Adult Complex: Exam 1

Etiology + patho: DIC

• Abnormal response to normal clotting cascade

• de stimulated by a disease process/disorder

• Chronic/subacute disease is most often seen in patients with long-standing illnesses

• Fibrin split products inhibit normal blood clotting by

  • Coating platelets + interfering with platelet function

  • Interfering with thrombin → disrupting coagulation

  • Attaching to fibrinogen → interfering with processes needed to form stable clots

Risk factors: acute DIC

• Acute leukemia

• Metastatic solid tumors

• Acute hemolysis from infection/immunologic disorders

• Mismatched blood transfusion

• Abruptio placentae

• Amniotic fluid embolism

• HELLP syndrome

• Septic abortion/pregnancy

• Shock (anaphylactic, cardiogenic, hemorrhagic)

• Acute anoxia

• Extensive burns/trauma

• Heatstroke

• Hepatitis

• Postop tissue damage

• Prosthetic devices

• Severe head trauma

• Snake bites

• Transplant rejections

• Vascular disorders

Risk factors: subacute DIC

• Metastatic cancer

• Myeloproliferative/lymphoproliferative cancers

• Retain dead fetuses

Risk factors: chronic DIC

• Cancer

• Liver disease

• Lupus

Clinical manifestations: DIC

• Bleeding

  • Pallor

  • Petechiae

  • Purpura

  • Oozing blood

  • Venipuncture site bleeding

  • Hematoma

  • Occult bleeding

  • Tachypnea

  • Hemoptysis

  • Tachycardia

  • Hypotension

  • GI bleeds

  • Abdominal distention

  • Bloody stools

  • Hematuria

  • Vision changes

  • Dizziness

  • Headache

  • Mental status change

  • Bone/joint pain

• Thrombotic

  • Cyanosis

  • Ischemic tissue necrosis

  • Hemorrhagic necrosis

  • Tachypnea

  • Dyspnea

  • Pulmonary emboli

  • ECG changes

  • Venous distention

  • Abdominal pain

  • Paralytic ileus

  • Kidney damage + oliguria → failure

  • Delirium

  • Coma

Diagnostic findings: DIC

• Prolonged

  • PT

  • PTT

  • aPTT

  • Thrombin time

• Decreased

  • Fibrinogen

  • Platelets

  • Antithrombin III (AT III)

  • Factor assays (may be misleading; factors V + VIII increased with inflammation)

  • Plasminogen + tissue plasminogen activator

  • Proteins C + S

• Increased

  • D-dimers

  • Fibrin split products

• Schistocytes present on peripheral blood smear

Interprofessional care: DIC

• It’s essential to diagnose, stabilize, treat underlying causative disease/problem, and control ongoing thrombosis and bleeding quickly

• If chronic disease is diagnosed in patients who aren’t bleeding, no treatment is needed

  • Treatment of underlying disease may be enough to reverse disease

• When patients are bleeding, therapy is directed toward providing support with needed blood products while treating primary disorder

• Blood products are given cautiously based on specific component deficiencies to patients with serious bleeding, are high risk for bleeding, or need invasive procedures

• Blood products support (platelets, cryoprecipitate, fresh frozen plasma) is usually reserved for patients with life-threatening bleeding

  • Cryoprecipitate replaces factor VIII + fibrinogen; can be given if fibrinogen is low and there’s potentially dangerous/active bleeding

  • Fresh frozen plasma is only given to patients with significant bleeding + prolonged PT + aPTT; replaces all clotting factors except platelets and is a source of antithrombin

• Patients with thrombosis are often treated by anticoagulation with heparin or low-molecular-weight heparin

  • It’s used to treat DIC when benefits (reduced clotting) outweigh risk (further bleeding)

• AT III can be useful in severe DIC, though it increases bleeding risk

• Chronic DIC is controlled with long-term heparin use

Nursing care: DIC

• Be alert to disease development, especially when risk factors are present

• Early detection of bleeding + clotting is a primary goal

• Assess for signs of external/internal bleeding and signs that microthrombi may be causing clinically significant organ damage

• Underlying causes must be managed while providing supportive car

• Minimize tissue damage + protect patients from bleeding sources

• Prompt admin of prescribed therapies is crucial; give blood products + meds correctly

Common issues for ICU patients + families

• Fear + anxiety

• Pain

• Impaired communication

• Sleep

• Sensory/perceptual problems

• Need for spiritual assistance

• Need for simple + honest knowledge on condition progress/care plan

• Need for consistency of care

• Setting of unrealistic needs/expectations

• Confusion on needs for various ICU equipment

• Family feelings of helplessness/uselessness

• Need for privacy

Etiology + patho: hypovolemic shock

• Occurs from inadequate fluid volume in the intravascular space to support adequate perfusion

• Types

  • Absolute - Fluid loss via hemorrhage, GI loss, fistula drainage, diabetes insipidus, or diuresis

  • Relative - Fluid volume movement from vascular → extravascular space; third spacing

    • Fluid shifts (burns, ascites)

    • Internal bleeding

    • Mass vasodilation (sepsis)

    • Blood/fluid pooling (GI obstruction)

Clinical manifestations: hypovolemic shock

• Tachycardia

• Decreased:

  • Preload

  • Cardiac output

  • Central venous pressure

  • Pulmonary artery wedge pressure

  • Cap refill

  • Cerebral perfusion → anxiety, confusion, agitation

  • Urine output

• Increased systemic vascular resistance

• Absent bowel sounds

• Tachypnea → bradypnea (late sign)

• Pallor + cool, clammy skin

Etiology + patho: cardiogenic shock

• Occurs when either systolic/diastolic dysfunction of the heart’s pumping results in reduced cardiac output, stroke volume, and BP

• Causes

  • Diastolic dysfunction

  • Dysrhythmias

  • Structural factors

  • Systolic dysfunction

Clinical manifestations: cardiogenic shock

• Tachycardia

• Hypotension

• Narrow pulse pressure

• Increased systemic vascular resistance → increased oxygen consumption

• Tachypnea

• Crackles, from pulmonary congestion

• Increases in:

  • Pulmonary artery wedge pressure

  • Stroke volume variation

  • Pulmonary vascular resistance

• Peripheral hypoperfusion

  • Cyanosis

  • Pallor

  • Weak peripheral pulses

  • Cool + clammy skin

  • Delayed cap refill

• Decreased renal blood flow → sodium + water retention and decreased urine output

• Impaired cerebral perfusion → anxiety, confusion, agitation

Etiology + patho: obstructive shock

• Develops when a physical obstruction to blood flow occurs with a decreased cardiac output

• Causes

  • Right ventricular compression → restricted diastolic filling

    • Cardiac tamponade

    • Tension pneumothorax

    • Superior vena cava syndrome

  • Abdominal compartment syndrome

  • Pulmonary embolism

  • Right ventricular emboli

Clinical manifestations: obstructive shock

• Tachycardia

• Hypotension

• Decreased:

  • Preload + cardiac output

  • Bowel sounds (may be absent)

  • Cerebral perfusion → anxiety, confusion, agitation

  • Urine output

• Increased systemic vascular resistance + central venous pressure

• Tachypnea → bradypnea (late)

• Shortness of breath

• Pallor + cool, clammy skin

Etiology + patho: neurogenic shock

• Hemodynamic phenomenon that can occur in 30 mins of a spinal cord injury, and lasts up to 6 weeks

