CARDIOVASCULAR DISORDER

ADULT HEALTH NURSING –II

GENERIC BSCN YEAR-II SEMSETER IV

Farhana Nisar
Lecturer
Dow Institute of Nursing & Midwifery

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OBJECTIVES:
By the end of the session students will be able to know:

1. Review the anatomy& physiology of cardiovascular system.

2. Discuss the causes, Pathophysiology and manifestation of the following cardiovascular disorders.
3. Discuss the diagnostic, medical and surgical management of the below mentioned disorders.
4. Basic ECG interpretation
5. Apply nursing process including assessment, planning, implementation and evaluation of care
provided to the clients with cardiovascular disorders.
6. Develop a teaching plan for a client experiencing disorders of the cardiovascular and lymphatic
system.

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 Aneurysm
 Coronary artery disease
 Atherosclerosis
 Angina pectoris
 Hypertension
 Endocarditis
 Myocarditis
 Pericarditis
 MI
 Heart failure
 Varicose vein & venous thrombosis
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ANATOMY AND PHYSIOLOGY

 The cardiovascular system delivers oxygenated blood to tissues and removes waste products.
 The heart, controlled by the autonomic nervous system, pumps blood to all organs and tissues of the
body.

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HEART

 Hollow, muscular organ

 Size of a closed fist.
 Located between the lungs in the mediastinum, it’s about 5 (12.5 cm) long and 31/2 (9 cm) in
diameter at its widest point.
 Weighs between 8.8 and 10 oz (250 to 285 g).
 Spans the area from the second to the fifth intercostal space.

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PERICARDIUM

 The pericardium has 2 layers

 Visceral layer (inner) and a parietal (outer)
 The space between the two layers contains 10 to 30 ml of serous (pericardial) fluid, which prevent
from friction

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STRUCTURE OF THE HEART WALL

 The heart wall is made of 3 layers

 Endocardium
 Myocardium
 Epicardium

Heart chambers
 The heart has four chambers — two atria and two ventricles

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VALVES
 The heart has two sets of valves:

Atrioventricular (between atria and ventricles) — tricuspid valve on the heart’s right
side and mitral (bicuspid) valve on its left

Semilunar — pulmonary valve (between the right ventricle and pulmonary artery) and
aortic valve (between the left ventricle and aorta).

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CONDUCTION SYSTEM OF HEART

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BLOOD CIRCULATION

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TYPES OF CIRCULATION

1. Coronary circulation
2. Pulmonary circulation
3. Systematic circulation
4. Portal circulation

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 CORONARY ARTERIES
 The right main coronary artery:
 The right atrium and ventricle
 The inferior portion of the left ventricle
 The posterior septal wall
 Sinoatrial and atrioventricular nodes

 The left main coronary artery consists of two major branches, the left anterior
descending and the circumflex arteries.
 The left anterior descending artery
 anterior wall of the left ventricle
 anterior ventricular septum
 apex of the left ventricle.
 The circumflex artery
 left atrium
 lateral and posterior surfaces of the left ventricle.
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HEART SOUNDS

 The first heart sound (S1) is heard as the atrioventricular valves close and is heard loudest at the apex
of the heart.
 The second heart sound (S2) is heard when the semilunar valves close and is heard loudest at the
base of the heart
 A third heart sound (S3) may be heard if ventricular wall compliance is decreased and structures in
the ventricular wall vibrate; this can occur in conditions such as heart failure or valvular regurgitation.
 A fourth heart sound (S4) may be heard on atrial systole if resistance to ventricular filling is present;
this is an abnormal finding, and the causes include cardiac hypertrophy, disease, or injury to the
ventricular wall.

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AUTONOMIC NERVOUS SYSTEM

 Stimulation of sympathetic nerve fibers releases the neurotransmitter norepinephrine, producing an

increased heart rate, increased conduction speed through the atrioventricular node, increased atrial
and ventricular contractility, and peripheral vasoconstriction. Stimulation occurs when a decrease in
pressure is detected.
 Stimulation of the parasympathetic nerve fibers releases the neurotransmitter acetylcholine, which
decreases the heart rate and lessens atrial and ventricular contractility and conductivity. Stimulation
occurs when an increase in pressure is detected.

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TERMINOLOGIES

 AFTERLOAD :The force against which the heart has to pump (peripheral resistance) to eject blood
from the left ventricle
 ARTERIAL PRESSURE : The pressure of the blood against the arterial walls. Pressure can be measured
indirectly by sphygmomanometer or directly by arterial catheter.
 BARORECEPTORS: Specialized nerve endings (also called pressoreceptors) located in the walls of the
aortic arch and carotid sinuses. They are affected by changes in the arterial blood pressure (BP).
Increases in arterial pressure stimulate baroreceptors and the heart rate and arterial pressure
decrease.

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 Cardiac output : The total volume of blood pumped through the heart in 1 minute. The normal cardiac
output is 4 to 7 L/minute.
 Conductivity: The ability of the heart muscle fibers to propagate electrical impulses along and across
cell membranes.
 Mean Arterial Pressure (MAP): An approximation of the average pressure in the systemic circulation
throughout the cardiac cycle; used in hemodynamic monitoring. Mean arterial pressure must be
between 60 and 70 mm Hg for adequate organ perfusion.
 Pulse Pressure : The difference between the systolic and diastolic pressure. Normal pulse pressure is
30 to 40 mm Hg.
 Stroke Volume : The amount of blood ejected from the left ventricle with each contraction. The
normal stroke volume is 70 to 130 mL/heartbeat.

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 Postural (Orthostatic) Hypotension: A blood pressure decrease of more than 10 to 15 mm Hg of the

systolic pressure or a decrease of more than 10 mm Hg of the diastolic pressure and a 10% to 20%
increase in heart rate. Postural hypotension occurs when the client’s blood pressure is not maintained
adequately when moving from a lying to a sitting or standing position.

 Preload : The volume of blood stretching the left ventricle at the end of diastole. Preload is

determined by the total circulating blood volume and is increased by an increase in venous return to
the heart.

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DIAGNOSTIC TESTS
Cardiac marker studies

 Cardiac markers (enzymes and proteins)

 After infarction, damaged cardiac tissue releases significant amounts of enzymes into the blood
 These cardiac enzymes include
I. Creatine kinase (CK)
II. Ischemia-modified albumin (IMA)
III. Myoglobin
IV. Troponin I and T

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CREATINE KINASE (CK)
 Heart muscle, skeletal muscle, and brain tissue all contain CK.
 CK-BB------- in brain & nerve tissue
 CK-MM---- in skeletal muscles
 CK-MB------ in the heart muscle

 CK-MB levels rise 4 to 8 hours after the onset of acute MI

 Peak in 12 to 24 hours, and may remain elevated for up to 96 hours.

