Вы находитесь на странице: 1из 6

CARDIAC CONDITIONS

HYPERTENSION
I.
A.

General Medical Background


Definition
Persistent elevation of the systolic
arterial blood pressure above
140mmHg or diastolic blood pressure
above 90mmHg.

B.

Classification
Stages of
HTN

Prehypertens
ion
Stage 1
Stage 2
Stage 3
C.

D.

Systolic
Blood
Pressure
(mmHg)
120-30

Diastolic
Blood
Pressure
(mmHg)
80-89

130-140
140-160
>160

90-100
100-110
>110

Epidemiology
The most prevalent cardiovascular
disease in the United States.
Most powerful contributors to
cardiovascular morbidity and
mortality.
76 million Americans have HTN.
Blacks highest prevalence
Etiology
Primary (essential) HTN diagnosed
when there is no known cause for the
elevation in BP values and exists in
approximately 90%-95% of all patients
with HTN. (Includes Genetic factors,
environmental, stress, diet, obesity,
alcohol consumption, lifestyle)
Secondary (non-essential) HTN is
caused by an identifiable medical
problem such as renal, endocrine,
vascular, or neurological complications
and exists in approximately 5% to 10%
of all patients with HTN.

E.

F.

G.

H.

Diagnosis
Physical Examination
High blood pressure (HBP) is
diagnosed
using
a
blood
pressure test.
I.
Differential Diagnosis
Acutely
Less acutely dangerous
Dangerous
Stroke
Obstructive uropathy
Aortic Dissection Hyperthyroidism
Drug
Sleep Apnea
Intoxication
Cushing Syndrome
Drug Withdrawal Primary
Renal Failure
hyperaldosteronism
Thyroid Storm
Renovascular
hypertension
Essential hypertension
J.

Clinical Manifestation
Exertional dyspnea
Fatigue
Impaired exercise tolerance
Tachycardia
Chest discomfort
Elevated BP
Complications
Heart failure
Renal failure

Prognosis

Most individuals diagnosed with


hypertension will have increasing blood
pressure (BP) as they age.
Mild to moderate hypertension, if left
untreated, may be associated with a risk of
atherosclerotic disease in 30% of people and
organ damage in 50% of people within 8-10
years after onset.
Death from ischemic heart disease or stroke
increases progressively as BP increases. For
every 20 mm Hg systolic or 10 mm Hg
diastolic increase in BP above 115/75 mm
Hg, the mortality rate for both ischemic heart
disease and stroke double
II.
A.

Pathophysiology/Pathomechanics
A mechanism manifests with normal or
reduced cardiac output and elevated
systemic vascular resistance due to
increased vasoreactivity.
Another (and overlapping) mechanism
is increased salt and water
reabsorption (salt sensitivity) by the
kidney, which increases circulating
blood volume.

Dissecting aneurysms
PVD
Retinopathy
Stroke

General Healthcare Management


Medical, Surgical and Pharmacologic
Beta-adrenergic blockers
Alpha-adrenergic blockers
Angiotension-converting
enzyme (ACE) inhibitors
Diuretics
Vasodilators
Calcium channel blockers

B.
Other
Healthcare
(Rehabilitation/Supportive)
Lifestyle modifications
Weight reduction
Sodium restriction
Moderation of alcohol intake
Regular aerobic exercise
III.
Physical
Therapy
Examination,
Evaluation & Diagnosis
A.
Points of Emphasis in Examination
BP Monitoring is crucial and should be
done both at rest and during exercise.
B.

Problem List
Exertional dyspnea

Fatigue
Impaired exercise tolerance
Tachycardia
Chest discomfort

IV.
A.

Physical Therapy Prognosis


Plan of Care
Aerobic exercise to achieve:
Lesser HR and systolic BP
increase with submaximal work,
Improve functional capacity,
Efficient O2 consumption.

B.
1.

Intervention (including rationale)


Modality
If HTN is associated with
Edema, IPC to reduce edema.
IFC to cause muscular
contraction to increase the
circulation of fluids back to the
central circulating system.

