6.1. Quiz II COMBINED Inflam, Cardio, Pulm

Cardiac Disease

Learning Objectives

• Define normal structure, circulation, and function of the heart.

• Recognize signs, symptoms, and risk factors of cardiovascular disease.

• Compare and contrast etiology, risk factors, pathogenesis, and clinical manifestations of diseases.

• Describe rehabilitation implications for each of the diseases affecting heart muscle.

• Discuss differences between sexes in cardiovascular disease.

• Conclude when it is appropriate to refer patients with cardiac disease.

Layers of the Heart

• Pericardium

• Myocardium

  • Middle muscular layer of the heart.

  • Primary mover of the heart.

• Epicardium

  • Thin layer of elastic connective tissues and fat.

  • Contains the coronary arteries.

• Endocardium

  • Most inner layer of the heart.

  • Lining of the chambers of the heart.

Coronary Arteries

• Originate from the aorta and supply blood to the heart.

  • Left main

  • Left anterior descending

  • Circumflex

  • Right main

  • Posterior descending

Anatomic Region of Heart & Coronary Artery Association

• Inferior: Right coronary artery

• Anteroseptal: Left anterior descending

• Anteroapical: Left anterior descending (distal)

• Anterolateral: Circumflex

• Posterior: Right coronary artery

Circulation of Blood through the Heart

• Lungs

• Pulmonary Veins

  • Only veins with oxygenated blood

• Left Atrium

  • Bicuspid/Mitral Valve

• Left Ventricle

  • Aortic Semilunar Valve

• Aorta

• Body Tissues

• Vena Cava

• Right Atrium

  • Tricuspid AV Valve

• Right Ventricle

  • Pulmonary Semilunar Valve

• Pulmonary Arteries

Valves of the Heart

Atrioventricular

• Tricuspid and Bicuspid (Mitral)

• Located between the atria and corresponding ventricle.

Bicuspid (Mitral)

• Located between the left atrium and ventricle.

Tricuspid

• Located between the right atrium and ventricle.

• Anterior, Septal, and Posterior cusps

Semilunar

• Pulmonary and Aortic

• Located between ventricles and corresponding artery.

Pulmonary

• Located between the right ventricle and pulmonary trunk.

• Left, right, anterior cusps

Aortic

• Located between the left ventricle and ascending aorta.

• Left, right, posterior cusps

Conduction System

• Goal is sequential atrioventricular contraction

  • SA Node

  • Internodal Pathways

  • Atria Contracts

  • AV node

  • Ventricles

  • Bundle of His

  • Purkinje Fibers

  • Ventricles contract

Electrocardiogram (ECG)

• P wave

  • Atrial contraction

• PR Interval

  • Seconds from the beginning of the P wave to the QRS segment

• PR segment

  • Conduction through atria and delay of AV node

• QRS Complex

  • Ventricular contraction

• T Wave

  • Ventricular recovery/relax

• QT Interval

  • Time of ventricular contraction and relaxation

Key Terms and Definitions

• Blood Pressure

  • $Cardiac\ Output \times Total\ Peripheral\ Resistance$

  • $TPR$ = diameter of vessels and viscosity of blood

• Systolic Pressure

  • Highest arterial pressure of cardiac cycle

  • Immediately after contraction of left ventricle

• Diastolic Pressure

  • Lowest arterial pressure of cardiac cycle

  • Occurs between heart contractions

• Stroke Volume

  • Volume ejected after each heart contraction

  • Influenced by preload, afterload, and contractility (inotropy)

• Cardiac Output

  • Volume of blood ejected each minute

  • $Stroke\ volume \times HR$

  • 5-6 L/min at rest

• Ejection Fraction

  • Amount of blood left in ventricle per contraction

  • Normal: 50-70%

Cardiovascular Disease Prevalence

• Risk Factors

  • Hypertension

  • High serum cholesterol levels

  • Smoking

  • Sedentary lifestyle

  • Poor diet patterns

  • Overweight/obesity

• 1 in 4 deaths in the U.S. due to cardiovascular disease

• Leading cause of death in the U.S.

• Coronary heart disease – most common type of heart disease

• ~735,000 individuals in the United States have myocardial infarctions each year

Ischemic Heart Disease

• Also known as Coronary Artery Disease (CAD) or Coronary Heart Disease (CHD)

  • Pathology

    • Narrowed/blocked arteries in the area of heart supplied becomes ischemic/injured

    • Myocardial infarction may result

    • Narrowing caused by Arteriosclerosis

      • Thickening and loss of elasticity of arterial walls

      • Atherosclerosis

        • Most common type

        • Accumulation of fatty deposits in the inner layer of arteries

• Coronary Vascular vs. Coronary Artery vs. Cerebrovascular Coronary Artery Disease

Pathogenesis

• Arterial wall damage by harmful blood substances and/or hypertension

• Injury leads to infiltration of macromolecules such as cholesterol into smooth muscle cells

• Platelets attracted

  • Thrombus formation

• Thrombus can rupture, narrow, or block artery

Coronary Artery Disease Risk Factors

Non-Modifiable

• Family history

• Age (40+)

• Sex

• Ethnicity

• Infection

  • Chlamydia Pneumonia

  • Helicobacter pylori

  • ½ US have antibodies for above

Modifiable

• Smoking

• High Cholesterol

• Obesity

• Hypertension

• Physical Activity

• Glucose metabolism

• Hormonal status

• Psychologic factors

• Alcohol Abuse

Coronary Artery Disease Prevention

• Atherosclerosis begins in adolescence and young adulthood

  • Address modifiable risk factors early

• Moderate-intensity exercise at least 30 minutes 5-7 days/week

  • Decreased risk for:

