Heart Failure and PE

What is heart failure?

means the heart can’t pump enough blood to meet the body’s needs. Blood backs up, Organs don’t get enough oxygen. and Fluid builds up in lungs or body

• Inadequate cardiac output

• Inadequate tissue perfusion

• increased diastolic filling pressure → increased in pulmonary capillary filling

It’s not that the heart stops — it’s that it works too hard and too poorly.

Why does heart failure happen? Common cause

• Long-standing high blood pressure

• Coronary artery disease (CAD)

• Heart attack (MI)

• Valve problems (mitral/aortic)

• Cardiomyopathy

• Pulmonary hypertension

• Pericarditis

Think: anything that increases workload or damages the heart muscle.

How it work and result too much work load? What is cardiac output?

The heart struggles with:

• Preload → how much blood fills the heart

• Afterload → how hard the heart has to pump against pressure

In HF:

• Kidneys think blood flow is low

• They retain sodium & water

• This increases preload

• More fluid = more stress on the heart

Cardiac output- the volume of blood pumped from each ventricle per minute

increased preload and afterload can result to?

What is baroreceptor?

This is the body’s EARLY response when cardiac output drops (like in Heart Failure).

The body is trying to save blood pressure and perfusion.

Signals are sent to the CNS → SNS increases heart activity → SNS causes vasoconstriction → SNS increases preload → Kidneys release renin

What happens in the body?

• Heart pumps poorly → ↓ cardiac output

• Body panics

• Activates:

  • Sympathetic Nervous System (SNS) release epinephrine and norepinephrine→ ↑ HR, vasoconstriction, contractility, and conduction ← B1 receptor stimulated

  • RAAS system → In kidney; retain sodium & water

• Short-term help (B1 help the heart to pump more) → long-term harm

• Fluid overload + worsening HF

What induces excretion of sodium by the kidney?

Natriuretic Peptide

Atrial natriuretic (ANP)

–Increases sodium excretion – secreted by muscle cells in the atria.

Brain natriuretic peptide (BNP)*

–Hormone secreted by the cardiomyocytes in the ventricles in response to an increase ventricular blood volume.  

Key indicator to diagnosis of HF?

Brain natriuretic peptide (BNP)*

> 100 = HF

Heart failure is a chronic (long-term) process where the heart is stuck in a loop it can’t escape. What are those?

1⃣ Afterload on the Left Ventricle increases

Afterload = how hard the LV must push to eject blood.

In HF:

• Blood vessels are constricted

• Blood pressure is higher

• The LV must work harder to pump forward

🧠 Think: pumping against a tight hose

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2⃣ Cardiac workload increases

Because afterload is high:

• LV uses more energy

• LV needs more oxygen

• Muscle gets tired and stiff

The heart is overworking every beat.

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3⃣ Stroke volume decreases

Stroke volume = blood pumped per beat

Because the LV is weak or stiff:

• Less blood leaves the heart

• More blood stays behind

• Ejection fraction drops

This is the failure part of heart failure.

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Why this becomes a vicious cycle

• ↓ Stroke volume → ↓ cardiac output

• Body senses poor perfusion

• SNS + RAAS activate

• ↑ Vasoconstriction → ↑ afterload

• ↑ Fluid retention → ↑ preload

• Heart stretches and weakens

➡ And the cycle continues.

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LV ejection fraction of HF patient

The percentage of blood pumped out of the LV with each beat.

35% or less

• Reduced EF which causes an increase in residual end-systolic volume

• *The more a myocardial fiber is stretched during filling, the more it shortens during systole and the greater the force of the contraction

Left and right HF Overview

What is left HF?

• Heart does not “pump” effectively

• Accumulates in the pulmonary (backward)

• Hydrostatic pressure builds

• Fluid is forced from the capillaries into the interstitial and alveolar spaces causing edema.

Sign and Symptoms of left HF

Left HF: Lungs- blood backs up

•Mnemonic: "DO CHaP"

•D → Dyspnea

•O → Orthopnea

•C → Cough/Crackles

•H → Hemoptysis (frothy sputum)

•a → Adventitious lung sounds (Crackles)

•P → Pulmonary congestion

Paroxysmal nocturnal dyspnea- severe shortness of breath that wakes individuals from sleep

What is right HF?

