UERM BSPT-2017

MS 1

Topic: CARDIOVASCULAR REHABILITATION Lecturer: Dr. Ej Agsaoay

I. DISEASES

Effects of aging on the heart:1. Sigmoid septum - ↓ ventricular cavity size outflow

obstruction2. Valve sclerosis & calcification leading to stenosis (aortic valve)3. Valve degenerative changes leading to insufficiency (mitral

valve)4. ↓ myocyte number & ↑ interstitial fibrosis causing reduced

contractility and compliancePathophysiology:

1. Failure to pump2. Blood flow obstruction (valvular insufficiency) & regurgitant flow 3. Shunts (RL: Lung bypassing or LR: volume overload)4. Abnormal cardiac conduction & rupture

CONGESTIVE HEART FAILURE (CHF) Unable to maintain output sufficient for the metabolic

requirements of the body or at elevated filling pressures. Forward failure: diminished cardiac output Backward failure: blood in the venous system Compensatory mechanisms:

Frank-Starling mechanism: Increased filling pressures dilate the heart, ↑ functional cross-bridge formation within sarcomeres and ↑ contractility

Myocardial hypertrophy with increased expression of contractile apparatus proteins

Activation of neurohumoral systems Systolic dysfunction: (most frequent) progressive deterioration

of myocardial contractile function, MI Diastolic dysfunction: inability of the heart chamber to relax

and fill during diastole, hypertrophy (>65 yo, F>M)

LEFT-SIDED HEART FAILURE Ischemic heart dse, HTN, aortic & mitral valve dse, intrinsic

myocardial dse Manifested by:

Pulmonary congestion and edema due to regurgitant flow or impaired pulmonary outflow

Left atrial dilation with atrial fibrillation Reduced renal perfusion Hypoxic encephalopathy

RIGHT-SIDED HEART FAILURE Most commonly caused by LSHF with biventricular CHF Tricuspid or pulmonic valve dse , intrinsic pulmonary vascular

dse R ventricular outflow obstruction

Manifested by: R atrial & ventricular dilation & hypertrophy Edema (feet, ankles, sacrum) Hepatomegaly (nutmeg appearance) w/ hypoxia,

centrilobular necrosis cardiac necrosis Congestive splenomegaly with deposits & fibrosis Renal congestion

CONGENITAL HEART DISEASE (CHD) Most common among children. Present at birth (faulty

embryogenesis at 3-8 wks of gestation) Sporadic genetic abnormalities (heart structure defects) Deletion of chromosome 22q11.2 (DiGeorge syndrome) 3rd &

4th pharyngeal pouches Most common cause: Trisomy 21 (Down syndrome) Direct hemodynamic squelae w/ retarded dev’t Divided into: obstruction and shunts

OBSTRUCTIONS Abnormal narrowing of chambers, valves, or vessels Complete obstruction = atresia

1. COARCTION OF THE AORTA Bicuspid aortic valce M>F, 2:1 Coarctations are common in Turner syndrome L ventricular hypertrophy Preductal – infantile form Postductal – adult form

2. PULMONARY STENOSIS AND ATRESIA 3. AORTIC STENOSIS AND ATRESIA

Abn cusps

RIGHT-TO-LEFT SHUNTS Hypoxia & cyanosis, paradoxical emboli (venous emboli),

finger and toe clubbing (aka hypertrophic osteoarthropathy), polycythemia

1. TETRALOGY OF FALLOT Ventricular septal defect Pulmonary stenosis w/ R ventricle outflow

obstruction / hypertrophy Overriding aorta

2. TRANSPOSITION OF THE GREAT ARTERIES Aorta and pulmonary systemic circulations Venous and systemic blood mixes thru ductus

arteriosus and a patent foramen ovale

LEFT-TO-RIGHT SHUNTS Prolonged shunt medial hypertrophy ↑ vascular

resistance reaches systemic levels R-to-L shunt occurs (aka Eisenmenger syndrome)

1. ATRIAL SEPTAL DEFECT Most common congenital cardiac anomaly in adults

2. PATENT FORAMEN OVALE Small hole from a defective postnatal closure of the

fossa ovalis flap (paradoxical emboli)3. VENTRICULAR SEPTAL DEFEC

Most common overall Associated with TOF

4. PATENT DUCTUS ARTERIOSUS

L subclavian artery Allows blood flow bet aorta & pulmonary artery

during fetal dev’t (normally closes w/in 1-2 days of life)

Machinery-like heart murmur

ISCHEMIC HEART DISEASE (IHD) Mismatch between cardiac demand and vascular supply of

oxygenated blood Reduced coronary blood flow Increased myocardial demand Hypoxia Arteriosclerosis – arterial wall thickening and loss of elasticity Atherosclerosis – progressive dse & lesions of large to medium

sized muscular and elastic arteries; chronic narrowing of the coronary lumens by plaque rupture leading to vessel thrombosis; weakening the underlying vessel wall leading to aneurysm formation

