Med Surg Test 2 Lecture 2
Cardiac Assessment
Neck Vessels: Carotid Artery Assessment
1. Palpation (feeling the pulse)
 Only palpate one side at a time (to avoid cutting off blood flow to the brain).
 When it comes to other pulses you would palpate both sides at the same time to see if
they are equal, the only exception is the carotid pulse
 Use gentle pressure.
2. Auscultation (listening with stethoscope)
 Ask the patient to hold their breath so you don’t mistake lung sounds for the carotid pulse
sounds
 Use the bell of the stethoscope lightly (pressing too hard can create a false bruit sound).
 Listen for a bruit (pronounced brewy)
o This is a whooshing sound caused by blood flow through a narrowed artery.
o It’s heard when the artery is partly blocked (50–67%).
o If the artery is fully blocked, the bruit disappears (no blood flow = no sound).
Normal: Blood flow in the arteries is silent (you shouldn’t hear anything).
Abnormal: If you hear a bruit (whooshing sound), it means turbulent blood flow, usually
from narrowing/partial blockage of the artery.
narrowing.
completely occluded (100% blocked), you will not hear a bruit because no
blood is moving at all. That is worse than a bruit.
Silence can mean two totally different things:
1. Normal, healthy artery → Silent because blood is flowing smoothly.
2. Completely occluded artery → Silent because no blood is flowing at all.
How do you tell the difference?
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You don’t rely on auscultation alone.
You also palpate (feel) the carotid pulse:
o If you feel a strong pulse + silence → normal.
o If you feel no pulse + silence → complete occlusion (bad).
Neck Vessels – Jugular Venous Pulse (JVP)
1. Positioning the patient
 Have them lying back at a 30–45° angle.
 Turn their head slightly away from the side you are checking.
 Shine a light across the neck to make the vein pulsation easier to see.
2. What to look for
 A normal JVP should not rise more than 3 cm above the sternal angle.
 If pulsation is greater than 3 cm, this may mean fluid overload or right-sided heart failure.
3. Changes with position
 As the patient sits up, the jugular veins should flatten and disappear.
 If they stay distended (bulging), that’s abnormal and suggests increased central venous
pressure.
Preload: How much blood is filling the ventricles right before the heart contracts to pump it out
to the body (or to the lungs on the right side). It’s pretty much the stretch/filling of the heart just
before it pumps blood out.
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Right side preload: Blood coming back from the body into the right atrium/ventricle
(goes to the lungs).
Left side preload: Blood coming back from the lungs into the left atrium/ventricle (goes
out to the body).
When the jugular veins are distended, it means:
 There’s a lot of blood backed up in the veins.
 The right side of the heart is having trouble handling the blood returning to it.
 So by looking at the jugular veins, you can estimate how much blood volume (preload) is
in the system.
The Precordium
Precordium: The area on the chest wall directly over the heart and great vessels, such as the
aorta and pulmonary artery. It is the region where you inspect, palpate, and auscultate in order to
assess the heart. When performing a cardiac exam with a stethoscope, you are working on the
precordium.
- When inspecting the anterior chest, focus on the apical impulse (PMI = point of maximal
impulse). This is usually found at the 4th or 5th intercostal space (ICS), just medial to the
left midclavicular line (MCL).
- In simple words, the apical impulse (PMI) is on the left rib cage, about the 4th or 5th rib
down, usually just under the nipple
- To assess it, place one fingertip over the area and feel for the impulse. Normally, the PMI
should feel like a gentle tap, about 1 cm by 2 cm in size.
- To better feel the apical impulse (PMI), position the patient lying on their left side (left
lateral position), which brings the heart closer to the chest wall.
- If you feel a sustained (“longer, stronger”) forceful thrusting, this is called a heave or lift.
A heave/lift means the ventricle is pushing very hard during systole (when it contracts).
This is usually a sign of ventricular hypertrophy (an enlarged, thickened ventricle).
The Precordium (Palpation)
• Palpate across the precordium: This means use your hand to feel over the entire chest area
where the heart is located (the precordium). You’re checking for any unusual pulsations or
vibrations.
