Adult Acute: Exam 3

Etiology + patho: Cushing syndrome

• Results from chronic exposure to excess corticosteroids, especially glucocorticoids

• Iatrogenic administration of exogenous corticosteroids is the most common cause

• Most cases of endogenous syndrome are due to an ACTH-secreting pituitary adenoma (Cushing disease)

Clinical manifestations: Cushing syndrome

• Related to excess corticosteroid levels

  • Weight gain, in the trunk, face, and cervical areas (centripetal obesity, moon face, buffalo hump)

  • Hyperglycemia

  • Muscle wasting → weakness

  • Osteoporosis → back pain

  • Weaker, thinner, easily bruised skin

  • Purplish-red striae, usually depressed below skin surface, on abdomen, breast, or buttocks

  • Delayed wound healing

• Related to mineralocorticoid processes

  • Hypokalemia

  • Hypertension

• Adrenal androgen excess

  • Severe acne

  • Development of male characteristics in women

  • Feminization in men

Diagnostic studies: Cushing syndrome

• Confirmation of increased plasma levels

  • Midnight/late-night salivary cortisol

  • Low-dose dexamethasone suppression

  • 24-hours urine cortisol

    • Urine cortisol >100 mcg/24 hrs = Cushing syndrome

• CTs/MRIs of the pituitary + adrenal glands can detect tumors

• Plasma ACTH levels can be low, normal, or high, depending on the underlying cause

  • High/normal levels can indicate Cushing disease

  • Low/undetectable levels indicate an adrenal/medication cause

Interprofessional care: Cushing syndrome

• Primary goal is normalization of hormone secretion

• Surgical therapy for tumor removal

• Drug therapy for patients who are poor surgery candidates/previous surgical failures

  • Goal is to suppress the synthesis + secretion of cortisol from the adrenal gland

  • Drugs

    • Ketoconazole/mitotane

    • Hydrocortisone/prednisone

    • Mifepristone

• If developed due to prolonged corticosteroid use:

  • Gradual discontinuation of drug therapy

  • Reduction of drug dose

  • Conversion to alternate-day dosing

Nursing management: Cushing syndrome

• Health promo

  • Focuses on IDing at-risk patients (those on long-term exogenous corticosteroids)

  • Teaching related to medication use and monitoring side effects is an important preventive measure

• Acute care

  • Assessment focuses on signs/symptoms of hormone and drug toxicity and complicating conditions (CVD, diabetes, infection)

  • Monitor/assess for:

    • Vitals

    • Daily weights

    • Glucose levels

    • Infection

    • Pain, loss of function, and purulent drainage

      • Signs/symptoms of inflammation may be minimal/absent

    • Thromboembolic events (pulmonary emboli)

  • Provide emotional support; changes in appearance can be distressing

  • Preop care

    • Control hypertension/glycemia

    • Correct hypokalemia

    • Implement high-protein diets to correct protein depletion

    • Include info about expected care postop

  • Postop care

    • Initiate VTE prophylaxis

    • Monitor BP and fluid/electrolyte balance, as they can be unstable due to hormone fluctuations

    • Monitor for hypertension/glycemia, bleeding, signs of infection, and delayed wound healing

    • Obtain morning urine samples at the same time each morning for cortisol measurement to evaluate surgery effectiveness

    • Patients are usually kept on bed rest until BP stabilizes

• Ambulatory care

  • Discharge teaching is based on patient’s lack of endogenous corticosteroids and resulting inability to react physiologically to stressors

  • Teach patients to always wear Medic Alert bracelet and carry medical ID and instruction in a wallet/purse

  • Teach patients to avoid exposure to

    • Extreme temps

    • Infections

    • Emotional situations

  • Teach patients to adjust their corticosteroid replacement therapy by their stress levels

Etiology + patho: Addison disease

• Primary adrenocortical insufficiency

• All 3 classes of adrenal corticosteroids are reduced

• Can present with other endocrine problems (autoimmune polyglandular syndrome; most common in white females)

Clinical manifestations: Addison disease

• Often don’t appear until disease has advanced

• Anorexia

• Nausea

• Progressive weakness

• Fatigue

• Weight loss

• Bronze-colored skin hyperpigmentation

  • Seen mainly in sun-exposed areas, pressure points, over joints, and in body creases (especially palmar)

• Abdominal pain

• Diarrhea

• Headache

• Orthostatic hypotension

• Salt craving

• Joint pain

• Irritability

• Depression

Diagnostic studies: Addison disease

• ACTH stimulation test

  • Used for diagnosis

  • Little/no increase in cortisol levels = Addison disease

• CRH stimulation test

  • Done when the response to the ACTH test is abnormal

  • High ACTH + no cortisol = Addison disease

• Lab findings

  • Hyperkalemia → Low voltage + peaked P waves on ECG

  • Hypochloremia

  • Hyponatremia

  • Hypoglycemia

  • Anemia

  • Increased BUN levels

• CTs/MRIs can ID other causes (tumors, fungal infections, TB, or adrenal calcification)

Interprofessional care: Addison disease

• Treatment focuses on managing underlying cause when possible

• Main treatment is often lifelong hormone therapy with glucocorticoids and mineralocorticoids

• Dietary salt intake is increased

• Glucocorticoids are usually given in divided doses

  • 2/3 in the morning, 1/3 in the afternoon

• Mineralocorticoids are given once daily, preferably in the morning

• Drug scheduling reflects normal circadian rhythm in endogenous hormone secretion and decreases side effects

Nursing management: Addison disease

• Patients need an increased dosage of corticosteroids in stressful situations to prevent addisonian crisis

  • Situations requiring corticosteroid adjustment

    • Fever

    • Flu

    • Tooth extraction

    • Rigorous physical activity

• Give written + verbal instructions on when to change doses

• Review stress management techniques

• Teach patients to notify provider if V/D occurs as may happen with gastroenteritis

