingham study, helped identify many factors that put an individual at risk for atherosclerosis. Risk factors are divided into three major categories: those that cannot be changed (heredity, male gender, and age), those that can be changed (high blood pressure, cigarette smoking, cholesterol levels, and inactive lifestyle) and contributing factors (diabetes, stress, obesity). Other factors that contribute to CAD include sleep apnea, high levels of triglycerides and high level of C-reactive protein. The more risk factors that an individual has, the greater the individual’s risk for CAD. All team members- the physician, nurse, physical

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therapist, case manager, social worker, nutrionist, and occupational therapist- should support the patient’s attempts to reduce risk factors.

Medical Management

A heart attack is a medical emergency and treatment with aspirin and oxygen is usually indicated before diagnosis. Nitroglycerin and other measures to control chest pain are included in these early measures. After emergency treatment, heart attack survivors are typically managed in a coronary care unit where they are closely observed for complications. Approximately 90% of persons who have suffered an MI will have arrhythmia. Heart failure, the development of blood clots (thrombosis and embolism), aneurysms, rupture of part of the heart muscle, inflammation of the sac around the heart (pericarditis), and even death are potential outcomes of MI. Close medical management is imperative.

Generally, patients are managed for 2 to 3 days after MI in an intensive care unit. Once their condition is stabilized, they graduate to a monitored hospital bed. Patients typically stay 4 to 6 days in the hospital after acute MI. Vital signs are monitored closely while activity is gradually increased. OT personnel may be called on to monitor the patient’s response to an activity and educate the patient about the disease process, risk factors and lifestyle modifications.

Various surgical procedures can correct the circulatory problems associated with CAD. Balloon angioplasty, also called percutaneous transluminal coronary angioplasty (PTCA), and coronary artery bypass grafting (CABG) are most common. During PTCA, a wire meth tube, called a stent may be implanted into the coronary artery to keep the artery open.

In PTCA, a catheter is inserted into the femoral artery and guided through the circulatory system into the coronary arteries. Radioactive dye is injected into the arteries, and the site of lesion is pinpointed. A balloon is then inflated at the site of the lesion to push the plaque against the arterial wall. When the balloon is deflated and the catheter removed, improved circulation to the myocardium usually results. Ensuring that the patient rests in bed for 8 hours after PTCA helps prevents hemorrhage from the femoral artery.

If a lesion is too diffuse or if an artery reoccludes after PTCA, CABG may be performed. The diseased section of the coronary arteries is bypassed with healthy blood vessels (taken from other parts of the body), thus improving the coronary circulation. In performing CABH, the surgeon usually open the chest wall by cracking the sternum and spreading the ribs to gain access to the

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heart. Postsurgical precautions to prevent trauma to the new graft sites, inclusions and sternum generally last about 8 weeks after surgery and include the following: avoiding Valsalva maneuvers (e.g. straining during a bowel movement), avoiding a rapid movement of the upper part of the body adhering to a 10-lb lifting restriction, wearing comprehensive hose, refraining from diving (which creates problems because of upper body torque), and traveling in a seat without an airbag when riding in a car, “Following CABG”, 85% of people have significantly reduced symptoms and a decreased chance of dying within 10 years.

Arrhythmias that cannot be controlled with medications may be managed by the insertion of a pacemaker in the chest. Wires are run from the pacemaker to specific spots on the heart. The pacemaker delivers a small electrical impulse to the heart muscles and sets the pace of the heart’s electrical conduction. The impulse may be set to deliver a regular impulse or to send an impulse only if the heart rate drops below a certain number of beats pr minutes (demand). Modern pacemakers can monitor physiologic responses such as BP and temperature. Implantable cardioverterdefibllators (ICD) may also be used to treat cardiac arrhythmias. An ICD can both pace the heart muscle and deliver a high-energy impulse to reset the heart muscle if certain dangerous arrhythmias develop.

When the heart’s pumping ability has become too comprised by CHF or cardiomyopathy, a heart transplant or heart-lung transplant may be considered. After the healthy tissue of a recently deceased person is harvested, the patient’s diseased organ (or organs) is removed and the harvested tissue is transplanted into the patient’s body. Transplant decrease the risk for organ rejection. Nearly 50% of all heart transplant recipients survive for 10 years. Most recipients resume normal lifestyles, but only about 40% return to work.

COMMON CARDIAC MEDICATIONS

It is important for the professional occupational therapy practitioner to know the purpose & side effects of cardiac medications that are prescribed to his clients so that he may be able to maximize client activity performance during intervention.