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ISCHEMIA-MODIFIED ALBUMIN (IMA)

 Onset of ischemia--- IMA reaches detectable levels in the blood

 IMA occurs significantly sooner than an increase in troponin or CK
 IMA levels don’t rise after tissue necrosis.
 This rapid increase means that IMA levels can be used to detect an MI sooner
 Levels return to normal within 6 hours of the resolution of ischemia.

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MYOGLOBIN

 Myoglobin is an oxygen-binding protein found in both the myocardium

and skeletal muscle.
 Levels may rise within 30 minutes to 4 hours
 Peak within 6 to 10 hours, and return to baseline by 24 hours.

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TROPONIN I AND TROPONIN T
 Troponin is a protein found in skeletal and cardiac muscles.
 Troponin I and troponin T, two isotypes of troponin, are found in the myocardium.
 Troponin T may also be found in skeletal muscle.
 Troponin I, exists in the myocardium
 Troponin levels rise within 3 to 6 hours after myocardial damage.
 Troponin I peaks in 12 hours, with a return to baseline in 3 to 10 days
 Troponin T peaks in 12 to 48 hours, with a return to baseline in 7 to 10 days.

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CARDIAC CATHETERIZATION:

Definition: Invasive procedure to visualize and assess the heart's blood vessels and chambers.
Procedure:
 A catheter is threaded through blood vessels into the heart.
 Contrast dye injected for imaging.

Purposes:
 Diagnostic: Evaluate coronary artery disease, valve disorders, congenital heart issues.
 Interventional: Angioplasty, stent placement, valve repair.

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ELECTROCARDIOGRAM (ECG OR EKG):
Definition:
 Non-invasive test that records the electrical activity of the heart over a specific period.

Purpose:
 Evaluates heart rate, rhythm, and electrical conduction.
 Identifies abnormalities and assists in diagnosing cardiac conditions.

Procedure:
 Electrodes placed on the skin at specific locations.
 Records electrical impulses as waveforms on a graph.

Components of ECG:
 P Wave: Represents atrial depolarization.
 QRS Complex: Indicates ventricular depolarization.
 T Wave: Represents ventricular repolarization.
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ANEURYSM

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ANEURYSM
 An aneurysm occurs when an artery’s wall weakens and causes an abnormally large
bulge. This bulge can rupture and cause internal bleeding. Although an aneurysm can
occur in any part of your body, they’re most common in the:

 brain
 aorta
 legs
 spleen

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CAUSES
 Aneurysms commonly result from atherosclerosis, plaque formation is thought to
cause degenerative changes in the middle layer of arterial wall, leading to loss of
elasticity, weakening and eventual aortic dilation. Other causes include:
• Fungal infection (mycotic aneurysms) of the aortic arch
and descending segments
• Congenital disorders, such as coaractation of the aorta
• Trauma
• Syphilis
• Hypertension.

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PATHOPHYSIOLOGY

 Degenerative changes in the muscular layer of the aorta (tunica media) create a focal
weakness, allowing the inner layer (tunica intima) and outer layer (tunica adventitia)
to stretch outward.
 The resulting outward bulge is called an aneurysm.
 Blood pressure within the aorta progressively weakens the vessel walls and enlarges
the aneurysm.

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SIGNS AND SYMPTOMS

 Asymptomatic pulsating mass in the periumbilical area

 Possible systolic bruit over the aorta on auscultation
 Possible tenderness on deep palpation
 Lumbar pain that radiates to the flank and groin (imminent rupture).

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 If the aneurysm ruptures, look for:
• Severe, tearing abdominal and back pain
• Weakness
• Sweating
• Tachycardia
• Hypotension
• Circulatory collapse.

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DIAGNOSTIC TEST

 Ct scan
 Angiography
 Arteriography
 Ultrasound

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INTERVENTIONS

 Be alert for signs of rupture, which is life-threatening.

 Watch closely for any signs of acute blood loss, such as hypotension, increasing pulse and respiratory
rate, cool and clammy skin, restlessness, and decreased sensorium.
 If rupture occurs, get the patient to surgery immediately.
 Evaluate the patient. Note whether the patient is free from pain and if he has adequate tissue
perfusion with warm, dry skin; adequate pulse and blood pressure; and absence of fatigue.
 Tell the patient not to push, pull, or lift heavy objects until medically cleared by the surgeon.

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REFERENCES

Lippincott Williams & Wilkins. (2008). Medical-surgical nursing

made incredibly easy!. Philadelphia: Wolters Kluwer
Health/Lippincott Williams & Wilkins

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Coronary Artery Disease

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 Total Cholestrol (Rule of 50s)--- Also in Alphabetical order
 HDL >50 md/dl
 LDL <100 mg/dl
 Triglycerides <150 mg/dl
 Total Cholestrol <200 mg/dl

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ATHEROSCLEROSIS

The thickening and hardening of the vessel wall is caused by soft deposits of intra-
arterial fat and fibrin that hardens over time.

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OVERVIEW
 Development of plaque formation in Coronary artery ---can lead to restriction of
blood flow to the heart.
 Fatty plaques are caused by a condition called ATHEROSCLEROSIS which creates fatty
plaques in the artery walls.
 Happens overtime.
 Atherosclerosis can also lead to hypertension, chest pain, and heart failure.

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 RISK FACTORS
Controllable
Uncontrollable •High blood pressure
•High blood cholesterol
•Sex
•Smoking
•Hereditary
•Physical activity
•Race
•Obesity
•Age
•Diabetes
•Stress and anger

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SIGNS AND SYMPTOMS OF CAD
• Angina, the classic symptom of CAD, occurs as a burning, squeezing, or crushing
tightness in the sub-sternal or precordial chest.

• It may radiate to the left arm, neck, jaw, or shoulder blade.

• Women, however, may experience atypical chest pain.

Other signs and symptoms of CAD include:

• Nausea
• Vomiting
• Weakness
• Diaphoresis

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CAD TREATMENT

 Starts with least invasive and progress to most invasive.

1. Patient education (Avoid sodium, red meat, oily fried food)

2. Statins
3. Nitrates
4. Calcium Channel Blockers
5. Stent
6. Coronary artery bypass grafting (CABG)

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ANGINA PECTORIS
 Angina pectoris is Latin for “squeezing of the chest”
 Angina is chest pain or discomfort occurs due to decrease blood flow to
heart.
 It may feel like pressure or squeezing in your chest.
 The discomfort also can occur in your shoulders, arms, neck, jaw, or
back.

