Exam 4 critical care

Why would a patient require pacing:

Symptomatic bradycardia, high-grade AV block, sinus node dysfunction, and selected HF patient who benefit from resynchronization

Transcutaneous pacing

emergency bridge; pads deliver impulses through the chest wall.

• verify electrical and mechanical capture; anticipate analgesia/sedation for a conscious patient when feasible; continue searching for and treating cause of bradycardia

Temporary transvenous/epicardial

Short-term support while the cause is treated or recovery occurs

• secure connections, protect wires, monitor capture/sensing and the insertion site, and know the backup plan if pacing is lost

Permanent pacing

implanted generator and leads for ongoing rhythm support

• monitor for bleeding/hematoma, pneumothorax, infection, lead dislodgment, and recurrent bradycardia

Congenital heart defects: increased pulmonary blood flow

Left-to-right shunting sends extra blood to the lungs. ASD, VSD, PDA

• Typical physiology: left-to-right shunt —> pulmonary over circulation —> increased work of breathing, and when shunt is large, HF

• common nursing cues: tachypnea, diaphoresis with feeds, fatigue, poor weight gain, recurrent respiratory symptoms, murmur, and cardiomegaly

• Large untreated shunts can lead to pulmonary vascular disease and eventual shunt reversal

• urgency of treatment depends on defect size, symptoms, pulmonary pressures, ventricular effects, and growth

Congenital heart disease: decreased pulmonary blood flow

Right-to-left shunting or outflow obstruction reduces pulmonary oxygenation.

Tetralogy of Fallot

Congenital heart defect: mixed/parallel circulation

Oxygenated and deoxygenated blood must mix adequately for survival. TGA, truncus arteriosus, tricupsid atresia.C

Congenital heart defect: obstructed systemic blood flow

blood cannot move effectively from the heart into the systemic circulation. coarctation, critical aortic stenosis

Atrial septal defects

often subtle in childhood, may cause right-sided volume overload. suitable secundum ASDs may be closed by catheter device; others require surgery

ventricular septal defects

classically produces a harsh holosystolic murmur. large defects can cause significant pulmonary overcirculation and infant heart failure.

Small vs large ASDs and VSDs + Management

Small may close spontaneously or remain clinically insignificant

Large are followed for chamber enlargement, pulmonary hypertension, symptoms, and growth

• Management: nutrition support and diuretics for HF symptoms while awaiting spontaneous improvement or definitive closure

Patent ductus arteriosus

the ductus arteriosus remains open after birth, allowing blood to move from the aorta toward the pulmonary artery when systemic pressure exceeds pulmonary pressure

• possible findings: continuous murmur, bounding pulses, widened pulse pressure, tachypnea, feeding intolerance, and heart-failure signs when shunt is large

• In premature infants: pharmacologic closure with ibuprofen or indomethacin may be considered

• Do not confuse treatment of an unwanted PDA with prostaglandin E1, which is intentionally used to keep the ductus open in ductal-dependent lesions

What assessment findings indicate pulmonary overload or developing heart failure?

Tachypnea, increase WOB, diaphoresis during feeding, fatigue and poor feeding, poor weight gain or failure to thrive, recurrent respiratory infections, heart murmur and cardiomegaly, signs of fluid congestion or HF

Anticipated treatment for congenital haert defects

• observation for smaller defects when appropriate

  • they may close spontaneously or do not cause clinically significant symptoms

• nutrition support

  • high calorie feeds and monitoring weight gain to meet increased energy needs

• diuretics when heart failure/congestion develops

  • reduce fluid overload and pulmonary congestion develops

• transcatheter closure

  • a catheter-based device closes suitable defects, such as ASD, PDA, or some VSD

• surgical closure

  • used for defects that are too large, unsuitable for catheter closure, or require surgical correction

• indomethacin or ibuprofen for selected premature infants with PDA

  • not used to keep ASD and VSD open individually, only kept open if the duct needs to stay open as well

  • indomethacin/ibuprofen: helps close a PDA

  • prostaglandin E1: keeps the ductus arteriosus open in ductal-dependent congenital heart defects

tetralogy of fallot: major physiologic problem and why cyanosis occurs

four features: VSD, overriding aorta, right-ventricular outflow obstruction, and right-ventricular hypertrophy

physiology: RV outflow obstruction decrease blood flow to the lungs —> deoxygenated blood crosses the VSD right to left —> cyanosis and hypoxemia

tetralogy of fallot: recognize stable findings vs hypercyanotic/tet spell

stable findings: baseline cyanosis, clubbing overtime, poor growth, and exercise intolerance

tet spell: sudden worsening cyanosis, tachypnea, agitation, and hypoxemia

what might trigger a tet spell?