The following table lists the common cardiac medications to patients who have experienced recent cardiac distress.

CATEGORY COMMON NAMES PURPOSE & USES

REASON PRESCRIBED

Angiotensin II Losartan (Cozaar) Keep blood Control high

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receptor blockers (or inhibitors)

Irbestan (Avopro) pressure from rising by

preventing angiotensin II

from having an effect on the

heart

blood pressure & heart failure

β – blockers Atenolol (Tenormin) Propanolol (Inderal)

Decrease heart rate & cardiac output, lower

blood pressure an make heart

beat more slowly & with

less force

Treatment of abnormal cardiac rhythms & chest

pain

Calcium channel blockers

Amlodipine (Norvasc, Lotrel)

Diltiazem (Cardizem, Tiazac)

Interrupt movement of calcium into cells of the

heart & blood vessels

Treat high blood pressure, angina

& some arrhythmias

Diuretics (water pills)

Furosemide (Lasix)Hydrochlorothiazide

(Esidrix, HydroDIURIL)

Cause loss of excess water &

sodium by urination

Lower blood pressure, reduce edema in lungs &

extremitiesVasodilators Nitroglycerin

MinodixilRelax blood

vessels, increase supply

of blood & oxygen to the

heart while reducing its

workload

Ease chest pain

Digitalis preparations

Digoxin (Lanoxin) Increase the force of cardiac

contractions

Treatment of heart failure & arrhythmias,

atrial fibrillationStatins Statins

ResinsNicotinic acid

(niacin)

Lower blood cholesterol

levels

Lower LDL, raise HDL & lower

triglyceride levels

Anticoagulants Warfarin (Coumadin)

Decrease blood clotting time

Prevent clots from forming & prevent clots

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Antiplatelet agents

Aspirin Dipyridamole

Prevent clots by preventing

platelets from sticking together

Prevent clots after MI; with

unstable angina, ischemic stroke,

plaqueACE inhibitors Fosinopril

(Monopril)Expand blood vessels, lower

levels of angiotensin II;

make heart work easily

Treat high blood pressure & heart

failure

PSYCHOSOCIAL CONSIDERATIONSClients who have experience recent myocardial infarctions usually go

through phases of adjustment to their disability. They go through fear & anxiety when they are forced to confront their mortality. Sedatives reduce stress in these patients & allow rest for healing. However, once they are stabilized, the clients must face the reality of their physical limitations.

Once the clients are able to ambulate within the hospital & thus start to resume their normal activities, their feelings of helplessness start to subside. The clients feel more secure when familiar coping mechanisms allow them to respond to stress. However, some of these coping mechanisms are harmful & should be discouraged. This is where newly learned coping mechanisms are reinforced on the client, which will be taught by the intervention team.

Feelings such as denial are common with patients with cardiac disease. Clients exhibiting signs of this attitude need close monitoring during the recovery phase. The individual may ignore all precautions & could therefore stress & further damage their cardiovascular systems.

CARDIAC REHABILITATIONDuring the first one to three days after the myocardial infarction, the

client’s condition is stabilized. This acute phase is then followed by a period of early mobilization. During the Phase 1 of treatment (inpatient cardiac rehabilitation), clients are allowed to do low-level physical activities such as self-care. Cardiac & postsurgical precautions, instruction in energy conversation & graded activities, establishment for appropriate activity level at discharge are also done at this phase.

During the Phase 2 (outpatient cardiac rehabilitation), which begins at discharge, exercise can be advanced but client is closely monitored. Phase 3 consists of community-based exercise programs. However, some individuals

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require home treatment because they are not strong enough to tolerate outpatient therapy.

Implementation of cardiac rehabilitation induces benefits for clients. These include reduction of health care costs, & positive health effects. Reduced mortality according to some researches are also shown to result from cardiac rehabilitation. Patients with left ventricular dysfunction are also giving good feedbacks by improving physical work capacity. In addition, patients who acquired skills in relaxation & control of breathing were found to require fewer hospitalizations.

Early & accurate identification of signs & symptoms of cardiac distress are imperative to the well-being of the client. When signs of cardiac distress are manifested during activity, the activity should be stopped, patient should be allowed to rest, & emergency medical help should be sought if symptoms don’t resolve. The symptoms exhibited should be reported afterward to the team & future activity must be modified to decrease workload.

The Borg Rate of Perceived Exertion Scale is a tool used to measure perceived exertion. After a given activity, the client will be asked to appraise his/her feelings of exertion after the activity & give the activity a rating. The scale starts at “6” which shows no exertion at all, until “19”, which is extremely strenuous activity, equal to the most strenuous activity the patient has ever performed.