• Use the palmar aspect four fingers: Instead of using your fingertips, you place the flat pads of
your 4 fingers against the chest. This lets you feel vibrations or strong movements more clearly.
• Palpate the apex, left sternal border, & the base, searching for any other pulsations: You
don’t just check one spot, you move your hand across key areas:
Apex (bottom tip of the heart → near the 4th/5th rib, left side).
Left sternal border (alongside the sternum).
Base (upper part of the heart, near the 2nd intercostal spaces).
• A thrill is a palpable vibration & accompanies loud murmurs: A thrill feels like a vibration
or cat purring under your hand. It happens when blood flow is very turbulent. Thrills usually go
along with loud heart murmurs, which suggest significant valve problems. A murmur can be
quiet and only heard with a stethoscope (no thrill), or it can be loud enough to cause a palpable
vibration called a thrill. Murmur: The sound Thrill: The vibration
The Precordium: Auscultate the heart sounds
Identify the auscultatory areas: Where sounds produced by heart valves are heard best, not their
anatomic position.
The 4 main heart valve areas on the chest: Ape to man
 A: Aortic (right 2nd intercostal space, just next to the sternum)
 P: Pulmonic (left 2nd intercostal space, next to the sternum)
 E: Erb’s Point (left 3rd intercostal space)
 T: Tricuspid (left 4th intercostal space, near the sternum)
 M: Mitral (left 5th intercostal space, midclavicular line — same as PMI)
The “Z Pattern”
 You don’t just go straight down in a line.
 Instead, you inch your stethoscope in a Z pattern from the base to the apex & back.
1. Start on the right for Aortic,
2. Cross over to the left for Pulmonic,
3. Drop down a little to Erb’s Point,
4. Down again to Tricuspid,
5. Then over to the left side for Mitral
Note rate & rhythm
 First, listen to the overall heart rate (fast, slow, normal) and rhythm (regular vs irregular).
Identify heart sounds (S1 & S2)
 S1 (“lub”): Is best heard at the apex (bottom of the heart, near the PMI).
 S2 (“dub”): Is best heard at the base (top of the heart, near aortic/pulmonic areas).
Listen for murmurs
When listening for murmurs, describe them using these features:
 Location: Where on the chest is it heard loudest? (aortic, pulmonic, tricuspid, mitral)
 Timing: Does it happen during systole (heart squeezing) or diastole (heart filling/relaxing
 Intensity: How loud is it? (graded I to VI — softest to loudest).
 Pitch: Is it high, medium, or low frequency?
 Quality: What does it sound like? (musical, blowing, rumbling).
 Radiation: Does the sound travel? (a murmur heard at the apex might radiate to the axilla
or neck).
Murmurs : Intensity
 Grade 1: Barely audible
 Grade 2: Clearly audible
 Grade 3: Moderately loud
 Grade 4: Loud with a thrill
 Grade 5: Very loud with an easily palpable thrill
 Grade 6: Very loud, no stethoscope needed, palpable and visible thrill
A grade 3 murmur is considered moderately loud, meaning it is about the same loudness as the
normal heart sounds (S1 and S2), but you can still tell it apart because it has a different quality
— a whooshing or blowing sound instead of the normal “Lub–Dub.”
Grade 1–3: Heard only with the stethoscope (no vibration).
Grade 4–6: Loud enough that the turbulence can actually be felt as a vibration (thrill).
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S1 (“Lub”): Is made when the mitral and tricuspid valves close. It’s heard best at the apex
of the heart, especially over the mitral area. Both the mitral and tricuspid valves close
together to produce one sound.
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S1 = “Lub” (closure of mitral + tricuspid valves → start of systole).
S2 = “Dub” (closure of aortic + pulmonic valves →end of systole).
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Lub–Dub (quick): Systole.
Pause (longer): Diastole.
S1 → S2: Systole (shorter phase, heart squeezing).
S2 → Next S1: Diastole (longer phase, heart relaxing and filling).