• Teach patients the signs/symptoms of corticosteroid deficiency/excess (Cushing syndrome) and to report signs to provider so that drug dose can be adjusted

• Patients should wear and Medic Alert bracelet + carry a wallet card saying they have Addison disease so that appropriate therapy can be started in an emergency

• When patients are hospitalized, nursing care focuses on monitoring the patient while correcting fluid/electrolyte balance

• Complete medication history if see if any drugs interact with corticosteroids

  • Examples:

    • Hypoglycemics

    • Cardiac glycosides

    • Oral contraceptives

    • Anticoagulants

    • NSAIDs

• Addisonian crisis is a life-threatening emergency requiring aggressive management

  • Treatment is directed toward shock management and high-dose hydrocortisone replacement

  • Large volumes of IV fluids are given to reverse hypotension and electrolyte imbalances until BP returns to normal

Indications: corticosteroid therapy

• Adrenal gland hormone insufficiency

• Allergic reactions

• Autoimmune + inflammatory connective tissue, GI, and integumentary disorders

• Increased ICP

• Inflammatory lung diseases

Side effects: corticosteroid therapy

• Increased infection risk

• Delayed wound healing

• Hyperglycemia

• GI upset

• Peptic ulcer disease

• Hypertension + increased heart failure risk

• Osteoporosis → pathologic fractures

• Electrolyte imbalances (decreased calcium + potassium)

Patient teaching: corticosteroid therapy

• Follow diets high in protein, calcium (1500 mg/day), and potassium and low in fat + sugar

• Ensure adequate rest + sleep; take daily naps and avoid caffeine late in the day

• Exercise to maintain bone integrity

• Recognize edema + restrict sodium intake if it occurs

• Monitor glucose levels + signs of hyperglycemia

• Notify provider if heartburn after meals or epigastric pain that’s unrelieved by antacids occurs

• See optometrists yearly to assess for cataract development

• Use safety measures to avoid injury

• Maintain appropriate hygiene practices

• Avoid contact with sick/contagious people to prevent infection

• Inform all providers about long-term corticosteroid use

• Recognize need for higher medication doses in times of physical/emotional stress

• Never abruptly stop medication; addisonian crises can occur

Etiology + patho: cellulitis

• Inflammation of SQ tissues

• Can be a primary or secondary infection

• Often follows a break in the skin

• Staph aureus and strep are the usual causative agents

• Deep inflammation of SQ tissue from enzymes produced by bacteria

Clinical manifestations: cellulitis

• Hot, tender, red, edematous area with diffuse borders

• Chills

• Malaise

• Fever

Treatment: cellulitis

• Topical

  • Moist heat

  • Immobilization

  • Elevation

• Systemic

  • Antibiotic therapy

  • Hospitalization, if severe, for antibiotic therapy based on C&S testing

  • Progression to gangrene is possible if untreated

Etiology + patho: herpes zoster

• Caused by activation of varicella-zoster virus

• Incidence increases with age

• Potentially contagious to anyone who hasn’t had varicella or who is immunosuppressed

Clinical manifestations: herpes zoster

• Linear distribution along a dermatome of grouped vesicles + pustules on reddened base

• Usually unilateral on the trunk, face, and lumbosacral areas

• Burning, pain, and neuralgia preceding outbreak

• Mild/severe pain during outbreak

Treatment: herpes zoster

• Topical

  • Wet compresses

  • Silver sulfadiazine to ruptured vesicles

• Systemic

  • Antivirals within 72 hours of onset to prevent postherpetic neuralgia

  • Analgesia; mild sedation at bedtime

  • Gabapentin to treat postherpetic neuralgia

  • Usually heals without complications, but scarring + postherpetic neuralgia is possible

  • Vaccination to prevent shingles; one-time dose for adults 60+

Etiology + patho: scabies

• Caused by sarcoptes scabiei

• Mite penetrates stratum corneum + deposits eggs

• Allergic reaction to eggs, feces, and mite parts can occur

• Transmission occurs by direct physical contact, sometimes through shared personal items

• Rarely seen in dark-skinned people

Clinical manifestations: scabies

• Severe itching, especially at night, usually not on the face

• Presence of burrows, especially on interdigital webs, flexor surface of wrists, genitalia, and anterior axillary folds

• Red papules (may be crusted)

• Possible vesiculation

• Interdigital web crusting

Treatment: scabies

• 5% permethrin topical lotion; 1 overnight application with second application one week later

• Treat all family members + environment with plastic covering for 5 days

• Launder all clothes + linen with bleach

• Treat sexual partner

• Antibiotics, if secondary infections are present

• Possible residual itching up to 4 weeks after treatment

• Recurrence is possible if not adequately treated

Etiology + patho: candidiasis

• Caused by candida albicans

• Aka moniliasis

• 50% of adults are symptom-free carriers

• Appears in warm, moist areas (groin, mouth, submammary folds

• Immunosuppression allows yeast to become pathogenic

Clinical manifestations: candidiasis

• Mouth

  • White + cheesy plaque that resembles milk curds

• Vagina

  • Vaginitis + red, edematous, and painful vaginal wall

  • White patches

  • Vaginal discharge

  • Itching

  • Pain with urination/sex

• Skin

  • Diffuse, popular, red rash with pinpoint satellite lesions around edges of affected area

Treatment: candidiasis

• Azole antifungals or other specific medication (vaginal suppository or oral lozenge)

• Sexual abstinence or condom usage

• Skin hygiene to keep areas clean + dry

• Powder is effective on nonmucosal surfaces of skin to prevent recurrence

Etiology + patho: allergic contact dermatitis

• Type IV delayed hypersensitivity

• Absorbed agent acts an an antigen

• Sensitization occurs after 1+ exposures

• Lesions appear 2-7 days after allergen exposure

Clinical manifestations: allergic contact dermatitis

• Red papules + plaques

• Sharply circumscribed with occasional vesicles

• Itching

• Area of dermatitis often takes shape of the causative agent

Treatment: allergic contact dermatitis

• Topical/oral corticosteroids

• Antihistamines

• Skin lubrication

• Elimination of contact allergen

• Avoidance of irritating affected area

• Systemic corticosteroids if sensitivity severe

Clinical manifestations: leukemia

• Vary, but are usually related to:

  • Anemia

    • Fatigue

    • Shortness of breath

    • Pallor

    • Tachycardia

    • Systolic murmurs

  • Thrombocytopenia

    • Increased bleeding risk

    • Petechiae

    • Ecchymoses

    • Bleeding

  • Leukopenia

    • Increased infection risk

    • Fever

    • Lymphadenopathy

• Related to leukemic cells that infiltrate patient organs:

  • Splenomegaly

  • Hepatomegaly

  • Lymphadenopathy

  • Bone pain

  • Meningeal irritation

  • Oral lesions

Diagnostic studies: leukemia

• Diagnosis + classification

  • Peripheral blood evaluation

  • Bone marrow exams

• Determines presence of leukemic cells outside of blood + bone marrow

  • PET/CT scans

  • Lumbar puncture

Interprofessional care: leukemia

• Initial goal is to attain remission

• Combo chemo is the standard treatment

• Chemo stages

  • Induction

    • Induces remission by destroying all leukemic cells

    • Patients can become critically ill (neutropenia, thrombocytopenia, anemia)

  • Postinduction/postremission

    • Started after remission is achieved

  • Maintenance

    • Goal is to keep the body free of leukemic cells

• Corticosteroids

• Radiation therapy

• Immunotherapy/targeted therapy

• Bone marrow transplantation

  • Eliminates all leukemic cells using combos of chemo with/without total body irradation

  • Sources of bone marrow

    • Bone marrow

    • Peripheral blood

    • Umbilical cord blood

Nursing management: leukemia

• Obtain health history

  • Exposure to toxin

  • Chromosome abnormalities

  • Frequent infections

• Routine assessment

• Monitor:

  • Lab results

  • Chemo side effects

  • Bleeding

• Implement neutropenic precautions

• Address psychological needs; anxiety, fear, and depression are common

• Provide patient education

  • Medication management

    • Side effects are usually temporary

  • Infection prevention

    • Emphasize hand hygiene

  • Neutropenic precautions

    • Avoid uncooked foods (raw meat, fresh fruits/veggies)

  • Bleeding precautions

  • Set realistic treatment goals

Complications: leukemia

• Infection

• Sepsis

• Treatment failure (relapse)

• Treatment-related death

Clinical manifestations: lymphoma

• Onset is usually gradual

• Enlargement of cervical, axillary, or inguinal lymph nodes

  • Subsequent lymph node involvement is generally by spread to adjacent lymph nodes

  • Nodes are movable + nontender

    • Enlarged nodes aren’t painful unless they exert pressure on adjacent nerves

• Weight loss

• Fatigue

• Weakness

• Fever

• Chills

• Tachycardia

• Night sweats

• B symptoms; correlate with a worse prognosis

  • Fever

  • Drenching night sweats

  • Weight loss (>10% in 6 months)

• Rapid onset of pain at disease site, with alcohol ingestion

• Generalized itching without skin lesions

• Occur with mediastinal node involvement

  • Cough

  • Dyspnea

  • Stridor

  • Dysphagia

• Advanced disease

  • Hepatomegaly

  • Splenomegaly

• Anemia

Diagnostic studies: lymphoma

• Peripheral blood studies

  • Increased sedimentation rate

  • Hypercalcemia

  • Hypoalbuminemia

• Lymph node biopsy

  • Reed-Sternberg cell = Hodgkin lymphoma

• Bone marrow examination

• Radiologic studies

  • Help define all sites and determine the clinical stage of disease

• PETs/CTs

  • Disease staging

  • Assessment of therapeutic response

  • Distinguishment of residual tumor form fibrotic masses after treatment

Interprofessional care: lymphoma

• Treatments

  • Chemo

  • Biotherapy

  • Radiation therapy

  • Phototherapy

  • Topical therapy

• Treatment is guided by disease staging

• Stem cell transplants can be done

Nursing management: lymphoma

• Nursing care focuses on managing problems related to the disease, pancytopenia, and other side effects of therapy

  • Supporting patients though the consequences of treatment is important

  • Address physical + spiritual consequences

  • Reassure patients that infertility issues are addressed soon after diagnosis

Complications: lymphoma

• Infection

• Sepsis

• Treatment failure (relapse)

• Increased risk for secondary cancer later in life

• Treatment-related death

Clinical manifestations: multiple myeloma

• Often don’t appear until disease is advanced

• Skeletal pain

  • In pelvis, spine, or ribs

  • Triggered by movement

• Diffuse osteoporosis develops as the myeloma protein destroys bone

• Osteolytic lesions occur in the skull, vertebrae, long bones, and ribs

• Vertebral destruction → vertebral collapse of vertebrae with spinal cord compression

• Loss of bone integrity → pathologic fractures

• Bony degeneration → calcium loss form bones → hypercalcemia

  • Can cause renal, GI, or neurologic problems (polyuria, anorexia, confusion, and heart problems)

• Serum hyperviscosity syndrome leads to cerebral, lung, renal, and other organ dysfunction can occur

• High protein levels → renal tubular obstruction, interstitial nephritis, and renal failure

• Anemia

• Thrombocytopenia

• Neutropenia

• Immune dysfunction from replacement of normal bone marrow with plasma cells

• Neurologic problems → regional myeloma cell growth compression the spinal cord/cranial nerves or by perineuronal or perivascular deposition of the abnormal protein

Diagnostic studies: multiple myeloma

• Lab studies

  • M protein presence in blood + urine

  • Pancytopenia

  • Hypercalcemia

  • Bence Jones protein in urine

  • High serum creatinine

• Radiologic tests

  • MRI

  • PET scans

  • CT scans

• Bone marrow exams

• Urinalysis

• Skeletal bone surveys, MRI, and/or PETs and CTs show distinct areas of destroyed bone, generalized thinning of bones, or fractures