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FACTORS
 Usually caused by atherosclerotic disease
 Physical exertion
 Exposure to cold
 Eating a heavy meal
 Stress or any emotion-provoking situation, causing the release of adrenaline and
increasing blood pressure, which may accelerate the heart rate and increase the
myocardial workload

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TYPES OF ANGINA
 Stable angina: predictable and consistent pain that occurs on exertion and is relieved by rest
 Unstable angina (also called preinfarction angina or crescendo angina): symptoms occur
more frequently and last longer than stable angina. The threshold for pain is lower, and pain
may occur at rest.
 Microvascular - angina-like chest pain in a patient with normal coronary arteries that results
from impaired vasodilator reserve.
 Variant angina (also called Prinzmetal’s angina): pain at rest with reversible ST-segment
elevation; thought to be caused by coronary artery vasospasm
 Silent ischemia: objective evidence of ischemia (such as electrocardiographic changes with a
stress test), but patient reports no symptoms

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CLINICAL MANIFESTATIONS
 Feeling of indigestion
 heavy sensation in the upper chest that ranges from discomfort to agonizing pain
accompanied by severe apprehension and a feeling of impending death
 pain is often felt deep in the chest behind the upper or middle third of the sternum
(retrosternal area)
 Pain may radiate to the neck, jaw, shoulders, and inner aspects of the upper arms,
usually the left arm.

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DIAGNOSTIC TEST
• Blood tests: Lipoprotein profile: total cholesterol, LDL, HDL, triglycerides
• EKG: assesses if there are any changes in the ST segments or t-waves (shows if there is a
heart attack in the progress, previous heart attack, or compromised blood flow)

• ST segment depression: demonstrates ischemia that is reversible

• ST segment elevation: infarction where there is injury to the heart muscle

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 CARDIAC CATHERIZATION

A special catheter is inserted into the femoral or radial artery to assess for blockages in the artery. Dye
is injected into the coronary arteries to assess if they are blocked (coronary angiography)…moderate
sedation is used and the patient breathes on their own.

Cardiac doctor makes the decision if the artery needs:

 PCI (also called angioplasty): Percutaneous Coronary Intervention

Balloon angioplasty: inflates a balloon in the blocked artery to compress the plaque against the artery
wall and a stent is placed to allow blood to flow back through the artery.
 Atherectomy: removal of plaque from the artery

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NURSING INTERVENTIONS FOR CAD

Educating patient about treatment, preventive measure, medications,

and management

• Educate the patient about the significance and complications of CAD

• Modifying lifestyle:
 How to manage with diet (low fat, low calorie)
 Exercise program
 Smoking cessation and why it is important
 Weight loss
• Monitoring heart rate and blood pressure
• Signs and symptoms and when to seek help
• Education about procedures: EKG, stress test, heart cath, lipid profile
blood test
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MEDICATIONS FOR CAD
Antiplatelet meds: prevent clots from forming or growing which decrease the chances
of ischemia
• Aspirin: watching for GI bleeding.
• Plavix: for patients who can’t tolerate Aspirin or just had a stent placed

Nitrates:
• Nitroglycerin: dilates vessels to allow more blood to get the heart muscle. Educate
about how to take: sublingual (underneath the tongue)
• Take right when having chest pain
• Place one tab or one spray under the tongue
• If not relieved in 5 minutes take another dose of Nitro a 2nd dose and
• If not relieved in 5 minutes take another one for a 3rd dose. The patient is NOT
to take more than 3 total doses.

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Cholesterol lowering medication:
Statins “Lipitor, Crestor, Zocor” (goal: LDL less than 100 mg/dL) helps lower LDL,
total cholesterol, lower triglycerides, and increase HDL.

Beta blockers:
end in “lol” Propranolol, Metoprolol
lowers heart rate and blood pressure which reduces work load on the heart. This
will help decrease episodes of chest pain

ACE inhibitors:
end in “pril” Lisinopril
blocks the conversion of angiotensin I to angiotensin II which caused
vasodilation….lowers blood pressure…this decreases the workload on the heart.

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REFERENCES:
• “Angiotensin-Converting Enzyme Inhibitor (ACE Inhibitor)
Drugs”. Fda.gov. Web. 4 Sept. 2016.
• “How Can Coronary Heart Disease Be Prevented Or Delayed? –
NHLBI, NIH”. Nhlbi.nih.gov. Web. 7 Sept. 2016.
• Anatomy Of The Heart – NHLBI, NIH”. Nhlbi.nih.gov. Web. 2 Sept.
2016.
• “Heart Health Tests: Medlineplus”. Medlineplus.gov. Web. 2 Sept.
2016.
• “What Causes Coronary Heart Disease? – NHLBI, NIH”. Nhlbi.nih.gov.
Web. 3 Sept. 2016.
• Lippincott Williams & Wilkins. (2008). Medical-surgical nursing made
incredibly easy!. Philadelphia: Wolters Kluwer Health/Lippincott
Williams & Wilkins

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HYPERTENSION

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HYPERTENSION
 Definition: The amount of resistance of blood pumping through the body/arteries.

 Normal: <120/80 (looking at systolic & diastolic)

 Prehypertension: 120-139/80-89

 Stage 1 HTN: 140-159/90-99

 Stage 2 HTN: >160/>100

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CAUSES OF HYPERTENSION
 Primary/Essential Hypertension:

 Increased consumption of salt/alcohol

 Smoking/stress
 Family health
 Advanced aged
 Cholesterol high
 Too much caffeine intake
 Obese
 Restricting activity
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 Secondary Hypertension:

 Caused by a pre-existing issue:

 Pregnancy, Cushing Syndrome,
 Chronic Renal Failure
 Diabetes
 Hypo/hyperthyroidism
 Pheochromocytoma (tumor on adrenal gland which cause adrenaline/noradrenaline to be secreted
increase BP)
 Coarctation of the aorta (congenital defect main artery of the body is super narrow and this leads to
high blood pressure)

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NURSING ASSESSMENT OF HYPERTENSION

 Remember silent killer…probably be without symptoms

 Headache*
 Blurry vision*
 Chest Pain*
 Nose bleeds
 Ringing in the ears
 Dizzy
 *Most common symptoms

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NURSING INTERVENTIONS FOR HTN

 Assess: measure blood pressure (obtain in both arms…make sure patient has been in
a resting position for 5 minutes, no smoking…causes vasoconstriction), ask about
family history, and if they have any sensory changes
 Evaluate: blood pressure reading, dietary intake, body mass index (overweight)

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Educate:
 Limiting sodium, alcohol and caffeine in diet, quit smoking (vasoconstriction)
 start an exercise program (cardiovascular) for weight loss
 Importance of medication compliance
 Measuring blood pressure regularly and keeping a record.