S1 (“Lub”): Happens when the mitral and tricuspid valves close → this is the start of systole
→ the ventricles begin pumping blood out (left ventricle to the body, right ventricle to the lungs).
S2 (“Dub”): Happens when the aortic and pulmonic valves close → this is the end of systole
→ the ventricles have finished squeezing blood out.
Extra Heart Sounds
S3 (Ventricular Gallop)
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The S3 sound happens early in diastole (right after S2 and before the next S1) and is
caused by blood rushing into a ventricle that isn’t empty yet (partially filled).
 It sounds like a dull, soft, low-pitched noise, sometimes described as “distant thunder.”
 S2 is best heard with the bell of the stethoscope while the patient is lying on their left side
(left lateral position).
 The rhythm of S1–S2–S3 makes the heart sound like “Lub-dah-tah” or “slush-ing-in.”
 Can be normal in children, young adults, and adults up to age 30.
 In older adults, it usually means the ventricles have decreased compliance (they are stiff
and don’t relax well).
 An S3 can be the earliest sign of heart failure.
S4 (Atrial Gallop)
 S4 is a low-pitched sound, best heard with the bell of the stethoscope.
 It sounds like “Lah-dah-dup” or the phrase “a stiff wall.”
 It occurs late in diastole, right when the atria contract and push blood into the ventricles.
 The sound happens because the ventricles are stiff and noncompliant, so they don’t relax
and fill easily.
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S4 is usually abnormal and is associated with conditions that stiffen the ventricles like
coronary artery disease (CAD), cardiomyopathy, and systemic hypertension.
Extra Notes
- Systolic murmurs might sometimes be harmless, but diastolic murmurs are never normal,
they always need evaluation.
- Swooshing over the heart: Murmur (problem with a valve or blood flow inside the heart).
- Swooshing over an artery: Bruit (turbulent flow in that vessel, often from
narrowing/blockage).
- For low-pitched heart sounds, use the bell of the stethoscope. Place the bell over the apex
while the patient is turned onto their left side.
- In heart failure, the ventricles don’t completely empty during systole, which causes blood
to back up and leads to fluid overload symptoms
- At the very end of diastole, the atria contract and push the last bit of blood into the
ventricles. This is called the atrial kick, and it ensures the ventricles are completely filled
and ready to pump, leading into S1 and the start of systole again.
Heart Failure
Definition: Heart failure happens when the heart muscle (myocardium) is too weak or stiff to
pump enough blood to meet the body’s needs (metabolic needs of the body). Because of this, the
body does not get enough oxygen and nutrients, which causes symptoms such as tiredness and
poor circulation (inadequate tissue perfusion). It can also lead to fluid building up in the lungs,
legs, or other tissues, causing shortness of breath and swelling. Heart failure is when the heart
cannot keep up with the demands of the body, resulting in problems from both poor blood flow
and fluid buildup.
Cardiac Output (CO): Cardiac output is the amount of blood pumped from the ventricles in one
minute. It’s calculated by multiplying heart rate (HR) the number of beats per minute — by
stroke volume (SV) — the amount of blood pushed out with each beat. So, CO = HR × SV. This
tells us how effectively the heart is moving blood through the body. Average stroke volume: 70
Cardiac Reserve: Cardiac reserve is the heart’s ability to increase its output when the body
needs more blood and oxygen, like during exercise, stress, or illness. A healthy heart has a strong
reserve and can quickly pump more blood when needed. In heart failure, this reserve is reduced,
so the heart struggles to keep up with increased demands. If I run around the block, my heart
accommodates my body’s increased need for blood. In people with heart failure, the heart cannot
adjust to this demand, causes symptoms such as shortness of breath, dizziness, or chest pain.
Normal cardiac output: Is about 5 L/min, but the exact value can vary depending on a person’s
height and weight, since body surface area influences cardiac output.
Variables Affecting Cardiac Output
Heart Rate: The number of times blood is ejected from the ventricles in a minute. Affected by
the autonomic nervous system.
Stroke Volume: The amount of blood ejected with each heartbeat.