Constitutional Risk Factors: Age 40-60 y.o Gender: M>F : M < Post-menopausal F Genetics: familial hyperchosterolemia

Modifiable Risk Factors: Hypercholesterolemia; diet, exercise, alcohol intake,

statins HTN Smoking (one pack per day, doubles death rate) DM (accelerates atherosclerosis, doubles MI, ↑

stroke & extremity gangerene)

ANGINA PECTORIS (CHEST PAIN) Stable angina – chronic stable stenosis Prinzmetal angina – vasospasm Unstable (crescendo) angina – atherosclerotic plaque is

disrupted w/ thrombosis or vasospasm: harbinger of myocardial infarction

Causes : Blockage Spasm / partial occlusion of coronary arteries Aortic stenosis Hypertrophic cardiomyopathy Pulmonary HTN Primary myocardial dse

Characteristics : Visceral (poorly localized), squeezing, oppressive,

burning/heavy

Brief (2-10 mins.) Moderate intensity Typically substernal

MYOCARDIAL INFARCTION (HEART ATTACK) Myocyte cell death caused by vascular occlusion or intraplaque

hemorrhage or plaque rupture with thrombosis or embolization (coronary atrial occlusion causes myocardial ischemia)

60secs: ATP depletion (loss of function) 20-30mins: complete deprivation of blood flow leads to

irreversible myocardial injury 2-4hrs: severe flow compromised for long periods; salvage 6hrs: necrosis is complete “ST ECG elevation MI” Lysis of a thrombotic occlusion before full thickness infarction Reperfused myocardium shows contraction band necrosis due

to Ca overload & hyper-tetanic contraction Morphology :

Gross changes:o 6 to 12 hrs: MIs are unapparent but can be

highlighted by histochemical stains; triphenyltetrazolium chloride is a lactate dehydrogenase substrate; viable myocardium turns the substrate red-brown, while nonviable areas are pale.

o 18 to 24 hrs: Infarcted tissue becomes apparent, pale to cyanotic areas.

o 1 wk: Lesions become progressively more defined, yellow, and softened.

o 7 to 10 days: Hyperemic granulation tissue appears at the infarct edges

o 1 to 2 mos: White fibrous scar is usually well established.

Microscopic changes:o < 1 hr: Intercellular edemao 12 to 72 hrs: Dead myocytes become

hypereosinophilic with loss of nuclei (coagulative necrosis)

o 3 to 7 days: Dead myocytes are digested by invading macrophages.

o 7 to 10 days: Granulation tissue progressively replaces necrotic tissue.

o > 2 wks: Fibrous scar. Clinical Features:

S/Sx:o Chest pian, nausea, diaphoresis, dyspneao Serum elevation (creatine kinase MB [CK-

MB], troponins)o Silent MI: diabetic or geriatric

Risk Factors: <40 – 65 y.o, M>F (Nearly) all transmural MI affect the L ventricle Half of MI deaths occur within the 1st hr. Contractile dysfunction Arrhythmias Ventricular rupture occurs within the 1st 10 days (4-5

median days) Fibrinous pericarditis (Dressler syndrome) common

2-3 days after MI Mural thrombosis peripheral embolization LTPrognosis: residual L ventricular function

Therapeutic Intervention: Thrombolysis Stenting

Chronic Ischemic Heart Disease Post-MI

ARRHYTHMIAS Abnormalities in myocardial conduction: sustained or sporadic

(paroxysmal) Abnormal rhythm of the heart = heart pumps less SA node (originating from the atrium) Clinical Features:

Tachy/bradycardia (racing heart or palpitations) Irregular rhythm w/ normal ventricular contraction Chaotic depolarization w/o functional ventricular

contraction (ventricular fibrillation) Atrial fibrillation (fatal) Asystole Loss of cardiac output due to sustained arrhythmia:

o Near syncope (light-headedness)o Syncope (LOC)

SA node damaged + AV node dysfunctional = heart block

Long QT syndrome

HYPERTENSIVE HEART DISEASE Elevated pressures induce myocyte hypertrophy and interstitial

fibrosis that ↑ wall thickness and myocardial stiffness ↑ resistance with every contraction hypertrophic LV walls If not managed properly, walls will dilate and weaken Causes and Risk Factors:

o Genetics (FMHx)o Lifestyle & diet (smoking)o Hyperglycemia

Uncontrolled HTN: o Affects kidneyso Affects eyes (due to ↑ pressure: retina pops,

hemorrhage over retina, visual problems) Improperly Managed:

o Microangiopathy (small vessels damaged)o Retinopathy (blurred vision)o Glaucoma (↑ intraocular pressure)o Autonomic neuropathy (incontinence)o Peripheral neuropathy (pins and needles over finger

tips, affects peripheral vessels: poor distal circulation in feet and hands)

o Infections if with wounds: gangrene amputation = can’t save

o Hardening of vessels supplying kidney, M.I., atherosclerosis

SYSTEMIC (LEFT-SIDED) HYPERTENSIVE HEART DISEASE Most common cause of pulmonary venous hypertension Hypertrophy is an adaptive response to elevated pressures.