    • Coronary events

    • Ischemic stroke

    • Metabolic syndrome

    • Insulin resistance

    • Diabetes

  • Improves heart rate recovery

  • Lowers cholesterol levels

Coronary Artery Disease Diagnosis

• Cholesterol checks

  • Begin at 20 and recheck every 5 years

• Coronary angiography

  • X-ray with dye of arteries

• Echocardiography

  • Ultrasound imaging

• Stress echocardiography

• Exercise treadmill testing

  • $HR recovery = change\ from\ peak\ HR\ and\ 2\ minutes\ later$

    • 25 – 30 bpm = good, 50-60 bpm = excellent

    • Abnormal recovery = 4x as more likely to die from CAD

  • Decline of systolic pressure after graded exercise: correlates with CAD

Coronary Artery Disease Surgical Interventions

Coronary Stents

• Drug-coated metal stents with plastic coating

• Hold and release drugs that inhibit growth of endothelial cells

Coronary Artery Bypass Graft (CABG)

• Portion of vein or artery grafted onto coronary artery

• Bypasses blockage

Percutaneous Transluminal Coronary Angioplasty

• Opens occluded coronary artery without opening chest

• Involves double lumen balloon catheter

Implications for Rehabilitation

• Cardiac Rehab Phase 1-3

  • Inpatient, outpatient, maintenance

  • Discharge instructions

  • Sternal Precautions

  • Indications for Exercise

Sternal Precautions

• No pulling up in bed

  • Must roll side to side

• No pushing, pulling, or lifting > 5 to 10 pounds for 6 weeks.

  • Vacuuming, lifting children bets, moving furniture, opening doors etc.

• Move in the tube sternal precautions

  • No driving

  • Avoid horizontal abduction and extreme external rotation

• Cough with heart pillow for splinting

• Avoid using armrests to push up from chair

Angina Clinical Manifestations

• Pain or discomfort in chest

  • Substernal

  • Occasionally refers to the left scapular area

  • Patients will report

    • Squeezing

    • Burning

    • Pressing

    • Heartburn

    • Indigestion

    • Choking

  • Varies in intensity

  • Can last 1 to 15 minutes

  • Usually relieved by rest or nitroglycerine

Angina Pathogenesis

• Workload exceeds oxygen demand for various reasons

• Symptom of ischemia secondary to imbalance between cardiac workload

• 90% secondary to CAD

• Disruption of plaques can lead to occlusive thrombus

  • Unstable angina or Myocardial Infarction

Types of Angina

Stable or Chronic

• Demand ischemia

• Involves coronary arteries

• Predictable threshold of activity or stress

• Hot and cold weather may trigger

• 5 minutes or less is normal

• Use rest or nitroglycerine

Unstable

• Unpredictable

• Changes in intensity, frequency, or threshold

• Lasts longer than 15 minutes

• Symptom or worsening cardiac ischemia

Variant (Prinzmetal’s)

• Caused by coronary artery spasm

• No CAD

• Triggers

  • Stress, extreme weather, vasoconstriction meds, smoking/cocaine

• Nitroglycerine and calcium antagonists

Microvascular

• Involves coronary microvasculature

• Endothelial dysfunction = chest pain

• Most often postmenopausal

• Most severe and lasts the longest

• Often first noticed with ADL’s and emotional stress

Medical Management

• Diagnosis

  • History supported by relief with sublingual nitroglycerin

    • Long-acting nitrates allow increased exertion

• Treatment

  • Avoid provoking situations

  • Keep nitroglycerin for acute attacks

    • Decreases cardiac workload by decreased cardiac oxygen demand

    • Decreases preload and afterload

  • Medication to decrease heart rate and force of contraction

    • Decreased myocardial demand

  • Anticoagulants for unstable angina

  • Revascularization procedures

    • PTCA and CABG

Rehabilitation Implications

• Unstable angina requires immediate medical referral

• If known, need to have nitroglycerin on hand

  • Administer and sit down supported or in supine until symptoms resolve

  • Usually very quick

• Watch for orthostatic hypotension

  • Common side effect of medications

• Monitor vitals

  • Exercise below threshold

  • May be blunted heart rate responses

• Education

Myocardial Infarction

Pathogenesis

• Heart attack: development of ischemia with resultant necrosis of myocardial tissue

• Heart deprived of oxygen

• Leading cause of death among adults in the U.S.

• Same etiology and risk factors as CAD

• Angina due to CAD is predictive of Myocardial Infarction

• 80—90% is secondary to coronary thrombus due to the site of preexisting atherosclerotic stenosis

  • Other causes are cocaine use, vasculitis, aortic stenosis, coronary artery dissection

• Vessel becomes partially or completely blocked due to plaque

Clinical Manifestations

• Sudden sensation of pressure with crushing chest pain

• Often radiates to arm, throat, neck, and back

• Pain is constant

  • 30-60 minutes

  • Up to hours

• Pallor, Shortness of breath, diaphoresis

• Women

  • Sudden nocturnal shortness of breath

  • Chronic, unexplained fatigue

  • Unexplained anxiety

  • Indigestion

• Silent Myocardial Infarction

  • Associated with no pain

  • More common in older adults, all smokers, diabetes mellitus, and women

  • Vomiting, fever in the first 24 hours and persist for a week

Postinfarction Complications

• Arrhythmias

  • Most common (90%)

