Download Management of cardiovascular system

Survey
yes no Was this document useful for you?
   Thank you for your participation!

* Your assessment is very important for improving the work of artificial intelligence, which forms the content of this project

Document related concepts

Remote ischemic conditioning wikipedia, lookup

Cardiovascular disease wikipedia, lookup

History of invasive and interventional cardiology wikipedia, lookup

Electrocardiography wikipedia, lookup

Heart failure wikipedia, lookup

Cardiac contractility modulation wikipedia, lookup

Hypertrophic cardiomyopathy wikipedia, lookup

Arrhythmogenic right ventricular dysplasia wikipedia, lookup

Mitral insufficiency wikipedia, lookup

Lutembacher's syndrome wikipedia, lookup

Angina wikipedia, lookup

Cardiac surgery wikipedia, lookup

Antihypertensive drug wikipedia, lookup

Management of acute coronary syndrome wikipedia, lookup

Quantium Medical Cardiac Output wikipedia, lookup

Dextro-Transposition of the great arteries wikipedia, lookup

Coronary artery disease wikipedia, lookup

Transcript
Management of cardiovascular
system
On completion of this chapter, the learner will be able to:
1. Describe the pathophysiology, clinical manifestations, and treatment of
coronary atherosclerosis.
2. Describe the pathophysiology, clinical manifestations, and treatment of
angina pectoris.
3. Use the nursing process as a framework for care of patients with angina
pectoris.
4. Describe the pathophysiology, clinical manifestations, and treatment of
myocardial infarction.
5. Use the nursing process as a framework for care of patients with
myocardial infarction (acute coronary syndrome).
6. Describe the nursing care of a patient who has had an invasive
interventional procedure for treatment of coronary artery disease.
7. Describe coronary artery revascularization procedures.
8. Describe the nursing care of the patient treated with cardiac surgery.