Continued overload CHF History of HTN + L ventricular hypertrophy Interstitial fibrosis that also reduces compliance Congestion and peripheral edema

PULMONARY (RIGHT-SIDED) HEART DSE — COR PULMONALE Results from pulmonary HTN due to primary lung parenchymal

or vascular disorders Acute cor pulmonale – Pulmonary embolism R ventricular

dilation w/o hypertrophy Chronic cor pulmonale – R ventricular pressure overload & wall

thickens

VALVULAR HEART DISEASE (VHD) Degeneration (calcific aortic stenosis, mitral annular

calcification, mitral valve prolapse)

Inflammatory process (rheumatic heart dse) Infection (infective endocarditis) Changes secondary to MI (IHDmitral regurgitation)

1. CALCIFIC AORTIC STENOSIS Age-related; >70yo Mostly occurs in congenitally bicuspid valves “Wear and tear”

2. MITRAL ANNULAR CALCIFICATION Degenerative non-inflammatory calcific deposits F: >60yo

3. MITRAL VALVE PROLAPSE mitral valve leaflets are enlarged and floppy

“balloon back” (prolapse) into the LA during systole4. INEFECTIVE ENDOCARDITIS

RHEUMATIC FEVER AND RHEUMATIC HEART DISEASE Acute inflammatory dse occurring in children after group A

streptococcal infection (pharyngitis) Antigens are activated antibodies go to work

creates vegetation that go into the heart (especially in inner layers: endocarditis/myocarditis)

(65-70%) Solitary mitral involvement (20-25%) Combined aortic & mitral involvement Virtually the only cause of acquired mitral valve stenosis Vegetative valve dse Instead of proper closure of heart, there is still an opening

blood now flows in the opposite direction. Leads to regurgitation of oxygenated &

unoxygenated blood Auscultation: specific murmur will be heard Ventricular septal defect (VSD): congenital in nature

Heart is surrounded by air, entered pericardial sac causes pressure/compression cardiac tamponade (cannot expand properly)

Hypertrophic LV CHF Management:

Tonsillectomy Morphology:

Acute RFo Appears 10 days to 6wks after grp A strep

infectiono Occurs in children 5-15 y.o but first attacks

can occur in middle to later lifeo Focal inflammatory lesions (aka Aschoff

bodies [pancarditis]) consists of plump macrophages (aka Anitschkow cells) with abundant cytoplasm which the chromatin condenses into a ribbon (aka “caterpillar cells”)

o Inflammatory valvulitis characterized by beady fibrinous vegetations (verrucae) along the lines of valve closure

Chronic (or healed)o Diffuse fibrous thickening of valve leaflets

(“fishmouth” or “buttonhole” stenoses)o Thickened MacCallum plaques

Clinical Features: Diagnosis is based on Jones criteria Polyarthritis of the large joints Pancarditis Subcutaneous nodules Erythema marginatum of the skin Sydenham chorea Edematous LE & cyanosis (finger and toes) Dyspnea

Cough Pleural effusion Acitis: compression of fluid over stomach

Causes: Persistent or recurrent sore throat Endocarditis Severe aortic stenosis

DISSECTING ANEURYSM Abnormal vascular dilations/tear in the inner layer of the vessel

True aneurysm – bounded by all three vessel wall layers False aneurysm (pseudoaneurysm) – extravascular hematoma

that communicates with the intravascular space that was lost Dissection occurs when blood enters the arterial wall itself

(hematoma dissecting between layers) Extreme severe stabbing pain Pathogenesis:

Poor intrinsic quality of the vessel matrix o Marfan syndrome – inadequate fibrillin

synthesis, loss of elastic tissue matrixo Loeys-Dietz syndrome – likewiseo Ehlers-Danlos syndrome – defective

collagen cross-linking in scurvy Imbalance of matrix synthesis and degradatioin

Causes: Atherosclerosis (particularly in the abdominal aorta) HTN (ascending thoracic aorta) Syphilis Trauma Vasculitis Congenital defects Septic embolization infection (mycotic aneurysm)

1. ABDOMINAL AORTIC ANEURYSM (AAA) True aneurysm Male smokers, >50 yo Positioned below the renal arteries above the iliac

bifurcation Medial smooth muscle cell (SMC) loss & ↑ matrix

degradation Occlusion of a branch vessel, atheroembolism Inflammatory AAA – dense periaortic fibrosis

