Moses Quinanola ORAL REVALIDA 2nd SEMESTER

ABRUPTIO PLACENTAE
Definition:
 Premature separation of all or part of placenta resulting in hemorrhage.
 Separation
 Usually happens in 20 weeks of gestation
 Classification:
1. Extent of separation: Partial vs complete
2. Location: Marginal vs central
3. Clinical presentation: revealed, concealed, and mixed
4. Clinical Severity:
o Class 0 – asymptomatic
o Class 1 – Mild (represents approximately 48% of all cases)
o Class 2 – Moderate (represents approximately 27% of all
cases)
o Class 3 – Severe (represents approximately 24% of all
cases)
Etiology:
 Degeneration of Arteries
 Predisposing: Hypertension, blunt trauma, Age (>35 & <20), previous
abruption, male fetal sex
 Precipitating: Smoking, Drugs (cocaine & meth), multiparity

Symptomatology:
 Key characteristics: painful, dark red vaginal bleeding
Class 1:
No vaginal bleeding to mild vaginal bleeding
 Slightly tender uterus
 Normal maternal BP and heart rate
 No coagulopathy
 No fetal distress The Implantation Process:
Class 2:  Zygote travels to uterus  develops into morula  blastocyst 
 No vaginal bleeding to moderate vaginal bleeding reaches endometrial lining  zona pellucida sheds  trophoblast
 Moderate to severe uterine tenderness with possible tetanic and crypt development  apposition  adhesion 
contractions synciotrophoblast formation  chorion & chorionic villi development 
 Maternal tachycardia with orthostatic changes in BP and heart rate placental development & implantation
 Fetal distress o zona pellucida – thick transparent membrane surrounding
 Hypofibrinogenemia (ie, 50-250 mg/dL) ovum before implantation
Class 3: o Apposition – contact between trophoblast and endometrial
 No vaginal bleeding to heavy vaginal bleeding lining
 Very painful tetanic uterus o Adhesion – multiplication of trophoblastic cells into the
 Maternal shock endometrial lining following apposition
 Hypofibrinogenemia (ie, < 150 mg/dL) o Synciotrophoblast – nucleated trophoblastic cells growing
 Coagulopathy out to the endometrial lining that allows both endometrial
 Fetal death and trophoblastic cells to fully fuse or implant

Anatomy & Physiology: Diagnosis:

Pregnancy and development  Physical exam – to check uterine tenderness or rigidity
 Coitus  ovum + sperm  Fertilization  zygote  morula   Blood tests – to identify possible sources of vaginal bleeding
blastocyst  trophoblast  embryo  Fibrinogen study – pregnancy is associated with hyperfibrinogenemia.
<200mg/dL suggests severe abruption
 Kleihauer-Betke test – to help detect fetal red blood cells in maternal
circulation
 Ultrasonography – to asses bleeding in pregnancy, however it is a
sensitive modality for this purpose.
 Biophysical Profile (BPP) – used to evaluate patients with chronic
abruptions. BPP score <6 (maximum is 10) may be an early sign of
fetal compromise.

Treatment and Management:

 Initial Management of Abruptio Placentae
- Begin continuous external fetal monitoring for the FHT and
contractions
- Obtain intravenous access using 2 large-bore intravenous lines
- Institute crystalloid fluid resuscitation for the patient
- Type and crossmatch blood
- Begin a transfusion if patient is hemodynamically unstable after
fluid resuscitation
- Administer Rh immune globulin if patient is Rh-negative
- Begin course of corticosteroids for fetal lung maturity (if <37 weeks
AOG)
 Vaginal delivery – this is the preferred method of deliver for a fetus that
has died secondary to placental abruption. The ability to undergo NSVD
depends on patient’s hemodynamic stability
 Cesarean delivery – necessary for fetal and maternal stabilization
 Dietary modification – patient should be on NPO
 Medications:
- Tocolytics
 Nifedipine – calcium channel blocker that decreases
contractions
Moses Quinanola
 Magnesium sulfate – drug of choice for tocolysis for abruptio
placentae
- Corticosteroids (dexamethasone) – given when preterm delivery is
expected to decrease risk of neonatal respiratory distress
Prioritized Nursing Diagnoses with Interventions:
 Ineffective maternal and fetal tissue perfusion related to excessive
blood loss
- Monitor FHT continuously to provide information regarding fetal
distress and/or worsening of condition
- Administer oxygen by appropriate route as ordered to maximize
oxygenation of tissues
 Risk for shock related to significant blood loss
- Administer blood or blood products as indicated to rapidly restore
or sustain circulating volume and electrolyte balance.
- Monitor I&O to obtain data about renal perfusion and function and
the extent of blood loss.
 Acute pain related to separation of placenta from uterine wall
- Administer analgesics as indicated to promote pharmacological
pain management
- Monitor skin color and temperature and vital signs. There are
usually altered in acute pain
DIABETIC KETOACIDOSIS (DKA)
Definition:
 Is an acute, major life-threatening complication of diabetes mellitus that
mainly occurs in patients with type I Diabetes.
 Characterized by hyperglycemia, ketoacidosis and ketonuria
Etiology:
 Type I Diabetes
 Predisposing Factors: UTI, pneumonia, heart attack, physical or
emotional trauma
 Precipitating Factors: Problems with Insulin therapy, alcohol or drug
abuse, medications (corticosteroids and some diuretics)
Symptomatology:
 Hyperglycemia
 Ketoacidosis
 Ketonuria
 Excessive thirst
 Abdominal pain
 Nausea and vomiting
 Dehydration
 Altered mental status
 Metabolic acidosis (kussmaul’s respirations)
 Fruity scented breath
 Shortness of breath
Anatomy and Physiology: Endocrine Pancreas
 The pancreas is both an exocrine and an endocrine gland.
o Exocrine – secretes digestive enzymes
o Endocrine – secretes hormones glucagon, insulin,
somatostatin and pancreatic polypeptides
 Cells and Secretions in the Pancreatic Islets (Islet of Langerhans’s)
o Alpha cells – produces glucagon. Low blood sugar
stimulates the release of glucagon (Elevates blood sugar).
o Beta cells – produces insulin. High blood sugar stimulates
the release of insulin (Lowers blood sugar).
o Delta cells – produces somatostatin, inhibiting the release
of both insulin and glucagon.
o PP cells – secretes polypeptide hormones.
 Glucose is the key source of energy for the human body. Supply of this
vital nutrient is carried through the bloodstream to many of the body’s
cells.
 The brain can only utilize two forms of energy: Glucose and
Ketones
 Insulin acts as a key that allows glucose to enter the cell.
Diagnosis:
 Blood sugar levels – usually exceeds 250mg/dL
 Arterial Blood Gas – metabolic acidosis, low bicarbonate and low pH
 Blood Urea Nitrogen (BUN) – frequently increase
 Blood electrolyte tests – K levels are high, Na is low, Cl and Ph are low
 CBC – increased WBC count
 Serum Ketones – Acetest and Ketostix
 Urinalysis – high glucose and ketone levels in urine
 Chest X-ray
ORAL REVALIDA 2nd SEMESTER
 ECG – T wave changes
Treatment:
 Insulin Therapy – to regulate blood glucose levels and suppress ketone
bodies
 Intravenous therapy – to correct dehydration and replace salts loss
from urine
 Bicarbonate therapy
 Oxygen Therapy
Nursing Diagnoses with Interventions:
 Unstable blood Glucose Levels related to lack of diabetes management
o Monitor blood glucose levels q1 hour as indicated
o Monitor vital signs accordingly for hypo/hypertension,
tachycardia and respiration changes
 Fluid Volume Deficit related to hyperosmolar urinary losses
o Monitor intake and output q1 hour as indicated
o Increase oral fluid intake and regulate IVFs as ordered
 Ineffective Breathing Pattern related to increased blood pH
o Monitor ECG tracings and Arterial blood gases
o Administer supplemental oxygen via nasal cannula
 Altered Mental Status related to impaired metabolic process
o Monitor neurovital signs q1 hour as indicated
o Provide safety by keeping side rails up
 Fatigue related to decreased metabolic energy production