• Congestive Heart Failure

• Pericarditis

• Myocardial rupture

  • Fatal and most often left ventricle

• Thromboembolism

• Recurrent Infarction

• Sudden death

Medical Management

• Diagnosis

  • Clinical history, ECG interpretation, measurement of cardiac enzyme levels

    • Troponin most common

• Treatment

  • If during treatment – rapid response/code blue or call 911 if outpatient

    • Chew/swallow aspirin

    • Nitroglycerin if prescribed

    • Unlock door

    • Lied down

  • Early intervention is optimal

  • Reestablish blood flow

    • Acute: thrombolytics

    • Post-acute: Same as CAD (stints, bypass, angioplasty)

Rehabilitation Implications

• Activity recommended with graded progressions

• Cardiac rehab can lead to coronary artery collateral growth

• Specific dosages of aerobic, resistive, and flexibility exercises

• Sexual activity

  • Follow general recommendations for AHA

  • Orgasm: Physiologically equivalent to brisk walk/climbing a flight to stairs

  • 5 METS

• Early mobilization

  • Gentle and prevention complications

  • Usually within 24 hours

• Holding breath and Valsalva contraindicated

• Monitor vital signs!

• Special care

  • Patients on thrombolytics

• Education on precautions/contraindications

• Referral for mental health and wellness

Heart Failure

• Heart is unable to pump sufficient amount of blood to supply body’s needs

  • Due to disorders of:

    • Pericardium

    • Myocardium

    • Epicardium

    • Heart valves

    • Large coronary vessels

    • Metabolic abnormalities

  • May occur on both sides or predominantly one

    • Usually due to left ventricular dysfunction

  • Most common reason for hospitalization in ages 65+

Heart Failure Classifications

Left Ventricular Failure

• Congestive heart failure

• Leads to pulmonary congestion

Acute Right Ventricular Failure

• NOT due to other issues

• Leads to superior and inferior peripheral system congestion

Cor Pulmonale

• Heart disease due to underlying pulmonary condition

• Leads to right heart failure

Pathogenesis – Left Heart Failure

First Compensatory Stage

• To maintain normal cardiac output – chambers enlarge to hold more blood

• Ventricular dilation

• Limited dilation before the threshold resulting in decreased contractility

• Right ventricle continues as normal

• With reduced left ventricular function, a back begins to occur leading to pulmonary congestion/edema

• Dyspnea is for all people to some degree.

Second Compensatory Stage

• Sympathetic nervous system responds

• Stimulation of heart muscle to increase rate

• Leads to ventricular hypertrophy

• More oxygen is required to maintain increased heart rate

• Angina pectoris begins to occur due to ischemia with hypertrophic demands

Third Compensatory Stage

• Activation of the renin-angtiotensin- aldosterone system

• Kidneys begin to retain water and sodium due to decreased blood

• Further tissue edema

• Increased load on compromised heart

• When this stage finally fails, the patient reaches decompensated heart failure

Right Sided Heart Failure

• Often but not always due to left-sided heart failure

• Or can be right ventricle weakness and unable to empty

• Blood will back up into systemic circulation via superior and inferior vena cava

• Peripheral edema in legs, liver, abdominal organs

  • Ascites

• Very high venous pressure causes distention of vessels

  • Jugular vein distention

Congestive Heart Failure Medical Management

• Diagnosis

  • Clinical diagnosis

  • Symptom severity

  • Echocardiogram: primary diagnostic tool.

• Treat underlying cause

  • Diet, exercise, lifestyle

• Pharmacologic

  • Reduce heart workload

  • Increase cardiac muscle strength and contraction

  • Diuretics

• Surgery

  • CABG

  • Cardiac Transplant

  • Pacemaker

Physical Therapy Implications

• Monitor vital signs

• Peripheral edema

  • DO NOT COMPRESS

• Assess jugular vein distention

• Utilize the Borg Scale

• Positioning

  • Dependent position

  • Head of bed

• Slow progression

• Energy Conservation

• Patient education

• Psychosocial

Heart Valve Diseases

Valve Dysfunctions

Functional

• Congenital deformities

• Rheumatic fever

• Trauma

• Ischemia

• Prolapse

  • Enlarged valve leaflets bulge backwards

  • Mitral or Tricuspid

Anatomic

• Insufficiency

  • Regurgitation when the valve does not close properly

  • Blood flows back into the chamber

  • Dilation Occurs

• Stenosis

  • Valve does not open fully

  • Obstruction leads to chamber hypertrophy

Mitral Valve Stenosis

• Mild

  • Asymptomatic with left atrial pressure and cardiac output remain normal

• Moderate

  • Dyspnea and fatigue appear and left atrial pressure rises

    • Decreased cardiac output

• Severe

  • High left atrial pressure

    • Pulmonary congestion at rest

  • Dyspnea and fatigue, right ventricular failure

• Diagnosis

  • Echocardiogram

• Intervention

  • Pharmacologic: anticoagulants, antiarrhythmic agents

  • Surgery: valve replacement, balloon valvotomy

Mitral Valve Regurgitation (Insufficiency)

• Associated with female, lower BMI, older age

• May be asymptomatic until severe left ventricular dysfunction occurs

  • Exertional dyspnea

  • Exercise-induced fatigue

• Diagnosis

  • Clinical with auscultation

  • Echocardiogram

• Treatment

  • Mild – Diuretics, anticoagulants, anti-hypertensives

  • Moderate-Severe

    • Valve replacement/repair

  • Education

Mitral Valve Prolapse

• 50% are asymptomatic

• 40% are only mild to moderate symptoms

  • Fatigue

  • Palpitation

  • Dyspnea

• Not at greater risk for heart failure

• Treatment

  • Pharmacologic – antiarrhythmics

  • Exercise

  • Lifestyle education

  • Antibiotics before any invasive procedure

Arrhythmias

Ventricular

• Fibrillation

  • Often results in cardiac arrest

• Premature

  • Can be benign but should be documented

Atrial

• Fibrillation

  • Most common and can lead to stroke/failure

  • Blood clot will originate and travel

Heart Block

• Slowing or interruption of impulses from atria to ventricles

• Different degrees and types

Treatment

• Pharmacology

  • Many types, will learn more later

• Cardioversion

  • Synchronized electrical shocks

• Defibrillation

• Ablations

  • Catheterization threads wire to where arrhythmia originates and the area is destroyed