E. Pathophysiology
When patients are in heart failure and
the ventricle is ejecting low blood
volumes, blood begins to accumulate
within the ventricles, causing
congestion. This congestion increases
the Left-Ventricle End-Diastolic Volume
(LVEDV) and contributes to an
elevation in LV pressure.
The increased pressure is transmitted
retrograde toward the LA and the
pulmonary veins.
This increase in hydrostatic pressure in
the pulmonary veins causes fluid to
move from the veins into the
interstitial space of the lung, resulting
in pulmonary edema.

2.

Non-Modality
Patient Education
Risk factor modifications
Stretching
Aerobic Exercise (threadmills,
UE or LE ergometer, Airdynes,
rowing machines, walking,
running, calisthenics

F. Clinical Manifestations
Fatigue and weakness
Dyspnea
Acute pulmonary edema
Weak, rapid pulse
Rales, wheezing
Chest pain and palpitations

CONGESTIVE HEART FAILURE

G. Complications
Renal dysfunction
Arrhythmias
Angina and MI

The New York Heart Association


(NYHA) classification system categorizes
heart failure on a scale of I to IV, as follows:

D. Etiology
Most common cause of heart failure is
cardiac muscle dysfunction. Cardiac muscle
dysfunction is a general term describing
altered systolic and/or diastolic activity of the
myocardium that usually develops as a result
of an underlying abnormality within the
cardiac structure or function.

Physical Therapy Diagnosis

B. Classification

Women constitute half of all cases


because of their longer life
expectancy.

C.

I. General Medical Background


A. Definition
Congestive Heart Failure (CHF) is a
syndrome by impaired cardiac pump
function, resulting in inadequate systemic
perfusion and an inability to meet the bodys
metabolic demands.

Class I: No limitation of physical


activity
Class II: Slight limitation of physical
activity
Class III: Marked limitation of physical
activity
Class IV: Symptoms occur even at rest;
discomfort with any physical activity
C. Epidemiology
In the United States, heart failure
affects 5.7 million individuals.
6% to 10% of people older than 65
have heart failure

H. Diagnosis
Chest X-Ray
Laboratory test
Echocardiogram
I. Differential Diagnosis
Cardiogenic
Noncardiogenic
Pulmonary Edema
Pulmonary Edema
Acute cardiac event
(-) S3 gallop
S3 gallop
(-) Jugular venous
distension
Elevated jugular
venous pulsation
J. Prognosis
In general, the mortality following
hospitalization for patients with heart failure
is 22% at 1 year, despite marked
improvement in medical and device therapy.
Heart failure associated with acute MI
has an inpatient mortality of 20-40%.
II. General Healthcare Management
A. Medical, Surgical, Pharmacologic
Cardiac Resynchronization Therapy
(CRT)

Beta- blockers
ACE inhibitors
Vasodilators

B. Other Healthcare
(Rehabilitative/Supportive)
Myoplasty
Left Ventricular Assist Device (LVAD)
Biventricular pacing
III. Physical Therapy Examination,
Evaluation & Diagnosis
A. Points of Emphasis in Examination
The extremities are inspected for the
presence of edema. Bilateral Peripheral
edema may be a result of CHF.
Examination for the presence of
Jugular Venous Distension
- Patient is placed at a 45-deg
semirecumbent position.
- Pts head is turned away from
the side to be evaluated
- PT observes for a distension or
pulsations of the jugular vein 35 cm above the sternum
B. Problem List
Dyspnea
Fatigue
Weakness
Chest discomfort
Impaired exercise tolerance
IV. Physical Therapy Prognosis
A. Plan of Care
Efficiency of O2 consumption
Improve peripheral muscle strength
Reduce excessive accessory muscle
use and reduce the work of breathing
B. Intervention
1. Modality
IFC therapy to stimulate muscle
contraction
2. Non-Modality
Graded aerobic exercise program to
improve functional capacity
Strength training to increase
peripheral muscular strength
Breathing exercises to improve
breathing

ATHEROSCLEROSIS
I. General Medical Background
A. Definition
Disease of large and medium-sized arteries
and is characterized by dysfunction, vascular
inflammation, and the buildup of lipids,
cholesterol, calcium and cellular debris
within the intima of the vessel wall resulting
to plaque formation, vascular remodeling,
obstruction, abnormal blood flow and
diminished oxygen supply.
B.Complications
Stroke