2. THORACIC AORTIC ANEURYSM HTN

Aortic root dilation (aortic valve insufficiency) Dyspnea (airway) & dysphagia (esophagus) Cough and bone pain

3. AORTIC DISSECTION Sudden death due to massive hemorrhage or cardiac

tamponade Hypertensive (M), ages 40-60.yo (cystic medial

degeneration) Children with Marfan syndrome Trauma

CARDIAC PROBLEMSCARDIAC NON-CARDIAC

PAIN QUALITY Heaviness, burning, constricting, visceral

Sharp, piercing, muscular, dull ache

PAIN LOCATIONSubsternal, neck, hands, shoulders, epigastrium

Submammary left, apex of heart, right lower chest, discrete location

PAIN DURATION Angina: 2-10 mins, >20 mins to 24h

Infarct <20 sec, persistent w/o change

PRECIPITATING / AGGRAVATING

FACTORS

Exercise, excitement, stressful stimuli, cold temp., post-prandial

After completion of exercise, related to body positions, spontaneous

RELIEVING FACTORS Rest, Nitroglycerin Antacids, food, nonsteroidal analgesic

II. SURGERIES

ANGIOPLASTY

IMPLANT PLACEMENT (CONVERTER DEFIBRILLATOR) An implantable cardioverter-defibrillator (ICD) detects a rapid

heartbeat coming from the bottom of the heart

CORONARY ARTERY BYPASS GRAFT (CABG)

VALVULAR REPLACEMENT

HEART TRANSPLANT

III. REHABILITATION Process of enabling patients with cardiac disorders to resume

activity & productive lives within the limitation imposed by their dse.

Objectives: Restoration of physiologic, psychosocial, and

vocational status at optimal levels Prevent progression of dse Reduce risk of sudden cardiac death

Goal: Return to NORMAL lifestyle & role in the society

Team: Cardiologist PT OT Psychologist Social Worker Nurses Nutritionist

Components Exercise conditioning Psychosocial intervention Education Dietary counseling Use of meds

METS:

Standard measure of energy expenditure Metabolic equivalents Estimate amount of O2 consumed to perform

function 1 MET = 3.5 ml / kg / min O2 consumed

PRIMARY PREVENTION Lifestyle modification and education Cardiac risk factor identification and modification

Irreversible ReversibleGender (M) Sedentary lifestyle & smoking

Age HTNFMHx: Premature CAD

(<55yo) DM

PMHx:CAD, CVD, Occlusive PVD

Low HDL cholesterol (35mg/dL)Hypercholesterolemia (200mg/dL)Hypertriglyceridemia (250mg/dL)

Abdominal obesityMetabolic syndrome

HyperinsulinemiaHigh lipoprotein A

Dietary counseling Stress management training Exercise regimen

PHYSIOLOGY RECAP Aerobic Capacity (VO2max) – ability the individual to perform

exercise. Measure of work output. It is the work capacity of a person. (liters of O2 per minute)

Oxygen Consumption (VO2) – linear relationship with workload. Measured thru analysis of expired gases. It reaches steady state after 3-6 mins of exercise.

Heart Rate – linear increase in relation to VO2. It declines with age even with ongoing exercise. (Max HR = age – 220)

Stroke Volume – quantity of blood pumped with each heartbeat. SV increases during early exercise. Major determinant is diastolic filling time. SV is sensitive to postural changes.

Cardiac Output = HR x SV. In early exercise principal increase is via the Frank-Starling mechanism (SV) while in late exercise, it is by HR. CO is the primary determinant of VO2max

Myocardial O2 Consumption (MVO2) – O2 consumption of the heart. Usually estimated using the rate pressure product (RPP) = HR x SBP / 100

Peripheral Resistance – responsible for ↑ in systolic pressure and is a major contributor to myocardial wall tension& limiting bloodflow

PRINCIPLES OF AEROBIC TRAINING Intensity (target heart rate) Duration

Cardiac conditioning exercise program is usually 20-30 mins with 5-10 min warm up and cool down

Frequency 3-5x /week

Specificity Normal:

Aerobic capacity: ↑ VO2: no change Max CO: ↑ Resting CO: no change HR after AT: ↓ Max HR: no change SV: ↑ (at rest and all levels of exercise after AT)

MVO2: ↓ or no change (determined by angina threshold)

PR: ↓

ABNORMAL PHYSIOLOGY IN RESPONSE TO EXERCISEVO2max CO HR SV MVO2 PR

MI ↓ ↓ ↓ / ↑ / x ↓ / x ↓ ↑ / xIHD ↓ x / ↓ ↓ / ↑ / x ↓ / x ↓ ↓ / ↑ / xVHD ↓ ↓ ↑ / x ↓ / ↑ / x ↓ / x ↑ / xCHF ↓ ↓ ↑ / x ↓ ↓ ↑Arrhythmia ↓ / x ↓ / x ↓ / ↑ / x ↓ / x ↓ / x xTransplant ↓ ↓ ↓