o Advise patient to complete bed rest without bathroom
privileges as order
o Keep things close to patient’s reach and provide call bells
CEREBROVASCULAR ACCIDENT (CVA)
Definition:
 AKA stroke, is a sudden impairment of cerebral circulation in one or
more blood vessels.
Etiology:
 Idiopathic – cerebral thrombosis, embolism or hemorrhage
 Predisposing Factors: Age (>55 years), Race (Black Americans),
Hypertension, Family History of stroke, TIA, CVDs, DM
 Precipitating Factors: Cigarette Smoking, Increased alcohol intake,
sedentary lifestyle, hormonal contraceptives
Symptomatology:
 F – facial drooping
 A – arm weakness
 S – speech difficulties
 T – time
Anatomy and Physiology: Cerebrovascular System
 The brain receives its arterial supply from two pairs of vessels, the
vertebral and internal carotid arteries, which are interconnected in the
cranial cavity to produce an arterial circle (Circle of Willis)
 Crawling up the brain stem are the vertebral arteries, joining to form the
basilar artery
 The basilar artery crawls up the brain stem, pons and midbrain, forming
the circle of Willis
 The circle of Willis gives of the posterior cerebral, middle cerebral and
anterior cerebral arteries
 Joining the anterior cerebral arteries is the anterior communicating
artery, the artery that connects two anterior cerebral arteries
 The posterior cerebral arteries are communicated by the posterior
communicating artery
 Internal carotid arteries do not give off any branches, but forms the
Circle of Willis
Moses Quinanola ORAL REVALIDA 2nd SEMESTER
Diagnosis:  Precipitating Factors: Exposure to chemicals (benzene), long-term
 CT Scan – determines the type of CVA (Ischemic or hemorrhagic) treatment with alkylating substances and ionizing radiation, smoking,
 MRI – assists in identifying areas of ischemia or hemorrhage alcohol abuse, drugs
 Cerebral angiography – reveals disruption of cerebral circulation by
occlusion Symptomatology:
 Carotid Duplex – identifies severity of stenosis  Sudden onset of high fever
 PET Scans – identify areas of altered metabolism surrounding lesions  Thrombocytopenia and abnormal bleeding
not yet able to be detected by other diagnostic tests  Weakness and lassitude
 Lumbar Puncture – performed if there are no signs of increased ICP,  Pallor
reveals bloody CSF
 Chills and recurrent infections
 EEG – helps identify damaged areas of the brain
 Bone pain
 Headache, papilledema, facial palsy, blurred vision and meningeal
Treatment:
irritation
 Osmotic diuretics (Mannitol) – to reduce cerebral edema
 Hepatosplenomegaly
 Corticosteroids (Dexamethasone) – to reduce inflammation and
cerebral edema
Anatomy and Physiology: Hematologic System
 Thrombolytics (If Ischemic) – within 4 hours
 Hematopoiesis – is the formation of blood components.
 Anticonvulsants o Takes place in the bone marrow
 Aneurysm repair
 Blood Components:
 Percutaneous Transluminal Angioplasty or Stent Insertion – to open o Erythrocytes (RBCs) – carries oxygen and carbon dioxide
occluded Vessels
o Leukocytes (WBCs) – destroy and remove old cells as well
as pathogens and foreign bodies. There are different types
Nursing Diagnoses with Interventions
of white blood cells:
 Ineffective Cerebral Tissue Perfusion related to interruption of blood
 Basophils
flow
o Administer medications that can reduce cerebral edema  Eosinophils
(Mannitol) or thrombolytics (heparin) as ordered  Neutrophils
o Check vital signs and neurologic status, record  Monocytes
observations and report any significant changes to  B & T lymphocytes
physician. o Thrombocytes (Platelets) – responsible for blood clotting
1. Impaired physical mobility r/t neuromuscular impairment (coagulation)
o Instruct in use of side rails, overhead trapeze, roller pads,  Hematopoietic Stem Cells
walker, cane for position changes, transfers and o Myeloid cells:
ambulation  Monocytes
o Support affected body parts using pillows to maintain  Macrophages
position of function and reduce risk of pressure ulcers.  Neutrophils
 Impaired Verbal Communication related to impaired cerebral circulation  Basophils
o Provide alternative cues to communicate with patient  Eosinophils
o Refer to physical and speech therapy  Erythrocytes
 Dendritic Cells
 Self-care Deficit related to decreased strength or endurance
 Platelets
o Assist in activities of daily living
o Lymphoid cells:
o Provide cleansing bed bath and oral care daily
 T lymphocytes
 Risk for Unilateral Neglect related to sensory loss of part  B lymphocytes
o Change positions every two hours  Natural killer cells
o Place objects beside affected side o Immature – “blasts”
o Mature – “cytes”
LEUKEMIA
Definition:
 The cancer of the blood-forming tissues, including the bone marrow
and lymphatic system.
 Acute Leukemia – blood cells grow rapid. Patient shows symptoms
within weeks. Blood cells are very immature.
 Chronic Leukemia – blood cells grow slowly. Patient is asymptomatic
and will experience symptoms on late stage. Blood cells are slightly
immature but more mature compared to acute leukemia.