Heart attack (myocardial infarction)


Narrowing (stenosis)
Decreased blood flow to the legs
Decrease blood flow to the intestines
Ballooning of an artery

C. Epidemiology
-predominantly asymptomatic condition
-M>W
-40 years & above
D. Etiology
- Mechanism of atherogenesis remains
uncertain.
-response-to-injury is most widely accepted
explanation: endothelial injury causes
vascular inflammation and a fibro
proliferative response.
-MC in medium-sized arteries (heart, brain,
kidneys, legs)

E. Pathophysiology
Lipoproteins accumulate inside artery&
associate with proteogylcans -> modified
lipoproteins trigger inflammatory response
-> leukocytes adhere to endothelium ->
leukocytes migrate into intima -> smooth
muscle cells invade and accumulate in intima
surrounding fibrous cap of plaque
F. Risk Factors
Hypercholestrolemia
hypertension
cigarette smoking
diabetes
obesity
G. Clinical Manifestations
Affected Artery
Clinical
Presentation
Coronary Artery
Angina pectoris,
acute MI
Cerebral arteries
Cerebral ischemia,
stroke
Peripheral circulation Intermittent
claudication
Renal arteries
Hypertensive
vascular disease
H. Diagnosis
blood test
CT
MRI
Angiography
I. Prognosis
-depends on a number of factors:
-systemic burden of disease
-vascular bed(s) involved
-degree of flow limitation
II. General Healthcare Management
A. Medical, Surgical, Pharmacologic
Angioplasty
Stenting
Thrombolysis

Thrombectomy
CABG
HMg-CoA
Vitamin E

III. Physical Therapy Examination,


Evaluation & Diagnosis
A. Points of Emphasis in Examination
- may reveal a whistling sound (bruit)
- Diminished pulse
IV. Physical Therapy Prognosis
A. Plan of Care
Relieving symptoms
Reducing risk factors in an effort to
slow or stop the buildup of plaque
Lowering the risk of blood clots
forming
Widening or bypassing plaque-clogged
arteries
Preventing atherosclerosis-related
diseases

Mitral Regurgitation-Failure of the valve to close


completely allowing some blood to backflow during
systole; the sound is heard during systole
Mitral Valve Prolapse (valvular incompetency)Ballooning of the cusps back into the atrium during
systole as ventricular pressure increases.
Aortic stenosis-Narrowing of Aortic valve; limits amount of blood
ejected into the aorta during systole; the sound is heard over the
aortic valve during systole
Aortic Regurgitation-Failure of the aortic valve to close completely
allowing some blood to flow back into the left ventricle during
siastole. The sound is heard during diastole.

C.

Epidemiology
>40y.o.
M>F during premenstrual
period to younger than 40-50
y.o.
M=F during post-menstrual
period
Caucasians(whites) > Blacks
> Asians
Pt. with LDL to HDL ratios of
greater than 2:1

D.

Etiology

B. Intervention
-smoking cessation
-weight reduction
-exercise:
-walking
-aerobic exercise
CORONARY ARTERY DISEASE
V.

Arteriosclerosis, hyperplasia of
arterial muscles, coronary artery
spas, coronary artery thrombus,
age, gender, family hx of CAD,
race, DM, obesity, type A
personality, oral contraceptives,
cigarette smoking, hypertension,
hypercholesterolemia,
sedentary lifestyle

General Medical Background


A.

Definition
Is a focal, narrowing of coronary
artery which results to a
decrease in blood supply heart.
There is an imbalance
myocardial oxygen supply and
demand.

B.

Classification
Type
1/
Intimal
Arteriosclerosis
arteriosclerosis which affects
the innermost layer of the
vessels

Type 2/ Medical Sclerosis affects the middle layer of the


vessel
and
results
in
calcification and hypertrophy.
Individuals with this type of
arteriosclerosis
develop
pipestem or rigid arteries,
typically in the medium-sized
vessels. Blood flow is not
usually produced.

