Cardiomyopathy is a dysfunction of cardiac muscle that can be associated with coronary artery disease, hypertension, cardiotoxic agents, valvular disorders, and vascular or pulmonary diseases. Cardiomyopathies are classified into three groups by etiology and the abnormal physiology of the left ventricle.
Dilated or congestive cardiomyopathy (DC) – is characterized by ventricular dilation and impaired systolic contractile fuction. Emboli may occur because of blood stasis in the dilated ventricles. This is the most common type cardiomyopathy.
Hypertrophic cardiomyopathy (HC) – is characterized by inappropriate myocardial hypertrophy without ventricular dilation. Obstruction to left ventricular outflow may or may not be present.
Restrictive cardiomyopathy (RC) – is characterized by abnormally rigid ventricles with decreases diastolic compliance. The ventricular cavity is decreased, and clinical manifestations are similar to constrictive pericarditis.
Signs and Symptoms
Dyspnea
Fatigue
Dysrhythmias or conduction disturbances
Onset may be insidious or exhibited by sudden death.
Physical Examination
Vital signs
HR: increased, irregular rhythm
BP: increased or decreased, depending on underlying disease or degree of heart failure
RR: may be increased
Cardiovascular
Murmurs
S3 and/ or S4
Ectopy
Jugular vein distention
Pulmonary
Crackles
Dry cough
Acute Patient Care Management
Nursing Diagnosis: Decreased cardiac output related to left ventricular dysfunction and dysrhythmias.
Outcome Criteria
Patient alert and oriented
Skin warm and dry
Pulses strong and equal bilaterally
Capillary refill < 3 sec
BP 90 to 120 mm Hg
Pulse pressure 30 to 40 mm Hg
HR 60 to 100 beats/min
Absence of life-threatening dysrythmias
Urine output 30 ml/hr
CVP 2 to 6 mm Hg
Patient Monitoring
Obtain Bp hourly or more frequently if the patient's condition is unstable.
Monitor hourly urine output to evaluate effects of decreased cardiac output or pharmacologic intervention.
Analyze ECG rhythm strip at least every 4 hours and note rate.
Continuously monitor oxygen status with pulse oximetry.
Monitor patient activities and nursing interventions that may adversely affect oxygenation.
Patient Assessment
Obtain vital signs every 15 minutes during acute phase.
Assess the patient for changes in neurological function hourly and as clinically indicated.
Assess for skin warmth, color, and capillary refill time.
Assess for chest discomfort because myocardial ischemia may result from poor perfusion.
Assess heart and lung sounds to evaluate the degree in heart failure.
Diagnostic Assessment
Review ECG
Echocardiography
Cardiac catheterization
Patient Management
Provide oxygen at 2 to 4 L/min to maintain or improve oxygenation.
Minimize oxygen demand by maintaining the patient at bed rest.
Provide liquid diet on acute phase,
Administer diuretic as prescribed to reduce preload and afterload.
Monitor serum potassium before and after administration of loop diuretics.
Prophylactic heparin may be ordered to prevent thromboembolus formation secondary to venous poisoning.
Institute pressure ulcer prevention strategies secondary to hypoperfusion or vasoconstriction agents.
Acute peritonitis is an inflammatory process within the peritoneal cavity most commonly caused by a bacterial infection. Types of acute peritonitis include primary and secondary. Primary peritonitis, otherwise known as spontaneous bacterial peritonitis, most commonly occur in patients with cirrhosis and clinically significant ascites. Secondary peritonitis most commonly occurs as a result of spillage of intestinal, biliary, or urinary tract contents into the peritoneal space as a result of perforation, suppuration, or ischemic injury. Patients at risk for developing secondary peritonitis include those with recent abdominal surgery, a perforated ulcer or colon, a ruptured appendix or viscus, a bowel obstruction, a gangrenous bowel, or ischemic bowel disease.
Signs and Symptoms
Patient assuming a knee-flexed position and complaining of severe localized or generalized abdominal pain.
Nausea and vomiting
Physical Examination
Vital signs
HR: tachycardia
BP: hypotension
RR: increased and shallow
Temp : elevated
Neurologic
Normal to decreased mentation
Skin
Pale
Flushed
Diaphoretic
Cardiovascular
Pulse thready or wear or may be bounding in presence of fever.
Pulmonary
Breath sounds may be diminished secondary to shallow breathing.