(max)↓ ↓ ↑ / x

*x = unchanged 85% max HR achieved during ETT 60%, in frail & deconditions 5 methods:

Karvonen formula RPE / Borg scale 220 – age O2 consumption Work load method (METS) – defined by physiologic

response (HR or RPP) or in terms of exercise intensity (speed or resistance setting)

SAMPLE METSALDs METS

Sitting at rest 1Dressing 2-3Eating 1-2Hygiene (sitting) 1-2Hygiene (standing) 2-3Sexual intercourse 3-5Showering 4-5Tub bathing 2-3Walking: 1mph 1-2Walking: 2mph 2-3Walking: 3mph 3-3.5Walking: 3.5mph 3.5-4Walking: 4mph 5-6Climbing up stairs 4-7Bed making 2-6Carrying 18lb upstairs 7-8Carrying suitcase 6-7General housework 3-4Making lawn (push power mower) 3-5Ironing 2-4Snow shoveling 6-7

AVOCATIONAL ACTIVITIES METSBackpacking (45lb) 6-11

Competitive baseball 5-6Non-competitive baseball 4-5Competitive basketball 7-12Non-competitive basketball 3-9Card playing 1-2Cycling 5mph 2-3Cycling 8mph 4-5Cycling 10mph 5-6Cycling 12mph 7-8Cycling 13mph 8-9Karate 8-12Running 12min/mile 8-9Running 11min/mile 9-10Running 9min/mile 10-11Skiing cross-country 3mph 6-7Skiing cross-country 5mph 9-10Skiing downhill 5-9Skiing water 5-7Swimming (backstroke) 7-8Swimming (breaststroke) 8-9Swimming (crawl) 9-10Television 1-2Tennis (singles) 4-9

VOCATIONAL ACTIVITIES METSAssembly line work 3-5Carpentry (light) 4-5Carry 20-44lb 4-5Carry 45-64lb 5-6Carry 65-85lb 7-8Chopping wood 7-8Desk work 1.5-2Digging ditches 7-8Handyman 5-6Janitorial (light) 2-3Lift 100lb 7-10Painting 4-5Sawing hardwood 6-8Sawing softwood 5-6Sawing (power) 3-4Shoveling 10lb, 10/min 6-7Shoveling 14lb, 10/min 7-9Shoveling 16lb, 10/min 9-12Tools (heavy) 5-6Typing 1.5-2Wood splitting 6-7

DeLisa: PM&R (5th Ed.)

KARVONEN FORMULA Training Heart Rate = (MHR – RHR) intensity + RHR

MHR: Maximal heart rate: from stress test RHR: Resting heart rate

Intensity 60 – 85% If no stress test result:

Predicted MHR = 220-age In determining intensity (if on medication)

Rate of perceived exertion Metabolic equivalent levels

BENEFITS OF CARDIAC REHABILITATION Peripheral Training Effects

↑ O2 extraction by skeletal muscle ↑ utilization of O2 by active muscle ↑ maximal O2 consumption & physical work capacity

Myocardial Training Effects Improved ventricular contraction Improved myocardial perfusion Improved myocardial function Formation of collateral vessels

Other benefits Promote weight loss Increase HDL Decrease LDL & triglyceride Improve blood sugar level

OUTCOME Resumption of normal life

Improve functional status Return to work

7 Mets or higher = able to return to most jobs 5 – 7 Mets = household chores 3 – 4 Mets = not suited to work

Sexual activity: 2 flight of stairs

PHASES OF CARDIAC REHABILITATIONPhase

1Mobilization

Phase (in-patient) In-patient Stable Reduces anxiety and prepares

patient and family for discharge

Phase 2

Conditioning Phase (out-

patient)

Post hospital phase Physical rehabilitation for

resumption of habitual and occupational activities habitual and occupational activities

Requirement Stress Test

Phase 3

Maintenance Phase

(community-level)

Back to ADL Maintenance of Lifestyle Back to work

In-patient Stable & Early mobilization Reduces anxiety and prepares pt & family for discharge

WEGNER PROTOCOLDAYS STEPS ACTIVITY

1 Program introduction, PROM, ankle pumps, self-feeding

2 Dangle at the side of the bed

3 AAROM, upright sitting (15-30mins), light recreation, bedside commode

4Increased sitting time, light activities w/ minimal resistance, seated ADL activities, warm up-standing

5 Light activities w/ moderate resistance, unlimited sitting, seated ADL activities

3 to 5 6 Increased resistance, walking to bathroom, standing ADL, 1hr long group meetings

CARDIAC REHAB OF THE POST-MI PATIENT

7 Walking up to 100ft, standing warm-up exercises8 Increased walking, walk down stairs (not up)

9 Increased exercise program, review energy conservation, pacing techniques

10 Increased exercises w/ light weights & ambulation, education on home exercise program

11 Increased duration of activities

12 Walk down two flights of stairs, increased resistance in exercises

13 Continue activities, HEP teaching

14Walk up and down two flights of stairs, complete instruction in HEP, energy conservation, and pacing techniques

