Upload
arvin-ian-penaflor
View
222
Download
0
Embed Size (px)
Citation preview
8/8/2019 The HEART and its dysfunctions
http://slidepdf.com/reader/full/the-heart-and-its-dysfunctions 1/13
Anatomy of the Heart
Hollow muscular organ
Lies obliquely in chest, behind sternum in mediastinum
Varies in size, depending on persons size; usually the size of the persons f ist
Heart Wall
Epicardium outermost layer
Myocardium middle and thickest layer
Endocardium innermost layer that lines heart valve and chambers
Pericardium consist of f ibrous pericardium and serous pericardium
Heart Chambers
Right atrium Left Atrium
Right ventricle Left Ventricle
Heart Valves Atrioventricular valves
Tricuspid valve
Mitral valve (bicuspid valve)
Semilunar valves
Pulmonic valve
Aortic valve
Coronary Blood Supply
Right coronary artery
Left main coronary artery (LAD, left circumflex)
About 75% of total coronary venous blood flow leaves left ventricle by way of coronarysinus.
Cardiac cycle
Includes the cardiac events that occur from the beginning of one heart beat to the
beginning of the next
Ventricular diastole (relaxation)
Ventricular systole(contraction)
Cardiac Output
Amount of blood the left ventricle pumps into the aorta per minute
Measured by multiplying heart rate times stroke volume
Cardiac output is 4-8 L per minute
3 Factors that Determine Stroke Volume
Preload degree of stretch on muscle f ibers when they begin to contract
8/8/2019 The HEART and its dysfunctions
http://slidepdf.com/reader/full/the-heart-and-its-dysfunctions 2/13
Afterload amount of pressure left ventricle must work against to eject blood during
systole
Myocardial contractility ventricles ability to contract
Autonomic Innervation of the Heart
Sympathetic nerve stimulation causes release of norepeniphrine, which increases heart rate and
accelerates AV node conduction
Parasympathetic nerve stimulation causes release of acetylcholine, which slows heart rate and
conduction through AV node
Transmission of Electrical Impulse
Four key cell characteristics
Automaticity
Cells ability to spontaneously initiate an electrical impulse
Excitability
Cells ability to respond to an electrical impulse Conductivity
Cells ability to transmit an electrical impulse from one cell to another
Contractility
Cells ability to contract
Depolarization and Repolarization Cycle
Phase 0: Rapid Depolarization
Sodium moves rapidly into cell
Calcium moves slowly into cell
Phase 1:
Early
Repolarization
Sodium channels close
Phase 2: Plateau Phase
Calcium continues t flow in
Potassium continues to flow out
Phase3: Rapid Repolarization
Calcium channels close
Potassium flows out rapidly
Active transport via the sodium-potassium pump begins restoring potassium to the
inside of the cell and sodium to the outside of the cell
Phase 4: Resting Phase
Cell membrane is impermeable to sodium
Potassium moves out of the cell
8/8/2019 The HEART and its dysfunctions
http://slidepdf.com/reader/full/the-heart-and-its-dysfunctions 3/13
Electrical Conduction System of the Heart
Impulses travel from SA node through internodaltracts and Bachmanns bundle to AV node
From AV node, impulses travel trough Bundle of His, bundle branches, and to Purkin je f ibers
SA node generates impulses of 60-100beats/minute
AV node can f ire cat a rate of 40-60beats/minute
Purkin je f ibers can f ire at rate of 20-40beats/minute
ECG BASICS
Application of Electrodes
Choose site over soft tissues or close to the bone; not over bony prominences, thick
muscles or skin folds
Skin Preparation
Use rough patch on back of electrode , dry washcloth, or gauze pad to rub each site until
skin reddens
Clip areas of dense hair
For oily skin, clean each site with alcohol pad, letting it air dry
SINUS TACHYCARDIA
Sinus rhythm at a rate equal to or greater than 100bpm
Etiology
Situations of increased physiologic demand for oxygen that occur in association with
stress, exercise, pain f ever, anemia, hypoxia and shock
Hyperthyroidism, heart failure, myocardial infarction, pulmonary embolism, excessve
caff eine and medications
Treatment
Beta-blockers and calcium channel blockers
SINUS BRADYCARDIA
A sinus rhythm with a rate less than 60bpm
Etiology
Vagal stimulation, sleep
Hypothyroidism, hypothermia, electrolyte imbalance
Inf erior wall myocardial infarction
Sick sinus syndrome
Medications
Treatment
Atropine and epinephrine
Pacemakers may be required if drug therapy is ineff ective
8/8/2019 The HEART and its dysfunctions
http://slidepdf.com/reader/full/the-heart-and-its-dysfunctions 4/13
ATRIAL PREMATURE COMPLEXES
Results from a premature, ectopic, supraventricular impulse that originates somewhere
in the atria outside of the SA node.