• Simplest measure of staging + prognosis is based on blood levels of beta-2 microglobulin and albumin

  • Higher levels = poorer prognosis

Interprofessional care: multiple myeloma

• Treatments:

  • Corticosteroid

  • Chemo

  • Immunotherapy

  • Targeted therapy

  • Bisphosphonates

  • Bone marrow transplants

• Treatments relieve symptoms, produced remission, and prolongs life

Nursing management: multiple myeloma

• Major focus of nursing care relates to patient safety due to bone involvement and sequelae from bone breakdown

• Ambulation + adequate hydration are essential

  • Maintain output between 1.5 - 2 L/day

• Assess patient + implement pain control methods

• Assess + treat infections

• Provide psychological support

Complications: multiple myeloma

• Hypercalcemia

• Dehydration

• Fluid/electrolyte imbalance

• Renal damage

• Neuro changes (peripheral neuropathy)

Clinical manifestations: thrombocytopenia

• Many patients can be asymptomatic

• Bleeding, usually mucosal or cutaneous

  • Mucosal bleeding manifests as nosebleeds and gingival bleeds

  • Large bullous hemorrhages can appear on buccal mucosa due to lack of vessel protection by submucosal tissue

• Petechiae

  • Small, flat, red/reddish brown microhemorrhages

• Purpura

  • Occur when there’s many petechiae

• Bruising

• Internal bleeding

  • Weakness

  • Fainting

  • Dizziness

  • Tachycardia

  • Abdominal pai

  • Hypotension

Diagnostic studies: thrombocytopenia

• Patient history + assessment

• Lab studies

  • PT + aPTT can be normal, even in severe cases

    • Increases can indicate disseminated intravascular coagulation

  • Lactate dehydrogenase can be incrased

  • Platelet count <150k

    • <50k = prolonged bleeding

    • <20k = hemorrhage

• Assays

  • ITP-antigen specific

  • Platelet activation/function

  • PE4-heparin complex

• RBC morphology changes and pronounced reticulocytosis can be seen in thrombotic thrombocytopenic purpura

• Bone marrow exams can be done to assess if production problems are that cause of thrombocytopenia or when other tests are inconclusive

Interprofessional care: thrombocytopenia

• Treatments depend on cause

  • ITP

    • Corticosteroids

    • Immunoglobulins

    • Monoclonal antibodies

    • Immunosuppression

    • Splenectomy

  • TTP

    • Corticosteroids

    • Immunosuppression

    • Plasmapheresis

    • Splenectomy

  • HIT

    • Cease all admin of heparin, including flushes

    • Initiate anticoagulation (direct thrombin inhibitors)

    • Plasmapheresis

Nursing management: thrombocytopenia

• Health promo

  • Discourage use of OTC meds, especially aspirin

  • Encourage patients to seek care if manifestations of bleeding develop

  • Observe for early signs in patients on chemo

• Acute care

  • Assess for bleeding; evaluation + treatment is needed if present

  • Prevent/control hemorrhage

  • Administer platelets per orders

  • Monitor labs

    • Platelet count

    • Coagulation studies

    • Hemoglobin/hematocrit

  • If SQ injection is unavoidable, use small-gauge needles + apply direct pressure/ice packs after

  • Avoid IM injections

  • Teach patients the importance of adhering to self-care measures to reduce bleeding risk

Cardiac conduction system

SA node → AV node → bundle of His → L/R bundle branches → Purkinje fibers

How does the autonomic nervous system affect cardiac rhythm/contraction?

• SNS stimulation increases:

  • HR

  • Speed of impulse conduction through the AV node

  • Force of atrial + ventricular contractions

• PNS stimulation decreases HR by slowing impulses from the SA node + conduction through the AV node

How does electrolyte balance affect cardiac rhythm/contraction?

Imbalances (hyper/hypokalemia, hypocalcemia, and hypomagnesemia) can disrupt the cardiac conduction system and precipitate dysrhythmias

How are time, voltage, and HR measured on ECG strips?

• Small box = 0.04 sec horizontally; 0.1 mV vertically

• Large box = 0.20 sec horizontally; 0.5 mV vertically

sinus bradycardia

SA node fires <60 bpm; normal conduction pathway

Clinical associations: sinus bradycardia

• Can be normal in aerobically trained athletes and in some people during sleep

• Occurs in response to:

  • Valsalva maneuver

  • Hypothermia

  • Increased IOP

  • Vagal stimulation

  • Certain drugs (beta/calcium-channel blockers)

• Common associated diseases:

  • Hypothyroidism

  • Increased IOP

  • Inferior myocardial infarction

Clinical significance: sinus bradycardia

• Depends on how the patient tolerates it

• Manifestations:

  • Pale + cool skin

  • Hypotension

  • Weakness

  • Angina

  • Dizziness

  • Confusion

  • Shortness of breath

Interprofessional treatment: sinus bradycardia

• Hold/stop/reduce drugs, if caused by them

• Symptomatic patients receive IV atropine

  • If ineffective:

    • Transcutaneous pacing

    • Dopamine infusion

    • Epinephrine infusion

• Permanent pacemaker may be needed

sinus tachycardia

SA node firing rate is between 101-180 bpm; normal conduction

Clinical associations: sinus tachycardia

• Vagal inhibition

• Sympathetic stimulation

• Common stressors:

  • Exercise

  • Fever

  • Pain

  • Hypotension

  • Hypovolemia

  • Anemia

  • Hypoxia

  • Hypoglycemia

  • Myocardial ischemia

  • Heart failure

  • Hyperthyroidism

  • Anxiety

  • Fear

• Common affective meds:

  • Epi

  • Norepi

  • Atropine

  • Caffeine

  • Theophylline

  • Hydralazine

Clinical significance: sinus tachycardia

• Depends on patient tolerance of increased HR

• Manifestations

  • Decreased cardiac output:

    • Chest pain

    • Dizziness

    • Dyspnea

    • Hypotension

  • Increased oxygen consumption

  • Angina + increased infarction size can occur in patients with sinus tach + CAD or AMI

Interprofessional treatment: sinus tachycardia

• Underlying causes guide treatment

• Vagal maneuvers are used for clinically stable patients

• Meds that reduce HR + decrease oxygen consumption

  • Beta blockers (metoprolol)

  • Adenosine

  • Calcium channel blockers (diltiazem)

• Clinically unstable patients may need synchronized cardioversion

Clinical associations: SVT

• In normal hearts, can occur with:

  • Overexertion

  • Emotional stress

  • Deep inspiration

  • Stimulants (caffeine/tobacco)

• Rheumatic heart disease

• Digitalis toxicity

• CAD

• Cor pulmonale

Clinical significance: SVT

• Depends on associated symptoms

• Prolonged episodes + HRs >180 bpm can cause decreased cardiac output due to reduced stroke volume

• Manifestations:

  • Hypotension

  • Palpitations

  • Dyspnea

  • Angina

Interprofessional treatment: SVT

• Vagal stimulation

  • Valsalva maneuver

  • Coughing

• Drug therapy

  • IV adenosine

  • Beta/calcium channel blockers

• Patients who become hemodynamically unstable require synchronized cardioversion

Clinical associations: atrial flutter

• Rarely occurs in a healthy heart

• CAD

• Hypertension

• Mitral valve disorders

• Pulmonary embolus

• Chronic lung disease

• Cor pulmonale

• Cardiomyopathy

• Hyperthyroidism

• Meds

  • Digoxin

  • Quinidine

  • Epi

Clinical significance: atrial flutter

• High ventricular rates (>100 bpm) + loss of atrial “kick” (contraction coordinated with ventricular contraction) = decreased cardiac output

  • Can cause serious problems, such as heart failure, especially in patients with underlying heart disease

• Patients are at increased risk for stroke because thrombi can form in the atria from blood stasis

  • Patients receive warfarin/other anticoagulants to prevent stroke

Interprofessional treatment: atrial flutter

• Main goal is to slow the ventricular response by increasing AV block

  • Beta/calcium channel blockers are used

• Electrical cardioversion can convert atrial flutters to NSR in emergencies or electively

• Antidysrhythmic drugs convert atrial flutter to NSR

• Radiofrequency catheter ablation in an electrophysiology study (EPS) lab is the preferred treatment

  • Low-voltage, high-frequency electrical energy is used to ablate ectopic foci through a catheter in the right atrium, restoring NSR

Clinical associations: a-fib

• Underlying heart disease

  • CAD

  • Valvular heart disease

  • Cardiomyopathy

  • Hypertensive heart disease

  • Heart failure

  • Pericarditis

• Develops acutely with:

  • Thyrotoxicosis

  • Alcohol intoxication

  • Caffeine use

  • Electrolyte issues

  • Stress

  • After heart surgery

Clinical significance: a-fib

• Results in decreased cardiac output due to ineffective atrial contractions (loss of atrial kick) and/or rapid ventricular response

• Thrombi can form in the atria due to blood stasis

  • Embolized clots can move through arteries to the brain, causing strokes

Interprofessional treatment: a-fib

• Goals:

  • Decrease ventricular response (<100 bpm)

    • Priority

    • Meds:

      • Calcium channel blockers (diltiazem)

      • Beta blockers (metoprolol)

      • Amiodarone

        • Most commonly used for conversion to + maintenance of NSR

      • Digoxin

  • Prevent stroke

  • Convert to NSR, if possible

    • Some patients need drug/electrical conversion of a-fib to NSR

    • Electrical cardioversion can convert a-fib to NSR

    • If a patient is in a-fib for >48 hours, anticoagulation therapy with warfarin in needed for 3-4 weeks before cardioversion

      • Therapy continues for several weeks, as the procedure can dislodge clots + place the patient at risk for stroke

      • If no clots are found by transesophageal echocardiogram, anticoagulation therapy may not be needed

    • If drugs or cardioversion fail, long-term anticoagulation therapy is needed

      • Warfarin use requires monitoring for therapeutic levels (INR)

        • Alternative meds:

          • Dabigatran

          • Apixaban

          • Rivaroxaban

• For symptomatic patients refractory to drugs/cardioversion, radiofrequency catheter ablation, AV nodal ablation, and the Maze procedure are other options

Clinical associations: PVCs

• Stimulants (caffeine, alcohol, nicotine, aminophylline, epi, isoproterenol)

• Electrolyte imbalances

• Hypoxia

• Fever

• Exercise

• Emotional stress

• MI

• Mitral valve prolapse

• Heart failure

• Cardiomyopathy

• CAD

Clinical significance: PVCs

• Usually harmless in patients with normal hearts

• Indicate ventricular irritability for patients with CAD or AMI

• Can reduce cardiac output and lead to angina + heart failure for those with heart disease

  • Assess patient physiologic response

• Assess apical/radial pulse + determine the pulse deficit, as PVCs often don’t generate a sufficient ventricular contraction to result in a peripheral pulse

Interprofessional treatment: PVCs

• Relates to the underlying cause (oxygen for hypoxia, electrolyte replacement)

• Assess hemodynamic status to determine need for drug therapy

  • Drug therapy

    • Beta blockers

    • Lidocaine

    • Amiodarone

ventricular tachycardia

• Life-threatening, due to decreased cardiac output and risk for V-fib development

• 3+ premature ventricular contractions

Clinical associations: v-tach

• MI

• CAD

• Significant electrolyte imbalances

• Cardiomyopathy

• Long QT syndrome

• Drug toxicity

• CNS disorders

Clinical significance: v-tach

• Can be stable (patient has a pulse) or unstable (pulseless patient)