• When related to spinal cord injuries, is usually associated with a cervical/high thoracic injury

  • Injuries result in mass vasodilation without compensation due to loss of sympathetic nervous vasoconstrictor tone; results in blood pooling, tissue hypoperfusion, and impaired cell metabolism

Clinical manifestations: neurogenic shock

• Hypotension

• Bradycardia

• Inability to regulate body temp → heat loss

• Warm skin that cools due to heat dispersal after mass vasodilation → hypothermia

  • Skin feel is determined by ambient temp (poikilothermia)

• Dry skin

Etiology + patho: anaphylactic shock

• Acute, life-threatening hypersensitivity reaction to a sensitizing substance

• Reactions cause mass vasodilation, release vasoactive mediators, and increase capillary permeability

• Can lead to respiratory distress due to laryngeal edema/severe bronchospasm + circulatory failure from mass vasodilation

Clinical manifestations: anaphylactic shock

• Dizziness

• Chest pain

• Incontinence

• Lip/tongue swelling

• Angioedema

• Wheezing

• Stridor

• Flushing

• Pruritus

• Urticaria

• Anxiety

• Sense of impending doom

• Abdominal pain

• Cramping

• N/V/D

• Decreased LOC

Etiology + patho: septic shock

• sepsis - Life-threatening syndrome in response to infection; characterized by a dysregulated patient response with new organ dysfunction related to the infection

• Septic shock is a subset of sepsis; characterized by persistent hypotension despite adequate fluid resuscitation, and inadequate tissue perfusion that results in tissue hypoxia

• Mainly caused by bacteria, but can be caused by parasites, fungi, and viruses

Clinical manifestations: septic shock

• Tachycardia

• Hyper/hypothermia

• Myocardial dysfunction

• Biventricular dilation

• Decreased ejection fraction

• GI bleeding

• Paralytic ileus

• Altered LOC

• Agitation

• Coma (late)

• Decreased urine output

• Hyperventilation

• Crackles

• Respiratory alkalosis → acidosis

  • Patients hyperventilate initially to compensate until they can’t

• Hypoxemia

• Respiratory failure

• ARDS

• Pulmonary hypertension

• Warm + flushed skin → cool + mottled (late)

Interprofessional care: hypovolemic shock

• Provide supplemental oxygen

• Monitor ScvO2 or SvO2

• Rapid fluid replacement with 2 large bore peripheral IVs, intraosseous access, or central line

  • Initial resuscitation is calculated with the 3:1 rule (3 mL isotonic crystalloids for every 1 mL estimated fluid loss)

• Restore blood volume

• End points of fluid resuscitations

  • Central venous pressure: 15 mmHg

  • Pulmonary artery wedge pressure: 10-12 mmHg

• Correct causes

• Use warmed IV fluids, including blood products

Interprofessional care: cardiogenic shock

• Provide supplemental oxygen

• Intubate + establish mechanical ventilation, if needed

• Monitor ScvO2 or SvO2

• Restore blood flow with angioplasty + stenting, or emergent coronary revascularization

  • Until complete, support hearts to optimize stroke volume + cardiac output

• Reduce heart workload with circulatory assist devices (IABP, VAD)

• Drugs

  • Nitrates

  • Inotropes

  • Diuretics

  • Beta-blockers (contraindicated with reduced ejection fraction)

• Treat dysrhythmias

Interprofessional care: obstructive shock

• Maintain patent airway

• Provide supplemental oxygen

• Intubate + mechanically ventilate, if needed

• Treat cause of obstruction

• Fluid resuscitation, to provide temporary improvement in cardiac output + BP

• Treat obstruction cause

  • Mechanical decompression via tube/needle insertion treats

    • Pericardial tamponade

    • Tension pneumothorax

    • Hemopneumothorax

  • Pulmonary emboli are treated via anticoagulants, thrombolytics, or pulmonary embolectomy

  • Superior vena cava syndrome is treated via radiation, debulking, or mass/cause removal

  • Decompressive laparotomies are done for abdominal compartment syndrome for those with high intraabdominal pressures + hemodynamic instability

Interprofessional care: neurogenic shock

• Maintain patent airway

• Provide supplemental oxygen

• Intubate + mechanically ventilate, if needed

• Give fluids carefully; hypotension is unrelated to fluid loss

• Drugs

  • Vasopressors (phenylephrine)

  • Atropine (for bradycardia)

• Minimize spinal core trauma with stabilization

• Monitor temps

Interprofessional care: anaphylactic shock

• Maintain patent airway

• Provide supplemental oxygen

• Intubate + mechanically ventilate, if needed

• Aggressive fluid resuscitation with crystalloids

• Drugs

  • Epinephrine

  • Antihistamines

  • Histamine receptor blockers

  • Bronchodilators

  • Corticosteroids

• ID + remove offending cause

• Prevent via avoidance of known allergens

• Premedicate with history of prior sensitivity

Interprofessional care: septic shock

• Provide supplemental oxygen

• Intubate + mechanically ventilate, if needed

• Monitor ScvO2/SvO2

• Aggressive fluid resuscitation (30 mL/kg of crystalloids repeated if hemodynamic improvement occurs)

  • End points based on focused physical assessment and any 2 of:

    • ScvO2 >70

    • SvO2 >65

    • Central venous pressure: 8-12 mmHg

    • Cardiovascular ultrasound

    • Fluid responsiveness with passive leg raise/fluid challenge

• Drugs

  • Antibiotics

    • Broad-spectrum should be started in the first hour of sepsis/septic shock

    • Obtain cultures before, but do not wait for results in the first hour

  • Vasopressors (norepi; vasopressin addition for those refractory to initial treatment)

  • Inotropes (dobutamine)

    • Can offset the decrease in stroke volume + increase tissue perfusion

  • IV corticosteroids, for those who can’t maintain an adequate BP despite vasopressors and fluid resuscitation

  • Anticoagulants

• Monitor temps

• Control blood glucose

  • Should be maintained below 180 mg/dL

• Provide prophylaxis for stress ulcers + VTE

Nursing care: shock

• Neuro status

  • Assess q1-2h; best indicator of cerebral blood flow

  • Watch for manifestations of neuro involvement; note + report any subtle changes in mental status

  • Orient patients to person, place, time, and events on a regular basis

    • Reduce noise + lights to control sensory input

    • Keep day-night cycles of activity, and rest as much as possible

• Cardiac status

  • If unstable, continuously assess HR, rhythm, BP, central venous pressure, and pulmonary artery pressures

  • Continuously monitor ECGs

  • Assess heart sounds for S3/4 sounds or new murmurs

    • S3 = heart failure

  • Monitor skin for adequate perfusion; temp, color and/or moisture changes reflect hypoperfusion

  • Give meds as ordered

  • Assess patient reponse to fluid + drug admin as often as q5-10mins; adjust as needed

    • Decreased frequency as perfusion improves + patient stabilizes

• Respiratory status

  • Assess often to ensure adequate oxygenation, find complications, and provide data on acid-base status

  • Monitor rate, depth, and rhythms as often as q15-30mins

  • Assess breath sounds q1-2h + prn for changes indicative of fluid overload/secretion accumulation

  • Continuously monitor O2 sats

    • Attach probes to the ear, nose, or forehead; poor peripheral circulation renders finger reads unreliable