Etiology
Stress, caff eine, alcohol
Heart failure, myocardial ischemia, valvular diseases, coronary artery disease
Chronic lung disease, hyperthyroidism, inf ection Electrolyte abnormalities; use of medications
PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA
Has an atrial rate from 150-250beats/min
Etiology
Caff eine
Marijuana use
Electrolyte imbalance
Hypoxia
Physical or psychological stress
Signs and symptoms
Rapid apical and peripheral pulse rate Hypotension
syncope
ATRIAL FLUTTER
A supraventricular dysrhythmia characterized by the appearance of sawtooth-shaped
flutter waves at a rate between 250-400bpm.
Etiology
Hyperthyroidism
Valvular disease
Ischemic heart disease, acute myocardial infarction
Pericardial disease Acute pulmonary embolism
8/8/2019 The HEART and its dysfunctions
http://slidepdf.com/reader/full/the-heart-and-its-dysfunctions 5/13
Pulmonary disease
Congenital heart disease
ATRIAL FIBRILLATION
A supravenmtricular dysrhythmia characterized by multiple ectopic atrial foci,
uncoordinated atrial contractions, and a classically irregular ventricular rate
Etiology
Heart failure, ischemic heart disease
Valvular heart disease
Cardiomyopathy, alcohol, pericardial disease
Congenital heart disease
Sick sinus syndrome
Hypertension
Hyperthyroidism Lung disease
VENTRICULAR PREMATURE COMPLEXES
A premature ectopic impulse that originates somewhere in the ventricles below the
Bundle of His.
Herald lethal ventricular arrhythmia
CARDIOVASCULAR DYSFUNCTION
2 MAJOR GROUPS
1. Congenital heart disease
= includes primarily anatomic aberration present at birth that result in abnormal
cardiac function.
2. Acquired Cardiac Disease
= ref ers to disease processes or abnormalities that occur after birth and can be
seen in the normal heart or in the presence of congenital heart def ects.
