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Cardiovasculer Disorders 1
Cardiovasculer Disorders 1
Cardiovascular
System
At the end of the session you will be able to :
1. Discuss the function of cardiovascular systems
2. Identify Risk factors for cardiovasculardisease
3. describe causes, pathophysiology, diagnostic tests, and
treatments for several common cardiovascular disorders.
4. Identify the sign and symptoms of selected cardiac
disease
cells, remove metabolic waste products, and carry hormones from one
Age
Male gender
Family history
Race.
Age
to cardiovascular disease.
Cardiovascular Disorders
Cardiogenic shock
MI
Heart failure
Hypertension
blood pressure and blood flow to the kidneys, and I.V. dobutamine, agents that increase
myocardial contractility and cardiac output. I.V. nitroprusside, a vasodilator, may be used
Aging
Diabetes mellitus
Elevated serum triglyceride,
Hypertension& Obesity
Positive family history of CAD
Sedentary lifestyle
Smoking & stress
Use of amphetamines or cocaine.
Excessive intake of saturated fats, carbohydrates, or salt
Susceptibility increases with age
Elderly patients are more prone to complications
and death.
The most common complications after an acute MI include:
arrhythmias • cardiogenic shock • heart failure
causing pulmonary edema • pericarditis.
Other complications include: • rupture of the atrial
or ventricular septum, ventricular wall, or valves
MI results from prolonged ischemia to the myocardium with irreversible cell
damage and muscle death. Functionally, MI causes:
Reduced contractility with abnormal wall motion
Altered left ventricular compliance
Reduced ejection fraction
Elevated left ventricular end-diastolic pressure
All mis have a central area of necrosis or infarction surrounded by an area of
injury. The area of injury is surrounded by a ring of ischemia. Tissue
regeneration doesn’t occur after an MI because the affected myocardial
muscle is dead.
Scar tissue that forms on the necrotic area may
inhibit contractility. When this occurs, the
compensatory mechanisms (vascular constriction,
increased heart rate, and renal retention of sodium
and water) kick in to try to maintain cardiac output.
Ventricular dilation also may occur. If a lot of scar tissue
forms, contractility may be greatly reduced. The patient
may develop heart failure or cardiogenic shock.
The cardinal symptom of MI is persistent,
crushing substernal pain that may radiate to the left
arm, jaw, neck, or shoulder blades.
The pain is commonly described as heavy,
squeezing, or crushing and may persist for 12 hours
or more.
However, in some patients particularly elderly or
diabetic patients pain may not occur at all. In others,
it may be mild and confused with indigestion
Other clinical effects include:
• Mechanical disturbances in ventricular filling during diastole, due to blood volume that’s
too low for the ventricle to pump, occur in mitral stenosis secondary to rheumatic heart
disease or constrictive pericarditis and in atrial fibrillation.
Pathophysiology
• Infections, which increase metabolic demands and further burden the heart
• Anemia, which leads to increased cardiac output to meet the oxygen needs of
the tissues
• Increased physical activity, increased salt or water intake, emotional stress, or
failure to comply with the prescribed treatment regimen for the underlying
heart disease.
Cont…Factors favorable to failure
• Getting complicated
Eventually, sodium and water may enter the lungs, causing pulmonary
edema, a life- threatening condition. Decreased perfusion to the brain, kidneys,
and other major organs can cause them to fail. MI can occur because the oxygen
demands of the overworked heart can’t be met.
Signs and Symptoms of Heart Failure
• Fatigue
• Hepatomegaly.
Echocardiogram identifies the underlying cause as well as the type and severity of the
heart failure.
PAP monitoring shows elevated PAP, PAWP, and left ventricular end-diastolic pressure
in left-sided heart failure
Heart Failure Treatment
Rheumatic Fever and
04 Rheumatic Heart
Disease
Rheumatic Fever and Rheumatic Heart
Disease
Rheumatic fever develops commonly in childhood after infection of the upper
respiratory tract with group A beta hemolytic streptococci.
Rheumatic heart disease refers to the cardiac manifestations of rheumatic fever
and includes pancarditis (myocarditis, pericarditis, and endocarditis).
Highest in children between ages 5 and 15.
Cardiac involvement develops in up to 50% of patients.
CAUSE
• Throat cultures
Surgery:
• Corrective surgery, such as commissurotomy, valvuloplasty, or valve valvuloplasty
replacement. commissurotomy
Cardiomyopathy generally applies to disease of the heart muscle fibers, and it occurs in
three main forms:
1. Dilated Cardiomyopathy
2. Hypertrophic Cardiomyopathy (2 TYPES)
• common form is caused by aortic valve stenosis.
• hypertrophic obstructive cardiomyopathy (HOCM), is due to a genetic
abnormality.
