Transcript lesson8_fa03

Diseases of the Circulatory
System
University of San Francisco
Dr. M. Maag
©2003 Margaret Maag
Class 8-9 Objectives
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Upon completion of this lesson, the student
will be able to
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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
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http://www.heartsite.c
om/html/the_heart.ht
ml
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Coronary Vessels
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http://www.heartsite.c
om/html/lad.html
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Cardiac Conduction
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http://www.heartsite.c
om/html/electrical_act
ivity.html
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Review
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How does preload, afterload & contractility
influence stroke volume and determine
cardiac output?
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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.,
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1997).
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Review
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Cardiac Output (HR X SV)
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How does vascular resistance affect hemo
dynamics?
Arterial pressure
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Stroke volume: volume of blood ejected during
systole
Normal adult C.O. = 5 L/min.
The MAP is the average pressure in arteries
Blood pressure
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CO times TPR
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Arteriosclerosis
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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
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Hypertension
Decreased tissue perfusion
Aneurysms
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Atherosclerosis
Plaque Formation
Damaged endothelium
 Fatty streak formation
 Fibrous plaque develops
 Complicated lesion
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Atherosclerosis
(“fat scar” or “atheromas”)
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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
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Risk factors
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Total serum cholesterol > 240 mg/dL
• LDL cholesterol > 160 mg/dL
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Obesity
Smoking
DM
Hypertension
Decreased HDL
Decreased estrogen levels
Sedentary life style
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Atherosclerosis
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Patho: local vasospasm and thrombus formation
alter the hemodynamics
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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
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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
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Raynaud Phenomenon
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Local vasospasm of the small arteries
• secondary to systemic diseases
• Scleroderma, pulmonary hypertension, malignancy
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Raynaud Disease
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Primary vasospastic disorder
the digit turns white, blue, red
• pain, numbness & cold sensation may be present
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DVT
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Deep Vein Thrombosis
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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
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Prevention: ambulation following surgery!
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Coronary Heart Disease
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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
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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
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Dyslipidemia
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Disorders of lipoprotein metabolism, may be
manifested by
• > total serum cholesterol
• > LDL and triglycerides
• < HDL cholesterol concentration
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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
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Hyperhomocysteine
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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
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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”
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Blood pressure is the pressure exerted by the
blood on the arterial walls and is a reflection of
the ventricles as pumps (Hartshorn, 1997).
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Mean average: 120/80
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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
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Primary: “essential” = unknown cause = 90-95% of cases
 At risk:
• ASHD, > age, obesity, > lipids,> glucose levels, ETOH abuse
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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
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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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Hypertension
Clinical Symptoms
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Etiology: problem with C.O. & vessel resistance
Patho: > large artery stiffness; backward flow of blood as
it meets > resistance
Signs & Symptoms:
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“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
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Prevention: BP screening; modify risk factors
Tx: Early pharmacological intervention
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Diuretics: Lasix, Dyazide, Spironolactone (aldosteronereceptor 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
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Atherosclerotic brain infarction
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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 Infarction
A Complication of CHD
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“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”
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• evolves over 3 hours & causes irreversible cellular
damage and muscle death (necrosis)
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Myocardial Ischemia
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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
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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
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Prinzmetal angina: unpredictable chest pain at
rest or during sleep patterns
Silent Ischemia: no symptoms except ischemia
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Myocardial Ischemia
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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 Infarction
Clinical Symptoms
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> Cardiac Enzymes d/t myocardial ischemia
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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”
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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 Infarction
Sites
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Anterior Left Ventricle
 involves LAD (40 - 50%)
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Inferior/Posterior wall of Left Ventricle & Right
Ventricle
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RCA (30-40%)
Lateral wall of Left Ventricle
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LCA (15 - 20%)
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Arrhythmias
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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
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Stenosis- constricted
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Rheumatic heart disease
Congenital
Calcification
Regurgitant - insufficiency or incompetence
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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
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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.
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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
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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
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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),
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crackles, ashen skin color, ck. electrolytes
Right heart failure
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Output of the right ventricle is less than the input
from the systemic venous circuit
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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:
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dependent peripheral edema,
enlarged spleen & liver
fluid retention
ascites
pleural effusions, JVD, engorged venous & portal systems
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Cardiac Inflammation
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Myocarditis: forms scar tissue
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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:
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flu like symptoms; fatigue; dyspnea; chest pain, IDC (idiopathic
dilated cardiomyopathy), cardiac death
decreases ejection fraction (15%)
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Cardiac Inflammation
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Pericarditis
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Inflammation of pericardial sac layers
Trauma, viral, neoplasms,MI, flu, iatrogenic
At risk: renal failure, radiation therapy, drugs or postsurgical open heart
Pre-load is compromised d/t inflammation
S&S:
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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
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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
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