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PHARMACOLOGY FOR HYPERTENSION

 Thiazide Diuretics: End in “iazide” HCTZ (hydrochlorothiazide),

Diuril (Chlorothiazide)

 Work by removing water and sodium through the kidneys

 Not for patients in renal failure WATCH BUN and CREATININE Levels.
 Watch patients who are taking Lithium (increases chances of
Lithium toxicity)

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 ACE Inhibitors (Angiotension -Converting Enzyme Inhibitors): End in “PRIL”
Lisinopril

 Prevent vasoconstriction by blocking Angiotension 1 and 2

 Educate patient about a dry cough/taste changes
 Avoid potassium substitutes or supplement…this drug causes potassium retention
 Compliance very important due to rebound hypertension
 Captopril (increased risk of bleeding) and Moexipril…take 1 hour BEFORE a meal

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 ARBS (Angiotension Receptor Blockers): drugs that end in “sartan” ex:
Losartan (may be prescribed in place of ACE inhibitors if patient can’t
tolerate ACE Inhibitor)
 Works by causing vasodilation by blocking aldosterone and Angiotension
 Same side effects as ACEI (except dry cough)
 Increase k+ level

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 CCB (Calcium Channel Blockers): end in “dipine” Amlodipine, and
Cardizem, Verapamil
 Slow the heart rate to decrease the work load on the heart and cause
vasodilation which lowers blood pressure
 Watch HR: bradycardia
 Watch pts who have CHF or AV blocks

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 BB: Beta blockers: end in “olol” ex: Labetalol, Metoprolol

 Affects epinephrine and norepinephrine which blocks the sympathetic nervous

system of the heart , which helps dilates vessel which lowers blood pressure
 Not for patients with asthma and COPD because this medication blocks the receptors
in the lungs and causes bronchoconstriction
 Monitor Glucose levels in diabetics because it conceals the signs of hypoglycemia
 Monitor heart rate and for orthostatic hypotension

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COMPLICATION
 Left ventricular hypertrophy
 Angina
 MI
 Heart failure
 Stroke
 Transient ischemic attack
 Nephropathy
 Peripheral arterial disease
 Retinopathy
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REFERENCE:

Lippincott Williams & Wilkins. (2008). Medical-surgical nursing

made incredibly easy!. Philadelphia: Wolters Kluwer
Health/Lippincott Williams & Wilkins

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INFECTIOUS DISORDER: PERICARDITIS, MYOCARDITIS &
ENDOCARDITIS

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ENDOCARDITIS

Definition: Inflammation of the endocardium layer of the heart.

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PATHOPHYSIOLOGY
1. Most common causative organism: staphylococcus aureus and streptococcus
viridans.
2. A pathogen enters into the blood (from invasive procedure….dental work, central
line placement, implantable device) and the pathogen sticks to the platelets and
fibrin (thrombus).
3. The pathogen is able to grow.
4. As it grows, parts of the pathogen, platelets, and fibrin can break off. This can cause
a stroke.

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ETIOLOGY:

 Infective Endocarditis (IE):

 Bacterial (most common, especially Staphylococcus aureus and Streptococcus viridans).
 Fungal.
 Rarely, viral.
 Non-Infective Endocarditis:
 Usually associated with autoimmune disorders.

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SIGNS AND SYMPTOMS OF ENDOCARDITIS:
 Petechiae (tiny purplish red spots on the skin….from emboli)

 Anorexia (loss of appetite and enlarged spleen pushing on the stomach)

 Tired and weak

 High Fever & Heart Failure

 Night sweats, New cardiac heart murmur

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 Roth’s spots (white spots surrounded by
hemorrhage on the retina)
 Skin Findings in Endocarditis –
Palpable petechiae,
Splinter hemorrhages (nail bed lesions)
Janeway lesions (painless, macular spots on
the palms and soles)
Osler’s nodes (painful, purple nodules on the
pads of the finger and toes).
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NURSING INTERVENTIONS FOR INFECTIVE ENDOCARDITIS:
 Monitor:
 Embolic episodes of the spleen, renal, brain, pulmonary status:
 Spleen embolic: radiating abdominal pain that goes to the left shoulder
 Renal: flank pain in the groin with possible pus or blood in the urine
 Brain (stroke): changes in neuro status…confusion, speech difficulty
 Pulmonary: chest pain, shortness of breath, dyspnea, decreased oxygen saturation
 Signs and symptoms of heart failure
 Monitor vital signs especially temperature, heart rate, blood pressure, oxygen
saturation
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 Interventions:

 Collecting blood cultures to find out what type of microorganism is infecting the
patient…antibiotic treatment is based on this
 Administered IV antibiotics…type of antibiotics depends on the pathogen causing the
problem
 Example: Vancomycin or Rocephin (strong…usually need a central line because
patient will be on long term and go home on them…up to 4 weeks)

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REFERENCES:

 “Endocarditis | Infective Endocarditis | IE | Medlineplus”. Medlineplus.gov. Web. 19 Aug. 2016.

 “What Causes Endocarditis? – NHLBI, NIH”. Nhlbi.nih.gov. N.p., 2010. Web. 20 Aug. 2016.
 “What Is Endocarditis? – NHLBI, NIH”. Nhlbi.nih.gov. N.p., 2010. Web. 20 Aug. 2016.

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MYOCARDITIS

Myocarditis, a focal or diffuse inflammation of the cardiac

muscle (myocardium), may be acute or chronic.

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CAUSES
 Viral infections (most common cause in the united states), such as coxsackievirus A and B
strains and, possibly, poliomyelitis, influenza, rubeola, rubella, adenoviruses, and echoviruses
 Bacterial infections, such as diphtheria, tuberculosis, typhoid fever, tetanus, and
staphylococcal, pneumococcal, and gonococcal infections
 Hypersensitivity reactions, such as acute rheumatic fever and postcardiotomy syndrome
 Radiation therapy to the chest in treating lung or breast cancer
 Chronic alcoholism
 Parasitic infections, such as toxoplasmosis and, especially, south american trypanosomiasis
(chagas’ disease) in infants and immunosuppressed adults
 Helminthic infections such as trichinosis.

