Cardiac Rehab Midterm 3/13/25

Describe the Farmington Heart Study

- through NIH, people 30-62 put through extensive fitness and lifestyle evaluations

-f/u every 2 years

-enrolled children and grandchildren, etc. in study to track multiple generations

Initial Findings of Farmington Heart Study

-factors that increase CVD risk: smoking, high cholesterol, HTN, ECG abnormalities, obesity, menopause, diabetes

-PA reduces CVD risk

-revolutionary at the time

More recent findings of Farmington Heart Study

HTN has harmful brain effects

smoking cessation net positive despite weight gain

DNA sites w associated arrhythmias

high WBC = high A fib risk

How has cardiac rehab changed over time

stared as bed rest, progressed to clinical trails of supervised exercise, then pharm intervention, then rehab for multiple diseases, NOW emphasis on outcomes assessment rather than morbidity/mortality rates

Who benefits from Cardiac Rehab?

-MI

-coronary artery bypass graft surgery (CABG)

-stable angina pectoris

-valve repair/replacement

- Percutaneous Transluminal Coronary Angioplasty (PTCA)/coronary stenting

-heart or lung transplant

-those with pacemakers

-PAD

what does cardiopulmonary rehab entail?

-med evaluation

-prescribed exercise

-counseling

-behavior modification

-risk factor modification/education

Primary Prevention

intervening before MI

- surgery/medication

Secondary Prevention

preventing event from reoccurring

-cardiac rehab

benefits of cardiac rehab

IMPROVES: exercise tolerance, symptoms, lipids, QOL

REDUCES: cigarette smoking, stress, mortality

Phase 1 CR (who, what, where, goals)

Inpatient

-had MI or non invasive procedure

-conducted by PT, OT, nurses, EPs

-focused on ADLs while on heart monitor

GOALS

-ID those w inability to perform PA due to CVD

-offset bed rest effects

-surveillance

-return to ADLs

-safe discharge

-referral to outpatient

Phase 2CR (who, what, where, goals)

Outpatient

-36 sessions (3x over 12 wks)

-pt monitored by telemetry every session

-intro to behavior modification classes

GOALS:

-formal exercise and lifestyle PA

-supervision

-surveillance

-return to work activities

-education

Phase 3/4 CR (who, what, where, goals)

Maintenance (out of pocket)

GOALS:

-lifelong

-RF management

-reinforce Phase 2

-note responses/feelings

-decrease program frequency

-not monitored but supervised

Cardiovascular Disease

atherosclerotic process characterized by thickening of intimal layer of vessel wall caused by local accumulation of lipids

Contributors to CVD

-heredity, smoking, HTN, DM, high cholesterol, age, visceral adiposity

-endothelial injury, chemical trauma, low estrogen, high cortisol, sheer stress, immunological stressors

Fatty streaks characteristics

in intima layer first, asymptomatic, lumen still in tact

COMPOSITION: SM cells, lipids, fat droplets

foam cells

balloon w oxidation, precursor to raised fibrous plaque

complicated lesions

>70% occluded lumen with symptoms

Ischemia

Lack of blood supply

Myocardial Ischemia

deficiency of blood supply to the myocardium

Angina pectoris

episodic; reversible myocardial ischemia

-goes away at rest bc MVO2 decreases

-pain my radiate to left side

Contributors to angina pectoris

obstruction - arterial stenosis >70%

high metabolic demands that heart cant reach

low blood Hb

pulmonary disease

stable angina (s/s, Dx, Tx)

chronic exertional; reproducible w effort (high O2 demands)

-flow reserve of coronary arteries is limited

S/S: decline in CrP & ATP, impairment of ventricular contractility and diastolic relaxation

DX: resting ECG normal, stress test reveal ECG changes, arrhythmias, or fall in BP due to low V. contractility

TX: rest or nitroglycerin; monitor through RF

unstable angina (pre-infarction angina)

acute coronary syndrome (ACS) is LIFE THREATENING

-does not comletely occulde artery

S/S: crescendo angina, pain w min exertion/rest, pain after recent MI

DX: V arrhythmias, syncope, MI, high CrP

Tx: pharm or surgical intervention

-w/in one year, most pts have another event

Prinzmetal/Varient angina

caused by artery spasm

S/S at rest, usually morning

smoking/cocaine use - occurs bc artery segment is over reactive to vasoconstricting agents (NO or serotonin)