  • Assess ABGs

• Renal status

  • Initially, measure urine output q1-2h

  • Output <0.5 mL/kg/hr can indicate inadequate renal perfusion

  • Use trends in serum creatinine values to assess function

• Body temp

  • Monitor q4h if normal; if not, assess hourly

  • Use light covers + control room temps to keep patients comfortably warm

  • If temps exceed 101.5 F + patients are uncomfy/show signs of cardiac compromise, treat fevers with antipyretics + remove blankets

• GI status

  • Assess bowel sounds q4h

  • Monitor for abdominal distention

  • If NG tubes are placed, measure drainage + check for occult blood

  • Check all stools for occult blood

• Skin integrity

  • Perform bathing/other nursing measures carefully

  • Use clinical judgement in determining care priorities to limit demands for increased oxygen

  • Monitor trends in oxygen use during all interventions to assess patient tolerance of activity

  • Turn patients q1-2h + maintain good body alignment

  • Perform passive ROM 3-4 times/day to maintain joint mobility + help prevent breakdown

  • Perform oral care for intubated patients

    • Brush teeth/gums with a soft toothbrush q12h

    • Swab lips + mouth with a moisturizing solution q2-4h

• Emotional support

  • Monitor patient mental state + pain level; give meds to decrease anxiety + meds as ordered/needed

  • Be aware of possible spiritual needs

  • Keep caregivers/families informed of patient condition with simple + honest info

  • Maintain consistency + continuity of care with same treatment teams for each patient

  • Ensure + encourage caregivers/families to spend time with patients and participate in their care

systemic inflammatory response syndrome (SIRS)

Systemic inflammatory response to a variety of insults, including infection (sepsis), ischemia, infarction, and injury

multiple organ dysfunction syndrome (MODS)

• Failure of 2+ organ systems in an acutely ill patients such that homeostasis can’t be maintained without intervention

  • Results from SIRS

Clinical manifestations: SIRS/MODS

• Biventricular failure

  • Decreased BP, MAP, systemic vascular resistance

  • Increased HR, cardiac output, stroke volume

• Mass vasodilation

• Myocardial depression

• Sys/diastolic dysfunction

• Acute neuro status changes (confusion, disorientation, delirium)

• Fever

• Hepatic encephalopathy

• Seizures

• Hyper → hypoglycemia

• GI bleeds

• Hypoperfusion → decreased motility/paralytic ileus/ischemia

• Decreased intramucosal pH

• Potential translocation of gut bacteria

• Potential abdominal compartment syndrome

• Mucosal ulcers

• Hyperbilirubinemia

• Jaundice

• Increased:

  • Liver enzymes

  • Ammonia

  • Bleeding times

  • D-dimer

  • Fibrin split products

• Decreased albumin, prealbumin, transferrin

• Thrombocytopenia

• Renal hypoperfusion (prerenal AKI)

  • BUN/creatinine ratio >20:1

  • Increased urine osmolality

  • Increased urine specific gravity

• Acute tubular necrosis (intrarenal AKI)

  • BUN/creatinine ratio <10:1 - 15:1

  • Decreased urine osmolality

  • Urine specific gravity ~1.010

• ARDS

• Dyspnea (severe)

• Pulmonary hypertension

• Refractory hypoxemia

• Tachynpea

• V/Q mismatch

Interprofessional + nursing care: SIRS/MODS

• Prevent + treat infection

  • Early, aggressive surgery is recommended to remove necrotic tissue that can breed microbes

  • Aggressive pulmonary management reduces infection risk

  • Strict asepsis can decrease infection related to intraarterial lines, endotracheal tubes, Foleys, IVs, etc.

  • When suspected, start interventions to treat

    • Obtain cultures + start broad-spectrum antibiotics as ordered

    • Adjust therapy based on culture results

• Maintain tissue oxygenation

  • Sedation, mechanical ventilation, analgesia, and rest can decrease oxygen demands and should be considered

  • Treating fever, chills, and pain decreases oxygen demands

  • Oxygen optimization methods:

    • Individualize tidal volumes with positive end-expiratory pressure

    • Increase preload (via fluids) or contractility

    • Reduce afterload

• Nutrition + metabolic needs

  • Monitor plasma transferring + prealbumin levels to assess hepatic protein synthesis

  • Enteral nutrition is preferred; if contraindicated, parenteral is used

  • Keep glucose levels <180 mg/dL

• Support failing organs

  • Maintain comms with care team + caregivers/families about realistic goals/outcomes for patients with MODS

    • Withdrawing life support/starting end-of-life care may be ideal options

Diagnostic findings: shock

• Respiratory alkalosis (early)

• Metabolic acidosis (late)

• Base deficit (acidity)

• Positive blood cultures

• Increased:

  • BUN

  • Creatinine kinase

  • Creatinine

  • D-dimer

  • Fibrin split products

  • INR

  • PTT + PT

  • Thrombin time

  • Glucose (early)

  • Sodium (early)

  • Potassium (early)

  • Lactate level

  • Liver enzymes

  • Procalcitonin

  • Troponin

• Decreased:

  • Fibrinogen

  • Platelets

  • Glucose (late)

  • Sodium (late)

  • Potassium (late)

Interprofessional care: shock

• Oxygen + ventilation

  • Oxygen delivery depends on cardiac output, available hemoglobin, and arterial oxygen saturation

  • Supply is increased by

    • Optimizing cardiac output with fluid replacement and/or drugs

    • Increasing hemoglobin via blood transfusions

    • Increased arterial oxygen sats with supplemental oxygen + mechanical ventilation

  • Plan care to avoid disrupting balance of oxygen supply + demand

  • Space activities that increase oxygen use appropriately for conservation

• Fluid resuscitation

  • Should start with 1-2 large-bore IV catheters, an intraosseous access device, or a central venous catheter

  • Fluid choice depends on type + volume of lost fluid and patient clinical status

  • Fluid responsiveness is determined by clinical assessment

    • Assessments of end-organ perfusion (urine output, neuro function, peripheral pulses) provide more relevant data than BP

    • Monitor:

      • Vitals

      • Cerebral + abdominal perfusion pressures

      • Cap refill

      • Neuro status

      • Skin temp

      • BP + trends

      • Urine output

    • Passive leg raise challenges and inferior vena cava evals help monitor fluid response

      • Leg raises provide a transient increase in fluid volume of 150-500 mL by placing the patient supine and raising legs 45 degrees

      • Responses are monitored in 1-2 mins via cardiac output + index, stroke volume, stroke volume variation, etc.