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SIGN & SYMPTOMS
 Chest pain or chest discomfort
 Shortness of breath
 Swelling and/or edema
 Liver congestion
 Abnormal heartbeat (palpitations)
 Sudden death (in young adults)
 Fever (usually associated with an infectious process)

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TREATMENT
Corticosteroid therapy (to help reduce inflammation)
Cardiac medications, such as a beta-blocker, ACE inhibitor, or
ARB
Behavioral changes, such as rest, fluid restriction, and a low-salt
diet
Diuretic therapy to treat fluid overload
Antibiotic therapy

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REFERENCE

 Lippincott Williams & Wilkins. (2008). Medical-surgical nursing made incredibly easy!. Philadelphia: Wolters
Kluwer Health/Lippincott Williams & Wilkins

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PERICARDITIS
 Pericarditis is an acute or chronic inflammation that affects the pericardium, the
fibroserous sac that envelops, supports, and protects the heart
 The layers are:
 Fibrous pericardium
 Serous pericardium which has two layers
 Parietal pericardium
 Serous fluid is between the parietal and visceral layer

 Visceral pericardium (also called the epicardium)

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CAUSES
 Infectious Causes:
 Viral (most common, such as Coxsackievirus).
 Bacterial.
 Fungal.
 Non-Infectious Causes:
 Autoimmune disorders.
 Trauma.
 Cancer.

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 Risk Factors:
 Viral Infections:
 Common cold viruses.
 Autoimmune Disorders:
 Systemic lupus erythematosus (SLE).
 Rheumatoid arthritis.
 Recent Heart Attack:
 Post-myocardial infarction pericarditis

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SIGNS AND SYMPTOMS OF PERICARDITIS
 Remember “Friction”
 *Friction rub pericardial (sounds like a grating, scratching sound), Fever
 Radiating substernal pain to left shoulder, neck or back
 *Increased pain when in supine position (leaning forward relieves pain)
 *Chest pain that is stabbing (will feel like a heart attack)
 Trouble breathing when lying down (supine position)
 *Inspiration or coughing makes pain worse
 Overall feels very sick and weak
 Noticeable ST segment elevation
*most common signs and symptoms
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INTERVENTION
 Encourage complete bed rest.
 Assess pain in relation to respiration and body position to distinguish pericardial pain
from myocardial ischemic pain.
 Place the patient in an upright position to relieve dyspnea and chest pain.
 Provide analgesics and oxygen, as ordered.
 Monitor for Cardiac Tamponade (fluid compressing the heart):
 Pulsus paradoxus (during the inspiratory phase that is a 10 or greater mmHg drop in the systolic
blood pressure)
 Jugular venous distention with clear lungs
 Heart sounds are muffled (fluid buildup on the heart
 Tachycardia
 Hypotension
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COMPLICATIONS

 Pericardial Effusion:
 Accumulation of fluid in the pericardial sac.
 Cardiac Tamponade:
 Compression of the heart due to excess fluid in the pericardial sac.
 Constrictive Pericarditis:
 Long-term inflammation leading to a thickened and fibrotic pericardium.

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REFERENCE

 Lippincott Williams & Wilkins. (2008). Medical-surgical nursing made

incredibly easy!. Philadelphia: Wolters Kluwer Health/Lippincott
Williams & Wilkins

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MYOCARDIAL INFARCTION

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MYOCARDIAL INFARCTION

 The heart’s myocardial tissue layer dies from decreased blood flow.

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CAUSES:

 Blockage in the coronary artery from coronary artery disease (most common)
 Coronary spasms from illicit drug usage drugs like cocaine or uncontrolled
hypertension.
 Damage to the coronary artery due to coronary artery dissection.

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WHAT HAPPENS TO THE HEART MUSCLE AFTER AN MI?
 When a coronary artery becomes 100% blocked the muscle cells die. Cell death is irreversible after
about 30 minute. The cellsan never be replaced.

 Early signs of an MI…no physical changes to heart muscle yet (until about 6-8 hours), but when the
myocytes die cardiac enzymes are released:
 CK-MB (4 to 6 hours after MI),
 troponin (2-4 hours…most regarded)
 myoglobin (1 hours after injury…show injury but not too specific). are gone forever and can never be
replaced.
 ECG changes: ST segment elevation + depression and t-wave inversion

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SIGNS & SYMPTOMS OF MYOCARDIAL INFARCTION
 Chest pain (intense, heavy)
 Radiating chest pain that goes to left arm, jaw, back
 Unrelieved by nitroglycerin or rest (chest pain)
 Sweating (cold)
 Hard to breathe (shortness of breath)
 Increased heart rate, blood pressure or irregular heart rate
 Nausea with vomiting
 Going to be anxious and scared
*Women may not have heaviness on chest but feel SOB, pain in lower part of chest and
feeling extremely fatigue
*Silent MI: most common in diabetics due to diabetic neuropathy
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DIAGNOSTIC TEST
Cardiac Marker:
 Troponins: gold standard. They are drawn in a series (troponin levels will
elevate 2-4 after injury). They are usually drawn every 6 hours for 3 sets.
 Myoglobin: an early cardiac marker released after heart injury (1 hour
after injury).
 CK: protein released when there is muscle damage (not specific to just
the heart)…so CK-MB may be ordered to tell if it is the heart since CK-MB
represents heart muscle (it elevates 4-6 hr after injury).

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Heart Catherization
Echocardiogram
Stress test with Myocardial Perfusion Imaging
EKG

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NURSING INTERVENTIONS FOR MI
 Monitoring & Assessing Cardiovascular system:
 Obtain a 12-lead EKG, have continuous bedside cardiac monitoring
 Monitoring blood pressure and heart rate
 Place on oxygen via nasal cannula per MD order 2-4 L
 Working IV access (multiple…may start drips and administer other IV medications)
 Monitor respiratory system: lung sounds “crackles”..represent heart failure
 Strict bedrest (activity puts strain on heart)
 Collect cardiac enzymes as ordered by the physician

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 MEDICATION

 Antithrombotic agents: prevent formation of clot

 Antiplatelets: decrease platelets aggregation and thrombus formation
 Morphine: for chest pain relief
 Nitrates: Nitroglycerin causes vasodilation and increases blood flow to the heart

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 Ace Inhibitors: work by allowing more blood to get to the heart muscle. It work by blocking the
conversion of Angiotensin I or Angiotensin II (this causes vasodilation, lowers blood pressure, and
allows kidneys to secrete sodium because it decreases aldosterone)

 Beta blockers: decreases work load on the heart…slows heart rate and decreases blood pressure

 ARBS Angiotensin II receptor blockers: used in place of ACE inhibitors if patient can’t tolerate them

 ARBs work by blocking angiotensin II receptors which causes vasodilation. This lowers blood
pressure and helps the kidneys to excrete sodium and water (due to the affects that blocking
angiotensin II has on the kidneys…decreases aldosterone).