Pulmonary disorders increase pulmonary vascular resistance, raising afterload on the right ventricle and leading to right ventricular hypertrophy and failure (cor pulmonale).

What happens to the BODY when right-sided heart failure backs blood up into the systemic circulation?

• Liver -- Hepatocytes atrophy and necrosis because of high pressure.

• Portal system will have an increase in hydrostatic pressure = Ascites.

• Enlarged spleen and GI tract

• Kidneys and decreased glomerular filtration

• Fluid retention – aldosterone not metabolized

• Superior Vena Cava cannot drain

Management of Heart Failure

Nutrition Management

Thiazide Diuretic (if not acute for older adults to prevent dehydration)

CPAP in patients with sleep apnea

Ventricular assist devices

Pacer – biventricular pacing

Medication Management of left and right HF

Left HF

• CE inhibitors / ARBs / ARNIs (CORE meds)

• Beta blockers

• Diuretics

• Aldosterone antagonists

• Digoxin (selected patients)

Right HF

Diuretics (MOST IMPORTANT for RHF)

Treat pulmonary cause

ACE inhibitors & beta blockers

What is ACE inhibitor? (action, Contraindication, and s/e)

Suffix: pril

–Examples (Captopril, Lisinopril, Enalapril, Ramipril)

ACTION:  Suppress the RAAS system and prevent activity of ACE

–This causes Na and H2O to not be retained so sodium and BP will decrease; also dilates blood vessels

Contraindications

–Renal failure—can worsen renal failure—what should you monitor

S/E: and AE

–Angioedema-

–Cough—annoying but normal

–Elevated K+

Key teaching for ACE

–Avoid potassium containing foods/meds

•Don’t forget to teach about salt substitutes usually containing high potassium levels

–Monitor weight and assess for s/s of heart failure

–First Dose hypotension effect—change positions slowly, ask for assistance

What is ARBS?

Suffix:  sartan

•Examples: Valsartan, Losartan

• Similar to ACE inhibitors in use, patient education and nursing considerations but some key differences:

Action: Inhibits angiotensin II verses Ace inhibitors which inhibit ACE conversion of Angiotensin I to Angiotensin II

Produce fewer side effects

Does not have cough SE

Less risk for angioedema

• ACE inhibitors do not impact HR but ARBs decrease HR

What is Digoxin? (Action, s/e, what to monitor?)

•Allows heart muscles to contract more efficiently

Side effects include bradycardia, visual disturbances (diplopia, halo around lights, blurred vision, yellow vision, photophobia)

•Monitor serum digoxin levels

Therapeutic range 0.5 -2.0 ng/dL

•Monitor apical pulse for 1 minute

•If <60 bpm, withhold med and notify physician 

Digoxin toxicity (s/s, toxic level, monitor, antidote)

S/S

–Early: Gi manifestations (anorexia, nausea, vomiting, diarrhea) then heart rate abnormalities, visual disturbances

Toxic Level:

–Greater than 2.0

Risk Factors for Toxicity

–Hypokalemia—

Monitor levels

•Pt’s taking loop and thiazide diuretics

•Teach pts to eat foods high in potassium

Antidote

–Digibind

HESI MUST KNOW: DIURETICS

Key teaching management of HF

Daily weights (MOST IMPORTANT teaching)

How is it done?

Tell the patient to:

• Weigh every morning

• After urinating

• Before eating or drinking

• Same scale

• Same clothes (or no clothes)

• Same time every day

Consistency is EVERYTHING.

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When should the patient notify the HCP?

Call the provider if:

• Gain of 2–3 lb in 1 day

• OR 5 lb in 1 week

This usually means fluid retention, not fat gain.

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How do you confirm a patient’s report of weight gain?

If the patient says,

“I gained 6 pounds in 3 days”

You confirm by:

• Reviewing documented daily weights

• Comparing today’s weight to baseline

• Assessing for:

  • Edema

  • JVD

  • Crackles

  • Shortness of breath

Objective daily weights > patient feelings

Diet: Heart-Healthy / DASH DietMain goals:

• ↓ Sodium

• ↓ Fluid retention

• ↓ Blood pressure

• ↓ Cardiac workload

Limit sodium to ~2 g/day

Avoid salt substitutes if on ACE inhibitors or aldosterone antagonists (high potassium!).