crying, feeding, defecation/straining, or activity

tetralogy of fallot: priority interventions

• knee-chest position: increases systemic vascular resistance and reduces right to left shunting

• calm the child

• oxygen/support

• escalate care

tetralogy of fallot: purpose of IV fluids, morphine, beta blockers, or vasoconstrictors when prescribed

IV fluids improve preload, morphine calms the child, beta blockers reduce outflow tract spasm, vasoconstrictors increase SVR and reduce right to left shunting

tetralogy of fallot: definitive treatment and continued follow up

definitive treatment: surgical repair

long term care: lifelong congenital cardiology follow up due to risk of pulmonary valve dysfunction and arrhythmias

TGA, Truncus Arteriosus, and Tricuspid Atresia: why mixing of oxygenated and deoxygenated blood is necessary for survival in these defects

survival depends on mixing through an ASD/PFO, VSD, or PDA

TGA

Aorta arises from the right ventricle; pulmonary artery arises from the left ventricle. this creates 2 parallel circulations.

• assessment: newborn may have profound cyanosis with relatively little respiratory distress

• purpose of prostaglandin E1: maintains ductal patency when additional mixing is needed

• anticipated definitive surgical treatment: arterial switch operation, the definitive neonatal repair for most patients

Truncus arteriosus

one arterial trunk supplies systemic, pulmonary, and coronary circulation, a VSD is usually present

• combination of cyanosis and HF: due to mixing and excessive pulmonary blood flow

  • Early repair with VSD closure and creation of a right-ventricular to pulmonary artery pathway

Tricuspid atresia

Tricuspid valve is absent, so blood must cross an atrial communication

• ASD and VSD/PDA may be necessary for blood flow

• pulmonary blood depends of an VSD and/or PDA. PGE1 is used when pulmonary blood flow is ductal-dependent

• Treatment: usually needs staged single-ventricle palliation, such as Glenn/Fontan procedures

Coarctation: assessment findings to the physiology

• Upper-extremity hypertension

• Weak/delayed femoral pulses

• Low lower-extremity blood pressure/perfusion

Coarctation: neonatal deterioration when the ductus closes

Poor feeding, pallor, acidosis, oliguria, shock, weak lower-extremity perfusion

Coarctation treatment

• Prostaglandin E1 when ductal support is needed

• Catheter-based intervention or surgery

• Critical aortic stenosis can cause a similar low-output neonatal presentation; balloon valvuloplasty or surgery may be required

Coarctation: nursing priority

Continuous cardiorespiratory monitoring, IV access, temperature and perfusion assessment, and airway readiness because apnea and hypotension can occur

Compare manifestation of heart failure in an infant with those in an older child

• Infants: feeding is exercise, tachypnea and tachycardia, sweating during feeds, tires before finishing feeds, poor weight gain, irritability, hepatomegaly

• Older children: exercise intolerance, dyspnea and fatigue, abdominal distention, edema and JVD, cough/crackles and poor growth

Heart failure: findings for worsening perfusion

Altered mental status, delayed capillary refill, weak pulses, decreased urine output, worsening feeding tolerance, worsening respiratory status. A normal BP does not exclude low cardiac output

Heart failure: nursing interventions

Cluster care, allow rest, minimize prolonged crying, and pace activity. Provide small frequent high calorie feeds. limit exhausting feeding sessions; supplemental tube feeding may be needed. trend weight, i/o, urine output, electrolytes, renal function, respiratory status, and perfusion. diuretics are common for congestion. other afterload-reducing and HF therapies depend on the lesion and ventricular physiology. digoxin is used selctively, not automatically.

Heart failure: how would you know treatment is working?

• look for improving respiratory status, feeding tolerance, growth/weight trends, urine output, and perfusion

cardiac catheterization: assessments before the procedure

Verify NPO status, renal function/contrast considerations, baseline pulses and perfusion, hemoglobin/hematocrit, access plan, and informed consent

cardiac catheterization: post-procedure complicaations

monitor access-site bleeding, distal pulses, limb temperature/color, vital signs, rhythm, urine output, and hydration

cardiac catheterization: routine reassessment versus immediate escalation

immediate escalation: expanding hematoma, absent pulses, severe pain, hypotension, new neurologic changes