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 Cholesterol lowering medication
 Calcium Channel Blockers: This medications work by stopping the transport of
calcium to the myocardium and into smooth muscle which causes vasodilation on
the coronary arteries.

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REFERENCES

 How Is a Heart Attack Treated? – NHLBI, NIH. (2015). Nhlbi.nih.gov. Retrieved 25 September 2016, from
https://www.nhlbi.nih.gov/health/health-topics/topics/heartattack/treatment
 “Heart Attack Signs & Symptoms | Cdc.Gov”. Cdc.gov. N.p., 2015. Web. 25 Sept. 2016.
 “How Is A Heart Attack Diagnosed? – NHLBI, NIH”. Nhlbi.nih.gov. N.p., 2015. Web. 26 Sept. 2016.

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HEART FAILURE

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HEART FAILURE
 The heart is too weak to pump efficiently so it can’t provide proper cardiac output to
maintain the body’s metabolic needs.

 Results on the body: organs and tissues will suffer from the decreased blood flow,
pressure in the heart increases which over works the ventricles, body can become
congested with fluids (enter into congestive heart failure) that can cause life-
threatening complications.

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CAUSES OF HEART FAILURE:

 Faulty heart valves

 Arrhythmias: atrial fibrillation or tachycardia
 Infarction (myocardial)…coronary artery disease
 Lineage (congenital)…family history
 Uncontrolled Hypertension
 Recreational Drug Use (cocaine) or alcohol abuse
 Envaders (instead of Invaders): viruses or infections that attack the heart muscle

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TYPES OF HEART FAILURES:

 Left-Sided Heart failure: the left side of the heart cannot pump blood
out of the heart efficiently so blood starts to back-up in the lungs.
 Most common type of heart failure.
 Left-sided heart failure is likely to lead to right-sided heart failure.
 The left ventricle becomes too weak and doesn’t squeeze blood out
properly….the heart failure can be either SYSTOLIC OR DIASTOLIC.

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 Systolic: “Left ventricular systolic dysfunction” remember systolic is the contraction or “squeezing”

phase of the heart. In systolic dysfunction, there is an issue with the left ventricle being able to eject
blood properly out of the ventricle and the organs can’t get all that rich-oxygenated blood it just
received from the lungs. Patients will have a low ejection fraction.

 What is ejection fraction? Ejection fraction is a calculation used to determine the severity of heart

failure on the left side. A normal EF is 50% or greater meaning that more than half of the blood that
fills inside the ventricles is being pumped out. An EF can be measured with an echocardiogram, heart
cath, nuclear stress test. An EF of 40% or less is a diagnosis for heart failure.

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 Diastolic: “left ventricular diastolic dysfunction” remember diastole is the filling or

resting phase of the heart. In diastolic dysfunction, the ventricle is too stiff to allow
for normal filling of blood. Since there isn’t an issue with contraction but filling the
ejection fraction is usually normal.

 Left-sided heart failure will present with PULMONARY Signs and Symptoms.

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 Right-Sided Heart Failure: the right side of the heart cannot pump the “used” blood it received

from the body efficiently so it can’t get the blood back to the lungs to get replenished with
oxygen. The causes the blood to back up peripherally (legs, hands, feet, abdomen).

 Right-sided heart failure causes congestion of blood in the heart and this increases the

pressure in the inferior vena cava (which normally brings “used” blood back to the heart for
re-oxygenation). This built-up pressure causes the hepatic veins to become very congested
with blood which leads to hepatomegaly and swelling peripherally.

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  Right-sided heart failure is usually caused from left-sided heart

failure because of the increased fluid pressure backing up from the left side
to the right. This causes the right side of the heart to become overworked.

 Other causes: pulmonary heart disease “cor pulmonale” as a complication

from pulmonary hypertension or COPD.

 Right-sided heart failure presents with PERPHIERAL SIGNS AND SYMPTOMS.

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SIGN & SYMPTOMS OF LT-SIDED HEART FAILURE
 Difficulty breathing
 Rales (crackles)
 Orthopnea (cannot tolerate lying down…must sit-up to breath, especially while sleeping)
 Weakness (extremely tired and fatigued due to shortness of breath and heart can’t compensate for increased
activity)
 Nocturnal Paroxysmal dyspnea (awaking during sleep with extreme dyspnea)
 Increased heart rate (due to fluid overload and the heart is trying to get the blood to organs but it can’t because
of muscle failure)
 Nagging cough (can be frothy or blood-tinged sputum from fluid overload in the lungs…very bad sign)
 Gaining weight from the body retaining fluid…2 to 3 lb in a day or 5 lbs in a week

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RIGHT-SIDED HEART FAILURE:
 Swelling of legs, hands, liver, abdomen

 Weight gain

 **Edema (pitting)

 **Large neck veins (jugular venous distention)

 Lethargic (weak and very tired)

 Irregular heart rate (atrial fibrillation)

 Nocturia (frequent urination at night) lying down elevates the legs and allows the extra fluid to enter into the vascular system

which allows the kidneys to eliminate the extra fluid.

 Girth of abdomen increased (from swelling of the liver and building up fluid in the abdomen)…can’t breathe well and this

causes nausea and anorexia.