      • Positive = fluid responsive; more fluids needed

    • Warm IV solutions to prevent hypothermia

    • Large volumes of packed RBCs don’t have clotting factors

    • Assess for hypocalcemia + DIC

    • Replace clotting factors based on patient condition

• Drug therapy

  • Sympathomimetics

    • Most are called vasopressors

    • Can harm patients in cardiogenic shock by causing further heart damage and increasing dysrhythmia risk

    • Use is limited to patients who aren’t fluid responsive

      • Adequate fluid resuscitation is needed before treatment starts; vasoconstriction effects in patients with low blood volume will further reduce tissue perfusion

    • if hypotension persists after adequate fluid resuscitation, vasopressors and/or inotropes are given

    • Goal is to achieve + maintain a MAP of 65+ mmHg

    • Continuously monitor end-organ perfusion and serum lactate levels (q3h for first 6h) to ensure perfusion adequacy

  • Vasodilators

    • Most used drug is nitroglycerin

    • Used to decrease afterload → reduce heart workload + oxygen needs

    • Goal is to break harmful cycle of widespread vasoconstriction causing a decrease in cardiac output + BP, resulting in further sympathetic-induced vasoconstriction

    • Goal is to maintain MAP >65 mmHg

    • Monitor hemodynamic parameters + assessment findings, so fluids can increased, or vasodilators decreased if steep fall in cardiac output/BP occurs

• Nutrition therapy

  • Enteral nutrition should be started in the first 24 hours

  • Full calorie replacement isn’t recommended for previously well-nourished adults early in critical illness

    • Start patients with trophic feeds; small amounts of enteral nutrition (10 mL/hr)

  • Early enteral nutrition enhances GI perfusion and helps maintain integrity of gut mucosa

  • Parenteral nutrition is used only if enteral is contraindicated

  • Obtain daily weights; if patients have significant weight loss, rule out dehydration before adding more calories

  • Monitor serum protein, total albumin, BUN, serum glucose, and electrolytes

Causes: renal trauma

• Blunt

  • Sports injuries

  • MVCs

  • Falls

• Penetrating

  • GSWs

  • Stabbings

Diagnostic studies: renal trauma

• CT

• CT pyelography

Nursing care: renal trauma

• Assess cardiac status

• Monitor for shock

• Ensure adequate fluid intake + monitor I/O

• Provide pain relief

• Assess for hematuria + myoglobinuria

• Evaluate patient + vitals regularly

Etiology + patho: AKI

• Categories

  • Prerenal

    • Factors that reduce systemic circulation, causing decreased renal blood flow

      • Decreased blood flow → decreased glomerular perfusion and filtration

    • If decreased renal perfusion persists, the kidneys lose their ability to compensate, and tissue damage occurs (intrarenal damage)

    • Common causes

      • Cardiogenic shock

      • Dysrhythmias

      • Heart failure

      • MI

      • Anaphylaxis

      • Neuro injury

      • Septic shock

      • Embolism

      • Burns

      • Dehydration

      • Excess diuresis

      • GI losses

      • Hemorrhage

  • Intrarenal

    • Includes problems that cause direct damage to kidney tissue, resulting in impaired nephron function

    • Damage causes usually results from prolonged ischemia, nephrotoxins, hemoglobin released from hemolyzed RBCs, or myoglobin released necrotic muscle cells

    • Acute tubular necrosis (ATN) is the most common cause of intrarenal AKI in hospitalized patients

      • Can result from ischemia, nephrotoxins, or sepsis

    • Common causes

      • Allergies (antibiotics, NSAIDs, ACE inhibitors)

      • Infections

      • Contrast emdia

      • Meds

      • Hemolytic blood transfusion reaction

      • Malignant hypertension

      • Lupus

      • Prolonged prerenal ischemia

      • Thrombotic disorders

  • Postrenal

    • Involves mechanical obstruction of urine outflow

    • With obstructed urine flow, the urine refluxes into the renal pelvis, impairing kidney function

    • Prolonged obstruction can lead to tubular atrophy and irreversible kidney fibrosis

    • Common causes

      • BPH

      • Bladder cancer

      • Calculi formation

      • Neuromuscular disorders

      • Prostate cance

      • Spinal cord disease

      • Strictures

      • Trauma (back, pelvis, perineum)

Clinical manifestations: AKI

• Phases

  • Oliguric

    • Reduction in urinary output to <400 mL/day; usually occurs in 1-7 days of the injury to the kidneys

      • If caused by ischemia, it occurs in 24 hours

      • If caused by nephrotoxins, onset can be delated by up to a week

    • Phase lasts from 10-14 days, but can last months in some cases

    • Hypovolemia

    • Metabolic acidosis

    • Hyponatremia (excess → cerebral edema)

    • Hyperkalemia

      • Monitor for ECG changes (peaked T waves, wide QRS, ST depression)

    • Leukocytosis

    • Increased BUN + creatinine

      • Creatinine is a better indicator of development; is unaffected by other factors

    • Neuro problems

      • Mild: fatigue, difficulty concentrating

      • Sever: seizures, stupor, coma

  • Diruetic

    • Output can be between 1-3 L/day, but can be up to 5

    • Nephrons still aren’t fully functional despite increased output

    • High output is caused by osmotic diuresis from the high urea concentration in the glomerular filtrate and inability of tubules to concentrate the urine

    • In this phase, kidneys recover their ability to excrete waster, but not to concentrate urine

    • Hypovolemia/tension can occur from massive fluid losses

    • Patient who had an oliguric phase will have greater diuresis as kidney function returns

    • Large loss of fluid + electrolytes require monitoring for hyponatremia/kalemia and dehydration

    • Can last 1-3 weeks; acid-base, electrolyte, and waster product (BUN + creatinine) levels stabilize

  • Recovery

    • Begins when GFR increases, allowing BUN and creatinine levels to decrease

    • Major improvements occur in the first 1-2 weeks

    • It can take up to a year for kidney function to stabilize

    • Patient overall health, severity of injury, and number/type of complications influence recovery outcome

    • Older adults are less likely to have complete recoveries of kidney function

    • Patients who recovery fully can achieve clinically normal kidney function but stay in early stages of CKD

Diagnostic studies: AKI

• Changes in output and creatinine are known diagnostic indicators of AKI

  • Increased creatinine may not be present until there’s a loss of 50%+ of kidney function

    • The rate of increase is important as a diagnostic indicator in determining injury severity

• Urinalyses are key diagnostic tests

  • Urine sediment containing abundant cells, casts, or proteins suggest intrarenal disorders

    • Can be normal in pre/postrenal AKI

    • In intrarenal AKI, hematuria, pyuria, and crystals can be seen

  • Urine osmolality, sodium content, and specific gravity help in distinguishing causes of AKI

• Kidney ultrasounds are often the first test performed; it provides imaging without exposure to nephrotoxic contrast agents

  • It can also evaluate kidney disease and urinary tract obstruction

• Renal scans assess abnormalities in kidney blood flow, tubular function, and the collecting system

• CT scans show lesions, masses, obstructions, and vascular anomalies

  • Assess for shellfish/iodine allergy before testing

• Renal biopsies are the best way to confirm intrarenal AKI

• MRIs/MRAs with contrast are contraindicated by patients with kidney failure; gadolinium can be fatal

Interprofessional care: AKI

• First step is to determine if there’s adequate kidney perfusion

  • Loop diuretic therapy may be given

• If AKI is established, forcing fluids and diuretics won’t be effective/can be harmful

• Monitor I/O during oliguric phase

• General rule for calculating fluid restriction is to add all loss from the last 24 hours + 600 mL for insensible losses (sweating)

• Hyperkalemia is one of the most serious complications due to life-threatening dysrhythmias

• Insulin and bicarb are temporary measures for treating hyperkalemia by promoting a transient shift of potassium into cells, which will eventually diffuse back to the bloodstream

• Calcium gluconate raises threshold at which dysrhythmias occur, temporarily stabilizing the myocardium

• Sodium polystyrene sulfonate and dialysis rapidly remove potassium from the body

• If conservative therapy isn’t effective in treating AKI, renal replacement therapy can be used

  • Common indications for renal replacement therapy:

    • Volume overload, resulting in compromised cardiac and/or pulmonary status

    • High potassium level

    • Metabolic acidosis

    • BUN >120 mg/dL

    • Significant change in mental change

    • Pericarditis, pericardial effusion, or cardiac tamponade

  • Clinical status of the patients are the best guideline for renal replacement therapy