Anatomy of the Heart
Assessment of
Cardiovascular Function
− Cardiac output: Amount of blood pumped
by each ventricle in liters per minute.
* Normal cardiac output 5L/min in resting.
− Stroke volume: Is the amount of blood
ejected per heart beat.
* The average stroke volume is about 70 ml.
Cardiac output = Stroke volume x Heart beat.
=
70 ml
X (60-80) b/min.
Control of stroke volume:
− Stroke volume: Is primarily determined by
three factors:
Preload: It’s the degree of stretch of cardiac
muscle fibers at end of diastole.
Afterload: The pressure the ventricular
myocardium must overcome to eject blood
during systole.
Contractility: is a term used to denote the
force generating by contracting myocardium
under any given condition.
I-Assessment:
1- Health history and clinical
manifestation:
* Cardiac Symptoms:
- Chest discomfort.
-Shortness of breath or Dyspnea.
- Edema and weight gain.
- Palpitation (dysarrythmias).
- Fatigue.
- Dizziness and syncope.
I-Assessment:
2- Nutrition and metabolism:
Diets that are restricted in sodium, fat,
cholesterol, and calories.
3- Activity and Exercise:
If symptoms develop during exercise,
what are nature of exercise.
I-Assessment:
4- Physical examination:
-The examination, which proceeds logically from head to toe
can
be performed in about 10 min.
a- General appearance:
- The nurse observes the patients level of consciousness,
and thought process as an indication of the hearts ability to
propel oxygen to the brain.
b- Inspection of skin:
Pallor, cyanosis, Temp, reduce skin turgor, wounds.
c- Blood Pressure.
d- Arterial pulses:
Pulse rate, rhythm, and volume.
II- Cardiac Auscultation:
Heart Sounds:
The normal heart sounds, S1, S2, are
produced primarily by the closing of
the heart values.
a- S1= Closure of mitral and tricuspid valves.
b- S2= Closure of aortic and pulmonic
valves.
II- Cardiac Auscultation:
c- Gallop:
S3: Occurring during rapid ventricle filling is impeded during
diastole. e.g MI, CHF.
S4: When the ventricle is enlarged or hypertrophied and
therefore resistant to filling. e.g. CAD, aortic stenosis.
Note: S4 heard by bell of stethoscope only, they are heard best at
the apex.
d- Murmurs:
Are created by the turbulent flow of blood, the causes
turbulence may be a critically narrowed valve or
regurgitation of valves.
III- Diagnostic
Evaluation:
1- Laboratory Tests:
e.g Cardiac enzyme , blood chemistry (urea, creatinine,
serum electrolyte, coagulation studies, lipid profile.)
2- Chest x-ray and fluoroscopy.
3- Cardiac stress test:
To detect the ischemia, by increasing the metabolic
demands for oxygen.
4- Echocardiograph:
Is non invasive ultrasound test used to examine the size,
shape and motion of cardiac structures.
5- Cardiac Catheterization:
Is an invasive diagnostic procedure in which radiopaque
arterial and venous catheters are introduced into selected
blood vessels of the right and left sides of the heart.
III- Diagnostic
Evaluation:
6-Electro cardiography. (ECG)
Normal Components of the EKG Waveform
Normal Components of the EKG
Waveform
P wave
Indicates atrial depolarization, or contraction of the atrium.
Normal duration is not longer than 0.11 seconds (less than 3 small
squares)
QRS complex
Indicates ventricular depolarization, or contraction of the ventricles.
Normally not longer than .10 seconds in duration
T wave
Indicates ventricular repolarization
ST segment
Indicates early ventricular repolarization
PR interval
Indicates AV conduction time
Duration time is 0.12 to 0.20 seconds
Management of Patient with
Coronary Vascular Disease
Coronary Artery Disease:
The most prevalent type of cardiovascular
disease is coronary artery disease (CAD).
Coronary Atherosclerosis:
Is an abnormal accumulation of lipid , or
fatty substances and fibrous tissue in the
vessel wall.
Atheroma: Begins as fatty streaks, lipids
that are deposite on the intima of the arterial
wall.
Management of Patient with
Coronary Vascular Disease
Risk factors for (CAD):
Non modifiable risk factors:
*
*
*
*
Family history.
Increasing age.
Gender.
Race.
Modifiable risk factors:
*
*
*
*
High blood cholesterol.
Smoking.
Hypertension.
Diabetes mellitus.
* Obesity.
* Stress.
Management of Patient with
Coronary Vascular Disease
Angina Pectoris:
Is a clinical syndrome usually characterized
by episodes or paroxysm of pain or pressure
in the anterior chest, the cause is usually
insufficient coronary blood flow.
− Factors those are associated with a
typical angina pain:
* Physical exertion.
* Exposure to cold.
* Eating a heavy meal.
* Stress or any emotion- provoking