Clients’ perception of their illness can have an impact on their ability to make the changes in lifestyle necessary for healthy living after an acute coronary event. Individualized intervention plans that address the unique physical, social &psychologic concerns of client improve the integration of lifestyle changes & functional improvement.

Signs & Symptoms of Cardiac DistressSign/Symptom What to Look For

Angina Look for chest pain that may be described as squeezing, tightness, aching, burning or choking. Pain is generally substernal& may radiate to the arms, jaw, neck or back. More intense or longer-lasting pain forewarns of greater ischemia.

Dyspnea Look for shortness of breath with activity or at rest. Note the activity that brought on the dyspnea & the amount of time that it takes to

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resolve. Dyspnea at rest with a resting respiratory of greater then 30 bpm is a sign of acute congestive failure. The patient may require emergency medical help.

Orthopnea Look for dyspnea brought on by lying supine. Count the number of pillows that the patient needs to breathe comfortably during sleep.

Nausea/Emesis Look for vomiting or signs that the patient feels sick to the stomach

Diaphoresis Look for cold, clammy sweatFatigue Look for a generalized feeling of

exhaustion. See: Borg Rate of Perceived Exertion Scale in previous discussions

Orthostatic [hypotension] Look for a drop in systolic blood pressure & hypotension of greater than 10 mmHg with a change in position from supine to sitting or sitting to standing.

MONITORING RESPONSE TO ACTIVITY

When the patient’s response to an activity is being assessed, symptoms provide one indication that the patient is or is not tolerating the activity. HR, BP, rate-pressure product (RPP), and ECG readings are other measures that may be used to evaluate the cardiovascular system’s response to work.

Heart RateHR, or the number of beats per minute, can be monitored by feeling the patient’s pulse at the radial, brachial, or carotid sites. The radial pulse is located on the volar surface of the wrist, just lateral to the head of the radius. The brachial pulse is found in the antecubital fossa, slightly medial to the midline of the forearm. The carotid pulse, located on the neck lateral to the Adam’s apple, should be palpated gently; if overstimulated, it can cause the HR to drop below 60 beats per minute (bradycardia).

To determine HR, the clinician applies the second and third fingers (flat, not with the tips) to the pulse site. If the pulse is even (regular), the clinician counts the number of beats in 10 seconds and multiplies the finding by 6. The thumb should never be used to take a pulse because it has its own pulse. All clinicians who assess HR, as well as patients, should be able to note the evenness (regularity) of the heartbeat. HR can be regular or irregular. An

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irregular heartbeat may be described as regularly irregular, which means that there is a consistent irregular pattern (e.g., every third beat is premature), or it may be described as irregularly irregular, which means that there is no pattern to the premature or skipped beats. HR irregularities include skipped beats, delayed beats, premature beats, and beats originating from outside the normal conduction pathway in the heart. Although an irregular HR is not normal, many individuals function quite well with an irregular rate.

Blood PressureBP is the pressure that the blood exerts against the walls of any vessel as the heart beats. It is highest in the left ventricle during systole and decreases in the arterial system with distance from the heart. A stethoscope and BP cuff (sphygmomanometer) are used to indirectly determine BP. The BP cuff is placed snugly (but not tightly) around the upper part of the patient’s arm just above the elbow, with the bladder of the cuff centered above the brachial artery. The examiner inflates the cuff while palpating the brachial artery to 20 mm Hg above the point at which the brachial pulse is last fel.t with the earpieces of the stethoscope angled forward in the examiner’s ears, the dome of the stethoscope is placed over the patient’s brachial artery. Supporting the patient’s arm in extension with the pulse point of the brachial artery and the gauge of the stethoscope at the patients’ heart level, the examiner deflates the cuff at a rate of approximately 2 mmHg per second.

Rate Pressure Product is the product of HR and systolic BP. It is usually a five-digit number but is reported in three digits by dropping the last two. During any activity, the RPP should rise at peak and return to base line in recovery after five to ten minutes of rest.

ANATOMY AND PHYSIOLOGY OF RESPIRATION

The respiratory system consists of an upper respiratory tract (nose to larynx) and a lower respiratory tract (trachea onwards).The conducting portion transports air and includes the nose, nasal cavity, pharynx, larynx, trachea, and progressively smaller airways, from the primary bronchi to the terminal bronchioles. The respiratory portion carries out gas exchange and is composed of small airways called respiratory bronchioles and alveolar ducts as well as air sacs called alveoli

The respiratory system supplies the body with oxygen and disposes of carbon dioxide, filters inspired air, produces sound, contains receptors for smell, rids the body of some excess water and heat and helps regulate blood pH.