Transcatheter closure

selected ASD, PDA, and some VSDs

Balloon valvuloplasty

Selected congenital pulmonary or aortic stenosis

Balloon/stent therapy

Some coarctations

Surgical repair

TOF, TGA, truncus arteriosus, and complex septal/outflow lesionsS

Staged single-ventricle procedures

Glenn/Fontan pathways for lesions such as tricuspid atresia

Dilated Cardiomyopathy

Dilated: enlarged, week ventricle —> systolic failure

Recognize: dyspnea/orthopnea, edema, S3, fatigue, poor perfusion, arrhythmias

Diagnostic finding of echocardiography: ventricular dilation and reduced systolic function

Dilated cardiomyopathy anticipated treatments

• guideline-directed heart failure medications

• diuretics for congestion

• selected ICD/CRT

• LVAD/transplant evaluation in advanced disease

• Anticoagulation for specific indications such as AF or documented intracardiac thrombus, not automatically for all DCM patients

Evaluate improving respiratory status, congestion, activity tolerance, perfusion, renal function, and ventricular function

Peripartum cardiomyopathy

Recognize new heart failure developing late in pregnancy or during the months after delivery

Peripartum cardiomyopathy is a cause of dilated cardiomyopathy and reduced systolic function

Peripartum cardiomyopathy: why ACE inhibitors/ARBs/ARNI/mineralcorticoid receptor antagonist are avoided

Due to high risk of fetal toxicity, birth defects, and life-threatening complications

Hypertrophic cardiomyopathy

Thick myocardium —> impaired relaxation and sometimes dynamic outflow obstruction

Recognize: exertional dyspnea, chest pain, syncope, systolic murmur, AF/ventricular arrhythmias, family history of HCM or sudden death

Hypertrophic cardiomyopathy: why can dehydration or a sudden reduction in preload make obstructive HCM worse?

It can worsen dynamic outflow in obstructive HCM

Hypertrophic cardiomyopathy: anticipated treatments

• beta blockers (nonvasodilating beta blockers are common first-line therapy for symptomatic obstructive HCM)

• verapamil or diltiazem in selected patients

• selected calcium-channel blockers

• selected myosin inhibitor therapy

• ICD for selected high-risk patients

• septal myectomy or alcohol septal ablation for persistent obstruction

hypertrophic cardiomyopathy: findings indicating worsening obstruction or poor perfusion

Exertional symptoms, syncope/presyncope, or ventricular arrhythmias are important warning findings

restrictive cardiomyopathy

stiff ventricle —> severe filling problem, with relatively preserved contraction early

recognize: JVD, hepatomegaly, ascites, edema, fatigue/dyspnea, AF

restrictive cardiomyopathy: why excessive preload reduction can worsen cardiac output?

due to the heart’s rigid, non-compliant chambers, and fixed filling mechanics

restrictive cardiomyopathy treatment

Treating underlying cause and managing congestion carefully.

Avoid excessive preload reduction because it can worsen cardiac output

Advanced disease may require HF or transplant evaluation

Arrhythmogenic cardiomyopathy

Ventricular arrhythmias and sudden-death risk may dominate the presentation

Think ventricular arrhythmias, syncope, and sudden-death risk

Arrhythmogenic cardiomyopathy: Treatment

ICD therapy for selected high-risk patients

Recognize instability, ventricular arrhythmia, hypotension, pulmonary edema, or shock needs immediate intervention

Valve disorders: stenosis and regurgitation

Stenosis: valve does not fully open —> pressure overload behind the valve

Regurgitation: valve does not fully close —> backward blood flow and volume overload

Consequences: chamber hypertophy/dilation, AF pulmonary hypertension, HF, low cardiac output, or thromboembolic

Valve disorders: echocardiography

The foundation for determining valve severity and the effect on chambers and ventricular function. TEE, CT, cardiac MRI, stress testing, or catheterization may provide additional detail.

Trend symptoms and ventricular response, not just the murmur. New dyspnea, syncope, pulmonary edema, declining EF, chamber dilation, or pulmonary hypertension can indicate progression.

Mitral valve disease: stenosis

• Elevated left-atrial pressure can lead to pulmonary hypertension, dyspnea, AF, and thromboembolic risk

• Selected rheumatic mitral stenosis may be treated with percutaneous balloon mitral commissurotomy M

Mitral valve disease: regurgitation

• Blood flows backward from LV to LA during systole

• Causes left-atrial and left-ventricular volume overload and pulmonary congestion

• Acute severe MR can cause sudden pulmonary edema and shock

• Chronic MR may cause progressive dyspnea, fatigue, AF, or HF

• Severe MR may require surgical repair/replacement or transcatheter edge-to-edge repair (TEER) in selected patients

Aortic valve disease: stenosis

• Think dysnpea, angina, syncope when severe

• Causes LV pressure overload

• Treatment: surgical aortic valve replacement (SAVR) or transcatheter aortic valve replacement (TAVR), depending on patient factors and anatomy