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TESTS USED TO DIAGNOSE HEART FAILURE:
 BNP (b-type natriuretic peptide) blood test: a biomarker released by the ventricles when there is
excessive pressure in the heart due to heart failure.
 <100 pg/mL no failure
 100-300 pg/mL present
 300 pg/mL mild
 600 pg/mL moderate
 900 pg/mL severe
 Source ClevelandClinic.org

 Chest x-ray
 Echocardiogram
 Heart cath
 Nuclear stress test

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 Heart failure can be acute or chronic and can be triggered/exacerbated with:
 High salt intake or fluid (watch fluids)
 Infection
 Uncontrolled atrial fibrillation
 Renal failure

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NURSING INTERVENTIONS FOR HEART FAILURE
 Role: Assessing, monitoring, intervening, and educating

 Assessing:

 Assess patient for worsening symptoms (right-sided failure…peripheral swelling vs left-sided failure…pulmonary edema)

 Patient responsiveness to medication treatment:

 watch heart rate (Digoxin)

 respiratory status

 blood pressure (vasodilators cause hypotension)

 diuretics (strict intake and output, daily weights, monitor electrolyte levels, especially K+)

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 Monitoring:

 Fluid status (may be ordered a Foley catheter, if on diuretics)

 Cardiac diet (low in salt and fats)

 Fluid restriction (no more than 2 L per day)

 Lab values: watching BNP, kidney function BUN & creatinine, troponins levels, electrolytes (especially

potassium…if on Lasix: waste potassium and low potassium increases risk of digoxin toxicity)

 Edema in leg: Keep legs elevated and patient in high Fowler’s to help with breathing

 Safety (at risk for falls due to fluid status changes, swelling in legs and feet, and orthostatic hypotension)

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 Educating:

 Early signs and symptoms heart failure exacerbation

 Shortness of breath

 Weight gain

 Orthopnea

 Low salt (allowed 2-3 G sodium per day) and fluid restriction (no more than 2 L per day)

 Vaccination to prevent illness, such as annual flu and to be up-to-date with pneumonia vaccine

 Exercise aerobic (as tolerated)

 Daily weights (watch for no more than 2-3 lb per day and 5 lbs per week)

 Compliance with medications

 Smoking cessation

 Limiting alcohol

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ADMINISTERING MEDICATIONS:
 Ace Inhibitors (angiotensin-converting-enzyme inhibitors)

 ARBs (Angiotensin II receptor blockers)

 Diuretics

 Beta Blockers

 Anticoagulants

 Vasodilators

 Digoxin

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REFERENCES:

 “Heart Failure Fact Sheet|Data & Statistics|DHDSP|CDC”. Cdc.gov. N.p., 2016. Web. 12 Aug. 2016.
 “How Is Heart Failure Treated? – NHLBI, NIH”. Nhlbi.nih.gov. N.p., 2015. Web. 19 Aug. 2016.
 “Heart Failure Fact Sheet|Data & Statistics|DHDSP|CDC”. Cdc.gov. N.p., 2016. Web. 12 Aug. 2016.
 “How Is Heart Failure Diagnosed? – NHLBI, NIH”. Nhlbi.nih.gov. N.p., 2015. Web. 13 Aug. 2016.
 “What Causes Heart Failure? – NHLBI, NIH”. Nhlbi.nih.gov. N.p., 2015. Web. 13 Aug. 2016.

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VENOUS DISORDERS

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VARICOSE VEINS

 Varicose vein or varicosities

 Varicose veins are large, swollen veins that often appear on the legs and
feet. They happen when the valves in the veins do not work properly, so
the blood does not flow effectively.

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PATHOPHYSIOLOGY
 Superficial veins in the lower extremities become dilated and tortuous, with increase venous
pressure.
 As the vein enlarge, the valves are stretched and become incompetent, allowing venous blood flow to
be reversed.
 As back pressure increases and the calf muscle pump (muscle movement that squeezes venous blood
back toward the heart) fails, further venous distention results.
 The increased venous pressure is transmitted to the capillary bed, and edema develops.

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CLINICAL MANIFESTATION

 Discomfort
 Ache or pain after prolonged standing, relived by walking or by elevating
the limb.
 Feel pressure or a cramp like sensation in the legs
 Swelling

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COLLABORATIVE CARE
 Rest with the affected limb elevated
 Stocking
 Exercise
 Laser therapy
 Surgical: Ligation of the entire vein (usually the greater saphenous) and
dissection.

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DEEP VEIN THROMBOSIS
 Deep vein thrombosis, or DVT, is a blood clot that forms in a vein deep in the body.

Most deep vein clots occur in the lower leg or thigh. If the vein swells, the condition
is called thrombophlebitis. A deep vein thrombosis can break loose and cause a
serious problem in the lung, called a pulmonary embolism

 https://medlineplus.gov/deepveinthrombosis.html

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REFERENCE

Retrieved from:
https://medlineplus.gov/deepveinthrombosis.html

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VALVULAR HEART DISEASE

 Heart contains two atrioventricular valves (mitral and tricuspid) and two

semilunar valves (aortic and pulmonary valves)

 Valvular heart disease is defined according to stenosis or regurgitation or

prolapse

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 In regurgitation also called valvular incompetence or insufficiency),
incomplete closure of the valve leaflets results in the backward flow of
blood.
 Prolapse (of a valve): stretching of an atrioventricular heart valve leaflet
into the atrium during systole

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 In stenotic valve, the valve orifice is smaller, prevent the forward flow of
blood and creating a pressure gradient difference across an open valve.
 The degree of stenosis is seen in the pressure-gradient differences (i.e.,
the higher the gradient, the greater the stenosis).

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Valvular Heart Disease:
1. Mitral stenosis
2. Mitral regurgitation
3. Aortic stenosis
4. Aortic regurgitation
5. Tricuspid stenosis
6. Tricuspid regurgitation
7. Pulmonary stenosis
8. Pulmonary regurgitation

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MITRAL VALVE STENOSIS
Mitral stenosis is an obstruction of blood flowing from the left
atrium into the left ventricle.
CAUSES:
Rheumatic heart disease (most common)
Congenital mitral stenosis, rheumatoid arthritis and SLE (less
common)

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PATHOPHYSIOLOGY
 Normally, the mitral valve opening is as wide as the diameter of three fingers. In cases of marked stenosis, the

opening narrows to the width of a pencil.

 The left atrium has great difficulty moving blood into the ventricle because of the increased resistance of the

narrowed orifice; it dilates (stretches) and hypertrophies (thickens) because of the increased blood volume it
holds.

 Because there is no valve to protect the pulmonary veins from the backward flow of blood from the atrium, the

pulmonary circulation becomes congested. As a result, the right ventricle must contract against an abnormally
high pulmonary arterial pressure and is subjected to excessive strain. Eventually, the right ventricle fails.

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CLINICAL MANIFESTATIONS

Breathing difficulty (i.e, dyspnea)

Fatigue as a result of low cardiac output.
They may expectorate blood (ie, hemoptysis), cough, and
experience repeated respiratory infections.

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ASSESSMENT
The pulse is weak and often irregular because of atrial
fibrillation (caused by the strain on the atrium).
A low-pitched, rumbling, diastolic murmur is heard at the apex.
As a result of the increased blood volume and pressure, the
atrium dilates, hypertrophies, and becomes electrically
unstable, and the patient experiences atrial dysrhythmias.