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Breathing (pulmonary ventilation) consists of two cyclic phases: (a) inhalation, also called inspiration, draws gases into the lungs and (b) exhalation, also called expiration, forces gases out of the lungs.

The upper respiratory tract is composed of the nose and nasal cavity, paranasal sinuses, pharynx (throat), larynx and is composed of all parts of the conducting portion of the respiratory system.

Respiratory mucosa is a layer of pseudostratified ciliated columnar epithelial cells that secrete mucus and is found in nose, sinuses, pharynx, larynx and trachea. Mucus can trap contaminants while cilia move mucus up towards mouth.

A. Upper Respiratory TractThe nose is composed of (a) Internal nares which has an opening to the exterior, (b) External nares which has an opening to the pharynx, and (c) Nasal conchae which has folds in the mucous membrane that increase air turbulence and ensures that most air contacts the mucous membranes.

The nose has a rich supply of capillaries and warms the inspired air. It is composed of an olfactory mucosa where the mucous membranes contain smell receptors, respiratory mucosapseudostratified ciliated columnar epithelium containing goblet cells that secrete mucus which traps inhaled particles. Lysozyme kills bacteria and lymphocytes and IgA antibodies protect against bacteria.

The nose provides and airway for respiration, moistens and warms entering air, filters and cleans inspired air, a resonating chamber for speech, detects odors in the air stream. Rhinoplasty is the surgery to change shape of external nose

The paranasalsinuses is composed of four bones of the skull containing paired air spaces - frontal, ethmoidal, sphenoidal, and maxillary. It decreases skull bone weight, warms, moistens and filters incoming air, adds resonance to voice, communicates with the nasal cavity by ducts and is lined bypseudostratified ciliated columnar epithelium.

The pharynx is a common space used by both the respiratory and digestive systems. It is commonly called the throat and originates posterior to the nasal and oral cavities and extends inferiorly near the level of the bifurcation of the larynx and esophagus. It is a common pathway for both air and food. Its walls are lined by a mucosa and contain skeletal muscles that are primarily used for swallowing. Its flexible lateral walls are distensible in order to force swallowed

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food into the esophagus. The pharynx is partitioned into three adjoining regions: nasopharynx, oropharynx, and laryngopharynx.

The nasopharynx is the superior-most region of the pharynx. It is covered with pseudostratified ciliated columnar epithelium and is located directly posterior to the nasal cavity and superior to the soft palate, which separates the oral cavity. Normally, only air passes through. Material from the oral cavity and oropharynx is typically blocked from entering the nasopharynx by the uvula of soft palate, which elevates when we swallow. In the lateral walls of the nasopharynx, paired auditory/eustachian tubes connect the nasopharynx to the middle ear. The posterior nasopharynx wall also houses a single pharyngeal tonsil (commonly called the adenoids).

The oropharynx is the middle pharyngeal region. It is immediately posterior to the oral cavity and is bounded by the edge of the soft palate superiorly and the hyoid bone inferiorly. It is the common respiratory and digestive pathway through which both air and swallowed food and drink pass. It contains nonkeratinized stratified squamous epithelim. The lymphatic organs here provide the first line of defense against ingested or inhaled foreign materials. Palatine tonsils are on the lateral wall between the arches, and the lingual tonsils are at the base of the tongue.

The laryngopharynx is the inferior, narrowed region of the pharynx. It extends inferiorly from the hyoid bone to the larynx and esophagus and terminates at the superior border of the esophagus and the epiglottis of the larynx. It is lined with a nonkeratinized stratified squamous epithelium and permits passage of both food and air.

B. Lower Respiratory TractThe conducting airways are composed of the trachea, bronchi, up to terminal bronchioles while the respiratory portion of the respiratory system is composed of the respiratory bronchioles, alveolar ducts, and alveoli.

The larynx, the voice box, is a short, somewhat cylindrical airway ends in the trachea. It prevents swallowed materials from entering the lower respiratory tract, conducts air into the lower respiratory tract and produces sounds. It is supported by a framework of nine pieces of cartilage (three individual pieces and three cartilage pairs) that are held in place by ligaments and muscles.