ASSESSMENT
Health History Finding
1. Family history of congenital heart disorders
2. Presence of murmurs and age at which f irst noted
3. Feeding problems, including fatigue or diaphoresis during f eeding and poor weight gain 4. Respiratory diff iculties, including tachypnea, dyspnea, shortness of breath, cyanosis and
frequent respiratory inf ections
5.Chronic fatigue or exercise intolerance
6. Contact with known teratogens such as rubella during pregnancy
PHYSICAL ASSESSMENT
1. Growth abnormalities
2. Cyanosis
3. Clubbing of f ingers and toes
4. Periorbital and peripheral edema
5. Diminished peripheral pulses
6. Thready pulse
8/8/2019 The HEART and its dysfunctions
http://slidepdf.com/reader/full/the-heart-and-its-dysfunctions 6/13
7.Engorged neck veins
8.Abdominal distention, hepatomegaly, spleenomegaly
9. Tachycardia, bradycardia, tachypnea
10. Hypotension or unequal blood pressure in arm and legs
11. Murmurs, bruits, thrills
DIAGNOSTIC TEST
A. Cardiac Catheterization
Types:
1. Diagnostic Catheterization
2. Interventional Catheterization
3. Electrophysiology Studies
NURSING MANAGEMENT
Preprocedural Care
1. Accurate height and weight measurement
2. Obtain history of allergic reaction to iodine
3. Assess and mark pulses before the patient goes to the catheterization room 4. Baseline oxygen saturation using pulse oximetry
5. NPO for 4-6 hours or more before the procedure according to institutional guidelines
Postprocedural Care
1. Assess for pulses, especially below the catheterization site for equality and symmetry
2. Assess for the temperature and color of the aff ected extremity
3. Vital signs every 15 minutes
4. Assess the dressing
5. Assess for the fluid intake
6. Watch out for hypoglycemia
7. Keep on bed with aff ected extremity straight for 4-6 hours after venous catheterization and 6-8
hours after arterial catheterization8. Encourage to void
9. B. Chest radiograph
10. C. Electrocardiography
11. D. Transthoracic
12. * M-Mode
13. *Two-dimensional
14. E. Doppler
15. *Fetal
16. *Trans-esophageal
17. F. Angiography
18. G. Electrophysiology
H. Exercise Stress Test
CONGENITAL HEART DISEASE
Pre-natal Contributory Factors
1. Maternal rubella during pregnancy
2. Maternal alcoholism
3. Maternal age over 40 years
4. Maternal type 1 diabetes
Genetic Factor
1. Has a sibling with a heart def ect
2. Parent with CHD
3. Chromosomal aberration such as Down Syndrome
CLASSIFICATION OF CHD
A. Acyanotic
1. Increased Pulmonary Blood Flow
Atrial Septal Def ect
Ventricular Septal Def ect
Patent Ductus Arteriosus
Atrioventricular Canal Def ect
2. Obstruction to Blood Flow from the Ventricle
Coarctation of Aorta
Aortic Stenosis
Pulmonic Stenosis
8/8/2019 The HEART and its dysfunctions
http://slidepdf.com/reader/full/the-heart-and-its-dysfunctions 7/13
B. Cyanotic
1.Decreased Pulmonary Blood Flow
Tetralogy of Fallot
Tricuspid Atresia
2. Mixed Blood Flow
Transposition of Great Arteries
Total Anomalous Pulmonary Venous Return
Truncus Arteriosus
Hypoplastic Left Heart Syndrome
ATRIAL SEPTAL DEFECT
3 Types:
1. Ostium Primum
2. Ostium Secundum
3. Sinus Venosus Def ect
Manif estation
Murmur
Medical Management: Dacron Patch
Ventricular Septal Defect
Complication
1. CHF
2. Bacterial Endocarditis
3. Pulmonary Vascular Obstructive Disease
Management:
Palliative; pulmonary artery banding
Complete Repair
Atrioventricular Canal Defect
Consist of a low atrial septal def ect that is continuous with a high ventricular septal def ect and
cleft of the mitral and tricuspid valves
Surgical Treatment:
Patch closure of the septal def ect and reconstruction of the AV valve tissue
(either repair of the mitral valve cleft or fashioning of the AV valve)
Complication:
1. Heart block
2. Mitral regurgitation
3. Pulmonary hypertension
4. Congestive heart failure
Patent Ductus Arteriosus
Failure of the f etal ductus ateriosus to close within the f irst weeks of lif e
Complication:
1. Congestive Heart failure
2. Bacterial Endocarditis
3. Pulmonary Vascular Disease
Management:
1. Administration of Indomethacin
2. Surgical division or ligation of the patent vessel via a left thoracotomy
Coarctation of Aorta Localized narrowing near the insertion of the ductus arteriosus, resulting in increased
pressure proximal to the def ects and decresed pressure distal to the obstruction
Manif estation
Bounding pulses in arms
Weak or absent f emoral pulses
Cool lower extremities with lower blood pressure
Dizziness, headache, fainting and epistaxis
Complication:
1. Rupture aorta
2.Aortic aneurysm
3. Stroke
8/8/2019 The HEART and its dysfunctions
http://slidepdf.com/reader/full/the-heart-and-its-dysfunctions 8/13
4. Congestive heart failure
Management:
1. Resection of coarcted portion with end to end anastomosis of the aorta
2. Enlargement of the constricted section using a graft of prosthetic material or a
portion of the left subclavian artery.