Heart Failure : Physiology
Variables Affecting Stroke Volume
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Preload: The stretch of the ventricles at the end of diastole, caused by the amount of
blood in them. According to the Frank-Starling law, the more the heart muscle
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stretches, the stronger the contraction—up to a certain physiologic limit. Keep in mind
that you will get less blood pumped out if you stretch the myocardial fibers too much
Afterload: The resistance the ventricles must push against to eject blood into circulation.
Contractility: The heart muscle’s natural ability to shorten (squeeze) during systole.
Heart Failure : Etiology
Coronary Artery Disease (CAD): Narrowing or blockage of the coronary arteries (usually from
atherosclerosis), which reduces blood flow to the heart muscle.
Cardiomyopathy: Disease of the heart muscle that makes it harder for the heart to pump blood,
can cause the heart to become enlarged, thickened, or stiff.
Hypertension: Consistently high blood pressure that increases the heart’s workload and
damages blood vessels over time.
Valvular Disorders: Problems with one or more of the heart valves (stenosis, regurgitation, or
prolapse) that affect how blood flows through the heart.
New York Heart Association Classification of Heart Failure
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Class I: No symptoms; tolerates ordinary physical activity
Class II: Comfortable at rest; ordinary physical activity results in symptoms
Class III: Comfortable at rest; less than ordinary physical activity results in symptoms
Class IV: Symptoms may be present at rest; symptoms with any physical activity
Classification of Heart Failure
Systolic vs. Diastolic Heart Failure
Systolic Failure: Happens when the ventricle does not contract strongly enough to pump out
(eject) a sufficient amount of blood into the arterial system. The ejection fraction (EF) is less
than 40%. This is often seen when myocardial (heart muscle) cells are lost because of ischemia
that progresses to muscle necrosis, such as after a myocardial infarction (MI). Systolic HFrEF is
the most common functional type of heart failure
Diastolic Failure: Happens when the heart cannot fully relax during diastole, which disrupts the
normal filling of the ventricles. This results from increased ventricular stiffness caused by
hypertrophy, cellular changes, and impaired relaxation of the heart muscle.
Left-sided versus Right-sided Heart Failure
Left-Sided Heart Failure
 Most common type of heart failure.
 Caused by ventricular muscle damage or volume overload.
 Symptoms come from pulmonary congestion and decreased cardiac output (CO).
Key Manifestations in left sided heart failure:
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Early signs: Fatigue and activity intolerance.
Low CO symptoms: Dizziness, syncope.
Pulmonary congestion symptoms: Dyspnea, shortness of breath, cough, orthopnea
(trouble breathing lying flat), cyanosis.
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Lung sounds: Crackles and wheezes at the bases.
Heart sound: Possible S3 gallop.
Left = Lungs: Left-sided failure backs fluid into the lungs → causes breathing problems,
fatigue, and decreased perfusion.
Right-Sided Heart Failure
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Most common cause: Left-sided heart failure.
Primary causes: Pulmonary hypertension (cor pulmonale) or right ventricular (RV)
infarction.
Leads to right ventricle (RV) and right atrium (RA) distention → blood backs up into the
systemic venous system.
Blood Flow Reminder:
 Blood from the body enters the Right Atrium (RA) → moves through the tricuspid valve
into the Right Ventricle (RV) → pumped to the lungs to get oxygen.
 In right-sided failure, this process is impaired → blood backs up before it can get to the
lungs.
Key Manifestations:
 Edema: Swelling in feet/legs (if patient is upright) or sacrum (if patient is reclining).
 Organ congestion: Enlarged, tender liver; splenomegaly (enlarged spleen).
 GI symptoms: Anorexia, nausea.
 Urinary changes: Nocturia.
 Other: Fatigue.
 Neck veins: Increased central venous pressure (CVP) → jugular vein distention (JVD).
Biventricular Heart Failure
 Definition: Both ventricles (right and left) fail to function adequately.
 Symptoms: Combination of right- and left-sided heart failure signs.
 Breathing issues: May have paroxysmal nocturnal dyspnea (PND) and may be short of
breath at rest and with activity.
 Heart sounds: Both S3 and S4 may be heard on auscultation.