Nine c-rings of cartilage form the framework of the larynx thyroid cartilage – (1) Adam’s apple, hyaline, anterior attachment of

vocal folds, testosterone increases size after puberty cricoid cartilage – (1) ring-shaped, hyaline

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arytenoid cartilages – (2) hyaline, posterior attachment of vocal folds, hyaline

cuneiform cartilages - (2) hyaline corniculatecartlages - (2) hyaline epiglottis – (1) elastic cartilage

The muscular walls of the larynx aid in voice production and the swallowing reflex. The glottis is the superior opening of the larynx,epiglottis prevents food and drink from entering airway when swallowing. The larynx is composed of pseudostratified ciliated columnar epithelium.

In sound production, the larynx’s inferior ligaments are called the vocal folds. These are the true vocal cordsbecause they produce sound when air passes between them while the superior ligaments are called the vestibular folds. These are the false vocal cordsbecause they have no function in sound production, but protect the vocal folds. The tension, length, and position of the vocal folds determine the quality of the sound.There is intermittent release of exhaled air through the vocal folds. The loudness depends on the force with which air is exhaled through the cords. The pharynx, oral cavity, nasal cavity, paranasal sinuses act as resonating chambers that add quality to the sound and the muscles of the face, tongue, and lips help with the enunciation of words.

The trachea is a flexible tube also called windpipe that is 10 cm long. It extends through the mediastinum and lies anterior to the esophagus and inferior to the larynx. The anterior and lateral walls of the trachea supported by 15 to 20 C-shaped tracheal cartilages. The cartilage rings reinforce and provide rigidity to the tracheal wall to ensure that the trachea remains open at all times. The posterior part of tube lined by trachealis muscle and is lined by ciliated pseudostratified columnar epithelium.

At the level of the sternal angle, the trachea bifurcates into two smaller tubes, called the right and left primary bronchi. Each primary bronchus projects laterally toward each lung. The most inferior tracheal cartilage separates the primary bronchi at their origin and forms an internal ridge called the carina. When the trachea/pharynx becomes blocked, a small incision may be made in the trachea to allow air to pass freely into the lungs, the surgeon performs a tracheotomy.

The bronchial tree is highly branched system of air-conducting passages that originate from the left and right primary bronchi. It progressively branches into narrower tubes as they diverge throughout the lungs before terminating in terminal bronchioles. The incomplete rings of hyaline cartilage support the walls of the primary bronchi to ensure that they remain open. The right

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primary bronchus is shorter, wider, and more vertically oriented than the left primary bronchus and foreign particles are more likely to lodge in the right primary bronchus. The primary bronchi enter the hilus of each lung together with the pulmonary vessels, lymphatic vessels, and nerves. Each primary bronchus branches into several secondary bronchi (or lobar bronchi). The left lung has two secondary bronchi. The right lung has three secondary bronchi. They further divide into tertiary bronchi. Each tertiary bronchus is called a segmental bronchus because it supplies a part of the lung called a bronchopulmonary segment. With successive branching amount of cartilage decreases and amount of smooth muscle increases, this allows for variation in airway diameter. During exertion and when sympathetic division active the blood vessels undergo bronchodilation while mediators of allergic reactions like histamine cause bronchoconstriction. Epithelium gradually changes from ciliated pseudostratified columnar epithelium to simple cuboidal epithelium in terminal bronchioles 

RESPIRATORY ZONE OF LOWER RESPIRATORY TRACTMost of the tubing in the lungs makes up conduction zone and consists of nasal cavity to terminal bronchioles. The respiratory zone is where gas is exchanged and consists of alveoli, alveolar sacs, alveolar ducts and respiratory bronchioles

The lungs contain small saccularoutpocketings called alveoli. They have a thin wall specialized to promote diffusion of gases between the alveolus and the blood in the pulmonary capillaries. Gas exchange can take place in the respiratory bronchioles and alveolar ducts as well as in the alveoli, each lung contains approximately 300 to 400 million alveoli. The spongy nature of the lung is due to the packing of millions of alveoli together.

The respiratory membrane is composed of squamous cells of alveoli, basement membrane of alveoli, basement membrane of capillaries and the simple squamous cells of capillaries about .5 μ in thickness

CELLS IN ALVEOLUS Type I cells : simple squamous cells forming lining Type II cells : or septal cells secrete surfactant Alveolar macrophages

GROSS ANATOMY OF THE LUNGSEach lung has a conical shape. Its wide, concave base rests upon the muscular diaphragm. Its superior region called the apex projects superiorly to a point that is slightly superior and posterior to the clavicle. Both lungs are bordered by the thoracic wall anteriorly, laterally, and posteriorly, and supported by the rib cage. Toward the midline, the lungs are separated from

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each other by the mediastinum. The relatively broad, rounded surface in contact with the thoracic wall is called the costal surface of the lung.