Abdominal
Rebound tenderness with guarding
May have referred pain to shoulder
Rigid, distended abdomen
Bowel sounds decrease to absent
Acute Care Management
Nursing Diagnosis: Deficient fluid volume related to intravascular fluid shift to the peritoneal space and inability to ingest oral fluids.
Outcome Criteria
Central venous pressure 2 TO 6 MM Hg
BP 90 to 120 mm Hg
Mean arterial pressure 70 to 105 mm Hg
Pulmonary artery systolic 15 to 30 mm Hg
Pulmonary artery diastolic 5 to 15 mm Hg
HR 60 to 100 beats/min
Urine output 30 ml/hr
Patient Monitoring
Obtain pulmonary artery pressure and central venous pressure and monitor mean arterial pressure hourly or more frequently if the patient's hemodynamic status is unstable.
Not the patient's response to all therapy.
Monitor fluid volume status by measuring urine output hourly and measure nasogastric and other bodily drainage.
Determine fluid balance every 8 hours.
Continuously monitor ECG fir dysrhythmias resulting from electrolyte disturbances.
Patient Assessment
Assess tissue perfusion. Note level of consciousness, skin color and temperature, pulses, and capillary refill.
Assess hydration status: note skin turgor on inner thigh or forehead, condition of buccal membranes, and development of edema or crackles.
Assess the patient's abdomen for resolution of rigidity, rebound tenderness, and distention. Auscultate bowel sounds.
Diagnostic Assessment
Review serum sodium and potassium levels, which may become depleted with nasogastric suctioning or fluid shifts.
Review serial WBC count and differentiated to evaluate the course of action.
Patient Management
Administer crystalloid or colloid solutions to improve intravascular volume.
Replace potassium as ordered; validate adequate urine output before administration.
Keep the patient NPO during acute phase and before evaluation by a surgeon.
Provide nutritional support as indicated; most patient will benefit from postpyloric delivery of early enteral nutrients at a minimal hourly rate to prevent v=bacterial translocation and sepsis.
Administer antibiotics as prescribed after appropriate cultures obtained.
Endocarditis is an inflammation of the endocardium; it is usually limited to the memrane lining and the valves. The cause of endocarditis may be viral, fungal, or most commonly, bacterial. The most common organism is Streptococcus viridans. Vegetations (growths or lesion) may cause vulvular dysfunction, with mortality from endocarditis being as high as 25%.
Risk factors include any high-risk individual as a patient with valvular disese or mitral valve prolapse; undergoing any type of invasive procedure, especially dental surgery; any chronically ill individual, especially one who is immunosuppressed; any individual with previously damaged or congenitally malformed valves; any individual with prosthetic valves; and illicit drug users.
Signs and Symptoms
Nonspecific
Fever and flu like symptoms
Fatigue
Weight loss
Malaise
Night sweats
Physical Examination
Physical findings are not specific
The hallmark of endocarditis is a fever and a new murmur.
Signs and symptoms of heart failure may be present.
Acute Care Management
Nursing Diagnosis: Decreased cardiac output secondary to valvular dysfunction from infective process.
Outcome Criteria
Patient alert and oriented
Skin warm and dry
Pulses strong and equal bilaterally
O2 sat ? 95%
Nursing Interventions
Patient Monitoring
Monitor pulse pressure and central venous pressure hourly or more frequently if titrating pharmacologic agents.
Obtain Bp hourly or more frequently if the patient's condition is unstable.
Monitor hourly urine output to evaluate for responses to pharmacologic interventions.
Analyze ECG rhythm strip at least every 4 hours and note every rate.
Patient Assessment
Obtain HR, RR, and BP every hour or more frequently if the patient is exhibiting signs and symptoms of heart failure.
Assess for changes in neurological function hourly and as clinically indicated.
Assess skin for warmth, color, and capillary refill time. Assess distal pulses bilaterally for strength, regularity, and symmetry.
Diagnostic Assessment
Review BUN and creatinine levels to evaluate renal function.
Review endocardiography finding if available for valvular and ventricular function and presence of vegetation.
Review WBC counts to evaluate course if infection.
Patient Management
Provide supplemental oxygen at 2 to 4 L/min to maintain or improve oxygenation.
Minimize oxygen demand to decrease anxiety.
Maintain patient on bed rest if in acute hear failure.
Administer multi-I.V. antibiotic regimen as ordered.
Administer antipyretics as ordered and as needed.
Prepare the patient for anticipated surgical intervention to repair or replace affected valves.