  • Continuous renal replacement therapy has slower blood flow rates compared with intermittent hemodialysis

  • Intermittent hemodialysis is the preferred method when changes are needed emergently

    • Patients need anticoagulation therapy to prevent blood lotting when blood makes contact with the dialysis circuit

    • Rapid fluid shifts can cause hypotension

Nursing care: AKI

• Health promo

  • Monitor patient weight, I/O, and fluid/electrolyte balance

  • Assess + record extrarenal fluid losses from V/D, hemorrhage, and increased insensible losses

  • Aggressive diuretic therapy for fluid overloaded patients can lead to decreased renal blood flow

  • Monitor kidney function in patients taking potentially nephrotoxic drugs

    • Such drugs should be avoided in high-risk patients, but if unavoidable, they should be given in the smallest effective doses for the shortest possible periods

  • Caution patients about OTC pain meds (especially NSAIDs), as they can worsen kidney function in patients with mild CKD

  • ACE-inhibitors can decrease perfusion pressure and cause hyperkalemia

    • If other measures (diet changes/diuretics) can’t control hyperkalemia, ACE inhibitors may have to be reduced/stopped

    • However, they can be used to prevent proteinuria and progression of kidney disease, especially in diabetic patients

• Acute care

  • Holistic care is key, as AKI patients may have comorbid conditions

    • Help patients understand that AKI can affect all body functions

  • Assess for signs/symptoms of:

    • Hypervolemia in the oliguric phase

    • Hypovolemia in the diuretic phase

    • Potassium/sodium problems

    • Other electrolyte imbalances that can occur

  • Meticulous aseptic technique is critical for AKI, as infection is the leading cause of death

    • Assess for signs of local and systemic infection

    • If patients with renal failure have infections, they be afebrile

    • If antibiotics are given to treat infection, consider the type, frequency, and dosage, as the kidneys are the main route of excretion for many antibiotics

      • Dosages may be decreased depending on the patient’s level of kidney function

• Ambulatory care

  • Recovery is dependent on:

    • Potential failure of body systems

    • Patient’s general health + age

    • Length of the oliguric age

    • Severity of nephron damage

  • Regular evaluation of the kidney is necessary

  • Teach patients the signs/symptoms of recurrent kidney disease

  • Emphasize measures to prevent AKI recurrence

  • Long-term convalescence (3-12 months) can cause psychosocial and financial hardships on patient + family; make appropriate referrals for counseling

  • If kidneys don’t recover, patients will need chronic dialysis or a possible transplant

hemodialysis

• Artificial membranes are the semipermeable membranes

• AV fistulas + grafts

  • Fistulas

    • Usually created in the forearm + upper arm with an anastomosis between an artery and vein; fistula allows arterial blood to flow through the vein

    • Veins become arterialized, increasing in size + develop thickened walls

    • Maturation can take 6 weeks to months

    • Should be placed at least 3 months before starting hemodialysis

    • Preferred access for hemodialysis

    • Thrills can be felt on palpation; bruits heard on auscultation

  • Grafts

    • Made of synthetic materials they bridge between the arterial + venous blood supplies

    • Placed under the skin and surgically anastomosed between an artery and vein (usually brachial/antecubital

    • 2-4 weeks are usually needed for healing, but can be used sooner

    • More likely to get infected + form clots due to artificial material usage; may require surgical removal since it’s hard to resolve infection of synthetic material

  • Never obtain BPs, insert IVs/venipuncture extremities with AV access

    • Helps to prevent infection + clotting of the vascular access

  • Place signs in patient’s room + label arm with warning bands “No BP, blood draws/IV)

• Risks

  • Distal ischemia (steal syndrome) + pain, from too much arterial blood shunting from the distal extremity

    • Manifestations

      • Pain distal to access site

      • Numbness/tingling of fingers that can worsen during hemodialysis

      • Poor cap refill

      • Aneurysm + rupture, if left untreated

Complications: hemodialysis

• Hypotension

  • Often results from

    • Hypovolemia

    • Decreased cardiac output

    • Decreased systemic vascular resistance

  • Manifestations

    • Lightheadedness

    • N/V

    • Seizures

    • Vision changes

    • Chest pain, from cardiac ischemia

  • Treated by decreasing the volume of fluid removed and infusion normal saline

• Muscle cramps

  • Risk factors

    • Hypotension

    • Hypovolemia

    • High ultrafiltration rate

    • Low-sodium dialysis solution

  • Treated by reducing ultrafiltration rate and giving fluids (saline, glucose, mannitol)

    • Hypertonic saline isn’t recommended due to sodium load

• Blood loss

  • Causes

    • Blood not being completely rinsed form the dialyzer

    • Accidental separation of blood tubing, dialysis membrane rupture

    • Bleeding after removing the needles at the end of hemodialysis

    • Excess heparin admin or clotting problems

  • It’s essential to

    • Rinse back all blood

    • Avoid excess anticoagulation

    • Hold firm, but nonocclusive pressure on access sites until bleeding risk passes

• Hepatitis

  • Rare, but can still occur from breaks in infection control practices

  • Prevented by requirements of all patients + personnel in dialysis units to get hep B vaccine

Complications: peritoneal dialysis

• Exit site infection

  • Most often caused by Staph aureus or epidermidis

  • Manifestations

    • Redness at sire

    • Tenderness

    • Drainage

  • Superficially, usually resolve with antibiotics

  • If not treated quickly, SQ tunnel infections may progress + cause peritonitis → catheter removal

• Peritonitis

  • Results from contact contamination or exit site/tunnel infection

  • Often occurs due to improper technique when connections for exchanges are contaminated

  • Usually caused by S. aureus/epidermidis

  • Manifestations

    • Abdominal pain

    • Rebound tenderness

    • Cloudy peritoneal effluent + WBC count >100 cells/μL or bacteria in the peritoneal effluent shown by Gram stain/culture

    • V/D

    • Abdominal distention

    • Hyperactive bowel sounds

    • Fever

  • To determine effluent cloudiness, drain onto reading material; if it can’t be read = cloudy

  • Cultures, Gram stain, and WBC differential of effluent confirm diagnoses

  • Antibiotics can be given PO, IV, or intraperitoneally; patients usually outpatient

  • Repeated infections can result in adhesions + interfere with membrane ability to act as dialyzing surface

    • Can require removal of catheters + temporary/permanent change to hemodialysis

• Hernias

  • Result from increased intraabdominal pressure from dialysate volume

  • After repair, dialysis can resume after several days of small dialysate volumes + keeping patients supine

• Low back problems

  • Caused/worsened by increased intraabdominal pressure

  • Orthopedic biners + regular exercise programs for strengthening back muscles can help

• Bleeding

  • After catheter placement, it’s common for effluent after the first few exchanges to be pink/slightly bloody from trauma after catheter insertion

  • Bloody effluent over several days or new appearance of blood can indicated active intraperitoneal bleeding

    • If occurs; check BP + hematocrit

    • Can appear for menstruating/ovulating women; acknowledge + move on

• Pulmonary complications

  • Atelectasis, pneumonia, and bronchitis can occur from repeated upward displacement of the diaphragm → decreased lung expansion

  • Longer dwell times increased risk for pulmonary problems; frequent repositioning + deep-breathing exercises can help

• Protein loss

  • Proteins are lost in dialysate fluid; typical loss is 0.5 g/L, but can be up to 20 g/day