At day 3, HEP is introduced

Patients are rapidly evaluated for revascularization procedures The post-MI HR rise with activity should be kept to within

20bpm of baseline Any decrease of SBP rise within 10mmHg or more should be

considered worrisome and the exercise halted The ultimate goal of the phase I program is to condition the

patient to perform activities up to four METs, which is within the range of most daily activities at home after discharge

EJ AGSAOAY VERSIONSTEP METS PT OT

1 1 – 1.5 PROMAnkle pumps

Self – feeding; dangle legs, sitting at bedside

2 1.5 – 2.5 AROM Sit in chair 15 – 30 min

3 2.5 – 3.5 Warm up in standing, walk Set chair as frequent, walk

4 3 – 4 Walk 30m, teach pulse counting

Out of bed, walk to bathroom

5 3 – 4Walk 100m, min resistance, 5 steps stairs

Walk around as tolerated

6 3 – 5 Walk 150m bid, des 1 flight of stairs

Supervised tepid shower or bath

7 3 – 5 Walk 200m bid, up & down stairs

Continue with ward activities

IN-PATIENT REHABILITATION PHASE (PHASE I-B) Many rehab specialists will care for these patients Guidelines are often the same as phase I but the period of

recovery is longer. Exercise intensity is limited to a target heart rate. It is

determined during a low level ETT or from unknown limitations from the revascularization performed prior to discharge.

Done at 70% max HR or a MET lvl of 5

Borg

scale

TRAINING PHASE (PHASE II) Started after a symptom limited full level ETT or completion of

a revascularization procedure and return to full activities Achievement of 85% of max HR is generally regarded as safe

In pt’s with higher risks a THR of 65-75% of maximum can be safe and effective

3 sessions per week for approximately 8 weeks All exercise sessions should begin with stretching warm up

training exercise cool down. Post-hospital phase Physical rehabilitation for resumption of habitual &

occupational activities Requirement: Stress test

EXERCISE STRESS TEST Technique used to uncover cardiac problems (diagnostic test) Used also as screening device for older people about to begin

an exercise program (functional test) Done in a medical center or physician’s clinic Stress test is usually is done by treadmill but when patient is

unable to do weight-bearing (arthritis) or is an amputee patient, other forms of testing is done

Done with ECG attached and oxygen tank is reserved alongside with hemo-doctors who monitors the patient’s progress

Objective: Create an individualized exercise prescription for

optimal level of stimuli without exposure to risk. Graded exercise stress test:

Continuous – without rest between stages Discontinuous – used for the elderly

Protocols: BRUCE & KATTUS – indicated for individuals with

good performance MODIFIED BRUCE – for early testing post-coronary

event, low level test NAUGHTON / BALKE – low level test CORNELL – modification on Bruce

Other forms of stress testing: Electrocardiographic exercise ECG stress testing (Typical Echographic stress

testing) – “ECHO” Nuclear stress testing Pharmacologic testing (inducing stress using drugs) Isometric hand grip (sitting position)

Basic Principle: To increase MVO2 via physiological response to

exercise, which can induce ischemia that can be detected via the ECG

Basic requirement Allow testing of patients with very limited cardiac

reserve as well as those with excellent aerobic conditioning

Absolute Cardiac Contraindications1. Unstable angina with recent chest pain2. Untreated life threatening cardiac

arrhythmias3. Uncompensated CHF4. Advanced atrioventricular block5. Acute myocarditis or pericarditis6. Critical aortic stenosis7. Severe hypertrophic obstructive

cardiomyopathy8. Uncontrolled HTN9. Acute MI

10. Active endocarditis

Absolute Non-cardiac Contraindications1. Acute pulmonary embolus or pulmonary

infarction2. Acute systemic illnessRelative Contraindications1. Significant pulmonary HTN2. Significant arterial HTN3. Tachy or bradyarrhythmias4. Moderate valvular heart disease5. Myocardial heart disease6. Electrolyte abnormalities7. Left main coronary obstruction8. Hypertrophic cardiomyopathy9. Psychiatric disease