• Sustained v-tach causes a severe decrease in cardiac output due to decreased ventricular diastolic filling time and loss of atrial contractions

  • Results in:

    • Hypotension

    • Pulmonary edema

    • Decreased cerebral blood flow

    • Cardiopulmonary arrest

• Must be treated quickly, even with brief occurrences

  • Episodes can recur is prophylactic treatment isn’t started + v-fib can develop

Interprofessional treatment: v-tach

• Precipitating causes must be IDed and treated

• IV procainamide, lidocaine, or amiodarone is given if v-tach is monomorphic and the patient is clinically stable with preserved left ventricular function

  • Can also be given if polymorphic with a normal baseline QT interval

• IV magnesium, isoproterenol, phenytoin, or antitachycardia pacing is given for polymorphic v-tach with a prolonged baseline QT interval

  • Drugs that prolong QT interval should be stopped

  • Cardioversion is used if drug therapy fails

• Pulseless v-tach is lethal, and treated the same as v-fib (CPR + rapid defibrillation → vasopressor + antidysrhythmic admin if unsuccessful)

Clinical associations: v-fib

• AMI

• Myocardial ischemia

• Chronic diseases (heart failure; cardiomyopathy)

• Can occur during cardiac pacing or cardiac catheterization procedures due to catheter stimulation of the ventricle

• Can happen with coronary reperfusion after thrombolytic therapy

• Other causes:

  • Electric shock

  • Hyperkalemia

  • Hypoxemia

  • Acidosis

  • Drug toxicity

Clinical significance: v-fib

• Results in an unresponsive, pulseless, and apneic state

• Deadly if not treated immediately

Interprofessional treatment: v-fib

Immediate CPR + ACLS + defibrillation + definitive drug therapy

Paced rhythms

• Types

  • Temporary

  • External

  • Permanent

  • Internal

• Electrical stimulation to the myocardium that leads to cardiac contraction and adequate perfusion

• Pacemaker impulse can be atrial and/or ventricular; (dual-paced, if both)

• Observable on ECG tracings as “pacer spikes”

Etiology + patho: acute coronary syndrome

• Develops when chest pain from ischemia is prolonged + not immediately reversed

• Includes the spectrum of unstable angina, NSTEMI, and STEMI

• ST elevation represents myocardial injury that’s potentially reversible, but can progress to permanent necrosis of myocardium if not

Diagnostic studies: acute coronary syndrome/MI

• ECGs

  • Changes in the QRS complex, ST segment, and T wave caused by injury, ischemia, and infarction can develop slowly or quickly

• Serum cardiac biomarkers

  • Helps distinguish between unstable angina (negative) and NSTEMI (positive)

  • High-sensitivity cardiac troponin test (hs-cTn) provides more rapid detection of MI compared to conventional cardiac-specific troponin assays, allowing for quicker diagnosis

• Cardiac catheterization

  • Patients with STEMI must undergo catheterization in 90 minutes of ED presentation or receive thrombolytic therapy in 30 minutes in agencies without PCI capability

  • Patients with unstable angina or NSTEMI usually undergo catheterization during hospitalization to diagnose + evaluate disease extent; need isn’t emergent

Interprofessional care: acute coronary syndrome/MI

• Percutaneous coronary intervention (PCI)

  • First line treatment for confirmed STEMI

  • Goal is to open blocked artery in 90 minutes to limit infarction size

• Thrombolytic therapy

  • Indicated only for patients with a STEMI in facilities that don’t have cath labs/cath lab is too far for fast transport

  • Aims to limit infarction size by dissolving thrombus in coronary artery to reperfuse heart muscle

• Drug therapy

  • IV nitroglycerin

    • Initial treatment

    • SL admin can be used until IV prep is ready

      • Give once every 5 mins

    • Goal is to reduce angina pain + improve coronary blood flow

    • Decreases pre/afterload while increase heart myocardial oxygen supply

  • Morphine

    • Preferred choice for chest pain that’s unrelieved by nitroglycerin

    • Decreases cardiac workload by lowering myocardial oxygen consumption, reducing contractility, and decreasing BP + HR

  • Beta blockers

    • Decrease myocardial oxygen demand by reducing HR, BP, and contractility

    • Given to patients who aren’t at risk for complications of MI (cardiogenic shock, bradycardia, hypotension)

  • ACE inhibitors + angiotensin receptor blockers

    • Should be started in the first 24 hours if BP is stable and there aren’t any contraindications

    • Angiotensin receptor blockers are used if patients can’t tolerate ACE inhibitors

  • Antidysrhythmics

  • Antihyperlipidemics

  • Stool softeners

    • Prevent straining and resultant vagal stimulation from the Valsalva maneuver

      • Stimulation produces bradycardia + can provoke dysrhythmias

• Nutrition therapy

  • Patients can be NPO except for water until stable

  • Advance diet as tolerated to a low salt + sat-fat + cholesterol diet

Nursing management: acute coronary syndrome/MI

• Monitor vitals + pulse ox (every hour) during first few hours after admit to ICU/telemetry unit and closely thereafter, according to agency protocol

• Obtain 12-lead ECG + draw serial cardiac biomarkers

• Maintain bed rest according to agency policy and gradually increase activity unless contraindicated

• For patients with unstable angina + NSTEMI, heparin is used to prevent microemboli from forming + causing further chest pain

• For patients with STEMI, reperfusion therapy (PCI, thrombolytics) starts as soon as possible

• Manage pain as with nitroglycerin, morphine, or supplemental oxygen

• Maintain continuous ECG monitoring

• Asses for signs/symptoms of early heart failure

• Monitor I/O

• Promote rest + comfort for patients with any degree of heart damage; slowly increase physical activity

• Assist in recognizing + reducing anxiety

• Provide psychological support

• Provide patient education

Etiology + patho: MI

• Occurs due to an abrupt stoppage of blood flow through a coronary artery with a thrombus caused by platelet aggregation