Aortic valve disease: regurgitation

• Diastolic backflow causes LV volume overload

• Chronic disease may cause widened pulse pressure, exertional dyspnea, and progressive LV dilation

  • Medical therapy may support BP or HR management but does not correct severe valve disease

Pulmonic valve disease: stenosis

may be congenital and can be treated with balloon valvuloplasty

Pulmonic valve disease: regurgitation

• important in patients with previous TOF repair and may eventually require valve replacement

• progressive RV dilation or symptoms may lead to surgical or transcatheter pulmonary valve replacement

Tricuspid valve disease: regurgitation

often accompanies RV dilation or pulmonary hypertension

Findings: JVD, hepatomegaly, ascites, peripheral edema, and fatigue

Mechanical vs bioprosthetic valves

Mechanical: very durable; requires lifelong vitamin-k antagonist anticoagulation and INR monitoring. Direct oral anticoagulants are not used for mechanical valves

Bioprosthetic: less durable; structural degeneration can occur. Antithrombtic therapy depends on the valve, time since implantation, rhythm, and other indications

Why medication adherence and anticoagulation history matter before invasive or surgical procedures:

They directly determine a patient’s risk of catastrophic blood clots vs severe, life-threatening surgical bleeding

Consider bleeding risk, drug/food interactions, and prescribed antithrombotic plan

Prophylaxis reserved for high-risk

After valve intervention, monitor for:

Bleeding or vascular complication, stroke or new neurologic deficits, conduction abnormalities or heart block, especially after TAVR. New/worsening HR, arrhythmia, or hypotension. Hemolysis, paravalvular leak, or prosthetic valve dysfunction, infection/endocarditis.

Evaluate: improved symptoms, stable perfusion, appropriate valve function/gradients, and ventricular recovery

Palliative care

symptom relief, communication, and quality of life; occur alongside disease-directed treatment

Hospice care

comfort-focused care for patients approaching end of life under applicable eligibility criteria

Goals of end-of-life care

prolong life, a time-limited trial of treatment, comfort-focused care, or a combination

Nurses role in end of life care

Assess symptoms, advocate for the patient, communicate with families, and identify treatments that are no longer match documented goal

Terminial delirium: findings and reversible causes

• Findings: agitation, restlessness, hallucination, disorganized thinking, or fluctuating alertness

• Reversible causes: pain, urinary retention, constipation, medication effects, hypoxia, infection, or metabolic problems

Terminal delirium: nursing role

Calm communication, familiar people/objects, low stimulation, day-night cues, and safety strategies. Avoid restraints when possible

Medication may be needed if agitation causes significant distress or danger and nonpharmacologic strategies are insufficient

Provide family education and offer cultural, spiritual, social-work, chaplain, and bereavement support

Brain death/death by neurologic criteria, not coma

Requires a known catastrophic and permanent brain injury with coma, absence of brainstem function, and apnea

Spinal reflexes may remain because they do not require brain or brainstem function

Determination is performed by qualified medical professionals according to accepted standards and policy

Brain death: nursing role

Before evaluation: address confounders such as hypothermia, hypotension, sedatives/paralytics, intoxication, and major metabolic/endocrine disturbances

Nursing priorities during evaluation: maintain oxygenation, ventilation, hemodynamics, temperature, and metabolic stability. Communicate medication history and factors that may delay medication clearance. Continue airway, skin, eye, line, and device care

Monitor during apnea testing and report instability

Nurses do not independently determine BD/DNC

Organ donation: nurse role

Continue excellent patient care and physiologic support while following the appropriate referral/donation process

Keep end of life decisions separate from organ recovery decisions

Nurses do not independently determine donor suitability or independently negotiate donation with the family

Organ donation

The organ procurement organization evaluates suitability and coordinates donation

Donation types: after brain death, organ support continues. After circulatory death, withdrawal of life-sustaining treatment through separate process

Transplant

New graft dysfunction, fever, hemodynamic change, or abnormal labs require evaluation for rejection, infection, medication toxicity, or another complicationT

Before transplant

verify identity, consent, compatibility testing, infection status, medication, NPO status, and readiness for a potentially changing operative timeline

After transplant

• new graft dysfunction, fever, hemodynamic changes, or abnormal labs require prompt evaluation for rejection, infection, medication toxicity, or another complication

• Hyperacute rejection: minutes to hours, preexisting antibodies cause catastrophic graft injury

• Acute rejection: usually days to months but can occur later, may be treatable when detected early

• Chronic rejection: months to years; progressive fibrosis/vasculopathy causes gradual loss of graft function