Stem cell  Immature blasts  Mature specialized cells

 Blood cells decrease in size as they mature into specialized cells

Diagnosis:
Etiology:  Bone marrow aspiration – reveals proliferation of immature WBCs
 Idiopathic  CBC – shows thrombocytopenia and neutropenia
 Predisposing Factors: Sex (2x more common in women), Genetic o Hgb levels <11g/dL
factors, Family history of cancer, human retroviruses o Neutropenia <1,500/uL
o Lymphocytosis >10,000/uL
o Thrombocytopenia <150,000/uL
Moses Quinanola ORAL REVALIDA 2nd SEMESTER
 Differential WBC count – reveals cell types o Renal columns – cortex-like tissue extensions separating
 Lumbar Puncture – reveals leukemic infiltration to CSF the renal pyramids
 Biopsy – shows lymphocytic invasion o Renal pelvis – Medial to the hilum continuous with the
ureter leaving the hilum
Treatment o Renal artery – supply oxygen rich blood to the kidneys
 Chemotherapy
 Targeted Therapy (Imatinib) – stops action of a protein within leukemic
cells
 Radiation therapy
 Stem cell Transplant – procedure to replace diseased bone marrow
with health bone marrow

Nursing Diagnoses with Interventions

 Risk for infection related to immunosuppression
o Observe reverse isolation precaution when caring for
patient
o Administer prophylactic medications as prescribed
 Acute pain related to bone marrow proliferation
o Administer analgesics as prescribed
 Imbalanced nutrition: less than body requirements related to anorexia
and chemotherapy-induced emesis  The Nephrons
 Activity Intolerance related to reduced energy stores o Are structural and functional units of the kidneys
o Provide safety measures such as raising of side rails o Glomerulus – one of the main structures of a nephron
o Assist in active or give passive range of motion exercises forming a knot of capillaries
 Anxiety related to change in health status o Renal tubule
o Bowman’s capsule
NEPHROTIC SYNDROME o Podocytes – inner layer of the capsule enclosing the
glomerulus
Definition: o Collecting ducts – received the urine from the nephrons
 A kidney disorder characterized by proteinuria, hypoalbuminemia, o Proximal convoluted tubule – part of the tubule that is near
hyperlipidemia and edema caused by damage to the glomerulus. to the glomerular capsule
o Primary – nephrotic syndrome being specific to the kidneys o Loop of Henle – hairpin loop following the PCT that
o Secondary – being a renal manifestation of a systemic recovers water and Na from the urine
general illness. o Distal convoluted tubule
o Afferent arteriole – arises from a cortical radiate artery;
Etiology:
AKA “feeder vessel”
 Predisposing: Age (more common in children), focal segmental o Efferent arteriole – receive blood that has passed through
glomerulosclerosis, membranous nephropathy, SLE, diabetic kidney
the glomerulus
disease, amyloidosis, blood clot in kidney vein, heart failure, infection
o Peritubular capillaries – arise from efferent arterioles and
(HIV, HBV/C, malaria)
drains the glomerulus
 Precipitating: Medication (NSAIDS, antibiotics)