• STEMI - Caused by occlusive thrombi + result in ST elevation in ECG leads facing the area of infarction

• NSTEMI - Caused by nonocclusive thrombi + don’t cause ST elevations

Clinical manifestations: acute coronary syndrome/MI

• Pain/discomfort

  • Chest pain is often worse than with previous episodes of angina

  • Persistent + unlike other pains; described as a heavy, pressure, tight, burning, constricted, or crushing feeling

  • Can radiate to neck, lower jaw, arms, or back

  • Can occur with exertion or rest

  • Often occurs in the early morning hours

  • Usually lasts 20+ minutes

• SNS stimulation

  • Diaphoresis

  • Increased HR + BP

  • Vasoconstriction of peripheral blood vessels → ashen, clammy + cool skin

• Cardiovascular manifestations

  • Increased HR + BP, due to catecholamine release

  • Crackles

  • Jugular vein distention

  • Hepatomegaly

  • Peripheral edema

• Abnormally distant heart sounds

• N/V

• Fever

• Weakness/fatigue

• Indigestion

• Shortness of breath

• Older patients can experience:

  • Changes in mental status (confusion)

  • Shortness of breath

  • Pulmonary edema

  • Dizziness

  • Dysrhythmias

Etiology + patho: infective endocarditis

• Occurs when blood flow allows organisms to contact + infect previously damaged heart valves or other endothelial surfaces

• Most cases are caused by staph

• Risk factors

  • History of infective endocarditis

  • IV drug use

  • Having a prosthetic valve

  • Nosocomial infection from intravascular device use

  • Renal dialysis

Clinical manifestations: infective endocarditis

• Nonspecific + involve multiple organ systems

• Fever

  • Can be low grade or absent in older adults or those who are immunocompromised

• Chills

• Weakness

• Malaise

• Fatigue

• Anorexia

• Vascular signs

  • Splinter hemorrhages (black longitudinal streaks) in nail beds

  • Petechiae on conjunctivae, lips, buccal mucosa, palate, ankles, feet, antecubital, and popliteal areas

  • Osler’s nodes (painful, tender, red/purple, pea-sized lesions) on fingertips/toes

  • Janeway’s lesions (flat, painless, small, red spots) on fingertips, palms, soles, and toes

  • Roth’s spots (hemorrhagic retinal lesions)

• New/worsening systolic murmur

  • Usually absent in tricuspid endocarditis because right-sided heart sounds are too low to hear

• Heart failure

Diagnostic studies: infective endocarditis

• Health history

  • Ask patients if they’ve recently (in the last 3-6 months) had:

    • Dental procedures

    • Urologic procedures

    • Surgery

    • Gynecologic procedures, including childbirth

  • Note history of:

    • IV drug abuse

    • Heart disease

    • Infections

    • Heart catheterization

    • Heart surgery

    • Intravascular device placement

    • Renal dialysis

• Blood cultures, drawn on a period of 1 hours form 3 different venipuncture sites

• Echocardiography can show vegetations

Interprofessional care: infective endocarditis

• Antibiotic prophylaxis

• Drug therapy

  • Long-term treatment is needed to kill dormant bacteria in valvular vegetations

  • Complete removal of organisms takes weeks; relapses are common

  • Antibiotic therapy is based on blood culture results

• Valve replacement surgery is done in most cases

  • Surgical indications:

    • Valve dysfunction → heart failure

    • Emboli prevention

    • Uncontrolled infection

• Fevers that persist after treatment is managed with:

  • Aspirin

  • Acetaminophen

  • Fluids

  • Rest

Nursing management: infective endocarditis

• Assess:

  • Vitals

  • Heart sounds

  • Joint/muscle tenderness

  • Decreased ROM

  • Petechiae

  • Splinter hemorrhages

  • Osler’s nodes

  • General systems assessment, for hemodynamic or embolic complications

• Health promo

  • Tell patients to avoid people with infection, especially upper respiratory, and to report cold, flu, and cough symptoms

  • Stress importance of avoiding fatigue, planning rest periods, using good oral hygiene, and scheduling regular dental visits

  • Tell patient to inform providers scheduling invasive procedures about endocarditis history; prophylactic therapy may be needed

• Ambulatory care

  • Endocarditis generally requires antibiotics treatment for 4-6 weeks

  • Assess home setting for adequate support; patients getting outpatient IV antibiotics need vigilant home nursing care

  • Inform patient + caregiver about the importance of monitoring body temps

    • Persistent elevations can indicate ineffective antibiotic

  • Teach patient + caregiver to recognize signs/symptoms of complications (stroke, pulmonary edema, heart failure; change in mental status, dyspnea, chest pain, explained weight gain)

Etiology + patho: pericarditis

• Causes

  • Infection

  • AMI

  • Cancer

  • Dissecting aortic aneurysm

  • Myxedema

  • Radiation

  • Renal failure

  • Trauma

  • Dressler syndrome

  • Drug reactions

• Types

  • Acute

    • Develops rapidly, causing the pericardial sac to become inflamed + leak fluid (pericardial effusion)

    • Inflammation is the characteristic finding

  • Subacute

    • Occurs weeks/months after an event

  • Chronic

    • Pericarditis lasting >6 months

Clincal manifestations: pericarditis

• Progressive, severe, sharp chest pain

  • Often worse with deep inspiration and when lying flat; sitting up + leaning forward relieves it

  • Can radiate to neck, arms, or left shoulder; complicated differentiation from angina

    • One distinction is that pain can be referred to the trapezius muscle

• Dyspnea

  • Related to patient breathing in rapid, shallow breaths to avoid chest pain

  • Worsened by fever and anxiety

• Pericardial friction rub

  • Scratching, grating, high-pitched sound resulting from roughened pericardial and epicardial surfaces

  • Best heard with stethoscope at lower left sternal border of the chest with the patient leaning forward