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MITRAL VALVE PROLAPSE
Mitral valve prolapse, formerly known as mitral prolapse
syndrome, is a deformity that usually produces no symptoms.
Rarely, it progresses and can result in sudden death. Mitral
valve prolapse occurs more frequently in women than in men.

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PATHOPHYSIOLOGY
In mitral valve prolapse, a portion of a mitral valve leaflet
balloons back into the atrium during systole. Rarely, the
ballooning stretches the leaflet to the point that the valve does
not remain closed during systole (i.e., ventricular contraction).
Blood then regurgitates from the left ventricle back into the left
atrium (Braunwald et al., 2001).

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ASSESSMENT AND DIAGNOSTIC FINDINGS

Often, the first and only sign of mitral valve prolapse is

identified when a physical examination of the heart discloses an
extra heart sound, referred to as a mitral click.
The systolic click is an early sign that a valve leaflet is ballooning
into the left atrium.

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 MITRAL REGURGITATION

Mitral regurgitation involves blood flowing back from the left

ventricle into the left atrium during systole. Often, the margins of
the mitral valve cannot close during systole.

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PATHOPHYSIOLOGY:
 Mitral regurgitation may be caused by problems with one or more of the leaflets, A

mitral valve leaflet may shorten or tear.

 The chordae tendineae may elongate, shorten, or tear.

 The papillary muscle may rupture, stretch, or be pulled out of position by changes in

the ventricular wall (eg, scar from a myocardial infarction or ventricular dilation).

 The papillary muscle may be unable to contract because of ischemia. Regardless of

the cause, blood regurgitates back into the atrium during systole.
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SIGN AND SYMPTOMS:
 Chronic mitral regurgitation is often asymptomatic, but acute mitral regurgitation

(e.g., that resulting from a MI)

 Usually manifests as severe congestive heart failure. Dyspnea, fatigue, and weakness

are the most common symptoms.

 Palpitations, shortness of breath on exertion, and cough from pulmonary congestion

also occur.

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Assessment and Diagnostic Findings
 A systolic murmur is heard as a high-pitched, blowing sound at the apex.
 Echocardiography is used to diagnose and monitor the progression of mitral
regurgitation.
 Chest x-ray:
- enlarged LA,LV
- pulmonary venous congestion
– pulmonary edema

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 Cardiac catheterization: - dilated LA,LV - mitral regurgitation - pulmonary
hypertension - coexisting coronary artery disease

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AORTIC STENOSIS

Aortic valve stenosis is narrowing of the orifice between the left

ventricle and the aorta.
Causes: congenital, Rheumatic Fever, atherosclerosis

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CLINICAL MANIFESTATIONS
patients usually first have exertional dyspnea, caused by left
ventricular failure.
Other signs are dizziness and syncope because of reduced
blood flow to the brain.
Angina pectoris is a frequent symptom

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Assessment and Diagnostic Findings
 On physical examination, a loud, rough systolic murmur may be heard over the aortic
area. The sound to listen for is a systolic crescendo-decrescendo murmur, which may
radiate into the carotid arteries and to the apex of the left ventricle.

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AORTIC REGURGITATION

 Aortic regurgitation is the flow of blood back into the left ventricle from

the aorta during diastole.

 It may be caused by inflammatory lesions that deform the leaflets of the

aortic valve, preventing them from completely closing the aortic valve
orifice

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Pathophysiology

 In aortic regurgitation, blood from the aorta returns to the left ventricle during

diastole in addition to the blood normally delivered by the left atrium. The left
ventricle dilates, trying to accommodate the increased volume of blood.

 It also hypertrophies, trying to increase muscle strength to expel more blood with

above normal force—raising systolic blood pressure.

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SIGN AND SYMPTOMS:
 Aortic insufficiency develops without symptoms in most patients.
 Arterial pulsations that are visible or palpable at the carotid or temporal arteries.
 Exertional dyspnea and fatigue.
 Breathing difficulties (e.g., orthopnea, paroxysmal nocturnal dyspnea) at night.

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Assessment and Diagnostic Findings
 A diastolic murmur is heard as a high-pitched, blowing sound at the third or fourth intercostal space
at the left sternal border.

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TRICUSPID STENOSIS

 Decrease blood flow from right atrium to right ventricle due to narrow of the
tricuspid valve.
 Its Usually occur together with aortic or mitral stenosis.
 Decrease right ventricular output and decrease left ventricular filling.

R. Atrium enlargement & ↑systemic venous pressure

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Sign And Symptoms:
 symptoms of right-sided heart failure
 hepatomegaly
 ascites
 peripheral edema
 neck vein engorgement
 Decrease cardiac output
 fatigue, hypotension
 Raised JVP
 Mid-diastolic murmur (best heard at lower left or right sternal edge)

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TRICUSPID STENOSIS MANAGEMENT:
 Valve replacement
 Valvotomy
 Balloon valvuloplasty

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TRICUSPID REGURGITATION

 An insufficient tricuspid valve allows blood to flow back into the right atrium that
leads to venous congestion
 Decrease right ventricular output and decrease blood flow towards the lungs.

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Sign And Symptoms
 Oedema
 Hepatic enlargement (venous congestion)
 Raised JVP
 systolic murmur (left sternal edge)
 Triedness, fatigue and weakness

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PULMONARY STENOSIS

 Flow of blood to the pulmonary artery due to narrowing.

 Blood flow back to right ventricle and right atrium.
 Right ventricle hypertrophy to compensate for increase blood volume
and force blood to the pulmonary artery.

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Sign and symptoms:
 Fatigue
 Dyspnea on exertion,
 Cyanosis
 Poor weight gain or failure to thrive in infants hepatomegaly,
 Ascites,
 Edema

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PULMONARY REGURGITATION

 Blood Flow Back Into Right Ventricle:

 A Rare Condition Usually Associated With Pulmonary Hypertension
Which May Be
 Secondary Of The Disease Of Left Side Of The Heart
 Primary Pulmonary Vascular Disease

 Right ventricle and atrium hypertrophy

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DIAGNOSING VALVE DISEASE

 History and Physical Exam

 Echocardiography
 Cardiac Catheterization
 ECG

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NURSING MANAGEMENT/GOALS

 Maintaining normal cardiac function

 Monitoring Cardiac output, fluid volume excess
 Improving activity tolerance
 Educating patients on the disease process and preventative measures

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MITRAL VALVE REPAIR

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 References:
 Hinkle, J.L. & Cheever, K.H. (2018). Brunner &Suddarth's Textbook of Medical-Surgical
Nursing (10th ed.). Philadelphia: Wolters Kluwer

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