situation.
Angina: Pathophysiology
• Temporary and reversible> partial occlusion, spasm, or
thrombus
• Cells deprived of oxygen
• Cell membranes release histamines, kinins,specific
enzymes stimulating nerve fibers in cardiac muscle that
send pain impulses to CNS
• Pain radiates to upper body
• <30 minutes ischemia: adequate nutrients/oxygen
clears waste products
• > 30 minutes ischemia: irreversible damage
Angina Types:
• Stable Angina
– Most common and predictable; occurs with predictable
amount of activity or stress
– Occurs when work of heart is increased by physical
exertion, exposure to cold, stress
– Relieved by rest and nitrates
• Prinzmetal’s (variant)
– Atypical angina occurs unpredictability; not related to
activity and often at night
– Caused by spasm of coronary artery with or without
atherosclerotic lesion
Angina Types:
• Unstable Angina
– Occurs with increasing frequency, severity, duration
– Pain is unpredictable and occurs with rest, low
activity, stress
– At risk for myocardial infarction
• Silent Angina
– Asymptomatic ischemia, thought to very common
with CHD
– May occur with activity or mental stress
Angina Pectoris:
Clinical Manifestation:
*
*
*
*
Chest pain. (Retrosternal pain).
Weakness or numbness in the arms.
Shortness of breath.
Pallor, diaphoresis, dizziness or
light –headedness.
* Nausea, Vomiting.
* Anxiety.
Medical Management:
1-Pharmacologic Therapy:
a-Nitroglycerine: To decrease workload of the heart, and
coronary artery vasodilation.
b- Beta-adrenergic blocking agents: Such as propranolol
(Inderal),and atenolol(tenormine).To decrease heart rate,
blood pressure and myocardium contractility.
c- Calcium channel blocking agents: Such as nipedipia,
verpamil, and diltiazem.To decrease heart rate, decrease
workload of heart, and increase coronary artery perfusion.
d-Antiplatlates and anticoagulant medication.
* Aspirin prevent platelets aggregation.
* Heparin prevents the formation of new blood clots.
e-Oxygen administration.
Medical Management:
2- Invasive intervention and surgical management:
a- Percautanouse transluminal coronary
angioplasty (PTCA).
b- Coronary artery stent.
c- Atherectomy.
d- Coronary artery bypass graft. (CABG).
Myocardial Infarction:
Definition: Is a death of heart tissue caused by prolonging ischemia.
- Necrosis of myocardial cells; life‐threatening event
– Loss of functional myocardium affects heart’s ability to maintain
effective cardiac output
– AMI and other ischemic heart diseases cause majority of deaths
– Majority of AMI deaths occur during initial period post symptoms: 60%
within first hour, 40% prior to hospitalization
•
MI: Pathophysiology
Develops from atherosclerotic plaques in coronary arteries
• Occurs when blood flow blocked>prolonged tissue ischemia
and irreversible cell damage
• Prolonged ischemia> irreversible damage
• Cellular metabolism shifts from aerobic to anaerobic
metabolism producing hydrogen ions and lactic acid
• Dysrhythmias and decreased myocardial contractility cause
decreased stroke volume, cardiac output, blood pressure
and tissue perfusion
MI: Pathophysiology
• Areas of heart
– Particular coronary artery occluded determines area of
damage
– The specific infarct site predicts possible complications
and dictates appropriate therapy
– Specific artery and affected area of heart
• Left anterior descending artery: anterior wall of left
ventricle and part of interventricularseptum
• Left circumflex artery: lateral MI
• Right coronary artery: right ventricle, inferior and
posterior infarct
• Left main coronary artery: entire left ventricle
Myocardial Infarction:
Clinical Manifestation:
*
*
*
*
*
Sudden chest pain.
Sweating.
Nausea and vomiting.
Cool, pale.
Anxiety.
Diagnostic procedure:
* ECG.
* Echocardiogram.
* Laboratory test. eg. Cardiac enzyme
(CPK, LDH,Troponin.)
Medical Management:
The goal of medical management is to minimize
myocardial damage, preserve myocardial function
and prevent complication.
a- Emergent PTCA or stent.
b- Pharmacological therapy.e.g thrombolytics:
the purpose is to dissolve and lyses the thrombus in
coronary artery. (Reperfusion)
e.g. TPA (Tissue plasminogen activate),
Streptokinase.
c- Analgesic.
d- Oxygen administration.
Myocardial Infarction:
Nursing intervention:
* Relieving chest pain.
*
*
*
*
Improving respiratory function.
Promoting adequate tissueperfusion.
Reducing anxiety.
Managing and monitoring potential
complication.
Management of Patients With Complications From
Heart Disease
LEARNING OBJECTIVES
On completion of this chapter, the learner will be able to:

1. Describe the management of patients with chronic heart failure.

2. Use the nursing process as a framework for care of patients with
heart failure.

3. Describe the management of patients with acute heart failure.

4. Develop teaching plans for patients with heart failure.

5. Describe the management of patients with cardiogenic shock.

6. Describe the management of patients with thromboembolic
episodes, pericardial effusion and cardiac tamponade, and myocardial
rupture.

7. Demonstrate the techniques of cardiopulmonary resuscitation.

Cardiac Failure:
Congestive heart failure :( CHF)
Referred to as a cardiac failure, is the inability of the heart
to pump sufficient blood to meet the needs of the tissue for
oxygen and nutrient.
- The term “congestive heart failure” is most commonly used
when referring to Lt- sided and right-sided heart failure.
- Cardiac failure commonly occurs with disorders of cardiac
muscle that result in decrease contractile properties of the
heart, lead to decrease myocardial contractility include.
Myocardial dysfunction (especially from coronary
atherosclerosis), arterial hypertension, and valvular
dysfunction.
Left –Sided Cardiac failure:
Pulmonary congestion occurs when the left ventricle cannot pump
the blood out of the chamber. This increase pressure in the left
ventricle and decrease the blood flow from the left atrium. The
pressure in the left atrium increase, which decrease the blood
flow coming from the pulmonary vessels. The result increase in
pressure in the pulmonary circulation forces fluid into the
pulmonary tissue and alveoli.
Sings & Symptoms:
* Dyspnea on exertion.
* Orthopnea.
* Cough.
* Pulmonary Crackles.
* Restlessness and anxiety.
* Tachycardia.
Right sided heart failure:
The right side of the heart cannot eject blood, and thus can not
accommodate all the blood that normally returns to it from the venous
circulation.
Sings & Symptoms;
*
*
*
*
*
*
*
*
*
Edema of the lower extremities.
Wight gain.
Hepatomegally (enlargement of the liver).
Distended neck vein.
Ascites (an accumulation of fluid in the peritoneal cavity).
Anorexia and nausea.
Nocturia.
Weakness.
Pitting edema.
Heart Failure Diagnostics:
• Electrolytes.
• UA, BUN, creatinine
• LFTs
• ABGs
• ECG
• Echocardiography
Hemodynamic
Monitoring
• Intra-arterial pressure (art line; a line)
Direct and continuous monitoring of systolic,
diastolic, mean arterial pressure; arterial blood
sampling
• Central venous pressure (CVP)
Measures blood volume/venous return; reflects
right heart filling pressures
• Pulmonary artery pressure (PA; Swan-Ganz
catheter)
Evaluate left ventricular and overall cardiac
function
Medical Management:
The basic objectives in treating patients with congestive
heart failure are the following:
* Reducing the workload on the heart.
* Increasing the force and efficiency of myocardial
contraction.
Pharmacological Therapy:
a-ACE (Angiotinsin converted enzyme) inhibitors:
ACE inhibitors promote vasodilation and diuresis by
decreasing afterload and preload, they decrease the
work load of the heart.
b-Diuretic Therapy.
c-Digitalis. The most commonly prescribed forms of digitalis for
patients with CHF are digoxin (lanoxine) and digotoxin.
- The medication increases the force of myocardial
contraction and slows conduction through the AVnode.
d- Dobutamine (dobutrex):