Cardiomyopathy is a dysfunction of cardiac muscle that can be associated with coronary artery disease, hypertension, cardiotoxic agents, valvular disorders, and vascular or pulmonary diseases. Cardiomyopathies are classified into three groups by etiology and the abnormal physiology of the left ventricle.
Dilated or congestive cardiomyopathy (DC) – is characterized by ventricular dilation and impaired systolic contractile fuction. Emboli may occur because of blood stasis in the dilated ventricles. This is the most common type cardiomyopathy.
Hypertrophic cardiomyopathy (HC) – is characterized by inappropriate myocardial hypertrophy without ventricular dilation. Obstruction to left ventricular outflow may or may not be present.
Restrictive cardiomyopathy (RC) – is characterized by abnormally rigid ventricles with decreases diastolic compliance. The ventricular cavity is decreased, and clinical manifestations are similar to constrictive pericarditis.
Signs and Symptoms
Dyspnea
Fatigue
Dysrhythmias or conduction disturbances
Onset may be insidious or exhibited by sudden death.
Physical Examination
Vital signs
HR: increased, irregular rhythm
BP: increased or decreased, depending on underlying disease or degree of heart failure
RR: may be increased
Cardiovascular
Murmurs
S3 and/ or S4
Ectopy
Jugular vein distention
Pulmonary
Crackles
Dry cough
Acute Patient Care Management
Nursing Diagnosis: Decreased cardiac output related to left ventricular dysfunction and dysrhythmias.
Outcome Criteria
Patient alert and oriented
Skin warm and dry
Pulses strong and equal bilaterally
Capillary refill < 3 sec
BP 90 to 120 mm Hg
Pulse pressure 30 to 40 mm Hg
HR 60 to 100 beats/min
Absence of life-threatening dysrythmias
Urine output 30 ml/hr
CVP 2 to 6 mm Hg
Patient Monitoring
Obtain Bp hourly or more frequently if the patient's condition is unstable.
Monitor hourly urine output to evaluate effects of decreased cardiac output or pharmacologic intervention.
Analyze ECG rhythm strip at least every 4 hours and note rate.
Continuously monitor oxygen status with pulse oximetry.
Monitor patient activities and nursing interventions that may adversely affect oxygenation.
Patient Assessment
Obtain vital signs every 15 minutes during acute phase.
Assess the patient for changes in neurological function hourly and as clinically indicated.
Assess for skin warmth, color, and capillary refill time.
Assess for chest discomfort because myocardial ischemia may result from poor perfusion.
Assess heart and lung sounds to evaluate the degree in heart failure.
Diagnostic Assessment
Review ECG
Echocardiography
Cardiac catheterization
Patient Management
Provide oxygen at 2 to 4 L/min to maintain or improve oxygenation.
Minimize oxygen demand by maintaining the patient at bed rest.
Provide liquid diet on acute phase,
Administer diuretic as prescribed to reduce preload and afterload.
Monitor serum potassium before and after administration of loop diuretics.
Prophylactic heparin may be ordered to prevent thromboembolus formation secondary to venous poisoning.
Institute pressure ulcer prevention strategies secondary to hypoperfusion or vasoconstriction agents.
Acute peritonitis is an inflammatory process within the peritoneal cavity most commonly caused by a bacterial infection. Types of acute peritonitis include primary and secondary. Primary peritonitis, otherwise known as spontaneous bacterial peritonitis, most commonly occur in patients with cirrhosis and clinically significant ascites. Secondary peritonitis most commonly occurs as a result of spillage of intestinal, biliary, or urinary tract contents into the peritoneal space as a result of perforation, suppuration, or ischemic injury. Patients at risk for developing secondary peritonitis include those with recent abdominal surgery, a perforated ulcer or colon, a ruptured appendix or viscus, a bowel obstruction, a gangrenous bowel, or ischemic bowel disease.
Signs and Symptoms
Patient assuming a knee-flexed position and complaining of severe localized or generalized abdominal pain.
Nausea and vomiting
Physical Examination
Vital signs
HR: tachycardia
BP: hypotension
RR: increased and shallow
Temp : elevated
Neurologic
Normal to decreased mentation
Skin
Pale
Flushed
Diaphoretic
Cardiovascular
Pulse thready or wear or may be bounding in presence of fever.
Pulmonary
Breath sounds may be diminished secondary to shallow breathing.