Medical Management:
Captopril ACE inhibitor
Nursing Responsibility:
1. Monitor BP and pulse rate often
2. Give drug 1 hour before meals
3. Separate doses with antacids
4. If patient develops f ever, sore throat, leukopenia, hypotension or tachycardia
withhold dose and notify the prescriber.
5. Inform that light headedness may occur
6. Use in caution during hot weather
Propranolol- Beta blocker
Nursing Responsibility:
1. Monitor BP, ECG and heart rate and rhythm, especially when giving IV route 2. Give oral drug with meals
3. Before any surgical procedure, notify anesthesiologist that patient is taking propranolol
4. Do not stop the drug abruptly
Aortic Stenosis
Narrowing or stricture of the aortic valve, causing resistance to blood flow in the left
ventricle
Manif estation
Faint pulses
Hypotension
Tachycardia
Poor f eeding
Exercise intolerance
Chest
Dizziness
Murmur
Management:
1. Aortic valvotomy
2. Valve replacement
3. balloon angioplasty
Complication:
1. Aortic insuff iciency
2. Valvular regurgitation
3. Tearing of valve leaflets
4. Loss of pulse in catheterized limb
Pulmonic Stenosis
Management:
1. Transventricular valvotomy
2. Balloon angioplasty
TETRALOGY OF FALLOT The classic form includes 4 def ects:
Vetricular septal def ect
Pulmonic stenosis
Overriding aorta
Right ventricular hypertrophy
Clinical manif estation
Blue spells or tet spells
Clubbing of f ingers
Squatting
Poor growth
8/8/2019 The HEART and its dysfunctions
http://slidepdf.com/reader/full/the-heart-and-its-dysfunctions 9/13
Complication
Emboli
Cerebrovascular disease
Brain abscess
Seizure and loss of consciousness
Sudden death
TRICUSPID ATRESIA
There is no communication between the right atrium to the right ventricle
Clinical Manif estation
Cyanosis
Tachycardia
Dyspnea
Clubbing of f ingers
Management
Infusion of Prostaglandin E1 Modif ied Fontan Procedure
Systemic venous return is directed to the lungs through surgical connections
between thr right atrium and the pulmonary artery
TRANSPOSITION OF GREAT ARTERIES
The pulmonary artery leaves the left ventricle, and the aorta exits from the right
ventricle
TOTAL ANOMALOUS PULMORY VENOUS CONNECTION
The pulmonary veins are abnormally connected to the systemic venous circuit via the
right atrium or various veins draining toward the right atrium such as the superior vena
cava
ACQUIRED HEART DISEASES
TRUNCUS ATRESIA
Failure of normal septation and division of the embryonic bulbar trunk into the
pulmonary artery and the aorta, resulting in a single vessel that overrides both
ventricles
CONGESTIVE HEART FAILURE
Inability of the heart to pump an adequate amount of blood to the systemic circulation
at normal f illing pressures to meet the metabolic demands of the body.