    • Losses can increase as much 40 g/day during episodes of peritonitis as the membrane becomes more permeable

Etiology + patho: CKD

• Progressive + irreversible loss of kidney function

• Risk factors

  • Age 60+

  • Cardiovascular disease

  • Diabetes

  • Ethinicity

  • Exposure to nephrotoxic drugs

  • Family history

  • Hypertension

Clinical manifestations: CKD

• Uremia

  • Syndrome in which kidney function declines to the point that symptoms may develop in multiple body systems

  • Often occurs when GFR is 15 mL/min or less

• Polyuria

  • More likely to be caused by comorbid diabetes

• Urinary retention, with disease progression

• Anuria, with dialysis treatment

• Decreased GFR → increased BUN + creatinine

• Impaired glucose metabolism → mild/moderate hyperglycemia + hyperinsulinemia

• Dyslipidemia

  • Increased very-low-density-lipoproteins

  • Decreased HDLs

• Hyperkalemia

  • Fatal dysrhythmias can occur when levels reach 7-8 mEq/L

• Sodium changes

  • If large amounts of water are retained, dilutional hyponatremia occurs

  • Sodium retention → edema, hypertension, and heart failure

• Hypermagnesemia; problematic if patients ingest increased magnesium

• Metabolic acidosis, due to kidneys’ impaired ability to excrete excess acid from defective reabsorption + regeneration of bicarb

• Anemia

Diagnostic studies: CKD

• Dipsticks, to detect proteinuria or albuminuria

  • Persistent proteinuria (1+ protein 2+ times over a 3 month period) requires further resting

• Urinalysis, to detect RBCs, WBCs, protein, casts, and glucose

• Renal ultrasounds detect obstructions + determine kidney size

• Renal biopsy

• BUN

• GFR

• Serum creatinine + creatinine clearance

• Electrolytes

• Lipid profile

• H/H

Interprofessional care: CKD

• Drug therapy

  • Hyperkalemia

    • Restrict high-potassium foods + meds

    • IV glucose + insulin or 10% calcium gluconate to treat hyperkalemia

    • Sodium polystyrene sulfonate helps lower potassium levels in stage 4 CKD

    • Patiromer binds potassium in the GI tract

      • Delayed onset of action; don’t use in emergency situations

      • Give 6 hours before/after meds to avoid accidently binding

  • Hypertension

    • Weight loss

    • Lifestyle changes

    • Diet changes

    • Drugs depend on diabetes status

      • ACE inhibitors + ARBs can be given to patients with diabetes and those with nondiabetic proteinuria

        • Decrease proteinuria + delay CKD progression

        • Used cautiously; can decrease GFR + increase potassium levels

  • Mineral + bone disorder

    • Limit phosphorus intake

      • Restrictions usually not enforced until patients need renal replacement therapy; intake is restricted to 1 g/day

    • Give phosphate binders (calcium acetate/carbonate)

      • Bind phosphate in the GI tract + excrete in stool

      • Give with each meal for max effectiveness

      • Monitor for constipation

    • Supplement vitamin D

      • Assess vitamin D levels

    • Control hyperparathyroidism

      • Secondary hyperparathyroidism requires activated forms of vitamin D, as the kidneys can’t activate it

      • Calcimimetics increase sensitivity of calcium receptors in parathyroid glands; calcium is detected and lower serum → decreases PTH secretion

    • Do not use magnesium-containing antacids; kidneys are needed for excretion

  • Anemia

    • Exogenous erythropoietin (epoetin alfa), IV/SQ, 2-3 times/week

      • Higher doses increase risk for thromboembolic events + death from serious cardiovascular events

      • Use lowest possible doses

      • Do not give to patients with uncontrolled hypertension

      • Iron supplements are recommended if ferritin concentrations fall below 100 ng/mL

      • Blood transfusion are avoided unless patients had acute blood loss or symptomatic anemia (dyspnea, excess fatigue, tachycardia, palpitations, chest pain)

        • Increase antibody development + difficulty finding kidney donors for transplant

    • H/H levels can take 2-3 weeks to increase

  • Dyslipidemia

    • Statins lower LDL levels

      • Should be used for CKD patients, especially diabetics not yet on dialysis

    • Fibrates lower triglyceride levels + increased HDLs

• Nutrition therapy

  • Protein restriction

    • For CKD stages 1-4, many providers encourage diets with normal protein intake

    • High-protein diets + supplements should be avoided to not overwork diseased kidneys

    • Protein guidelines for peritoneal dialysis differ from hemodialysis due to protein loss through the peritoneal membrane

      • In peritoneal dialysis, protein intake must be high enough to compensate for losses to maintain nitrogen balance

  • Fluid restriction

    • Not usually done for CKD stages 1-5 not on hemodialysis

    • Diuretics are often used to reduce fluid retention

    • Patients on hemodialysis have a more restricted fluid intake than patients on peritoneal dialysis

      • Recommended intake depends on daily urine output

      • 600 mL (from insensible loss) plus an amount equal to the previous day’s urine output is allowed

      • Foods that are liquid at room temp are counted as fluid intake

    • Teach patients limit fluid intake so that weight gains are no more than 1-3 kg between dialyses

  • Sodium + potassium restriction

    • Teach patients to restrict sodium

    • Tell patients to avoid high-sodium foods

    • Salt substitutes should be avoided with potassium-restricted diets because they contain potassium chloride

    • Potassium restrictions depend on kidneys’ ability to excrete potassium

      • Range from 2k-3k mg

    • Teach hemodialysis patients to avoid foods high in potassium

    • Patients on peritoneal dialysis need oral potassium supplements due to losses with dialysis exchanges

  • Phosphate restriction

    • When patients have ESRD, phosphate is restricted to 1 g/day

    • When patients eat diets with protein, phosphate binders are given to control levels

Nursing care: CKD

• Assessment

  • Obtain complete histories of any existing kidney disease/family history of kidney disease

  • Obtain medication histories

    • Decongestants + antihistamines with pseudoephedrine and phenylephrine cause vasoconstriction → increased BP

    • Magnesium + aluminum from antacids can accumulate; salts in antacids can lead to hypertension

  • NSAIDs can contribute to AKI development + CKD progression, especially when taken in higher doses than recommended

  • Assess diet habits + discuss issues with intake

  • Measure height + weight; evaluate recent weight changes

  • Assess patient support systems

• Health promo

  • ID patients with risk factors

  • Diabetics should urine checked for albuminemia if routine urinalyses are negative for protein

  • Teach diabetics to report changes in urine appearance, frequency, or volume

  • If patients nephrotoxic drugs, monitor kidney function (BUN, creatinine, GFR)

• Acute care

  • Inpatients care is needed for complication management + kidney transplant

• Ambulatory care

  • Encourage patients to participate in their care

  • Teach patients + caregivers about diets, drugs, and follow-up care

  • Tell patients to avoid OTCs

  • Teach patients to take daily BP readings + watch for signs/symptoms of fluid overload, hyperkalemia, and other electrolyte imbalances

  • Collab with dieticians regularly to help diet planning

  • Explain the process of peritoneal/hemodialysis

  • Offer info on all treatment options to keep patients involve in decision-making + control

  • Tell patients that transplants are still options even on dialysis

  • Discuss palliative care as needed; focus discussion on moving from the curative approach to promotion care and consideration of hospice