• Pacemaker

  • Single chamber – right ventricle

  • Dual chamber – right ventricle and atrium

  • Biventricular

    • Resynchronization therapy: used with heart failure

Pulmonary Disease Notes

1. Impact of Lung Disease

• COPD is the 4th leading cause of death in the US.

• Over 50% of Americans with lung disease are undiagnosed.

• Lung disease directly impacts exercise and ADLs, requiring modifications to physical therapy recommendations.

• Smoking statistics:

  • 1960: 55% ♂ / 30% ♀

  • 2008: 22.8% ♂ / 18.5% ♀

  • 2016: 18.6% ♂ / 14.3% ♀

  • 2021: 13% ♂ / 10% ♀

• Patients with chronic respiratory disorders are at risk for acute exacerbations, ER visits, hospitalization, and co-morbidities.

• Chronic lung disorders result in chronic modification of ADLs and therapeutic interventions.

2. Leading Causes of Death in US (2021)

• 1. Heart disease

• 2. Cancer

• 3. Medical errors (under-documented)

• 4. COPD (Chronic lower respiratory disease)

• 5. Accidents

• 6. Stroke

• 7. Alzheimer’s disease

• 8. Diabetes

• 9. Influenza & pneumonia

• Kidney disease

4. Pulmonary A&P Review

• Upper airways: above larynx (vocal cords); includes nasopharynx, oropharynx, laryngopharynx.

• Vocal cords division.

• Lower airways: below larynx; includes conducting zone & respiratory zone.

5. Pulmonary A&P Review (Continued)

• Conducting Zone: Trachea -> Bronchi -> Bronchiole -> Terminal Bronchiole (23-24 bifurcations).

• Respiratory Zone: Respiratory bronchioles -> Alveolar Duct -> Alveolar Sac -> Alveoli.

• Respiratory Zone: Actual interface of alveoli with capillary beds (AC membrane) for exchange of CO2 and O2 with RBCs.

• O2/CO2 exchange (respiration).

• Gases diffuse from high concentration to low concentration.

  orr$</p></li></ul><h4 id="cfc8a2eb-2bfb-4548-8765-d95d01031e09" data-toc-id="cfc8a2eb-2bfb-4548-8765-d95d01031e09" collapsed="false" seolevelmigrated="true">6. Infrastructure of Alveolar-Capillary Interface</h4><ul><li><p>Alveolar Type I cell: compose the actual structure of the cell.</p></li><li><p>Alveolar Type II cell: produce surfactant to prevent alveolar collapse.</p></li><li><p>Alveolar Type III cell: alveolar macrophage (housekeeping).</p></li><li><p>Surface Area of Type I cells (300 million) is$70 m^2$(tennis court).</p></li></ul><h4 id="41a68330-93e9-4529-be1d-f3d6477aa423" data-toc-id="41a68330-93e9-4529-be1d-f3d6477aa423" collapsed="false" seolevelmigrated="true">7. Ventilation vs. Respiration</h4><ul><li><p>Respiration:$O2/CO2 exchange through A/C membrane in the Respiratory Zone.

• Ventilation: mechanical movement of gas in and out of lungs as a function of thorax musculature, lung compliance, and airway resistance.

• Control of ventilation: neuro-chemical through carotid bodies and CSF response through BBB.

• Hypercapnic drive vs. hypoxic drive.

8. Ventilatory Muscles

• Muscles of resting ventilation:

  • Inspiration: diaphragm.

  • Expiration: none (passive recoil of thorax).

• Muscles of active ventilation (accessory muscles):

  • Inspiration: sternocleidomastoid, external intercostals, scalene, trapezius, pectoralis major/minor.

  • Expiration: internal intercostals, transverse abdominis, external/internal obliques, serratus, latissimus dorsi.

9. Pulmonary Function Test (PFTs)

• Primary method for Dx/stage lung disease.

• Total Lung Capacity:

  • The Volume of Air in the Lungs After a Maximum Inhalation

• Tidal Volume:

  • The Volume of Air Inhaled or Exhaled During Normal Breathing

• Vital Capacity:

  • The Maximum Amount of Air a Person Can Exhale After a Maximum Inhalation

• Inspiratory Reserve Volume:

  • The Maximum Amount of Extra Air That Can Be Inhaled Above Tidal Volume

• Expiratory Reserve Volume:

  • The Maximum Amount of Extra Air That Can Be Exhaled Beyond Tidal Volume

• Residual Volume:

  • The Volume of Air Remaining in the Lungs After a Maximum Exhalation

10. Pulmonary Signs and Symptoms

• Sign (objective finding perceived by examiner) vs Symptom (subjective indicator of disease or change as perceived by the patient).

• Cough.

• Dyspnea.

• Abnormal sputum.

• Chest pain/discomfort.

• Hemoptysis.

• Cyanosis.

• Digital clubbing.

• Altered breathing patterns.

11. Digital Clubbing

• Fingers & toes.

12. Altered Breathing Patterns & Sounds

• Hyperventilation (hyperpnea vs. tachypnea).