Right-sided failure
The right ventricle is unable to pump blood eff ectively into the pulmonary artery
Left-sided failure
The left ventricle is unable to pump blood into the systemic circulation
Clinical manifestation of CHF
y Impaired Myocardial Function
Tachycardia
Sweating
Decreased urine output Fatigue
Weakness
Restlessness
Anorexia
Pale, cool extremities
Weak peripheral pulses
Decreased blood pressure
Cardiomegaly
Gallop rhythm
8/8/2019 The HEART and its dysfunctions
http://slidepdf.com/reader/full/the-heart-and-its-dysfunctions 10/13
Pulmonary Congestion
Tachypnea
Dyspnea
Retractions
Flaring nares
Exercise intolerance
Orthopnea
Cough, hoarseness
Cyanosis
Wheezing
Grunting
Systemic Venous Congestion
Weight gain
Hepatomegaly
Peripheral edema
Ascites
Neck vein distention
Therapeutic management
Improve cardiac functions
Administration of digitalis glycosides (digoxin)
ACE inhibitor results in decreased pulmonary and systemic vascular resistance,
decrease blood pressure, and a reduction in afterload
Remove accumulated fluid
Fluid restriction, sodium restriction
Administration of diuretics
Decrease cardiac demands
Limit physical activity
Preserving body temperature
Treating any inf ections
Reducing the effort of breathing
Improve tissue oxygenation and decrease oxygen consumption
Supplemental cool, humidif ied oxygen
ISCHEMIC HEART DISEASE
An imbalance between the supply and demand of the heart for oxygenated blood
Conditions that Aggravate Ischemia
Increase in cardiac energy demand
Lowered systemic blood pressure
4 Syndromes
1. Myocardial Infarction
2. Angina Pectoris
3. Chronic Ischemic heart disease
4. Sudden cardiac death
Epidemiology
1.Prevention achieved by modif ication of determinants
2. Therapeutic advances
3. Maintenance of normal blood glucose levels in diabetic patients
4. Postmenopausal estrogen replacement therapy 5. Lipid lowering and antioxidant therapy
6. Aspirin prophylaxis
Pathogenesis
1. Role of Fixed Coronary Obstruction
2. Role of Acute Plaque Change
3. Role of Coronary Thrombus
4. Role of Vasoconstriction
8/8/2019 The HEART and its dysfunctions
http://slidepdf.com/reader/full/the-heart-and-its-dysfunctions 11/13
ANGINA PECTORIS
Paroxysmal and usually recurrent attacks of substernal or precordial chest discomfort caused by
transient myocardial ischemia that falls short of inducing the cellular necrosis that def ines
infarction.
1. Stable Angina
Caused by reduction of coronary perfusion to a critical level by chronic
stenosing coronary atherosclerosis
Usually relieved by rest or nitroglycerine
2. Prinzmetal Variant Angina
Episodic angina that occurs at rest due to coronary artery spasm
Responds promptly to vasodilators, such as nitroglycerine and calcium channel
blockers
3. Unstable or Crescendo Angina
A pattern of pain that occurs with progressively increasing frequency, often
occurs at rest, and of more prolonged duration
MYOCARDIAL INFARCTION Also known as heart attack
Transmural
Involves full or nearly full thickness of the ventricular wall in the distribution of a
single coronary artery
Subendocardial Infarct
Ischemic necrosis limited to the inner one third of the ventricular wall
Risk Factors
Hypertension
Cigarette smoking
Diabetes mellitus
Genetic hypercholesterolemia
Blacks and white are aff ected equally
Men are signif icantly are at greater risk than women
Pathogenesis
1. Coronary Arterial Occlusion
Severe coronary atherosclerosis, acute atheromatous plaque change,
superimposed platelet activation, thrombosis and vasospasm.