    • Ask patient to hold their breath to distinguish from a pleural friction rub

Complications: pericarditis

• Pericardial effusion

  • Buildup of fluid in the pericardium

  • Can occur rapidly (chest trauma) or slowly (TB pericarditis)

  • Can compress nearby structures, if large

    • Pulmonary compression → cough, dyspnea, and tachypnea

    • Phrenic nerve compression → hiccups

    • Laryngeal nerve compression → hoarseness

  • Heart sounds are distant + muffled

  • BP is normal

• Cardiac tamponade

  • Develops as pericardial effusion volume increases and compresses the heart

  • Increasing compression results in:

    • Decreased cardiac output

    • Muffled heart sounds

    • Narrowed pulse pressure

    • Tachypnea

    • Tachycardia

  • Increased jugular venous pressures → neck vein distention

  • pulsus paradoxus - Large decrease in systolic BP during inspiration

Diagnostic studies: pericarditis

• ECGs

  • Diffuse ST segment elevations

  • Don’t show evolving changes like those in MI

• Echocardiogram

  • Determines presence of pericardial effusion or cardiac tamponade

• Doppler imaging + color M-mode

  • Assesses diastolic function

  • Diagnoses constrictive pericarditis

• CT/MRI

  • Visualize pericardium and pericardial space

• X-ray

  • Usually normal, but large pericardial effusion can appear as cardiomegaly

• Lab findings

  • Leukocytosis

  • Increased CRP + ESR

  • Increased troponin levels, which can indicate concurrent heart damage

• Fluid obtained from pericardiocentesis or tissue from a pericardial biopsy can determine cause

Interprofessional care: pericarditis

• Management is aimed at IDing + treating underlying problem and symptoms

• Antibiotics are used to treat pericarditis

• NSAIDs are used for pain + inflammation

• Corticosteroids are used for

  • Patients whose lupus caused pericarditis

  • Patients already taking them for autoimmune conditions

  • Patients who don’t respond to NSAIDs

• Aspirin is recommended for treatment after ST elevation

• Colchicine can help patients with pericarditis present for >10 days or who have recurrent pericarditis

Nursing management: pericarditis

• Manage patient pain + anxiety

  • Assess pain to distinguish from angina

    • Pain is usually found in the precordium or left trapezius region, is sharp, increases with inspiration + lying flat, and is relieved by sitting up + leaning forward

  • Keep patient on bed rest with head of bed raised to 45 degrees; provide overbed table for support

  • Antiinflammatories control pain

    • Give with food or milk

    • Tell patient to avoid alcohol due to GI bleed risk

  • PPIs can reduce stomach acid

  • Provide simple + complete explanation of procedures and possible causes of pain to reduce anxiety

• Monitor for signs of tamponade + prep for possible pericardiocentesis

Etiology + patho: DVT

• Localized platelet aggregation and fibrin entrap RBCs, WBCs, and more platelets to form a thrombus

• Frequent thrombus formation site is the vein’s valve cusp, where stasis occurs

• If thrombi only partially block veins, endothelial cells cover it and stop the thrombotic process

  • If they don’t detach, it undergoes lysis or become firmly organized and adherent in 5-7 days

• Causes

  • Virchow’s triad

    • Venous stasis

    • Endothelial damage

    • Hypercoagulability

Clinical manifestations: DVT

• Unilateral leg edema

• Pain

• Tenderness with palpation

• Dilated superficial veins

• Sense of fullness in the thigh/calf

• Paresthesia

• Warm skin

• Redness

• Fever

• Bilateral edema + cyanosis of legs (inferior vena cava involvement)

Diagnostic studies: DVT

• Lab studies

  • Activated clotting time

  • aPTT

  • INR

  • Bleeding time

  • Hemoglobin/hematocrit

  • D-dimer

  • Fibrin monomer complex

• Noninvasive venous studies

  • Duplex ultrasound

  • Venous compression ultrasound

• Invasive venous studies

  • CTV(enography)

  • Contrast venography

  • MRV(enography)

Interprofessional care: DVT

• Prevention

  • Early + aggressive ambulation is the easiest + most cost-effective method to reduce VTE risk

  • Patients on bed rest should be turned every 2 hours

  • Teach patients to flex + extend feet, knees and hips at least every 2-4 hours when awake

  • Patients (who can) should be out of bed + in a chair for meals and walk at least 4-6 times/day

  • TED hoses

    • Proper stocking use

      • Toe hole is under toes

      • Heel patch is over the heel

      • Thigh gusset is on the inner thigh

      • No wrinkles

      • Don’t roll down/cut/alter

    • Not recommended if VTE is already present

  • SCD

    • Can be used with TED hoses

    • Ensure correct fit by accurately measuring extremities

    • Ineffective if:

      • Applied incorrectly

      • Fit incorrectly

      • Inconsistently used

    • Can be removed for bathing, skin assessment, and ambulation

    • Not recommended if VTE is already present

• Drug therapy

  • Warfarin

    • Therapeutic effects monitored via INR measurements

    • Do not give with antiplatelets or NSAIDs; increased bleeding risk

    • Diets that vary in vitamin K intake can complicate achievement of target INR levels

  • Heparin

    • Can be given SQ for prevention or IV for treatment

      • IV use required monitoring of clotting status by measuring aPTT

    • Heparin induced thrombocytopenia (HIT) is a serious side effect

      • Diagnosed by measuring presence of heparin antibodies in blood

      • Treated by cessation of heparin therapy

    • LMWHs are less likely to cause HIT and osteoporosis

      • Usually don’t require ongoing anticoagulant monitoring/dose adjustment

      • Reversed by protamine

• Surigcal/interventional radiology

  • Surgeries:

    • Open venous thrombectomy

    • Inferior vena cava interruption

  • Percutaneous endovascular interventional radiology procedures can be used with catheter-directed thrombolytic therapy, especially for severely symptomatic patients with iliocaval/iliofemoral obstruction