  • Listen to patients + caregivers, letting them do most speaking, and pay attention to hopes + fears

hypertensive crisis

• Term that indicates either hypertensive emergency/urgency

• Crisis = SBP >180 and/or DBP >120 mmHg

hypertensive urgency

• No target organ damage + hospitalization may not be needed

• Associated with chronic, stable complications:

  • Stable angina

  • Chronic heart failure

  • Past MI/CVA with no threat of an acute event

hypertensive emergency

• Evidence of target organ disease + often need hospitalization for immediate, controlled BP reduction

• Complications

  • Encephalopathy

  • Intracranial/subarachnoid hemorrhage

  • Heart failure

  • MI

  • Renal failure

  • Dissecting aortic aneurysm

  • Retinopathy

Clinical manifestations: hypertensive crisis

• Severe headache

• N/V

• Seizures

• Confusion

• Coma

• Chest pain

• Dyspnea

• Encephalopathy → cerebral edema + disruption in cerebral function

• Retinal exudates, hemorrhages, and/or papilledema

• Renal insufficiency (ranges from minor injury → renal failure)

• Rapid cardiac decompensation (ranges from unstable angina → MI + pulmonary edema)

• Aortic dissection → sudden, severe chest + back pain with reduced/absent peripheral pulses

Interprofessional + nursing care: hypertensive crisis

• MAPs are often used to guide/evaluate therapy for hypertensive emergencies

• Initial goal is to decrease MAP by no more than 20-25% (110-115 mmHg)

• If patients are clinically stable, drugs can be titrated to gradually lower BP over 24 hours

  • Lowering BP too fast/much can decrease brain, heart, or renal perfusion → stroke, MI, or renal failure

• Patients with aortic dissection should have SBP lowered to less than 100-120 mmHg asap (if tolerated)

  • An exception are patients with acute ischemic stroke whose BP is lowered to allow for thrombolytic use

• Drug therapy

  • Vasodilators (nitroprusside)

    • Most effective at treating hypertensive emergencies

  • Adrenergic inhibitors (labetalol)

  • Meds given IV have rapid onsets of action; assess BP + HR q2-3mins during initial admin

• Hypertensive emergencies

  • Use A-lines or an automated, noninvasive BP machine to monitor BPs

  • Titrate meds per MAP/SBP as ordered

  • Monitor ECG for dysrhythmias + signs of ischemia/MI

  • Measure urine output hourly to assess renal perfusion

  • Patients may be kept on bedrest for safety (rising → severe cerebral ischemia → fainting)

  • Monitor heart, lung, and renal systems for decompensation caused by severe BP increases

  • Frequent neuro checks (LOC, pupil size/reaction, extremity movement) help detect changes in status

• Hypertensive urgencies

  • Can be managed with PO meds + outpatient follow-up within 24 hours

  • Initial decision for PO antihypertensives should be made based on underlying cause, patient characteristics, and comorbidities

  • Common meds

    • Captopril

    • Labetalol

    • Clonidine

      • Teach patients to change positions slowly

      • Patients should avoid hazardous activities; drowsiness is a side effect

      • Don’t stop taking abruptly; rebound BP increases possible

    • Amlodipine

• Acute care

  • Obtain baseline vitals (give oxygen per agency policy)

  • Start continuous BP + ECG monitoring

  • Auscultate heart + lungs

  • Establish IV access

    • Give antiheptensives as ordered

  • Obtain baseline labs

  • Measure urine output hourly

  • Keep patients on bedrest

  • Assess + record patient response to meds

• Once crises are resolved, it’s essential to determine the cause; patients will need appropriate management + teaching to prevent recurrence

  • Patients should seek immediate help for

    • Altered LOC

    • Unresponsiveness

    • High BP (>200/100 despite treatment)

• Not every patient with elevated BP will need emergent drug therapy/hospitalization

  • Letting patients sit for 20-30 mins in a quiet environment can significantly lower BP

  • PO meds can be given

  • Encourage patients to share concerns/fears, answer questions about hypertension

  • Reduce any adverse stimuli

Patho: heart failure

• Left sided heart failure

  • Most common form; results from inability of the left ventricle to either empty adequately during systole or fill adequately during diastole

  • Types

    • Systolic (reduced ejection fraction)

      • Results from:

        • Inability of the heart to pump blood effectively

        • Increased afterload

        • Cardiomyopathy

        • Mechanical problems

      • Hallmark sign is a decrease in left ventricular ejection fraction (usually <40%; can be down to 5-10%)

      • Left ventricle doesn’t generate enough pressure to eject blood through the aorta; ventricle eventually dilates + hypertrophies, reducing stroke volume → impairing output

      • Ventricle fails, causing blood to back up into the left atrium, then causing fluid accumulation in the lungs → pulmonary congestion + edema

    • Diastolic (preserved ejection fraction)

      • Results from the inability of the ventricles to relax + fill during diastole

      • Main cause is hypertension

        • Other risk factors

          • Older age

          • Female sex

          • Diabetes

          • Obesity

      • Ventricle stiffens, causing high filling pressures; decreased filling volume → decreased stroke volume → reduced output → pulmonary congestion

      • Diagnosis is based on:

        • Signs/symptoms of heart failure

        • Normal left ventricular ejection fraction

        • Evidence of left ventricular dysfunction via echocardiography/cardiac catheterization

• Right sided heart failure

  • Occurs when the right ventricle doesn’t pump effectively; blood backs up into the venous system and eventually into organs/tissues (peripheral edema, abdominal ascites, hepatomegaly, JVD)

  • Most commonly caused by left sided heart failure

    • Other causes

      • Infarction

      • Pulmonary embolism

      • Cor pulmonale (ventricular dilation + hypertrophy caused by pulmonary disease)

Clinical manifestations: acute decompensated heart failure

• Typically includes sign/symptoms related to pulmonary congestion + volume overload; ost commonly associated with left-sided heart failure

• Increased respirations (early)

• Decreased O2 sats (early)

• Tachypnea

• Progressive respiratory acidosis (lower PaO2, increased PaCO2)

• Pulmonary edema

  • Dyspnea

  • Orthopnea

  • Paroxysmal nocturnal dyspnea

  • JVD

  • Coughing

  • Anxiety

  • Pallor/cyanosis

  • Accessory muscle use

  • Pink + frothy sputum (severe)

  • Crackles/wheezing

  • Tachycardia + S3/S4 heart sounds

  • Hypo/hypertension, depending on severity

    • Hypotension indicates high severity + cardiogenic shock

  • Cool extremities

  • Hoarseness (Ortner sign)

Clinical manifestations: chronic heart failure

• Right sided

  • Increased HR

  • Anasarca (massive generalized edema)

  • Ascites

  • Edema

  • Hepatomegaly

  • JVD

  • Murnurs

  • Weight gain

  • Anorexia + GI bloating

  • Anxiety

  • Depression

  • Fatigue

  • Nausea

  • RUQ pain

• Left sided

  • Increased HR

  • S₃ + S₄ heart sounds

  • Confusion, restlessness

  • Dry, hacking cough

  • Pleural effusion

  • Pulsus alternans (alternating strong/weak pulses)

  • Shallow respirations

  • Anxiety

  • Depression

  • Dyspnea

  • Nocturia

  • Orthopnea

  • Paroxysmal nocturnal dyspnea

  • Fatigue

Complications: heart failure

• Pulmonary effusion

• Dysrhythmias + dyssynchronous contractions

  • A-fib is common + increases in prevalence with progression of severity

    • Increases stroke risk via thrombus formation promotion in the atria

  • Patients are at risk for ventricular dysrhythmias (v-tach/fib)