Symptomatology:
 TETRAD SIGNS: proteinuria (>3.5gday), hypoalbuminemia,
hyperlipidemia and edema (peripheral, periorbital, ascites or anasarca)
 Other signs and symptoms:
o Foamy urine due to excess protein
o Weight gain due to excess fluid retention
o Xanthelasma and xanthomata – cholesterol deposits in the
eyes and hands
o Fatigue
o Leukonychia striates
o Shortness of breath

Anatomy and Physiology: The Renal System:

 Functions of the kidneys:
o Filter  Urine Formation
o Waste processing o Glomerular filtration – water and solutes smaller than
o Elimination proteins are forced through the capillary walls and pores of
o Regulation the glomerular capsule into the renal tubule
o Tubular reabsorption – water glucose, amino acids and
o Production of enzymes and hormones
needed ions are transported out of the filtrate into the
o Conversion
tubule cells and then enter the capillary blood
 Anatomy of the kidney o Tubular secretion – hydrogen, potassium, creatinine and
o Location – located in the superior lumbar region extending
drugs are removed from the peritubular blood and secreted
from the T12 to the L3 vertebra. by the tubule cells into the filtrate.
o Position – the right kidney is lower than the left Diagnosis:
o Size – 12cm long, 6cm wide and 3cm thick  Blood chemistry (albumin, lipids, creatinine, BUN) – determines
o Adrenal gland – sits atop each kidney and is part of the hypoalbuminemia, hyperlipidemia and increased creatinine and BUN
endocrine system levels
o Fibrous capsule – encloses each kidney, giving them a  Urinalysis – determines proteinuria (>3g/day)
glistening appearance  Renal Biopsy – to determine type of nephrotic syndrome
o Perirenal fat capsule – fatty mass surrounding each kidney  Chest Xray – pleural effusion and edema
and acts to cushion it against blows  Kidney ultrasound
o Renal fascia – outermost capsule anchoring the kidney to  Physical Assessment – assess edema (peripheral, periorbital, ascites,
the muscles of the trunk wall anasarca), xanthelasama, xanthemata, leukonychia
o Renal cortex – outer region of the kidney
o Renal medulla – the inner region; darker with a reddish- Treatment:
brown are  Medical:
o Renal pyramids – triangular regions within the medulla
Moses Quinanola
o Antihypertensive (ACE inhibitors) – benazepril, captopril
and enalapril; reduce blood pressure and amount of
protein released in urine
o Diuretics – furosemide, spironolactone – control edema
o Antilipidemic – atorvastatin, simvastatin; lowers blood
cholesterol levels
o Anticoagulants – warfarin, heparin; help decrease blood
clotting
o Immunosuppressants – corticosteroids; decreases
inflammation
 Surgical:
o Nephrectomy
o Kidney transplant
 Management:
o Diet high in protein and low in salt
o Exercise
Nursing Diagnoses with Interventions:
 Fluid volume excess related to fluid retention
o Monitor I&O ratios to evaluate fluid loss and kidney
perfusion
o Administer albumin as prescribed to correct
hypoalbuminemia and reduce fluid retention
 Risk for infection related to loss of antibodies
o Observe aseptic technique: use of gloves and frequent
handwashing to prevent cross-contamination
o Evaluate
 Decreased cardiac output related to decreased venous return and
blood volume
o Monitor cardiac status
o Advise to increase oral fluid intake and regulate IVF
accordingly
CONGESTIVE HEART FAILURE
Definition:
 Occurs when the heart can’t pump enough blood to meet the body’s
metabolic needs and results in intravascular and interstitial volume
overload and poor tissue perfusion
 Types:
o Left-sided heart failure – ineffective left ventricular
contractile function; refluxes back into the left atrium, into
the lungs, causing pulmonary congestion.
o Right-sided heart failure – ineffective right ventricular
contractile function; refluxes back into the right atrium,
peripheral circulation, causing peripheral edema and
weight gain.
o Systolic dysfunction – left ventricle can’t pump enough
blood out to the systemic circulation during systole,
causing the ejection fraction to fail.
o Diastolic dysfunction – reduced ability of left ventricle to
relax and fill during diastole, causing the stroke volume to
fall.
Etiology:
 Predisposing: atherosclerotic heart disease, MI, hypertension, RHD,
CHD, ischemic heart disease, cardiomyopathy, valvular disease,
arrhythmias, COPD, thyrotoxicosis, sever infection, acute blood loss,