 Serious risks: High risk of sudden cardiac death.
 Complications: Can lead to cardiogenic shock and pulmonary edema.
Collaborative Care
Goals:
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Reduce cardiac workload
Improve cardiac pumping ability
Control fluid retention
Laboratory & Diagnostic Tests:
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Serum electrolytes, Liver function tests (LFTs), ABGs
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B-type natriuretic peptide (c-BNP):
o Elevated levels = poorer outcomes
o Normal (NL) = less than 100
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ProBNP:
o Age < 50 yrs: less than 450 pg/mL
o
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Age ≥ 50 yrs: less than 900 pg/mL
Chest X-ray: May show pulmonary congestion and cardiomegaly
Laboratory & Diagnostic Tests
Echocardiography (Echo):
 Ultrasound of the heart.
 Evaluates left ventricular (LV) function.
 Shows evidence of ventricular dilation (enlargement of the chambers) and hypertrophy
(thickening of the heart muscle).
 Can also estimate ejection fraction (EF), which is key for diagnosing systolic vs. diastolic
failure.
Electrocardiography (ECG or EKG):
 Measures the electrical activity of the heart.
 Primarily to check for Dysrhythmias
 Detects:
o Ventricular enlargement (changes in wave patterns)
o Dysrhythmias (irregular rhythms)
o Ischemia (poor blood flow to the heart muscle)
o Infarction (evidence of past or current heart attack)
Pharmacologic Management
Positive Inotropic Agents (increase contractility):
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Digoxin:
o Improves contractility by increasing calcium available for contraction.
o Slows heart rate (HR) and conduction through the AV node.
o Digoxin is an example of a vagotonic medication: Before giving it make sure the
apical is not below 60
o Digoxin enhances the vagus nerve activity, which slows heart rate
o Digoxin has a narrow therapeutic window, patients can get toxicity from it
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Dobutamine:
o Stimulates beta receptors → increases contractility.
Vasodilators (reduce afterload & workload of the heart):
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Nitrates: Tridil, Isordil, Nitrobid ointment
Hydralazine (Apresoline)
Milrinone (Primacor): Phosphodiesterase inhibitor that promotes vasodilation Given IV
Nitroglycerin (Nitro): Nitro works by decreasing preload. It does this through
vasodilation and venous pooling, which reduce the amount of blood returning to the hea
Natriuretic Peptides: Nesiritide (Natrecor)
 Reduces preload & afterload through vasodilation.
 Promotes diuresis.
 Given IV; requires close BP monitoring.
ACE Inhibitors (reduce preload & afterload; prevent ventricular remodeling):
 Enalapril maleate (Vasotec)
 Captopril (Capoten)
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Lisinopril (Prinivil, Zestril)
Angiotensin II Receptor Blockers (ARBs):
 Losartan (Cozaar)
 Candesartan (Atacand)
 Valsartan (Diovan)
 Irbesartan (Avapro)
Beta-Blocking Agents: Lower heart stress & prevent deadly rhythms.
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Action: Decrease myocardial workload and protect against fatal dysrhythmias by
blocking norepinephrine effects of the sympathetic nervous system (SNS).
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Examples:
o Metoprolol (Lopressor, Toprol XL)
o Carvedilol (Coreg): nonselective beta & alpha blocker
Diuretics
 Hydrochlorothiazide (Hydrodiuril, HCTZ): Thiazide diuretic
 Furosemide: Loop diuretic (potassium-wasting)
 Spironolactone: aldosterone antagonist (potassium-sparing)
Diuretics: Get rid of extra fluid.
 Thiazide: Mild, long-term control
 Loop: Strong, but wastes potassium
 Spironolactone: Spares potassium
Entresto (Sacubitril/Valsartan, ARNI)
Indication:
 Used in systolic heart failure (Class II–IV).
 Proven to reduce mortality.
How it Works (2 drugs in 1 pill):
1. Valsartan (Angiotensin II Receptor Blocker, ARB):
o Blocks the effects of angiotensin II.
o This leads to less water and sodium retention, less vasoconstriction, less cardiac
hypertrophy, and less fibrosis.
