Diseases of the Circulatory System

University of San Francisco

Dr. M. Maag©2003 Margaret Maag

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Class 8-9 Objectives Upon completion of this lesson, the student will be

able to describe the effects of aging on the cardiovascular system. investigate risk factors associated with CVD. formulate nursing interventions for CVD. determine the clinical manifestations of left and right heart

failure. discuss the etiology and manifestations of myocarditis and

pericarditis. identify the prevalence of atrial and ventricular arrhythmias.

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Anatomy & Physiology Review

http://www.heartsite.com/html/the_heart.html

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Coronary Vessels

http://www.heartsite.com/html/lad.html

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Cardiac Conduction http://www.heartsite.c

om/html/electrical_activity.html

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Review

How does preload, afterload & contractility influence stroke volume and determine cardiac output?

Preload: pressure created in the left ventricle at the end of diastole.

Afterload is the pressure or resistance to blood flow out of the left ventricle.

Contractility is the force of the ventricular contraction in order to eject the stroke volume. The ability of the muscle fibers to shorten (Hartshorn et al., 1997).

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Review

Cardiac Output (HR X SV) Stroke volume: volume of blood ejected during

systole Normal adult C.O. = 5 L/min.

How does vascular resistance affect hemo dynamics?

Arterial pressure The MAP is the average pressure in arteries

Blood pressure CO times TPR

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Arteriosclerosis

A chronic disease of the arterial system Thickening of the arterial walls and loss of

elasticity Causes a narrowing of the tunica intima that

can result in Hypertension Decreased tissue perfusion Aneurysms

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AtherosclerosisPlaque Formation

Damaged endothelium Fatty streak formation Fibrous plaque develops Complicated lesion

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Atherosclerosis(“fat scar” or “atheromas”)

Pathological process of arterial wall damage & occlusion of the artery with plaque formation

Plaque: accumulated monocytes & lipids at inflammatory sites along the tunica intima

Response to an arterial wall injury An inflammatory response affecting the aorta,

coronary arteries, and medium-sized arteries Leading cause of death from MI and CVAs

• 3/4 of deaths are r/t CVD

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Atherosclerosis Risk factors

Total serum cholesterol > 240 mg/dL• LDL cholesterol > 160 mg/dL

Obesity Smoking DM Hypertension Decreased HDL Decreased estrogen levels Sedentary life style

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Atherosclerosis Patho: local vasospasm and thrombus formation

alter the hemodynamics causing a change in flow and pressure real risk is the vulnerability to rupture thrombosis formation with subtotal or total vessel occlusion can cause angina or MI

Clinical symptoms: especially seen in the coronary, femoral, popliteal, dorsalis pedis & cerebral vessels < venous return; no pulses; skin pale & cool to

touch,distal to obstruction; paresthesia

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Peripheral Artery Disease

Buerger’s disease, also known as “thromboangiitis obliterans” Inflammatory disease of peripheral arteries Affects the small and medium arteries and

veins of upper and lower extremities High association with tobacco use http://www.nytimes.com/2003/06/10/health/10B

ROD.html

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Peripheral Artery Disease Raynaud Phenomenon

Local vasospasm of the small arteries• secondary to systemic diseases

• Scleroderma, pulmonary hypertension, malignancy

Raynaud Disease Primary vasospastic disorder the digit turns white, blue, red

• pain, numbness & cold sensation may be present

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DVT

Deep Vein Thrombosis Asymptomatic, however associated with risk

factors• Venous stasis: immobility, age, left heart failure• Vessel damage: trauma, IV medications• > Coagulation: pregnancy, oral contraception,

some cancers, coagulation disorders Prevention: ambulation following surgery!

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Coronary Heart Disease

The single leading cause of death of American males and females

• Every 29 mins. a person experiences a coronary event in this country

• Every minute someone will die from such an event

85% of the fatalities are > 65 y.o. Average age:65.8 (males) and 70.4 (females)

• 25% of men will die within 1 yr. of initial MI• 38% of women will die within 1 yr. of initial MI

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Coronary Heart Disease Dyslipidemia

Disorders of lipoprotein metabolism, may be manifested by

• > total serum cholesterol• > LDL and triglycerides • < HDL cholesterol concentration

Causal relationship between > cholesterol levels and CHD.