Left lung is divided into 2 lobes by oblique fissure and is smaller than the right lung. The cardiac notch accommodates the heart. Right lung is divided into 3 lobes by oblique and horizontal fissure and is located more superiorly in the body due to liver on right side.

PLEURA AND PLEURAL CAVITIESThe outer surface of each lung and the adjacent internal thoracic wall are lined by a serous membrane called pleura. The outer surface of each lung is tightly covered by the visceral pleura while the internal thoracic walls, the lateral surfaces of the mediastinum, and the superior surface of the diaphragm are lined by the parietal pleura. The parietal and visceral pleural layers are continuous at the hilus of each lung.

The potential space between the serous membrane layers is a pleural cavity. The pleural membranes produce a thin, serous pleural fluid that circulates in the pleural cavity and acts as a lubricant, ensuring minimal friction during breathing. Pleural effusion is pleuritis with too much fluid

BLOOD SUPPLY OF LUNGS pulmonary circulation bronchial circulation – bronchial arteries supply oxygenated blood to

lungs, bronchial veins carry away deoxygenated blood from lung tissue superior vena cava

Response of two systems to hypoxia – Pulmonary vessels undergo vasoconstrictionBronchial vessels like all other systemic vessels undergo vasodilation

RESPIRATORY EVENTSPulmonary ventilation is the exchange of gases between lungs and atmosphere. External respiration is the exchange of gases between alveoli and pulmonary capillaries. Internal respiration is the exchange of gases between systemic capillaries and tissue cellsThere are two phases of pulmonary ventilation:

a. Inspiration, or inhalationis a very active process that requires input of energy. The diaphragm, contracts, moving downward and flattening, when stimulated by phrenic nerves.

b. Expiration, or exhalation is a passive process that takes advantage of the recoil properties of elastic fiber. ・ The diaphragm relaxes. The elasticity of the lungs and the thoracic cage allows them to return to their normal size and shape. Forced expiration requires active contraction of abdominal muscles to compress the viscera and

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squeeze the diaphragm upward in the thorax and further enforced by flexing torso forward and pressing with the arm on the chest or abdomen

MUSCLES THAT ASSIST WITH RESPIRATIONThe scalenes help increase thoracic cavity dimensions by elevating the first and second ribs during forced inhalation. The ribs elevate upon contraction of the external intercostals, thereby increasing the transverse dimensions of the thoracic cavity during inhalation. Contraction of the internal intercostals depresses the ribs, but this only occurs during forced exhalation. Normal exhalation requires no active muscular effort. Other accessory muscles assist with respiratory activities. The pectoralis minor, serratus anterior, and sternocleidomastoid help with forced inhalation, while the abdominal muscles (external and internal obliques, transversusabdominis, and rectus abdominis) assist in active exhalation.

BOYLE’S LAW The pressure of a gas decreases if the volume of the container increases, and vice versa.When the volume of the thoracic cavity increases even slightly during inhalation, the intrapulmonary pressure decreases slightly, and air flows into the lungs through the conducting airways. Air flows into the lungs from a region of higher pressure (the atmosphere) into a region of lower pressure (the intrapulmonary region).When the volume of the thoracic cavity decreases during exhalation, the intrapulmonary pressure increases and forces air out of the lungs into the atmosphere.

VENTILATION CONTROL BY RESPIRATORY CENTERS OF THE BRAIN The trachea, bronchial tree, and lungs are innervated by the autonomic nervous system. The autonomic nerve fibers that innervate the heart also send branches to the respiratory structures. The involuntary, rhythmic activities that deliver and remove respiratory gases are regulated in the brainstem within the reticular formation through both the medulla oblongata and pons.

RESPIRATORY VALUESA normal adult averages 12 breathes per minute = respiratory rate (RR). The respiratory volumes are determined by using a spirometer.

LUNG VOLUMES TIDAL VOLUME (TV): Volume inspired or expired with each normal

breath. = 500 ml INSPIRATORY RESERVE VOLUME (IRV): Maximum volume that can

be inspired over the inspiration of a tidal volume/normal breath. Used during exercise/exertion.=3100 ml

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EXPIRAT0RY RESERVE VOLUME (ERV): Maximal volume that can be expired after the expiration of a tidal volume/normal breath. = 1200 ml

RESIDUAL VOLUME (RV): Volume that remains in the lungs after a maximal expiration CANNOT be measured by spirometry.=1200 ml

LUNG CAPACITIES INSPIRATORY CAPACITY ( IC): Volume of maximal inspiration: IRV +

TV = 3600 ml FUNCTIONAL RESIDUAL CAPACITY (FRC): Volume of gas

remaining in lung after normal expiration, cannot be measured by spirometry because it includes residual volume: ERV + RV = 2400 ml