2. Sacubitril (Neprilysin inhibitor):
o Increases the effects of natriuretic peptides (natural hormones that lower fluid and
pressure).
o This leads to more diuresis, more vasodilation, less aldosterone release, and less
fibrosis.
Entresto: Two drugs in one pill.
 Valsartan stops the harmful RAAS effects.
 Sacubitril boosts the helpful natriuretic peptides
Calcium Channel Blockers (CCBs)
First-generation CCBs:
 Use: Helpful in diastolic heart failure.
 Contraindicated in systolic heart failure (they can make the pumping problem worse).
 Verapamil (Calan, Isoptin)
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Nifedipine (Adalat, Procardia)
Diltiazem (Cardizem, Tiazac)
Second-generation CCBs (dihydropyridines):
 Use: May be used in patients with nonischemic cardiomyopathy
 Action: Cause vasodilation, which reduces systemic vascular resistance.
 Amlodipine (Norvasc)
 Felodipine (Plendil)
Diastolic HF: First gen CCBs are useful.
Systolic HF: Avoid first-gen, but second-gen may be used in certain patients.
Management of the patient with heart failure
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Low sodium diet: Limit sodium intake to 2–3 grams per day to help reduce fluid
retention. Frane said 2 grams
Supplemental oxygen: Used as needed depending on the degree of pulmonary
congestion and hypoxia.
Activity restriction: During acute episodes of heart failure, activity may be limited to
bed rest to reduce cardiac workload and allow the heart to recompensate (recover).
Treatment of Heart Failure
Coronary artery revascularization (for CAD): Restores blood flow to the heart muscle
(angioplasty or CABG).
Ventricular Assist Devices (VADs): Mechanical pumps that help the ventricles circulate blood
when the heart is too weak.
ICD (Implantable Cardioverter Defibrillator): Detects and shocks life-threatening
dysrhythmias to prevent sudden cardiac death.
Cardiac Resynchronization Therapy (CRT): Biventricular pacemaker that makes both
ventricles contract at the same time, improving efficiency.
Surgical options:
o Pericardiectomy: Removal of part of the pericardium (for constrictive
pericarditis).
o Valve surgery: Repair or replace damaged heart valves.
o Ventricular aneurysmectomy: Removal of a weakened, bulging area of the
ventricle.
Heart transplantation: Final option for end-stage heart failure when other treatments fail.
Nursing Care
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The major nursing goal in heart failure is to reduce oxygen demand of the heart, which
means making the heart work less hard, so it needs less oxygen.
- The nurse’s role focuses on reducing heart workload, preventing fluid overload, and
supporting safe activity.
Priority nursing problems:
Decreased cardiac output: The heart cannot pump enough blood to meet the body’s needs.
Fluid volume excess: Extra fluid builds up in the body due to poor pumping, leading to edema
and pulmonary congestion.
Activity intolerance: Patients tire easily and may develop shortness of breath or fatigue with
even mild exertion.
Client teaching for heart failure
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Diet: Reinforce the need for a low sodium, high potassium diet to manage fluid balance
and prevent complications.
Medications: Stress the importance of taking each medication as prescribed. Teach about
dosage, actions, and possible side effects.
Diagnostics: Explain the purpose and preparation for diagnostic examinations so the
patient understands their role in care.
Activity & energy conservation: Explain why activity restriction may be necessary and
teach methods to conserve energy. Encourage safe, prescribed exercises to strengthen the
heart muscle and improve aerobic capacity
Warning signs: Review the signs of cardiac decompensation (worsening heart failure)
that must be reported to the physician immediately.
Home care considerations
Advise the client and family to notify the physician immediately if any of the following occur:
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Weight gain: Greater than 3–5 lbs in a week or increased swelling (fluid retention).
Dizziness or blurred vision: Possible poor perfusion or medication side effect
Shortness of breath or cough: May indicate fluid buildup in the lungs
Palpitations: Possible dysrhythmias
Decreased urine output: Kidneys may not be perfusing well due to heart failure
Ongoing care:
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Stress the importance of lifelong medical follow-up.