• Cholesterol lowering Rx reduces lipid content of atherosclerotic plaque (e.g. Simvastatin)

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Coronary Heart Disease Hyperhomocysteine

Due to a genetic lack of the enzyme that breaks down homocysteine

And/or a nutritional lack of folate, cobalamin, or pyridoxine

• < levels of folic acid, B12, B6 hampers the natural breakdown of homocysteines

Causes the arteries to narrow and harden Check serum levels Encourage a diet rich in folate and B vitamins

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Hypertension“a cause of pump failure”

Blood pressure is the pressure exerted by the blood on the arterial walls and is a reflection of the ventricles as pumps (Hartshorn, 1997).

Mean average: 120/80

Hypertenison: consistent BP > 140/90 (adults) • staged according to severity • 140/90: watch out for children and people with

poor diet & lack of exercise (“suspicious”)

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Hypertension

Primary: “essential” = unknown cause = 90-95% of cases At risk:

• ASHD, > age, obesity, > lipids,> glucose levels, ETOH abuse hypertension accelerates atherosclerosis & vice versa 41.4% of white females (55-64) are hypertensive 63% of black females (55-64) are hypertensive 50 million Americans (6 and older) have HBP 1 in 5 Americans has HBP Mortality: 1999 (males: 40% & females: 60%) Cigarette smoking increases risk of atherosclerosis Genetic and environmental factors

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Hypertension

Secondary: specific to a disorder renal disease or renal artery stenosis neoplasia: Wilm’s Tumor phenochromacytoma: adrenal medulla tumor pregnancy: “eclampsia” > protein diets (> lipid levels)

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HypertensionClinical Symptoms

Etiology: problem with C.O. & vessel resistance Patho: > large artery stiffness; backward flow of blood as

it meets > resistance Signs & Symptoms:

“Silent killer” : no signs and symptoms Some: headache, epistaxis, or orthostatic hypotension

Target organs will begin to deteriorate• cardiac failure, left ventricular hypertrophy, CVA,

PVD, renal failure, retinopathy

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Hypertension

Prevention: BP screening; modify risk factors Tx: Early pharmacological intervention

Diuretics: Lasix, Dyazide, Spironolactone (aldosterone-receptor blocker)

Vasodilators to < peripheral resistance: Minipress or Cardizem

Ace inhibitors to interrupt RAAS: Captopril ,Vasotec• Drastically reduces the incidence of CVAs

> BP & left ventricular hypertrophy > mortality rates in both genders

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Cerebral Vascular Accident Atherosclerotic brain infarction

Most common type of complete stroke• 61% of all “strokes” (excluding TIAs)• Approximately 4,600,000 stroke survivors • Stroke rate < by 13% from ‘89 to ‘99

• However the actual number of deaths rose 8.6%

• More common in men vs. women, except in the later years of life

• 1999 stroke mortality• male: 64,485

• female: 102,881

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Myocardial InfarctionA Complication of CHD

“Ischemia with death to myocardium d/t lack of blood supply from the occlusion of coronary artery and its branches” (Hartshorn, 1997)

imbalance between myocardial oxygen supply and demand

imbalance is result of atherosclerosis, coronary artery vasospasm, thrombus, or dysrhythmias

prolonged ischemia is called an “infarction”• evolves over 3 hours & causes irreversible cellular

damage and muscle death (necrosis)

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Myocardial Ischemia Angina Pectoris

• 6,400,000 Americans experience angina d/t a lack of blood flow to the heart

• 2,400,000 males and 4,000,000 females

Stable angina-• Predictable chest discomfort on exertion or under mental or

emotional stress• Generally substernal and confused with indigestion, pain in jaw,

neck, and/or shoulder• Pain is relieved with rest/nitroglycerin

Prinzmetal angina: unpredictable chest pain at rest or during sleep patterns

Silent Ischemia: no symptoms except ischemia

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Myocardial Ischemia Leads to dysrhythmias, heart failure, sudden death ECG changes: ST depression, T wave inversion ,

and ST segment elevation Infarction leads to cell death & irreversible damage Clinical presentation: angina, vasovagal reflexes,

cool, pale, diaphoretic ECG changes: p.1015

• ischemia (st depression)• Zone of injury r/t (st elevation)• Zone of infarction/necrosis (> q wave)

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Myocardial InfarctionClinical Symptoms

> Cardiac Enzymes d/t myocardial ischemia CK: “creatine kinase” onset = 2-6 hrs after MI LDH: “lactate dehydrogenase” = 12 hrs after MI AST: “asparate transaminase” + 6-8 hrs after MI Troponin: protein marker for early detection of MI