It stimulates the beta1-adrenergic receptor, and its major
action to increase cardiac contractility.
e- Other Medication. e.g Anticoagulant, Beta-adrenergic
blockers (propranolol,atenolol)
Aneurysm:
Is an abnormal widening or ballooning of apportion of a blood vessel,
the blood vessel wall becomes weaker in this location.
Causes and Risks:
*
*
*
*
Aneurysms are either congenital or acquired.
Hypertension.
Atherosclerosis disease.
Pregnency, associated with formation and or rupture
of splenic artery aneurysms.
Signs & Symptoms:
* Swelling with a pulsatile (throbbing) mass at site of
aneurysms are often seen.
* In case of rupture, hypotesion, high heart rate and
light headedness are seen; the risk of death from
rupture is high.
Aneurysm:
Sings and Tests:
* Physical Examination.
* Ultrasound Examination.
* CT-scan. (Abdomen).
Treatment:
* Surgical excision is generally
recommended.
Management of Patients With Structural, Infectious, and
Inflammatory Cardiac Disorders
On completion of this chapter, the learner will be able to:
1. Define valvular disorders of the heart and describe the pathophysiology,
clinical manifestations, and management of patients
with mitral and aortic disorders.
2. Describe types of cardiac valve repair and replacement procedures used
to treat valvular problems and the care needed by patients who
undergo these procedures.
3. Describe the pathophysiology, clinical manifestations, and management
of patients with cardiomyopathies.
4. Describe the pathophysiology, clinical manifestations, and management
of patients with infections of the heart.
5. Describe the rationale for prophylactic antibiotic therapy for patients
with mitral valve prolapse, valvular heart disease, rheumatic
endocarditis, infective endocarditis, and myocarditis.
Infectious Disease of the
Heart:
Rheumatic Endocarditic:
− It is results directly from rheumatic fever caused by group A
Streptococcal infection.
− The disease affects all bony joint, producing polyarthritis; the
heart is also a target organ and is where the most serious
damage occurs.
− Rheumatic endocarditis are not infectious in origin rather they
represent reaction occurring in response to hemolytic streptococci,
Leukocytes accumulate in the affected tissue and
forms nodules, which are replaced by scars, gradually thicker
than normal and preventing them from closing completely
result in leakage, a condition called valvular regurgitation.
− The most common site of valvular regurgitation is the mitral
valve.
Rheumatic Endocarditic:
Prevention and Treatment:
− Early and adequate treatment of streptococcal infections.
− Long term antibiotic therapy is the treatment of choice.
− Penicillin administered parentally remains the medication
of choice.
Infectious Disease of the
Heart:
II- Myocarditis:
Is an inflammation process involving the myocardium.
− Myocarditis can cause heart dilatation, thrombi on the heart wall.
Medical Management:
− Antibiotic Therapy (penicillin).
− Same used for congestive heart failure.
III- Pericarditis:
Refers to an inflammation of the pericardium, the membrane
sac enveloping the heart.
Clinical Manifestation:
− Sever pain may be felt beneath the clavicle and in the neck
and left scapular region. Pericardial pain is aggravated by breathing.
Medical Management:
− Antibiotic therapy.
− Analgesic and NSAID. e.g indomethacin(indocin).
•VALVUALR HEART DISEASE