• Hypoventilation (hypopnea vs, bradypnea).

• Stridor (high-pitched inspiratory sound).

• Wheeze (musical expiratory sound).

• Crackles (known as rales, crackling inspiratory sound).

13. Aging and the Respiratory System

• Normal physiologic changes.

• Senile emphysema (shrinking “tennis court”).

• Chest wall compliance decreases (ribs ossification, joints stiffening).

• Elastic recoil of lungs decreases (loss of muscle fiber).

• Overall decreased ventilatory capacity with reduced VC, increased RV, decreased exercise tolerance (increased DOE and SOB).

14. Classification of Lung Diseases

• Physiology of Restrictive vs. Obstructive Lung Disease.

• Both classified/diagnosed through patient Hx, chest assessment, CXR, ABGs, and PFTs.

• Restrictive Pulmonary Disease: generally the “inability to take a deep breath” due to restriction (stiffening) of lung tissue or the thorax or neurological disorder.

• Obstructive Pulmonary Disease: generally the “inability to exhale each breath completely” due to a reduced expiratory airflow from obstruction of the airways.

15. Obstructive Lung Disease

• Acute or Chronic; Reversible or Non-reversible.

• Termed COPD in US and COLD in Europe.

• Prolonged expiratory time required by patient to empty lungs due to thoracic pressure dynamics.

• Following heart disease, 2nd most debilitating disease of adults under 65 and 3rd leading cause of death (Pack-Years > 60).

• Environmental irritants cause exacerbations & increase morbidity/mortality rates.

• Diagnosis/management of COPD recognized world-wide using Global Initiative for Chronic Obstructive Lung Disease (GOLD) standards through NHLBI and WHO.

16. Acute Obstructive Lung Diseases

• Acute bronchitis: inflammation of trachea and bronchi with a bacterial or viral etiology.

• Asthma: potentially reversible obstructive airways disease caused by increased Raw due to hyperactivity in the presence of personal airway triggers; may potentially return to normal lung function.

• Croup and epiglottis: acute obstruction of upper airways.

17. Chronic Obstructive Lung Diseases

• Chronic bronchitis, emphysema, asthma.

• Term COPD used when CB and emphysema present concurrently.

• Also cystic fibrosis (CF), bronchiectasis, bronchiolitis.

18. Emphysema

• Anatomic Definition: permanent destruction of alveoli, connective tissue, and capillary beds resulting in hyper-inflation (air trapping) with loss of elastic recoil of lung tissue.

• Centrilobular: cigarette smoking (60 pack-yrs).

• Panlobular: genetic (alpha1-antitrypsin deficiency)

• Loss of elasticity and alveoli -> air trapping -> barrel chest (1:1) -> increased WOB/DOE -> weight loss/difficulty eating -> accessory muscle hypertrophy.

• Progressive anatomic changes:

  • Loss of “tennis court” AC interface -> increased pulmonary vascular resistance -> cor pulmonale -> increased pedal edema, palpable liver, JVD’s in neck.

  • Increased SOB at rest -> increased sedentary lifestyle.

21. Emphysema PFTs Diagnosis & Staging

• Increased lung volumes.

• Reduced expiratory flow rates.

• Decreased diffusion capacity due to loss of capillary beds.

• Limitation of thoracic cage expansion and diaphragmatic excursion.

• V/Q ratio near normal due to focused work on breathing. Pursed-lip breathing helps keep alveoli from collapsing. Described as “pink puffer.”

• Tx: Disease is progressive with low flow O_2 primary support, possible corticosteroids during exacerbations, inhaled bronchodilators when indicated, when cor pulmonale presents < 6 months survival.

22. Chronic Bronchitis

• Clinical definition: chronic productive cough for 3 months out of year for 2 consecutive years.

• Chronic irritation of airways -> inflammation, edema, excessive mucous production, hyperplastic mucous glands, physical obstruction of large and small airways by mucous, normal mucous clearance impeded due to increased viscosity.

• Initially NORMAL alveoli!

• Cyanosis “Blue Bloater” characteristics with poor ventilation.

• Hypercapnea and hypoxia increase pulmonary vascular pressure resulting in early cor pulmonale.

• Polycythemia, digital clubbing, similar PFT changes as seen with emphysema except normal diffusion rates.

• Treatment: O_2$, mucolytic Rx, bronchodilators, corticosteriods, low-carb diet, chest physiotherapy or postural drainage/percussion.</p></li></ul><h4 id="c98c197e-520a-4a53-bbf0-40d51c110b08" data-toc-id="c98c197e-520a-4a53-bbf0-40d51c110b08" collapsed="false" seolevelmigrated="true">23. COPD Implications for PT</h4><ul><li><p>Chest physical therapy: postural drainage, breathing techniques (pursed-lip breathing), segmental resistance, breathing exercises to strengthen ventilatory muscles (inspiratory/expiratory trainers), physical training to combat general deconditioning, posture training.</p></li><li><p>Instruct in energy conservation.</p></li><li><p>Monitor$O_2$saturation and HR.</p></li></ul><h4 id="28c49fa3-27c0-421f-bbed-f6b851ec12bf" data-toc-id="28c49fa3-27c0-421f-bbed-f6b851ec12bf" collapsed="false" seolevelmigrated="true">24. Asthma</h4><ul><li><p>Characterized by airway hyperreactivity to various external/internal stimuli with recurrent episodes of intermittent reversible airway obstruction due to bronchospasm and mucous production.</p></li><li><p>Extrinsic (Allergic/Type I): most common in children, due to IgE documented An/Ab rxt.</p></li><li><p>Intrinsic (Non-Allergic/Type II): adult onset, triggered by cold air, exercise, emotions, drugs.</p></li><li><p>Prevalence doubled in US since 1980 and increased by 400$O2/CO2$exchange, hypoxia results with ñWOB.</p></li><li><p>Tx: diuretics,$O_2, Beta 1 & 2 Rx.