VITAL CAPACITY (VC): Volume of maximal inspiration and expiration: IRV + TV + ERV = IC + ERV = 4800 ml

TOTAL LUNG CAPACITY (TLC): The volume of the lung after maximal inspiration. ハ The sum of all four lung volumes, cannot be measured by spirometry because it includes residual volume: IRV+ TV + ERV + RV = IC + FRC = 6000 ml

INNERVATION OF RESPIRATION

The trachea, bronchial tree and lungs are innervated by the autonomic nervous system. The autonomic nerve fibers that innervate the heart also send branches to the respiratory structures. The pulmonary plexus is composed of the sympathetic innervation which causes bronchodilation and parasympathetic innervation which causes bronchoconstriction. The involuntary, rhythmic activities that deliver and remove respiratory gases are regulated in the brainstem.

CHRONIC LUNG DISEASE

o Common chronic disorders of the lungs for which pulmonary rehabilitation is typically prescribed include chronic obstructive pulmonary disease (COPD) and asthma.

o COPD is characterized by: Damage to the alveolar wall Inflammation of the conducting airway Includes emphysema, peripheral airway disease, chronic

bronchitiso Emphysema – condition in which alveoli becomes enlarged or

ruptured, usually because of a restriction during expiration or a decrease in elasticity of the lungs.

o Chronic emphysema

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Men; ages 45 -65 yo who have a history of chronic bronchitis, smoking, working in areas of high levels of air pollution, or exposure to cold

Progresses = becomes dyspnea which occurs at resto Physiologic changes that occur with peripheral airway disease

Inflammation Fibrosis Narrowing of terminal airways of lungs

o Common clinical manifestations Coughing Spitting up mucus

o May develop into emphysema or evolve in to a full-fledged COPD

o Chronic bronchitis is diagnose after a 2yr period of repeated episodes, lasting longer than 3mos of mucus producing cough of unknown origin

o Cigarette smoking has a direct relationship with the development of the disease

Clinical manifestations increases aNd the pack-year history increases

Pack –year = no. of packs of cigarettes per day X no. ofyrs smoking

o Asthma Irritability of the bronchotracheal tree Onset: episodic Experience wheezing, shortness of breath Some have a genetic predisposition Allergic causes: pollens, respiratory irritants (perfume,

dust, cleaning agents) First clinical manifestation: BRONCHOSPASM due to

exposure to cold air/exercise Irritation of the airways leads to narrowing of the air

passages and interferes with ventilation o the alveolar sacs.

If obstruction of the airway is significant enough, a reduction in oxygen levels in the bloodstreams will result in HYPOXIA

Untreated= death PULMONARY RISK FACTORS

o SMOKING

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o Other environmental irritants Air pollution Chemical exposure Dust

MEDICAL MANAGEMENTo COPD is a progressive, chronic diseaseo Onset – insidiouso Evaluate patient’s medical history and perform a physical

examinationo Assess history of smoking and occupational exposure to

respiratory irritantso Blood work and x-ray examination – to further asses clinical

statuso Medications:

Anti-inflammatory Bronchodilators Expectorants

o Flu shots and pneumonococcal vaccines are recommendedo Oxygen therapy may also be prescribed at a low rate

SIGNS AND SYMPTOMS OF RESPIRATORY DISTRESSo DYSPNEA - most obvious sign of breathing difficultyo Shortness of breath even at resto Unable to utter a short phrase without grasping for airo Extreme fatigueo Nonproductive cougho Confusiono Impaired judgmento Cyanosis

Pulmonary Rehabilitation

The goal of pulmonary rehabilitation is to stabilize or reverse the disease process and return the patient’s function and participation in activity/occupation to the highest capacity. A multidisciplinary rehabilitation team working with the patient can design an individualized intervention program to meet this end. Accurate diagnosis, medical man- agement, therapy, education, and emotional support are components of a pulmonary rehabilitation program. OT personnel are frequently part of the patient’s team, which is headed by the patient and also includes the physician, nurse, and the patient’s family and social supports. Respira- tory therapists, dietitians,

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physical therapists, social workers, and psychologists may also be team members. Roles of team members vary slightly among facilities. Knowledge of spe- cialized pulmonary treatment techniques is imperative for each team member when treating persons with pulmonary disease.

Intervention Techniques

1. Dyspnea Control Postures

Adopting certain postures can reduce breathlessness. In a seated position, the patient bends forward slightly at the waist while supporting the upper part of the body by leaning the forearms on a table or the thighs. In a standing position, relief may be obtained by leaning forward and propping oneself on a counter or shopping cart.