Referral to home care services may be appropriate.
Connect the client and family with community organizations for education, resources,
and psychosocial support.
Acute Pulmonary Edema 
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Definition: Abnormal accumulation of fluid in the interstitial tissue and alveoli of the
lungs. It’s like the patient is drowning. Needs immediate treatment
Causes:
o Cardiac: Myocardial infarction (MI), acute volume overload, valvular disease.
o Non-cardiac: Acute respiratory distress syndrome (ARDS), trauma, sepsis, drug
overdose, neurologic causes (CVA, head trauma).
Medical emergency: Fluid in alveoli makes the client essentially “drown” in their own
lung fluid. Immediate treatment is required.
Acute Pulmonary Edema – Pathophysiology & Manifestations
Pathophysiology:
 Increased hydrostatic pressure in pulmonary capillaries forces fluid into interstitial tissues
and alveoli.
 This fluid buildup impairs lung expansion and gas exchange.
Signs & Symptoms:
 Severe dyspnea and shortness of breath – It is a medical emergency
 Severe hypoxia
 Noisy breathing, bubbling respirations.
 Jugular vein distention (JVD).
 Cyanosis, cool and clammy skin.
 Productive cough with pink frothy sputum.
 Crackles throughout the lungs.
 Tachycardia, hypotension.
 Ventricular gallop (extra heart sound). S3 – One of the earliest signs of heart failure
 Extreme anxiety and panic.
 Confusion or lethargy (due to cerebral hypoxia).
Diagnostic Evaluation – Pulmonary Edema
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Chest X-ray: Shows interstitial edema, fluid in alveoli, and possible cardiomegaly.
Echocardiogram: Detects underlying structural/valvular disease and evaluates left
ventricular function. (This test can wait, not needed immediately)
Blood cultures: Obtained if infection (like sepsis) is suspected as the cause.
Cardiac enzymes (troponin, CK-MB, CK2): Checked if acute myocardial infarction is
suspected as the trigger. Also the ROMI panel, to rule out an MI.
12 Lead (views) EKG: To check for an MI
Management of Acute Pulmonary Edema
Goals: Improve oxygenation, reduce pulmonary congestion, and stabilize cardiac function.
Oxygen therapy: The goal is to increase oxygen levels (oxygen tension) and relieve hypoxemia.
Patients are usually started on high-flow oxygen, often with a non-rebreather mask that can
deliver close to 100% oxygen concentration. If hypoxemia persists, noninvasive ventilation such
as BiPAP may be used to improve oxygenation and reduce the work of breathing.
Reduce fluid volume: Diuretics (furosemide) and vasodilators decrease preload and pulmonary
congestion. A single IV dose can produce a very brisk diuresis, sometimes removing 2 liters of
fluid within a few hours.
Improve contractility: Cardiac glycosides (digoxin) or beta agonists (dobutamine) may be used
if cardiac output is low. Dobutamine is a positive inotropic drug that increases myocardial
contractility and improves cardiac output with an onset of 1–2 minutes, whereas digoxin has a
much slower onset of 30 minutes to 2 hours.
Identify and correct underlying causes: Treat precipitating conditions such as MI, valvular
disease, or infection to prevent recurrence.
Decrease anxiety: Calming measures and sometimes medications since anxiety worsens dyspnea
and oxygen demand.
Notes Frane said
Normal Heart Rate: The normal resting heart rate is 60–100 beats per minute, with the most
typical range being in the 80s.
Anticholinergics: These medications block the effect of the vagus nerve, which normally slows
the heart rate, so the result is an increased heart rate.
Preload: Preload is the amount of blood returning to the heart during diastole. Because veins
return blood to the heart, anything that affects venous return will affect preload.
Effects on Preload: IV fluids will increase preload by expanding circulating blood volume.
Diuretics will decrease preload by reducing circulating volume.
Afterload: Afterload is the resistance the left ventricle must overcome to pump blood out into
the systemic circulation. It is mainly influenced by arterial tone and systemic vascular resistance.