age (>80), sex (more common in men), race (African americans)
 Precipitating: pregnancy, severe physical or mental stress, smoking,
drugs, improper diet, sedentary lifestyle
Symptomatology:
 Left-sided heart failure – “DO CHAP”
o Dyspnea – typically occurs during rest
o Orthopnea
o Cough – initially dry and nonproductive. Large frothy,
sputum, which is sometimes pink, may be produced,
usually indicating severe pulmonary congestion
o Hemoptysis
o Adventitious breath sounds (crackles)
o Pulmonary congestion
 Right-sided heart failure – “AW HEAD”
o Anorexia and Nausea – due to engorgement and venous
stasis within the abdominal organs
o Weight gain – due to fluid retention
ORAL REVALIDA 2nd SEMESTER
o Hepatomegaly – venous engorgement of the liver
o Edema (Bipedal)
o Ascites – increased pressure within the portal vein
o Distended neck vein – increased venous pressure
Anatomy and Physiology: The Cardiovascular System
 Functions of the heart:
o Managing blood supply
o Producing blood pressure
o Securing one-way blood flow
o Transmitting blood
 Structures of the Heart:
o Weight – approximately the size of a person’s fist and
weighs less than a pound
o Mediastinum - the medial cavity of the thorax
o Apex – directed toward the left hip and rests on the
diaphragm, approximately at the level of the 5th intercostal
o
space
Base
o Pericardium – double-walled sac and enclosing the heart
o Fibrous pericardium – loosely fitting superficial part of the
pericardium, protecting and anchoring the heart to the
diaphragm and sternum
o Serous pericardium
 Layer of the Heart:
o Epicardium – visceral and outermost layer
o Myocardium – muscular, middle layer
o Endocardium – innermost layer
 Cardiac cycle and heart sounds
o Systole – heart contraction
o Diastole – heart relaxation
o Cardiac cycle – events of one complete heartbeat, during
which both atria and ventricles contract then relax
o Length – beats approximately 75 times per minute,
normally about 0.8 seconds
o Mid-to-late diastole – the cycle starts with the heart in
complete relaxation; the pressure in the heart is low, and
blood is flowing passively in and through the atria into the
ventricles from the pulmonary and systemic circulations;
the semilunar valves are closed, and the AV valves are
open; then the atria contract and force the blood remaining
in their chambers into the ventricles.
o Ventricular systole – shortly after, the ventricular
contraction begins and the pressure within the ventricles
increases rapidly, closing the AV valves; when the
intraventricular pressure is higher than the pressure in the
large arteries leaving the heart, the semilunar valves are
forced to open, and blood rushes through them out of the
ventricles; the atria are relaxed, and their chambers are
again filling with blood.
o Early diastole – at the end of the systole, the ventricles
relax, and the semilunar valves snap shut, and for a
moment the ventricles are completely closed chambers;
the intraventricular pressure drops, and the AV valves are
forced open; the ventricles again begin refilling rapidly with
blood, completing the cycle.
o First heart sound – the first heart sound, “lub”, is caused by
the closing of the AV valves
o Second heart sound – the second heart sound, “dub”,
occurs when the semilunar valves close at the end of the
systole.
 Cardiac output
Moses Quinanola
o It is the amount of blood pumped by each side of the heart
in one minute. It is the product of the heart rate and stroke
volume.
o Stroke volume – volume pumped out by a ventricle with
each heartbeat
o Starling’s Law of the Heart – states that the critical factor
controlling the stroke volume is how much the cardiac
muscles are stretched before they contract; the more they
are stretched, the stronger the contraction will be; and
anything that increases the volume or speed of venous
return also increases stroke volume and force of
contraction.
ORAL REVALIDA 2nd SEMESTER
Nursing Interventions with Diagnoses:
 Decreased cardiac output related to altered myocardial contractility and
structural changes
 Impaired gas exchange related to alveolar-capillary membrane
changes
 Ineffective breathing pattern related to alveolar-capillary membrane
changes
 Fluid volume excess related to sodium and water retention
 Activity intolerance related to imbalanced O2 supply and demand