TX: Ca channel blockers - inhibit thrombosis formation

Asymptomatic (Silent) angina

w/o pain/ischemia w/o symptoms

-observed during avionics monitoring (24 hr heart)

TX: nitrate and betablockers

Myocardial Infarction (MI)

artery 100% occluded; no blood to heart muscle

-worse if higher in heart

S/S unresolved pain, sometimes w dyspnea, nausea, vomiting, diaphoresis, weakness

DX: Hx, symptoms, serial serum enzymes, ECG

TX: rapid management to limit size and scope of damage; rapid perfusion and use of antithrombolytics/ PTCA

Causes: ischemia, thrombosis, trauma leading to blood loss

Most danegrous arrhythmias

VT, VF, SVT

Deep Vein Thrombosis (DVT)

clot forms in extremity, usually calf, from inactivity

-can cause pulm embolism

Mural Thrombosis

forms in ventricular wall post mI

-can lodge in visceral arteries and infarct other organs/limbs

S/S: sudden pain/numbness/coldness of extremity

TX: surgical embolectomy

Papillary muscle rupture

mitral valve insufficiency

intraventricular septal rupture

tunnel-like lesion through septum

ventricular aneurysm formation

due to insubstantial repair of rupture

DX/TX of heart structural damage

congestive heart failure (CHF) and surgical intervention

Pericarditis

occurs 2-3 days post MI

S/S: intense pain aggravated by breathing and relieved by sitting upright

-if fluid accumulates, can compress heart resulting in cardiac tamponade

TX: aspiration of fluid, steroids, pain killers, antibiotics

cardiac tamponade

high external pressure restricting diastolic filling and decreasing CO and arterial pressure

What causes most deaths w/in the hour of an MI

V. fib, cardiogenic shock if >40% myocardium is necrotic

Sudden Cardiac Death

unexpected, w/o prior symptoms or S/S of <6hrs

Causes: Vt of VF w/ unrecognized CAD

RF: v electrical instability, CAD, abnormal LV fx

TX: CPR and defib w/in 4 min, AICD placement w or w/o pacemaker, pharm agents

Congestive Heart Failure (CHF)

inability of heart to maintain CO

-associated w CAD, HTN, valve disease, congenital heart disease

acute CHF

rapid failure of heart pump

S/S: dyspnea at rest, orthopnea, pulm congestion, edema

Chronic CHF

develops gradually, chronic fluid/salt retention by kidneys

-leading cause of hospitalization in >65 yrs

-leads to end organ failure

Compensated CHF

maintain CO through compensatory mechanisms and pharm intervention

S/S: rapid HR, pallor diaphoresis

Intractable CHF

heart fails despite therapies

low CO: EF< 20%

TX: heart transplant

normal lung size

4-6L

Imaging used to DX pulm diseases

chest x ray, CT, echocardiogram

Chest X ray

used to find cause of SOB, CP, chronic cough, fever

DX: pneumonia*, heart failure, cancer

computerized tomography (CT)

higher detail than an x ray (used as a f/u); shows size/shape/position of lung structures; can identify tumor, fluid, pulm embolism, emphysema*

echocardiogram

evaluate pressure on right side of heart due to pulmonary hypertension

3 pulmonary function tests

spirometry, oximetery, stress test

spirometry

a measurement of total forced vital capacity & how quickly air can be moved out of lungs

oximetery

02 saturation in arterial blood

hypoxia classification via oximetery

<94% - needs o2 supplementation

Diseases that affect airways - obstructive

COPD, acute bronchitis, cystic fibrosis

Diseases that affect air sacs - restrictive

difficulty fully expanding lungs

interstitial lung disease (alveoli damage), obesity, scoliosis, neuromuscular diseases

diseases that fall under COPD

chronic bronchitis, emphysema, asthma

what is the leading cause of COPD

cigarrette smoking

Emphysema

bronchoscopic Lung Volume Reduction (BLVR) - reduced hyperinflation

when less air flows out of airways due to COPD...