2. Response of the Myocardium
Consequences and Complications of Myocardial Infarction
1. Contractile dysfunction
Left ventricular failure with hypotension, pulmonary vascular
congestion, pulmonary edema
2. Arrhythmias
Sinus bradycardia or tachycardia, ventricular premature contractions or
ventricular tachycardia, ventricular f ibrillation, or asystole
3. Myocardial rupture
Results from the mechanical weakening that occurs in necrotic and
subsequently inflamed myocardium
4. Pericarditis
5. Right ventricular infarction
6. Infarct extension
7. Infarct expansion
8. Mural thrombus 9. Ventricular aneurysm
10. Progressive late heart failures
Nursing interventions:
Encourage assessment of food intake and eating patterns to help identify areas that can
be improved
Discuss therapeutic lif estyle changes, dietary recommendations, emphasizing the role of
the diet in heart disease
Encourage gradual but progressive dietary changes
Discourage use of high fat, low-carbohydrate, or other fad diets for weight loss
Encourage reasonable goals for weight
8/8/2019 The HEART and its dysfunctions
http://slidepdf.com/reader/full/the-heart-and-its-dysfunctions 12/13
Discuss risk factors for CHD, stressing that changing or managing those factors that can
be modif ied reduces the clients overall risk for the disease
y Discuss the immediate benef its of smoking cessation
y Help the client identify specif ic sources of psychosocial and physical support for smoking
cessation, dietary, and lif estyle changes
y Discuss the benef its of regular exercise for cardiovascular health and weight loss
y Provide information and teaching about prescribed medication such as cholesterol-
lowering drugs.
y STATINS= assess for muscle pain and tenderness
report digoxin toxicity
do not use for pregnant
women
Nicotinic acid
Give oral preparation with meals and accompanied by a cold beverage to
minimize GI eff ects
Administer with caution to clients with active liver disease, peptic ulcer disease,
gout or type 2 diabetes Monitor blood glucose, uric acid levels and liver function test during treatment
HYPERTENSION
BLOOD PRESSURE
- pressure exerted by blood on walls of the
blood vessels
- determined by CO, PVR, viscosity of the
blood, and the amount of circulating
blood volume
FACTORS THAT LEADS TO HPN
1. S
NS
overstimulation2. Alteration in baroreceptors and chemoreceptors
3. Increase in hormone
4. Changes in kidney function
Primary HPN
- chronic elevation of blood pressure
Secondary HPN
- a sign of another problems such as
kidney abnormality tumor of adrenal
gland, or a congenital def ect of the aorta
Isolated Systolic HPN
- a systolic pressure of 160 mmHg or
greater and a diastolic pressure of
90mmHg or less
Signs and Symptoms of HPN
1. Often none
2. Increase BP, bloody nose, severe anxiety or
shortness of breath
Diagnosis of HPN
1. Previous diagnosis of HPN
2. Presence of signs and symptoms, history of kidney or heart disease and current use of medication, increase BP
Risk Factors
Non-modif iable
1. family history of hypertension
2. age plaque build-up among elderly
3. ethnicity African-American (respond to
diuretics), European-Americans
chemical imbalances (respond to be beta blockers), Japanese-Americans
high sodium content of the diet, stress and cigarette smoking)
Modif iable Risk Factors
1. Weight reduction
8/8/2019 The HEART and its dysfunctions
http://slidepdf.com/reader/full/the-heart-and-its-dysfunctions 13/13
2. Meal Planning
- salt intake
- caff eine
- intake of potassium (orange, banana,
brocolli), magnesium (spinach, nuts,
seeds, whole grains), calcium (milk,
yogurt, spinach)
3. Alcohol consumption
4. Exercise control hypertension by reducing weight,
decreasing peripheral resistance, and decrease body fat
5. Smoking
Therapeutic and Intervention
1. Lif estyle modif ication
2. Drug Theraphy
a. Diuretics increase urine output by
inhibiting sodium and water reabsorp-
tion by the kidneyPatent teaching:
1. Antihypertensive therapy must usually be
continued for the rest of their lives.
2. care
Complications:
1. Coronary Artery Disease
2. Atherosclerosis
3. Myocardial Infarction
4. Heart Failure
5. S
troke 6. Kidney Damage
7. Eye Damage
8. . Blood pressure should be well controlled before any invasive procedure
9. 4. Antihypertensive medication should be resumed as soon as possible after the procedure
10. Hypertensive emergency:
- a severe type of hypertension characterized
by elevation in SBP greater than 180mmHg
and diastolic BP greater than 120
- patients who are untreated, fail to comply with
antihypertensive therapy, or stop their
medication abruptly