Type 3/ Arteriolar Sclerosis


affects small blood vessels
with characteristic changes in
both the media and intima.
Blood flood is reduced and
Htn results.
Common Valvular Problems
Mitral stenosis-Narrowing of mitral valve; blood from
the left atrium will have difficulty draining onto the left
ventricle during diastole. The sound is heard over the
mitral valve during diastole.

E.

Pathophysiology/Pathomechanics
The main pathophysiology of
CAD is arteriosclerosis which
starts with Virchows triad:
stasis, endothelial injury &
hypercoagulable state. Injury to
the endothelial lining of the
coronary
arteries
causes
platelets and WBC to converge
at the damaged lining and
absorbs oxidized cholesterol
forming a fatty streak that
narrow the arterial lumen.
Brcause the arterial lumen
narrows gradually, collateral
circulation develops and helps
maintain myocardial perfusion
distal to the obstruction. When
myocardial demand for oxygen
is more than the collateral can
supply, myocardial metabolism
shifts from aerobic to anaerobic
producing lactic acid which
stimulates pain nerve endings.
The
patient
experiences
worsening angina that requires
rest and medication for relief.
Lacking oxygen, the myocardial
cells die. Thos decreases
contractility, stroke volume and

blood
pressure.
Excessive
damage to the left ventricle may
impair the ventricles ability to
pump, allowing blood back up in
to the left atrium and eventually
into the pulmonary veins and
capillaries. When this occurs,
the patient may be dyspneic,
orthopneic,
tachypneic and
cyanotic.

F.

G.

H.

I.

VI.

Clinical Manifestation
Angina pectoris
Myocardial infarction
Sudden cardiac death
Congestive heart failure
Complications
Arrhythmias an irregular
cardiac rhythm. The most
common form of arrhythmic
death is an acute M.I. is
ventricular fibrillation.
Pump Failure
Cardiac Rupture this
complication nearly always
is a fatal as it results in
overwhelming
cardiac
tamponade.
Cardiac
tamponade is a condition
wherein
there
is
an
excessive amount of fluid in
the
pericardial
space
choking
the
heart,
preventing
it
from
contracting and relaxing
Shock
Diagnosis
History and physical
examination
MRI, Coronary Angiograph,
Stress test
Angina symptoms
Prognosis
The prognosis of patients with
CAD is primarily determined by
two variables: the extent of
coronary disease in terms of the
number of vessels affected by
the disease and the extent of
left ventricular damage present
due to previous MI.

General Healthcare Management


A.
Medical, Surgical and Pharmacologic
Angina pectoris
- nitrates/ nitroglycerine
- beta blockers
- clacium blockers
- PTCA ( Percutaneous
Transluminal Angioplasty)
- CABG (Coronary Artery
Bypass Graft)
B.
Other Healthcare
(Rehabilitation/Supportive)
Inpatient Cardiac Rehabilitation: this
begins on admission of patient to the
hospital and continues until patient is
discharge.

VII.
Physical Therapy Examination, Evaluation &
Diagnosis
A.
Points of Emphasis in Examination
Specifically for cardiac patients,
observation should include facial
appearance, specific skeletal
abnormalities, coloration of the skin, and
appearance of the knuckles, elbows,
knees and Achilles tendon where
swelling or deposit of cholesterol may
appear. Observe for abnormal
pulsations palpation and auscultaion

VIII.

B.

Problem List
Pain Management
Weight Management

C.

Physical Therapy Diagnosis


History and physical
examination

Physical Therapy Prognosis


A.
Plan of Care
Self-care
Resumption of upright sitting
Selected arm and leg exercises
to improve flexibility and muscle
tone
B.

Intervention (including rationale)


In-hospital phase
Step-ladder program
Prevent complications of
bedrest and resume
functional activities.
Convalescent Phase
Walking or Bicycling
Gradually increase exercise
endurance

Training Phase
Stretching and Aerobic
exercise
Maintain endurance
achieved

Sources:
Sullivan, S, Schmitz, T, and Fulk, G: Physical
Rehabilitation, ed. 6, F.A Davis Company (P)
LTD., Philadelphia, 2014
Medscape App
http://www.nhlbi.nih.gov/health/healthtopics/topics/atherosclerosis/treatment.html