Regurgitation: blood flow backward through the valve.
(valve do not close completely).
Prolapse: stretching the valve leaflet into the atrium during
systole.
Stenosis: narrowing or obstruction of a cardiac valve’s
orifice.
Medical Management :
*Valvuloplasty
*Comissurotomy
*Valve replacement
Cardiomyopathies

Is a heart muscle disease associated
with cardiac dysfunction.



Dilated cardiomyopathy (dilation of the
ventricles)
Hypertrophic cardiomyopathy (increase in
size and mass of heart muscle)
Restrictive cardiomyopathy (diastolic
dysfunction caused by rigid ventricular
walls)
Medical Management


Heart transplantation
Mechanical assistive devices
Assessment and Management of Patients
With Hypertension
LEARNING OBJECTIVES ●
On completion of this chapter, the learner will be able to:
1. Define blood pressure and identify risk factors for hypertension.
2. Explain the difference between normal blood pressure and
hypertension and discuss the significance of hypertension.
3. Describe the treatment approach for hypertension, including
lifestyle changes and medication therapy.
4. Use the nursing process as a framework for care of the patient
with hypertension.
5. Describe the necessity for immediate treatment of hypertensive
crisis.

Hypertension


It is a systolic blood pressure greater than
140 mmHg and a diastolic pressure 90 mmHg
based on average two or more readings
Types


Primary Hypertension (essential hypertension):
high blood pressure of unidentified cause
Secondary Hypertension: high blood pressure
from an identified cause
Identifiable causes of
hypertension






Sleep apnea
Drug induced or related causes
Chronic kidney disease
Primary aldosteronism
Vascular disease
Thyroid disease
Clinical manifestation



Often no signs and symptoms
Late signs are retinal hemorrhages,
arteriolar narrowing, cotton-wool
spots, papilledema
Pathological changes include
coronary artery disease, kidney
damage, and cerebrovascular
involvement
Lifestyle modification to manage
Hypertension




Weight reduction
Dietary sodium reduction
Physical activity
Moderation of alcohol consumption
Medical Management
Goal is to achieve BP 140/90 mm
Hg. or lower
 Pharmacologic therapy includes:
diuretics, beta-blockers, or both

Hypertensive Crises
Hypertensive Emergency- BP must
be lowered immediately to prevent
damage to target organs. E.g. MI,
ICH, Aortic aneurysm
 Hypertensive Urgency- BP must be
lowered within a few hours.

Vascular Disorders and Problems of
Peripheral Circulation
Pump failure
 Alterations in blood and
lymphatic vessels
 Circulatory insufficiency of
the extremities

Health history and clinical
manifestations
Intermittent claudication
 Rubor, loss of hair, dry skin,
ulcerations, and edema
 Pulses

Diagnostic Evaluation
Doppler Ultrasound Flow Studies
 Exercise Testing
 Computed Tomography and
Angiography
 Magnetic Resonance Angiography
 Angiography

Arterial disorders
Arteriosclerosis: hardening of arteries
 Atherosclerosis
Management






Prevention by dietary modifications and
exercise to reduce lipid levels
Medications
Surgical management
Radiologic interventions
Peripheral Arterial Occlusive
Disease




Legs are most frequently affected
Hallmark symptom is intermittent claudication
Pharmacologic therapy is to increase RBC flexibility,
reduce blood viscosity, inhibit platelet aggregation,
inhibit smooth muscle cell proliferation, and
increase vasodilation
Surgical management includes vascular grafting or
endarterectomy
Arterial Embolism and Arterial
Thrombosis




Acute vascular occlusion may be caused by
trauma or result of invasive interventions
Arterial emboli most often caused by atrial
fibrillation, MI, or other heart dysfunction
Medical management is anticoagulation
Surgical management is emergency
embolectomy
Venous Disorders
I- Varicose Veins:
Are abnormally dilated, tortuous, superficial veins
caused by incompetent venous valves.
- In normal veins, valves in the veins keep blood moving
forward toward the heart. With varicose veins, the
valves do not function properly, allowing blood to
remain in vein.
- This process usually occurs in lower extremities
(saphenous veins, it can occur else where in the body. e.g.
esophageal varices.
I- Varicose Veins:
Causes:
* Prolong standing.
* A hereditary weakness of vein wall.
* Increasing the pressure within abdomen.
Clinical Manifestation:
*
*
*
*
Dull aches.
Muscle cramps.
Increase muscle fatigue.
Ankle edema.
Medical Management:
* Surgery for varicose vein.
Venous Disorders
II- Chronic Venous Insufficiency:
Is a condition in which the veins do not
efficiently return blood from the lower limbs back
to the heart.
- Venous insufficiently involves one or more veins.
- The valves in the vein usually channel the flow
of blood toward the heart .When these are
damaged, the blood leaks and pools in the legs
and feet.
Chronic Venous Insufficiency:
- Clinical Manifestation:
*
*
*
*
Edema.
Alterd pigmentation.
Pain.
Stasis dermatitis.
- Medical and Nursing Management:
* Elevating the legs.
* Walking should be encouraged.
* Compression of the legs with elastic
pressure stocking.
Venous Disorders
III- Thrombophlebitis:
Is vein inflammation related to a blood clot.
Causes:
* Local irritation. e.g. IV line.
* Infection in or near vein.
Clinical Manifestation:
* Tenderness over the vein.
* Pain in the part of the body affected.
* Skin redness.
Medical Management:
*
*
*
*
Analgesic.
Anticoagulants.
Non steroidal anti-inflammatory drugs (NSADs).
Antibiotics.