MI: 20 - 60% are “silent” skin is cool, clammy, pale, & diaphoretic Color of skin is dusky, ashen, hyperthermic SOB, dyspnea, tachypnea, hypotension, anxious, denial, depression, “impending doom or death”, nausea,

vomiting

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Myocardial InfarctionSites Anterior Left Ventricle

involves LAD (40 - 50%) Inferior/Posterior wall of Left Ventricle & Right

Ventricle involves RCA (30-40%)

Lateral wall of Left Ventricle involves LCA (15 - 20%)

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Arrhythmias

12 lead ECG is useful in identifying dysrhythmias Pattern of electrical current identifys location of

ischemia, myocardial injury & detection and confirmation of an infarct

Anginal attack: T-wave inversion; ST-segment depression; minor ST elevation when ischemia is severe and progressive

MI: Q waves; PVCs; V-tach; V-fib; Atrial flutter; atrial fib; Bundle Branch Block; second or third-degree block; sinus tach or bradycardia

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Valvular Dysfunction Stenosis- constricted

Rheumatic heart disease Congenital Calcification

Regurgitant - insufficiency or incompetence The valve leaflets fail to shut completely Stimulates chamber dilation and myocardial

hypertrophy• Compensatory mechanism to increase the pumping of the

heart

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Cardiac Failure Inability of the heart to contract with adequate rate & force

to pump enough blood to meet the metabolic needs of the body’s tissues circulatory failure (hypo-perfusion)

Forward effects: C. O. systolic dysfunction: inability of left heart to pump blood into

circulation results in a decreased systemic blood pressure compensation: alerts the RAAS & SNS

Backward effects: emptying of Left Ventricle diastolic dysfunction: d/t volume overload of L.V. volume in pulmonary veins & capillary bed impaired gas exchange

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Congestive Heart Failure Left sided: failure of the left ventricle to pump the

blood received from the R side of the heart pulmonary circuit becomes congested with

blood MOST common cause is MI; Systemic

Hypertension; Cardiomyopathy S&S: Dyspnea, SaO2 decreases, RR increases,

DOE, pink-tinged sputum, acute anxiety fatigue, weakness, dizziness d/t SaO2 & C.O.,

othopnea, “Cardiac Asthma” (wheezing), crackles, ashen skin color, ck. electrolytes

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Right heart failure Output of the right ventricle is less than the input

from the systemic venous circuit congested venous circuit ensues: poor forward flow major cause of RHF is LHF results in > central venous pressure or hepatomegaly COPD, ARDS, Cystic Fibrosis

S&S: dependent peripheral edema, enlarged spleen & liver fluid retention ascites pleural effusions, JVD, engorged venous & portal systems

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Cardiac Inflammation

Myocarditis: forms scar tissue inflammation & injury of myocardium without ischemia caused by an infection with virus or bacterial protein that triggers

an autoimmune attack on myocardial cells CMV, HIV, Hep B, coxsackievirus TB, B-hemolytic strep, slamonella, lyme disease fungi: candidiasis, histoplasmosis, chalmydia

S&S: flu like symptoms; fatigue; dyspnea; chest pain, IDC (idiopathic

dilated cardiomyopathy), cardiac death decreases ejection fraction (15%)

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Cardiac Inflammation

Pericarditis Inflammation of pericardial sac layers Trauma, viral, neoplasms,MI, flu, iatrogenic At risk: renal failure, radiation therapy, drugs or post-

surgical open heart Pre-load is compromised d/t inflammation

S&S: fever, severe chest pain upon deep inspiration,

pericardial effusion, pericardial friction rubs; cardiac tamponade with pulsus paradoxus : < systolic

BP during inspiration

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References

American Heart Association. 2002 Heart and Stroke Statistical Update. Dallas, Tex.: American Heart Association; 2001.

Bullock, B. A. & Reet, L. H. (2000). Focus on Pathophysiology. Philadelphia: Lippincott.

Corwin, E.J.(2000).Handbook of pathophysiology. Baltimore: Lippincott.

Hansen, M. (1998). Pathophysiology: Foundations of disease and clinical intervention. Philadelphia: Saunders.

Hartshorn, J. C., Sole, M. L., & Lamborn, M. L. (1997).Introduction to critical care nursing.Philadelphia: Saunders.

Huether, S. E., & McCance, K. L. (2002). Pathophysiology. St. Louis: Mosby.

http://www.heartsite.com Illustrations in this presentation used are from HeartSite.com