 Coronary Circulation
o Inferior/superior vena cava  Right atrium  tricuspid
valve  right ventricle  Pulmonary Valve  Lungs 
Pulmonary veins  Left Atrium  Mitral valve  Left
Ventricle  Aortic valve  Aorta  rest of the body

Diagnosis:
 Chest x-ray – show increased pulmonary vascular markings, interstitial
edema, or pleural effusion and cardiomegaly
 Electrocardiography (ECG) – indicates hypertrophy, ischemic changes,
or infarctions
 Blood tests – Liver function test, Serum creatinine and BUN, APTT-PT
 Brain natriuretic peptide (BNP) assay – blood test to establish
diagnosis of heart failure; elevated levels indicate heart failure
 Echocardiography – reveal left ventricular hypertrophy, dilation and
abnormal contractility
 Pulmonary artery monitoring – (LSHF) elevated pulmonary artery and
pulmonary artery wedge pressures, left ventricular end-diastolic
pressure; (RSHF) elevated atrial pressure or central venous pressure
 Radionuclide ventriculography – reveal and ejection fraction less than
40%; in diastolic dysfunction, the ejection fraction may be normal

Treatment:
 Medical
o Diuretics – to reduce total blood volume and circulatory
congestion
o ACE inhibitors – dilates blood vessels and decrease
systemic vascular resistance
o Vasodilators – may be given to patients intolerable of ACE
inhibitors
o Digoxin (Lanoxin) – strengthens myocardial contractility
o Beta-adrenergic blockers – prevent cardiac remodeling
o Nesiritide – to augment diuresis and decrease afterload
o Dopamine/dobutamine – reserved for those with end-stage
heart failure or those with awaiting heart transplantation
 Surgical
o Surgical valve replacement, coronary artery bypass
grafting, percutaneous transluminal coronary angioplasty
or stenting.
o Dor procedure (partial left ventriculectomy) – removal of
nonviable heart muscle to reduce the size of the
hypertrophied ventricle
o Mechanical ventricular assisted device (VAD)
o Internal cardioverter-defibrillator implantation
o Biventricular pacemaker
o Cardiac transplantation
 Management
o Alternate periods of rest with periods of activity
o Sodium-restricted diet with small, frequent meals
o Antiembolism stockings to prevent venostasis
o Oxygen therapy