2. Pursed-Lip Breathing

Pursed-lip breathing (PLB) is thought to prevent tightness in the airway by providing resistance to expiration. This technique has been shown to increase use of the diaphragm and decrease accessory muscle recruitment.5 Persons with COPD sometimes instinctively adopt this technique, whereas others may need to be taught it. Instructions for PLB are as follows:

3. Diaphragmatic Breathing

Another breathing pattern, which calls for increased use of the diaphragm to improve chest volume, is diaphragmatic breathing. Many persons learn this technique by placing a small paperback novel on the abdomen just below the xiphoid process (base of the sternum or breastbone). The novel provides a visual cue for diaphragmatic movement. The patient lies supine and is instructed to inhale slowly and make the book rise. Exhalation through pursed lips should cause the book to fall.

4. Relaxation

Progressive muscle relaxation in conjunctions with breathing exercises can be effective in decreasing anxiety and controlling shortness of breath. One technique involves tensing muscle groups while slowly inhaling and then exhaling twice as slowly through the lips. It is helpful to teach the patient a sequence of muscle groups to tense and relax. One common sequence involves tensing and relaxing first the face; followed by the face and neck; then the face, neck, and shoulders; and so on, down the body to the toes. A calm, quiet, and comfortable environment is important for the novice in learning any relaxation technique. Biofeedback in conjunctions with relaxation therapy promotes more timely masterly of relaxation skills.

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5. Other Treatment and Considerations

Physical therapists are generally called on to instruct patients in chest expansion exercises, a series of exercises intended to increase the flexibility of the chest. Percussion and postural drainage use gravity and gentle drumming on the patient’s back to loosen secretions and help drain the secretions from the lungs. By isometrically contracting the arms and hands while they are placed on the patient’s thorax, the therapist may transmit vibration to the patient. Vibration is performed during the expiratory phase of breathing ad helps loosen secretions. Percussion and postural drainage, however, be contraindicated on acutely ill patients and those who are medically unstable

Humidity, pollution, extremes of temperature, and stagnant air have deleterious effects on persons with respiratory ailments. The therapist and patient should take these factors into consideration when planning activity.

EVALUATION

I. REVIEW OF MEDICAL RECORDSA review of the medical record will identify the patient’s medical history, social history, test results, medications, and precautions.

II. PATIENT INTERVIEWThoughtful, probing questions will help the patient and the therapist identify areas of concern and lay the groundwork for establishing mutually agreeable goals. The therapist should observe the patient for signs of anxiety, SOB, confusion, difficulty comprehending, fatigue, abnormal posture, reduced endurance, reduced ability to move, and stressful family dynamics. Clarification of symptoms before treatment can prove invaluable should symptoms arise. Asking patients to describe a typical day will reveal problems that are meaningful and relevant to the patient. Also patient’s cognitive and psychosocial status will become apparent.

III.CLINICAL EVALUATIONIts purpose is to establish the patient’s present functional ability and limitations. Clients with impairments in the cardiovascular system will require monitoring of HR, BP, signs and symptoms of cardiac distress, and possibly ECG readings during an assessment of tolerance to postural changes and during a functional task.

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CARDIOVASCULAR RESPONSE TO ACTIVITY

APPROPRIATE INAPPROPRIATEHEART RATE Increases with ax to

no more than 20 beats/min above the resting heart rate (avg: 60-100 beats/min)

HR >20beats/min above the RHR with ax; RHR >120; HR drops or does not rise

BLOOD PRESSURE Systolic blood pressure rise with ax

SBP >220 mm Hg postural hypotension (>10-20 mm Hg drop in SBP; decrease in SBP

SIGNS AND SYMPTOMS

Absence of adverse symptoms

Excessive SOB; angina; nausea and vomiting; excessive sweating; extreme fatigue; cerebral sx

Individuals with disorders involving the reparatory systems should be monitored closely for signs and symptoms of respiratory distress. Example: (1) an increased awareness of normal breathing such as during an anxiety attack, (2) an increase in the work of breathing (3) an abnormality in the ventilatory system (4) SOB (5) cyanosis (6) nasal flaring (7) increased/decreased breathing rate (8) increased/decreased O2 saturation.

SOURCE:

PEDRETTI’S OT PRACTICE SKILLS FOR PHYSICAL DYSFUNCTION, 7TH

ED., EDITED BY HEIDI PENDELTON, WINIFRED SCHULTZ-KROHN

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