1. Treadmill2. Bicycle ergometry3. Upper extremity ergometry4. Pharmacologic agents

Components: Deisgn with 3-5 minutes stages to achieve steady

state response Start with warm-up and end with coold down Refrain from holding handrails as isometric hand grip

cause exaggerated heart response

CATEGORY

SELF CARE

OCCUPATION

RECREATIONAL CONDITIONING

PHYSICAL

Very light1 – 3 mets

EatingWashingDressing

Sitting- typingStanding – store clerk

Light craft. Golf, Billiards

Walking at 3kph, stationary bike

Light5 mets

Warm showerCleaningPreparing meals

Light carpentryStacking of light objects

Playing pianoSocial dancingFishing

Walking at 5-6kph light calisthenics

Mod7 mets

Hot showerStair climbingScrubbing

CarpentryShoveling earth

BadmintonTennisSkating

Walking at 7-8kphswim

METHODS OF EXERCISE CONDITIONING Interval conditioning – involves work followed by prescribed

rest interval Circuit conditioning – work performed on a number of exercise

modalities, with or without rest Circuit-interval conditioning – combined circuit & interval

training Continuous training – Imposes submaximal energy

requirement that is consistent throughout the training

INTENSITY LOW MODERATE HIGHMET 2 – 4 3.0 – 6.5 5.0 – 8.5Intensity THR

65% to 75%THR70% to 80%

THR75% to 85%

MAINTENANCE PHASE (PHASE III) Most important part. If the pt stops from exercises the benefits

gained from phase II can lost in a few weeks. Perform exercises at THR for at least 30mins 3x a week (for

low-level exercises, 5x a week) ECG monitoring is not necessary Back to ADLs and work Lifestyle maintenance

CARDIAC REHAB IN SPECIAL CONDITIONS

Benefits: ↑ ischemic threshold, coronary collaterals &

fibrinolysis Improved LV function ↓ serum catecholamines & platelet aggregation

ANGINA PECTORIS The goal of rehabilitation in angina is to use the training

effectively to improve the efficiency of exercise performance below the anginal threshold

Rehab program can begin at phase II Aimed at increasing work capacity decrease disability

caused by recurrent chest pain

POST-CORONARY ARTERY BYPASS GRAFTING Symptom-limited cardiac stress test is useful in determining the

level of tolerated exercise, especially if the revascularized pt has a non-diagnostic thallium or EKG stress test.

Exercise can be performed at 3-4 weeks after surgery Can be similar to the post-MI rehab program

PHASE I1. Intensive mobilization in the immediate post-op period2. Progressive ambulation and daily exercises3. Discharge planning and exercise prescription for the

maintenance stage

Start: sitting upright, active leg exercises & mobilization out of bed

Rapid progression: supervised ambulation (150-200ft) Advanced: independent ambulation by the 3rd day

PHASE II Usually conducted at home or as outpatient. High risk pts may require IB rehab program (may have

had a neurological or other complications)

IV. ANAPHY

HEART Systole

Heart muscle contracts or beats pumps blood out of heart

1st Stage – the right and left atria contract at same time, pumping blood to LV and RV

2nd Stage – ventricles contract together to propel blood out of the heart

Diastole Heart Muscle Relaxes before next heartbeat This allows blood to fill up the heart again

HEART VALVES One-way valve at its exit that prevents BACKFLOW of blood

Tricuspid Valve – Exit of RA Pulmonary Valve – Exit of RV Mitral Valve – Exit of LA Aortic Valve – Exit of LV

Chordae Tendinae (Heart Strings) – found in mitral and tricuspid valve which attach to papillary muscle to prevent back flow and eversion of valve into atrium during ventricular contraction

If backflow happens: Regurgitation happens – mixture of Oxygenated and Unoxygenated blood: Pt may appear cyanotic

HEART SOUNDS Auscultation: What makes noises in the heart Valves Closing:

Atrioventricular/AV: Mitral and Tricuspid (S1) Semilunar: Aortic and Pulmonic (S2)

Heart’s valves open and close -> “Lub-DUB” First Sound (S1) “Lub” – made by the mitral and tricuspid

valves closing at the beginning of systole Second Sound (S2) ”Dub” – made by aortic and pulmonary

valves closing at end of systole/ beginning of diastole

HEART SOUNDSLOCATION OTHER NOTES ABNORMALITIES

S1Systolic (Mitral & Tricuspid)Loudest at apex

Closing of AV valves; coincides with carotid artery and R wave

Accentuated:- anemia - hyperthyroidism - mitral stenosisDiminished: - 1st degree heart block

S2Diastolic (Aortic & Pulmonic)Loudest at base

Closing of SV valves

Split S2 – end of inspiration; occurs every 4th heart beat; fading in with inhalation; fading out with exhalation & LBB

EXTRA HEART SOUNDSLOCATION OTHER NOTES DISEASES

S3“VENTRICULAR

Diastole ventricular

- Bell at apex - Low pitched

- Heart failure- Pulmonary

GALLOP” filling- Supine/Left side-lying

congestion- Shunting- Anemia

S4 “ATRIAL GALLOP”

Precedes S1 at the next cycle

- Bell at M/T- Supine

- Hyperthyroidism- Aortic stenosis- CAD

S3 + S4 = “SUMMATION GALLOP”