Abdominal
Rebound tenderness with guarding
May have referred pain to shoulder
Rigid, distended abdomen
Bowel sounds decrease to absent
Acute Care Management
Nursing Diagnosis: Deficient fluid volume related to intravascular fluid shift to the peritoneal space and inability to ingest oral fluids.
Outcome Criteria
Central venous pressure 2 TO 6 MM Hg
BP 90 to 120 mm Hg
Mean arterial pressure 70 to 105 mm Hg
Pulmonary artery systolic 15 to 30 mm Hg
Pulmonary artery diastolic 5 to 15 mm Hg
HR 60 to 100 beats/min
Urine output 30 ml/hr
Patient Monitoring
Obtain pulmonary artery pressure and central venous pressure and monitor mean arterial pressure hourly or more frequently if the patient's hemodynamic status is unstable.
Not the patient's response to all therapy.
Monitor fluid volume status by measuring urine output hourly and measure nasogastric and other bodily drainage.
Determine fluid balance every 8 hours.
Continuously monitor ECG fir dysrhythmias resulting from electrolyte disturbances.
Patient Assessment
Assess tissue perfusion. Note level of consciousness, skin color and temperature, pulses, and capillary refill.
Assess hydration status: note skin turgor on inner thigh or forehead, condition of buccal membranes, and development of edema or crackles.
Assess the patient's abdomen for resolution of rigidity, rebound tenderness, and distention. Auscultate bowel sounds.
Diagnostic Assessment
Review serum sodium and potassium levels, which may become depleted with nasogastric suctioning or fluid shifts.
Review serial WBC count and differentiated to evaluate the course of action.
Patient Management
Administer crystalloid or colloid solutions to improve intravascular volume.
Replace potassium as ordered; validate adequate urine output before administration.
Keep the patient NPO during acute phase and before evaluation by a surgeon.
Provide nutritional support as indicated; most patient will benefit from postpyloric delivery of early enteral nutrients at a minimal hourly rate to prevent v=bacterial translocation and sepsis.
Administer antibiotics as prescribed after appropriate cultures obtained.
Endocarditis is an inflammation of the endocardium; it is usually limited to the memrane lining and the valves. The cause of endocarditis may be viral, fungal, or most commonly, bacterial. The most common organism is Streptococcus viridans. Vegetations (growths or lesion) may cause vulvular dysfunction, with mortality from endocarditis being as high as 25%.
Risk factors include any high-risk individual as a patient with valvular disese or mitral valve prolapse; undergoing any type of invasive procedure, especially dental surgery; any chronically ill individual, especially one who is immunosuppressed; any individual with previously damaged or congenitally malformed valves; any individual with prosthetic valves; and illicit drug users.
Signs and Symptoms
Nonspecific
Fever and flu like symptoms
Fatigue
Weight loss
Malaise
Night sweats
Physical Examination
Physical findings are not specific
The hallmark of endocarditis is a fever and a new murmur.
Signs and symptoms of heart failure may be present.
Acute Care Management
Nursing Diagnosis: Decreased cardiac output secondary to valvular dysfunction from infective process.
Outcome Criteria
Patient alert and oriented
Skin warm and dry
Pulses strong and equal bilaterally
O2 sat ? 95%
Nursing Interventions
Patient Monitoring
Monitor pulse pressure and central venous pressure hourly or more frequently if titrating pharmacologic agents.
Obtain Bp hourly or more frequently if the patient's condition is unstable.
Monitor hourly urine output to evaluate for responses to pharmacologic interventions.
Analyze ECG rhythm strip at least every 4 hours and note every rate.
Patient Assessment
Obtain HR, RR, and BP every hour or more frequently if the patient is exhibiting signs and symptoms of heart failure.
Assess for changes in neurological function hourly and as clinically indicated.
Assess skin for warmth, color, and capillary refill time. Assess distal pulses bilaterally for strength, regularity, and symmetry.
Diagnostic Assessment
Review BUN and creatinine levels to evaluate renal function.
Review endocardiography finding if available for valvular and ventricular function and presence of vegetation.
Review WBC counts to evaluate course if infection.
Patient Management
Provide supplemental oxygen at 2 to 4 L/min to maintain or improve oxygenation.
Minimize oxygen demand to decrease anxiety.
Maintain patient on bed rest if in acute hear failure.
Administer multi-I.V. antibiotic regimen as ordered.
Administer antipyretics as ordered and as needed.
Prepare the patient for anticipated surgical intervention to repair or replace affected valves.
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