• Prognosis: potentially reversible, but may lead to respiratory failure.

46. RLD – Tuberculosis (TB)

• Was once leading cause of death in U.S.

• Still one of top causes of death in world.

• 15,000 new cases annually in US (250-300 in Alabama).

• Caused by infection with Mycobacterium tuberculosis.

• Characterized by granulomas, caseous necrosis, and cavity formation.

• Transmission: airborne.

• Primary versus secondary infection.

• Multi-drug resistant TB.

47. TB (Continued)

• At-risk groups:

  • Immunocompromised

  • Crowded living conditions

48. TB Transmission

• Primary TB: inhalation of Mycobacterium tuberculosis from infected (Secondary TB).

• + TB skin test denotes exposure.

• Body forms Ghon foci calcification around MTB.

• Time bomb? May choose to tx with INH x 1 year.

• Secondary (post-Primary or Reactivation):

  • Not due to exogenous infection, rather reinfection of endogenous TB.

• TB treatable but difficult to recognize.

• Symptoms subtle, easy to ignore, nonspecific (eg, cough, phlegm production, weight loss, dyspnea, night sweats, fever, malaise, anorexia).

• Diagnosis: H&P, TB skin test, chest radiograph, microscopic examination and culture of sputum.

• During Secondary Infection, person is extremely contagious and should be placed in respiratory isolation until after 10-14 days of anti-TB Rx.

• Pharmacologic tx:

  • Agents that inhibit bacterial protein synthesis on DNR/RNA (INH, rifampin, pyrazinamide).

  • Agents that inhibit bacterial DNA/RNA synthesis and function (eg, ethambutol, rifampin).

• Recommended duration: 6-9 months.

• Rx side effects may include liver damage, hepatitis, temporary blindness (optic nerve toxicity), temporary loss of hearing.

• RESPIRATORY ISOLATION (mask only).

51. RLD: Aspiration Pneumonia

• Aspiration: inhalation of foreign material, usually food, drink, or vomit; common sequelae of stroke, seizure.

• Aspiration pneumonia: inflammation of lungs that results from aspiration.

• Introduction of aerobic and anaerobic bacteria into lungs, difficult to treat/resolve.

52. RLD: Acute Respiratory Distress Syndrome (ARDS)

• Acute respiratory failure due to systemic or pulmonary insult (eg, sepsis, trauma, major surgery).

• Also called adult respiratory distress syndrome, shock lung, hyaline membrane disease (adult or newborn), diffuse alveolar damage.

• Often fatal (80% mortality rate for patients >35 yrs and 20% fatal for patients <35 yrs).

• Pathogenesis: damage to alveolar epithelium and capillary endothelium→ pulmonary edema → “drowning” at cellular level.

• Onset: within 12-48 hrs, w/ initial presentation of ↑ RR (shallow, rapid).

• Characterized by dropping SaO2$while increasing$FIO2.

• Neonates benefit from surfactant replacement Rx.

• Adults do not benefit form surfactant Rx.

Injury, Inflammation, Healing and Repair

Learning Objectives

• Describe the mechanisms of cell/tissue injury.

• Compare the different means of cellular adaptation.

• Explain the cellular responses associated with inflammation.

• Describe the process of tissue healing.

• Define factors that affect tissue healing.

• Compare & contrast the phases of healing.

Cell Injury

• Reversible or irreversible.

• Factors affecting return to homeostasis:

  • Mechanism of injury.

  • Length of time injured without intervention.

  • Severity of injury.

Mechanism of Cell Injury

• Ischemia

• Infectious Agents

• Immune Reactions (Hypersensitivity, Autoimmune)

• Genetic Factors

• Nutritional Factors

• Physical Factors

• Mechanical Factors

• Chemical Factors

Mechanisms of Cell Injury - Ischemia

• Blood flow below the minimum necessary to maintain cell homeostasis and metabolic function.

  • ↓$blood flow</p></li><li><p>$↑$metabolism</p></li></ul></li><li><p>Reduction in oxygen supply (partial: hypoxia, total: anoxia).</p></li><li><p>$↓$nutrients</p></li><li><p>$↓waste removal

  • Arterial obstruction and narrowing by atherosclerosis and/or intravascular clot called thrombus.

  Mechanisms of Cell Injury - Infectious Agents

  • Bacteria, viruses, mycoplasma, fungi

  Mechanisms of Cell Injury - Immune Reactions

  • Hypersensitivities

    • Overactive immune reactions → mild allergy reaction or life-threatening anaphylactic reactions.

  • Autoimmune

    • Immune system attacks self.

  Mechanisms of Cell Injury - Genetic Factors

  • Alters the structure or # of chromosomes that leads to multiple abnormalities (Down’s Syndrome/ Trisomy 21).

  • Single mutations of genes: changes in the amount or functions of proteins (Sickle Cell Disease).

  • Multiple gene mutations: interact with environmental factors and multifactorial disorders result. (Hypertension, Type II DM).

  Mechanisms of Cell Injury - Nutritional Factors

  • Imbalances in essential nutrients → cell injury or death.

  • Abnormal levels of vitamins/minerals, protein malnutrition (kwashiorkor), reduced (anemia) or excessive (free radicals) iron.