SOUNDS PITCH ABN LOCATION POSITION

Clicks HighTensing of chordae tendinae

ApexUse diaphragm; sitting/standing

Snaps High

Stenosis; stenotic valve attempts to open

Apex (after S2)

Use diaphragm

RubsHarsh, scratching, scraping

Pericardial Friction Rub

Lower base (R&L 2nd ICS)

Use diaphragm; sit upright then lean forward

HEART’S BLOOD SUPPLY Two main coronary arteries (arises from Aorta)

Left Main Coronary Arteryo Divides into Left Ant. Desc. Branch)o Then into Left Interventricular brancho Left circumflex arteries

Right Coronary Artery Any blockage over CA’s will cause chest pain, infarction of

heart muscle (take note of anatomical variations)

HEART’S ELECTRICAL SYSTEM Pacemaker cells

Cells that have the ability to generate electrical activity on their own.

These cells do this more than once per second to produce a normal heartbeat of 72 bpm

! Or if 60 below, Bradycardic Sinoatrial Node (SA Node)

Natural Pacemaker of Heart Found in RA / Right Atrium

Specialized fibers Conducts electrical impulse from pacemaker (SA

node) to the rest of the heart

WHAT MAKES THE HEART BEAT? Electrical activity produces electrical waves and can be

measured. The measurement is typically represented as a graph called an

electrocardiogram (ECG) Place leads on parts of chest (each lead corresponds to a

specific location) Chest leads provide a different view of the electrical activity

with the heart

EKG TRACING P-Wave

Coincides with the spread of electrical activity over the atria and the beginning of its contraction

Atrial Depolarization P-Wave absence

QRS Complex Coincides with the spread of electrical activity over

the ventricles and the beginning of its contractions Ventricular Depolarization

T – Wave Coincides with the Recovery phase of the ventricle Ventricular Repolarization

P-R Interval – take note of the time/duration. If too long: Conduction problems

S-T Segment – look at this area for possible M.I. EKG paper is a grid where time is measure along the

horizontal axis Each small square is 1mm in length and represents

0.04 seconds Each larger square is 5mm in length and represents

0.2 seconds Voltage is measured along the vertical axis – 0mm is equal to

1mV in voltage Q – Wave – the first downward wave of the QRS complex

(often absent) R – Wave – the Initial Positive Deflection S – Wave – the negative deflection following the R wave

EKG TRACING PATHOLOGIC Atrial Fibrillation (!Picture of ECG)

Electrical signals are scattered, disorganized Heart pumps irregularly Atrial Flutter

Ventricular Tachycardia (EMERGENCY) – must give electrical current to pt to correct electrical activity

Ventricular Fibrillation (EMERGENCY) – must give electrical current to pt to correct electrical activity

DISEASES Signs and Symptoms:

Syncope / Dizziness Chest pain / Angina Murmur Weakness Hypertension Fatigability (! Not specific, could also be endocrinal

or respiratory prob, so RULE OUT!) Syncope

Temporary and brief LoC that results of sudden fall in BP

Common symptoms: o Black Outo Dizzinesso Lightheadednesso Drowsinesso Fainting after meal or exerciseo Falling of no reasono Grogginesso Wobbly or weak when standing

Rule out weakness 2ndary to heart problem Could be dizzy because of lack of food Angina

o Temporary type of pain over chesto Pressure or discomfort over area

o Due to presence of ischemia

MURMUR Caused by change in direction of blood flow or turbulence Abnormal valves Damage

Deformed, Narrowed or stenotic Incompetent, back flow or regurgitant flow

Septal defect Other causes: Pregnancy, rheumatic heart disease, Htn, fever,

thyrotoxicosis, anemia

Murmurs — longer than a heart sound; vibrating, blowing & mumbling noise— best heard at pulmonic area— pt sitting up then lean forward/left side-lying

A. Location and timing Auscultate from the loudest & farthest side until heard Systole? (Pansystolic) Diastole? (Pandiastolic) Midiastole? Late

systole?B. Pitch

High – diaphragm Low – bell

C. Pattern Cresendo – ↑ blood flow velocity Decresendo – ↓ blood flow velocity Cresendo-Decresendo – ↑ loudness followed by softness

D. Quality Musical/blowing/harsh/rasping/rumbling/machine-like

E. Implications Stenosis – impaired heart valve opening Regurgitant – impaired heart valve closing

F. Intensity Grade 1 – barely audible Grade 2 – audible but quiet & soft Grade 3 – moderately loud w/o thrill Grade 4 – loud w/ thrill Grade 5 – very loud w/ thrill Grade 6 – loud enough to hear w/o a steth

THROMBOANGITIS OBLITERANS (BUERGER’S) Smoking causes constriction of arteries (Vasospasm) Could cause affectations of distal parts (Feet, hands) Venous scan of chronic smoker

Narrowing and obstruction of vessels Does not flow to ankle and feet anymore (So things

like wound healing cannot be done properly