Discharge to Home in Heart Failure

Indications of poor perfusion

Examples from your slide:

• Fatigue

• Angina (chest pain)

• Activity intolerance

What does this mean?

Poor perfusion = organs aren’t getting enough oxygenated blood.

This tells the nurse:

• Cardiac output is still limited

• Patient may not tolerate normal activity

• Risk for falls, injury, worsening HF

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Nursing implications (assessment & interventions)

You should:

• Assess vital signs with activity

• Monitor for:

  • SOB

  • Dizziness

  • Chest pain

  • Excessive fatigue

• Adjust activity level

• Teach energy conservation

• Coordinate home support if needed

NCLEX clue: Fatigue = ↓ cardiac output

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Assess ability to perform ADLs

ADLs = bathing, dressing, toileting, cooking, walking.

What are you looking for?

Ask:

• “Can you shower without stopping?”

• “Do you get short of breath getting dressed?”

• “Can you walk to the bathroom safely?”

If patient cannot perform ADLs independently:

• They may need:

  • Home health nursing

  • Physical therapy

  • Assistive devices

  • Family support

Safety + independence = discharge readiness

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Energy conservation strategies (VERY TESTABLE ⭐)

Teach the patient to:

Plan & pace

• Schedule activities with rest periods

• Do hardest tasks in the morning

• Sit instead of stand when possible

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Reduce energy use

• Keep frequently used items within reach

• Avoid unnecessary trips up/down stairs

• Use shower chair, raised toilet seat if needed

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Control breathing

• Stop activity if SOB

• Use pursed-lip breathing

• Avoid rushing

Memory trick: “Do less, rest more, breathe better”

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Assess nutritionWhat are you looking for?

• Excess sodium intake

• Poor appetite or early satiety

• Unintentional weight gain or loss

• Understanding of DASH / low-sodium diet

Ask:

• “What did you eat yesterday?”

• “Do you read food labels?”

• “Who prepares your meals?”

Red flags 🚩:

• Processed foods

• Fast food reliance

• No understanding of sodium limits

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Assess home environment

You’re looking for:

• Stairs (can patient manage them?)

• Bathroom safety

• Access to scale for daily weights

• Transportation to appointments

• Ability to obtain medications

Unsafe home = ↑ risk of:

• Falls

• Non-adherence

• Readmission

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Assess understanding of disease

Ask teach-back questions:

• “What symptoms should make you call your provider?”

• “Why do you weigh yourself daily?”

• “What foods should you avoid?”

You want to see:

• Understanding of:

  • Daily weights

  • Medication purpose

  • Diet

  • Symptom reporting

If they can’t explain it → teaching isn’t done.

What is pulmonary edema?

Pulmonary edema happens when fluid leaks into the lungs (alveoli) instead of staying in blood vessels.

➡ Oxygen can’t move well
➡ Gas exchange fails
➡ The patient feels like they’re drowning in air

What causes PE?

Fluid overload

• Too much fluid in circulation

• Often from heart failure, renal retention, or excess IV fluids

The heart can’t handle the volume → blood backs up into lungs.

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Acute MI

• Sudden loss of left ventricular pumping ability

• Blood backs up into pulmonary circulation

• Pressure forces fluid into alveoli

Heart suddenly fails → lungs pay the price

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Mitral valve disease

• Blood leaks backward from LV → LA → lungs

• Pulmonary pressure rises

• Fluid shifts into lung tissue

What nurses must assess EARLY for PE?

Key early assessment findings:

• Crackles (especially bases)

• Dyspnea at rest

• Disorientation or confusion

• Restlessness

• Anxiety

Confusion = low oxygen to the brain (late sign!)

If PE is left untreated what’s gonna happen?

• Severe hypoxia

• Pink, frothy sputum

• Respiratory failure

• Cardiac arrest

This is why crackles + SOB at rest = act NOW

Nursing priority for PE

Airway and breathing FIRST

• Sit patient upright

• Apply oxygen

• Call provider / rapid response