Transplant: Nursing priorities

medication adherence and infection prevention, monitor therapeutic drug levels and renal/metabolic toxicity, promptly evaluate new organ dysfunction

Chronic hypertension

present before pregnancy or diagnosed before 20 weeks of gestational

Gestational hypertension

new hypertension after 20 weeks without proteinuria or other diagnostic feature of preeclampsia

Preeclampsia

New hypertension after 20 weeks with proteinuria or new maternal end-organ dysfunction

Superimposed preeclampsia

chronic hypertension with new or worsening features of preeclampsia

eclampsia

new-onset seizure associated with preeclampsia when another cause is not more likely

postpartum preeclampsia

preeclampsia that develops or persists after delivery including after discharge

Worsening gestational disease

• Bp: 160/110 is maternal emergency if persistent

• RUQ pain: rising liver enzymes

• Hematologic: falling platelets, hemolysis

• Renal: decreased urine output, rising creatinine

• Respiratory: dyspnea, crackles, increased oxygen requirement, pulmonary edema

• Priority: recognize worsening trends and escalate early

BP trends, CBC/platelets, renal function/urine output, AST/ALT, proteinuria, hemolysis studies, and fetal assessment

• Serum creatinine, electrolytes, and urine output

• AST/ALT for liver injury

• Urine protein-to-creatine ratio >0.3 or 24 hour urine protein > 300 mg

• If HELLP is suspected: LDH, bilirubin, peripheral smear, hemoglobin

• Fetal growth assessment and fetal surveillance based on gestational age and severity

• Preeclampsia can occur without proteinuria when new organ dysfunction is present

Labetalol

treats hypertension; monitor BP and HR

Use caution with bradycardia, heart block, decompensated heart failure, or reactive airway disease

Hydralazine

Treats severe hypertension; monitor for hypotension, tachycardia, headache, and fetal heart rate changes.

Nifedipine

extended release for ongoing BP control; immediate-release orally for urgent severe BP treatment.

Do not give immediate-release nifedipine sublingually

Magnesium sulfate

prevents or treats seizures

monitor respirations, oxygenation, consciousness, deep tendon reflexes, urine output, and renal function

not primary med for severe hypertension

calcium gluconate

antidote for clinically significant magnesium toxicity. stop magnesium and support airway/ventilation

corticosteroids (betamethasone/dexamethasone)

promote fetal lung maturation when preterm delivery is anticipated. do not delay urgent delivery just to complete steroids

Eclampsia: nursing role

• stay with patient, call for help, protect from injury

• position laterally when feasible; prioritize airway and oxygenation

• suction only as needed; never place objects in the mouth

• administer magnesium sulfate promptly per emergency protocol

• treat persistent severe hypertension with a rapid-acting antihypertensive

• assess for stroke, intracranial hemorrhage, aspiration, pulmonary edema, placental abruption, and feta. compromise

  • prioritize: stabilize mother first, delivery follows stabilization; seizure alone does not automatically require cesarean delivery

postpartum preeclampsia

• can first develop after birth, including after discharge

• warning signs: severe headache, visual changes, severe BP, confusion, seizure, dyspnea, or pulmonary edema

  • postpartum fluid shifts can worsen pulmonary edema

postpartum preeclampsia: nursing role

continue BP, neurologic, respiratory, renal, and bleeding assessment

treat persistent severe BP urgently; use magnesium when seizure risk remains high

teach patients to seek urgent evaluation for severe headache, vision changes, breathing difficulty, seizure, or severe hypertension

ensure timely postpartum BP follow-up

HELLP syndrome

watch for RUQ pain, falling platelets, rising liver enzymes, hemolysis, oliguria, bleeding, or altered mental status

HELLP = hemolysis, elevated liver enzymes, low platelets

can occur with preeclampsia, sometimes without severe hypertension or proteinuria; may also present postpartum

HELLP nursing role

anticipate stabilization, serial labs, BP/seizure management, blood products as needed, delivery when indicated

continue monitoring after delivery because labs may worsen temporarily before improving

watch for DIC, hepatic hematoma/rupture, kidney injury, pulmonary edema, and hemorrhage

HELLP diagnosistics

serial CBC/platelets

liver enzymes

renal function

coagulation studies

fibrinogen

hemoglobin

LDH

bilirubin

HELLP treatment

stabilize airway, breathing, circulation, BP, and seizure risk; magnesium sulfate when indicated; prepare blood products if needed

give corticosteroids for fetal lung maturation when appropriate; do not delay urgent delivery

definitive treatment: delivery after stabilization when indicated