HYPERTROPHIC CARDIOMYOPATHY
Dyspnea
Fatigue,
Angina
Irregular pulse
Peripheral pulse with a characteristic double impulse (pulsus biferiens)
CLINICAL MANIFESTATION
HOCM RESTRICTIVE CARDIOMYOPATHY
• Fatigue
• Systolic ejection murmur
• dyspnea
• Angina • Orthopnea
• Syncope • Chestpain
• Activity intolerance • Edema
• Abrupt arterial pulse secondary to vigorous • liver engorgement
left ventricular contractions • peripheral cyanosis
• Pallor
• Irregular pulse
• S3 or S4 gallop rhythms due to heart failure
• Systolic murmurs
DIAGNOSTIC TESTS
• ECG and angiography rule out ischemic heart disease. ECG may also show biventricular
hypertrophy, sinus tachycardia, atrial enlargement, and, in 20% of patients, atrial
fibrillation.
• Chest X-ray may reveal cardiomegaly associated with any of the cardiomyopathies.
• Cardiac catheterization with possible heart biopsy can be definitive with HOCM.
• Diagnosis requires elimination of other possible causes of heart failure and arrhythmias.
TREATMENTS
DILATED CARDIOMYOPATHY
Treatment seeks to correct the underlying causes and to improve the heart’s pumping ability.
Diuretics are commonly given with an ACE inhibitor to reduce fluid retention.
Treatment may also include oxygen, a sodium-restricted diet, and bed rest.
valve replacement
Ventricular myotomy
TREATMENTS
RESTRICTIVE CARDIOMYOPATHY
identifiable cause.
ETIOLOGY
1. Primary Hypertension Secondary hypertension
Advancing age . Brain tumor, quadriplegia, and head injury
Diabetes mellitus . Coarctation of the aorta
excess renin Excessive alcohol consumption
Excessive alcohol consumption Family history. Gestational hypertension
High intake of saturated fat . Hormonal contraceptives,
High intake of sodium Mineral deficiencies Cocaine
(calcium, potassium, and magnesium) Antinflammatory drugs.
Obesity Pheochromocytoma, cushing’s syndrome,
Sedentary lifestyle Sleep apnea Hyperaldosteronism, andthyroid, pituitary,
Stress Tobacco use Or parathyroid dysfunction.
Race (most common in blacks) Renal artery stenosis and parenchymal disease
PATHOPHYSIOLOGY
• Several theories help to explain the development of hypertension. It’s thought to arise
: Changes in the arteriolar bed that cause increased
resistance
abnormally increased tone in the sensory nervous system that originates in the
vasomotor system centers, causing increased peripheral vascular resistance .
• In chronic renal disease. Insult to the kidney from chronic glomerulonephritis or renal
artery stenosis interferes with sodium excretion, the renin-angiotensin-aldosterone system
, or renal perfusion, causing blood pressure to increase.
Clinical Manifestation
hypertension usually produces no secondary hypertension to have clinical
symptoms, (SILENT KILLER): manifestations of the primary disease.
Signs and symptoms may include: (Other clinical effects don’t appear until
Blood pressure complications develop as a result of vascular
Throbbing occipital headaches upon changes in target organs. These effects include) :
waking Left Ventricular Hypertrophy
Drowsiness Angina
MI
Confusion
Heart Failure
Vision problems(blurry vision as a
Stroke
result of retinal damage)
Transient Ischemic Attack
Nausea.
Nephropathy
Peripheral Arterial Disease
Retinopathy
DIAGNOSTIC TESTS
Serial blood pressure measurements may be useful.
• In urinalysis, protein, red blood cell (RBC), and WBC levels may indicate
glomerulonephritis.
• Elevated blood glucose levels may indicate diabetes.
• Complete blood count may reveal anemia (causes a high-output state resulting in
hypertension) or polycythemia (increases the risk of hypertension and stroke).
• Lipid profile reveals elevated total cholesterol and low-density lipoprotein levels.
Serum potassium levels are less than 3.5 mEq/L, indicating adrenal dysfunction
(primary hyperaldosteronism).
ECG may show left ventricular hypertrophy or ischemia.
• Chest X-ray may show cardiomegaly.
TREATMENT
Lifestyle modification including :
Weight reduction, use of a dietary approaches to stop hypertension (DASH) diet.
Learning relaxation techniques,
Exercising regularly,
Quitting smoking, and
Limiting alcohol use.
Medication
Drug therapy for uncomplicated hypertension usually begins with :
a thiazide diuretic,
an ACE inhibitor, or
a beta adrenergic blocker.
Other antihypertensive drugs include:
angiotensin II receptor blockers,
alpha-receptor blockers,
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