-alveoli lose elasticity

-walls btwn alveoli destroyed

-walls of airways become thick/inflamed

-airways produce more mucus than usual

TX for COPD

-airway valves

-coil placement

-combo drugs

Impact of smoking on lung function

decreases dynamic lung fx

increases asthma/wheezing

asthma

inflames and narrows airways; causes wheezing, chest tightness, SOB, coughing

populations at risk for COVID complications

asthma, COPD, interstitial lung disease

Pulm Rehab

evidence based, multi disciplinary, comprehensive intervention for those w respiratory diseases, are symptomatic, or have decreased ADLs

Pulm Rehab is designed to

decrease symptoms, optimize fx status, increase participation, decrease healthcare costs

What disease benefits the most from pulm rehab

COPD

PR outcomes

physical TR

breathing TR

medication/O2 management

nutritional/psychological support

2 types of barriers to pulm rehab

non attendance and non adherence

who is most likely to not attend pulm rehab

women, current smoker, lives alone

who is most likely to not adhere to pulm rehab

extremes of age, current smoker, LTOT use, poor status

PR differences from CR

-specific focus on breathing difficulties and disease symptoms

-disease management and reduction of dependence on meds/dr visits

-education about O2 therapy, breathing retraining, symptom assessment/knowledge

When did the Framingham Heart Study begin?

1948

What did researchers do initially in the FHS?

Full Physical evaluation and lifestyle consultation

Who is cardiac rehab for?

- Heart attack

- Heart surgery

- Heart failure

- ICD fitted

- Coronary Angioplasty

Phase 1 of Cardiac Rehab

Acute (monitoring)

Phase 2

Sub acute (conditioning) Outpatient

*monitored on telemetry

Phase 3 (Usually not covered by insurance)

TR and maintenance (intensive rehab) Community-based

Psycho-social benefits are valuable

Phase 4 (Usually not covered by insurance)

Disease prevention

(prevention program)

Primary Prevention

Surgical procedure/medication to prevent it from happening in the FIRST PLACE

Secondary prevention

Keeping event from reoccurring (pharmacological, medical, physical, psychological, social*)

What is MI?

Myocardial Infarction (heart attack)

What is telemetry?

Electric monitoring of the heart (ECG)

What is cardiac rehab?

Multidisciplinary approach to care/management of cardiac problems (trying to get the pt. back to normal/previous level of function)

what type of disease is Atherosclerosis

Diffuse disease

Atherosclerosis

Plaque build up in any bld vessel (usually arteries)

Main contributors to atherosclerosis

- Hereditary

- Smoking

- HTN

- Diabetes (type I & II)

- High Chol

- Age

- Visceral adiposity (fat around organs)

Other contributors to atherosclerosis

- Endothelial injury

- Chemical trauma (environmental inhalants)

- High cortisol

- Areas of sheer stress (bld damages arteries from high pressure)

Do fatty streaks impede bld flow through arteries?

No

Fatty streaks (contain foam cells)

Primarily in the intima; asymptomatic; lumen still patent

When do we start getting fatty steaks (contain foam cells)?

infancy

Plaque

Raised Fibrous plaque: lesion of yellow-gray; elevated lump that thickens and ↓ lumen. Process can progress to occlude artery

Myocardial Ischemia

Lack of bld flow to cells

Angina

Lack of bld flow

Angina Pectoris

Chest pain (bc heart isn't getting enough O2)

symptoms of Angina Pectoris

Pain in chest, neck, jaw, left side (arm), and back

Dyspnea

Shortness of breath

Syncope

Fainting

Contributors to myocardial ischemia

- Arterial stenosis

- ↓ bld hemoglobin

- Pulmonary disease

Stenosis

Narrowing

Stable angina

chronic effort angina, predictable

Diagnosis of Stable Angina

ECG = normal, stress test = CP, ST segment depression/elevation, arrhythmias, or fall in BP from ↓ Ventricular contractility

Tx (treatment) for Stable Angina

rest 5-10 minutes or NTG (nitroglycerin)