  Mechanisms of Cell Injury - Physical Factors

  • Trauma: blunt trauma (massive brain contusions, internal organs, blood loss …)

  • Physical agents: extremes of temperature (burn, frostbite), radiation, electricity

  Mechanisms of Cell Injury - Physical Stress

  • Physical stress exceeds tolerance of the tissue.

  • Overstretch, compression, friction, anoxia

  Mechanisms of Cell Injury - Chemical Injury

  • Toxic substances lead to chemical injury

  • Mercury poisoning, agents used in chemotherapy, drug overdose

  Types of Cell Injury

  • Reversible injury: when stress is small and duration is short à cell is able to cover homeostasis after stress removal

  • Irreversible injury: when stress is of sufficient magnitude or duration à cell is unable to adapt

  Adaptation

  • The ability to alter mechanisms and regain homeostasis in the altered environment by cells or tissues

  • Alterations with sub-lethal stress over a period of time

  • Cellular adaptation characteristics:

    • Change in cell size, #, or function

    • Increases ability to survive

  Cellular Adaptations

  • Common cellular adaptations

    • Atrophy: Reduction in cell and organ size due to vascular insufficiency, reduction in hormone levels, malnutrition, immobilization, and pain

    • Hypertrophy: Increase in size (skeletal muscle, cardiac cell hypertrophy)

    • Hyperplasia: Increase in # of cells → increased tissue size (uterus during pregnancy, skin callus, prostate enlargement)

    • Metaplasia: Conversion of an adult cell; change in form or function (smoker respiratory epithelium)

    • Dysplasia: Pre-neoplastic alteration; ↑ in number with altered cell morphology, and loss of histological organization (chronically injured area)

  Inflammation

  • Normal secondary response to cell injury followed by healing & repair

  • Viral role in host defense mechanism against pathogens protecting host from infection/injury

  • Purpose: mobilize & transport the body’s defenses essential for healing to occur

    • Removal of injurious agent

    • Removal of cellular debris (dead cells)

    • Initiation of healing process

  • Intertwined with process of repair

    • Stimulates response for healing

  • Involves complex set of vascular, neurologic, & cellular responses

  Acute Versus Chronic Inflammation

  • Acute Inflammation

    • Sudden onset with short duration; self limiting

    • Exudation of fluid and plasma protein (edema), migration of leukocytes (neutrophil)

    • Clinical manifestations: redness, swelling, increased temperature, pain, decreased function, increased Muscle Tone or Spasm

  • Chronic Inflammation

    • Long duration: weeks, months, or years

    • Causes:

      • Extensive necrosis

      • Underlying cause not addressed

      • Chronic overuse

      • Repeated trauma

      • Low-grade, persistent immune reactions

      • Autoimmune diseases

    • Hallmark in tissue: accumulation of macrophages, lymphocytes, & plasma cells

    • Much greater scar formation

  Components of Inflammatory Response - Vascular alterations

  • Vasoconstriction of small arteries supplying injured area

    • Due to neural reflex

    • Short duration, ~ 10 minutes

  • Vasodilation

    • Long duration

    • ↑$blood flow to injured area (thus$↑$blood volume) → hydrostatic pressure$↑$</p></li><li><p>Transudation results: leakage of low-protein fluid from vasculature into the injured tissue (transudate)</p></li><li><p>Erythema, warmth, and edema</p></li><li><p>Exudation: extravascular fluid with high-protein</p></li></ul></li></ul><h4 id="2f753e7f-4d76-44d8-a3e9-1e639c93f68b" data-toc-id="2f753e7f-4d76-44d8-a3e9-1e639c93f68b" collapsed="false" seolevelmigrated="true">Components of Inflammatory Response - Leukocyte Accumulation</h4><ul><li><p>$↓ protein & fluid in vasculature (due to transudation) → engorgement of red blood cells in vessels → stasis

    • Stasis: slowing or cessation of blood flow

    • During stasis, leukocytes accumulate and adhere to endothelial cells of blood vessel walls at injury site (margination)

    • Actively pass through the vascular walls, migrating out of vessel into interstitial space without damage to vessel wall (diapedesis or oozing)

    • Diapedesis due to leukocytes attraction to chemotactic agents in interstitial space at site of injury (chemical stimulus)

    • Leukocyte locomotion process: chemotaxis

    Summary of Inflammatory Response

    • Tissue Injury → Vaso Constriction → Vasodilation → Transudation → Stasis → Margination → Diapedesis → Chemotaxis → Phagocytosis

    Chemical Mediators

    • Responsible for the vascular & leukocyte responses with acute inflammatory response

    • Released from inflammatory cells or plasma

      • Cell-derived – generated from inflammatory cells

      • Plasma-derived – generated by plasma protease (enzymes that act as catalyst in breakdown of proteins)

    • Multi-functional effects on blood vessels, inflammatory cells, other body cells

    • Vasodilation, vasoconstriction, vascular permeability change, activation of inflammatory cells, chemotaxis, cytotoxicity, affect fever & pain

    Cell-Derived Mediators

    • Histamine

      • Endothelial Contraction - Increased membrane permeability

      • Vasodilator (Strong)

      • Potent bronchoconstrictor

      • Stored in mast cells, basophils, platelets

    • Serotonin

      • Vasoconstriction

      • Effects overridden by histamine

    • Cytokines

      • Wide range of inflammatory actions & systemic actions

      • Moderate activity/function of other cells

    • Prostaglandins

      • Lipids made at sites of tissue damage with hormone-like effects

      • Mediators of fever/pain responses associated with inflammation, constriction or dilation blood vessels

      • Clot formation

    • Chemokines

      • Specific types of cytokines

      • Chemoattractants for leukocytes, neutrophils, monocytes (direct the leukocytes to the pathogen)