• Hepatomegaly

• Cardiorenal syndrome

  • Reduced cardiac output → decreased renal perfusion + GFR and increased serum creatinine

  • RAAS activation → water + sodium retention

• Anemia

  • Mainly caused by chronic kidney insufficiency

  • Renal vasoconstriction → less erythropoietin production → anemia

  • Can worsen cardiac function due to increased workload via tachycardia, fluid retention, and increased stroke volume

• Hepatomegaly

• Renal failure

• Left ventricular thrombus

Diagnostic studies: heart failure

• Echocardiogram

• ECGs

• Ambulatory heart monitors

• Chest x-rays

• 6-min walk test

• Multigated acquisition (MUGA) scan

• Cardiopulmonary exercise stress test

• Cardiac MRI

• Cardiac catheterization/angiogram

• Lab studies

  • BNP + N-terminal prohormone of BNP

  • Liver function tests

  • Thyroid function tests

  • CBC

  • Lipid profile

  • Kidney function tests

  • Urinalysis

• Polysomnography, to ID obstructive sleep apnea

• Endomyocardial biopsy during catheterization to evaluate for infection/disease in patients with unexplained, new-onset heart failure

Interprofessional care: acute decompensated heart failure

• Continuously monitor + assess vitals, O2 sats, weight, mentation, ECGs, and indicators of volume overload + decreased organ perfusion

  • Indicators

    • Edema

    • Ascites

    • JVD

    • Positive hepatojugular reflux test

    • S3 heart sounds

    • Crackles

    • Hypoxia

    • Worsening renal function

• Assess ED patients q4h for adequate oxygenation

• Place dyspneic patients in high-Fowler’s

• Unstable patients go to the ICU

  • ECGs, O2 sats, vitals, and urine output are assessed hourly

• Nonpharm therapies

  • Ultrafiltration (aquapheresis)

    • Used for patients with volume overload when diuretics haven’t worked

  • Hemodialysis

    • Used for volume overload + renal failure

  • Pacemaker implantation

• Drug therapy

  • Diuretics

    • First line for treating patients with volume overload

  • Vasodilators (nitroprusside)

    • Record baseline BP + continuously monitor during admin

    • Arterial BP monitoring is recommended

    • Infuse slowly; too rapid infusion can drop BP too fast + cause hypotension

    • Side effects

      • Headahce

      • Dizzines

      • Nausea

      • Agitation

      • Restlessness

    • Monitor for toxic thiocyanate levels if infusion is >3 mcg/kg/min

  • Morphine

  • Positive inotropes

Interprofessional care: chronic heart failure

• Supplemental oxygen helps meet oxygen needs + improves O2 sats

  • Continuous pulse oximetry monitors the needs for + effectiveness of therapy

• Physical + emotional rest allows for energy conservation + decreased oxygen demand

  • Degree of rest depends on heart failure severity

    • Severe = bed rest

    • Mild/moderate = Ambulation + restricted activity

      • Encourage participation in prescribed activities with adequate rest periods

• Drug therapy

  • ACE inhibitors

    • First line drugs to decrease mortality, hospitalization, and symptoms in patients with HFrEF

    • Side effects

      • Symptomatic hypotension

      • Persistent dry cough

      • Hyperkalemia

      • Angioedema

      • Renal insufficiency (high doses)

    • Monitor renal function + potassium levels

  • ARBs

    • For patients who can’t tolerate ACE inhibitors

    • Similar side effects to ACE inhibitors, but without coughing

  • Aldosterone antagonists (spironolactone)

    • Monitor potassium levels

    • Use cautiously in patient on digoxin; hyperkaleia can reduce digoxin effects

    • Teach patients to avoid high potassiu foods

    • Assess males for gynecomastia

  • Beta blockers

    • Improvements are dose-related; highest tolerated doses are given

    • Used cautiously in patients with volume overload

    • Major side effects

      • Worsening heart failure symptoms

      • Hypotension

      • Fatigue

      • Bradycardia

  • Digitalis

    • Better outcomes occur with digoxin levels <0.9 ng/mL

    • Doses should be based on body mass renal function, and concomitant meds

    • Monitor renal function + potassium levels

  • Diuretics (symptom management)

    • Loop

      • Potential problems

        • Low potassium levels

        • Ototoxicity

        • Possible allergic reaction in patients sensitive to sulfa-type drugs

    • Thiazides

      • Can severely lower potassium levels

    • For chronic heart failure, patients get the lowest effect doses

      • Side effects

        • Dehydration

        • Hypotensino

        • Orthostasis

        • Renal problems

        • Electrolyte imbalances

Nursing care: heart failure

• Assessment

  • Obtain drug history

    • OTCs know to pose significant risk to heart failure patients

      • NSAIDs

        • Increased sodium retention → worsen heart failure

      • High dose aspirin

      • Ephedrine

      • Pseudoephedrine

      • Diet pills

  • Obtain diet history to assess heart failure related issues

  • Review medical history for other chronic health problems that can exacerbate heart failure

• Health promo

  • Lifestyle modifications start with weight management, diet, and regular exercise

  • Encourage recommended vaccinations

• Acute care

  • Successful heart failure care depends on several principles

    • HF is progressive

    • Treatment plans are made with quality of life goals

    • Symptom management depends on adherence to self-management protocols

    • Precipitating factors, etiologies, and contributing conditions must be addressed

    • Complex care needs often require care access settings, increasing risk for fragmented care

    • Support systems are essential to treatment plan success

• Ambulatory care

  • Include patient + family in overall care plan

    • Assist in developing a clear action plan for response to signs/symptoms of impending exacerbation

  • Teach patients the basic mechanisms of action of meds and signs of drug toxicity in layman’s terms

    • Patients should understand when to hold HR-lowering meds

    • Teach patients on diuretic and/or potassium supplement meds the signs/symptoms of hypo/hyperkalemia (weakness, fatigue, constipation, muscle cramping)

  • Tailor exercise programs based on what patients enjoy doing

    • Teach about the importance of rest periods, especially after exertion, and energy-conserving behaviors

    • Consult with PT/OT as needed

Indications: intraaortic balloon pumps (IABPs)

Indications: ventricular assist devices (VADs)

Interprofessional + nursing care: IABPs/VADs

arterial lines

Complications: arterial lines

pulmonary artery (Swan-Ganz) catheters

central venous catheters

Nursing care: hemodynamic monitoring

Clinical associations: sinus bradycardia

Clinical significance: sinus bradycardia

Treatment: sinus bradycardia

Clinical associations: sinus tachycardia

Clinical significance: sinus tachycardia

Treatment: sinus tachycardia

atrial flutter

Clinical associations: atrial flutter

Clinical significance: atrial flutter

Treatment: atrial flutter

a-fib

Clinical associations: a-fib

Clinical significance: a-fib

Treatment: a-fib

v-tach

Clinical associations: v-tach

Clinical significance: v-tach

Treatment: v-tach

v-fib

Clinical associations: v-fib

Clinical significance: v-fib

Treatment: v-fib

Clinical associations: asystole

Clinical significance: asystole

Treatment: asystole

3rd degree heart block

Clinical associations: 3rd degree heart block

Clinical significance: 3rd degree heart block

Treatment: 3rd degree heart block