    Plasma-Derived Mediators

    • Blood Coagulation Cascade

      • Plasma proteins bandage injuries with clots (coagulation)

      • Disassemble (lyse)

      • Thrombin → Fibrinogen to fibrin

    • Fibrinolytic System

      • Activated by fibrinolysin

      • Dissolves clots

    • Bradykinin

      • Inflammatory Mediator

      • Peptide that causes vessel dilation and pain

    • Complement System

      • Plasma proteins dormant in blood, interstitial fluid, & mucosal surfaces

      • Activated by foreign protein & antigen-antibody complex

      • Vasodilation, leukocytes migration, opsonization

    Tissue Healing

    • Begins soon after tissue injury/death

    • Tissue healing occurs either by regeneration (regrowth of original tissue) or by repair (formation of a connective tissue scar)

    • Complex and influenced by many components

    • Components

      • Fibronectin

      • Proteoglycans

      • Elastin

      • Collagen

    Fibronectin

    • One of the first proteins to provide structural support that stabilizes the healing tissue - most common type of cell in connective tissue

    • Most important functions:

      • Formation of scaffold

      • Provision of tensile strength

      • “glues” other substances/cells together

    • Binds to fibrin: protein that makes up blood clots present in injured tissue

    • Attracts fibroblasts & macrophages by chemotaxis

    • Stimulated fibroblasts secrete more fibronectin

    • Binds to proteoglycans and collagens à stabilizes healing tissues

    Proteoglycans & Elastin

    • Proteoglycans

      • Proteins secreted by fibroblasts early during tissue repair reaction

      • Bind to fibronectin & collagen: helps stabilize the healing tissue

      • Aid in hydration of tissue

    Collagen

    • Most important protein to provide structural support and tensile strength most tissues and organs à Give stability to healing tissues

    • 28 different types: each type has special function

      • Type I: most common form, found in all body tissues, structurally very strong, predominant in tendons/bones & mature scars

      • Type II: predominant in cartilaginous tissue & bone physis (growth plate)

      • Type III: provides support for developing capillaries / makes tissues strong but supple, & elastic

      • Type IV: forms basement membrane to which other cells are anchored

    Factors Affecting Tissue Healing

    • Growth Factors

      • Proteins that regulate several cellular reactions involved in healing: cell proliferation, differentiation, & migration

    • Nutrition: vitamin A, vitamin B, vitamin C, zinc, protein, and carbohydrates

    • Vascular supply

    • Presence of Infection

    • Immune reactions

    • Age

    • Comorbidities / medications

    • Smoking

    Phases of Healing

    • Within 24 hours after dead tissue removal:

      • Hemostasis

      • Inflammation

      • Proliferation

      • Remodeling (maturation)

    Hemostasis

    • Hemostasis is the first step, occurring immediately after acute injury as body tries to stop bleeding

    • Vessels constrict to restrict the blood flow

    • Platelets plug formation

    • Coagulation cascade: formation of blood clot – thrombus

    Inflammation

    • Serves vital role in healing process

    • Protective and curative features

    • Begins once blood clot forms

    • Suffix = “-itis”

    • Functions

      • Inactivate injurious agent

      • Breakdown/remove dead cells

      • Initiate tissue healing

    Proliferation

    • Reconstruction step with endothelial cell proliferation

    • Purpose: establish vascular network to transport O_2$$ & nutrients & support metabolism of healing tissue

    • Characterized by formation of granulation tissue, angiogenesis, wound contraction and process of epithelialization

    • Occurs 3-5 days following injury

    • Overlaps with inflammatory phase

    • Angiogenesis: formation of new blood vessels, involving the migration, growth, and differentiation of endothelial cells, which line the inside wall of blood vessels

    Remodeling (Maturation)

    • OCCURS AFTER 2-3 WEEKS – 2 YEARS

    • SCAR TISSUE REDUCED & REMODELED: SMOOTHER, STRONGER, LESS DENSE, LESS RED TISSUE

    • COLLAGEN FIBERS REMODELED: PRODUCED, BROKEN DOWN, REARRANGED – GROWING STRONGER (BUILD TENSILE STRENGTH AND ELASTICITY OF THE SKIN)

    • 3 MAIN REMODELING STEPS: TISSUE CONTRACTION & CONTRACTURE, TISSUE REGENERATION, TISSUE REPAIR

    Tissue Contraction & Contracture

    • Extracellular matrix draws together: healing tissue contracts

    • Tissue defect size is shrinking

    • Due to specialized fibroblasts: myofibroblasts that accumulate in wound margins

    • Tissue contraction approximates the margins of the healing tissue – wound closing

    • Contracture: excessive shrinkage – can limit mobility

    Tissue Regeneration

    • Regeneration: The process of replacement of dead cells by new cells

    • Regrowth of original tissue

    • Restores normal tissue structure and function

    • Occurs due to healthy cell mitosis (cell division)

    Tissue Repair

    • Most healing involves regeneration & tissue repair

    • Tissue repair: replacement by connective tissue scar

    • Dense, irregular laying down of collagen

    • Occurs with damage beneath epidermis

    • Scar tissue: 70-80% as strong as original tissue, less vascular

    • Scar function dependent upon stresses applied during healing

    Physical Therapy & Scar Tissue

    • EXERCISE!

      • Scar remodeling occurs with stress (stretch/strengthening exercises)

      • Realignment of collage fibers to become stronger

    • Pressure

    • Myofascial release

    • Deep transverse friction tissue mobilization

    • Lubrication

    • Stretching

    • Kinesiology tape

    • Therapeutic Pulsed Ultrasound