Vasodilators and Blood Pressure: Always check blood pressure before administering
vasodilators. The systolic blood pressure should be at least 100 (some physicians may allow 90
as the cutoff). If no specific parameters are ordered, use 100 as the safe cutoff.
Coronary Artery Disease (CAD): CAD occurs when there is not enough oxygen delivery to the
myocardial tissues, usually due to narrowed or blocked coronary arteries.
Cardiomyopathy: Cardiomyopathy is an umbrella term for disorders of the heart muscle, which
impair the heart’s ability to pump effectively.
Hypertension: Long-term hypertension increases the workload of the left ventricle, which can
eventually lead to left ventricular failure.
Kidneys: The kidneys are very sensitive to blood flow and normally receive about 25% of
cardiac output. If they do not get adequate blood flow, they release renin, which activates the
RAAS system to increase blood pressure and volume.
ACE inhibitors and ARBs: they block the RAAS system, helping reduce fluid overload and
blood pressure. These medications are recommended for patients with heart failure.
Systolic heart failure: Occurs due to a problem with contractility, meaning the ventricle cannot
pump effectively.
Ejection fraction (EF): The percentage of end-diastolic volume ejected from the ventricle with
each beat. Example: If the ventricle fills with 140 mL of blood and ejects 70 mL, the EF is 50%.
Myocardial infarction: Causes damage to the myocardial muscle, which decreases the heart’s
ability to pump effectively.
The right ventricle: Pumps blood into the lungs for oxygenation.
Sudden cardiac death: Death that occurs as a result of a life-threatening dysrhythmia
Implantable cardioverter-defibrillator (ICD): Should be placed if the ejection fraction (EF) is
less than 30%, because it can deliver a shock if a life-threatening dysrhythmia occurs.
Positive inotropic agents: Medications that improve contractility of the heart muscle.
Beta blockers: Reduce the chance of ventricular fibrillation by slowing the heart rate and
decreasing vascular resistance, which lowers the workload on the heart. They are especially
beneficial in heart failure because they decrease myocardial oxygen demand and allow the heart
to fill more effectively, leading to improved long-term outcomes.
Metoprolol: A selective beta-1 blocker, it primarily blocks the beta-1 receptors in the heart.
Heart failure: The inability of the heart to contract and meet the body’s metabolic demands.
Diuretics: Often used to reduce fluid overload. Hydrochlorothiazide (HCTZ) may be tried first.
If a stronger effect is needed, they may use furosemide (Lasix, the most potent loop diuretic) or
spironolactone (a potassium-sparing diuretic). Always monitor potassium levels, especially if the
patient is also on digoxin since low potassium increases the risk of digoxin toxicity.
Calcium channel blockers (CCBs): Only indicated in patients with diastolic heart failure. They
should not be given in systolic heart failure since they can worsen contractility problems.
Crackles (rales): These are a classic sign of left-sided heart failure because blood backs up
into the pulmonary circulation, causing fluid to leak into the alveoli → pulmonary
congestion/edema → crackles on auscultation.
Extremity edema: This is a hallmark of right-sided heart failure because blood backs up into
the systemic venous circulation, leading to dependent edema (legs, ankles, sacrum if bedridden),
jugular venous distention, and hepatomegaly.
Beta Blockers: Selective vs. Non-Selective
Selective Beta Blockers (Beta-1 only – heart):
 Target only beta-1 receptors in the heart.
 Effects: Lower heart rate, contractility, and oxygen demand.
 Safer in asthma/COPD since they don’t block lung beta-2 receptors.
 Examples: Metoprolol, Atenolol, Esmolol, Bisoprolol.
Non-Selective Beta Blockers (Beta-1 + Beta-2):
 Block both beta-1 (heart) and beta-2 (lungs, vessels).
 Effects: Lower heart rate and contractility but also cause bronchoconstriction and
vasoconstriction.
 Avoid in asthma/COPD due to risk of bronchospasm.
 Examples: Propranolol, Nadolol, Carvedilol, Labetalol.
Why important in Heart Failure:


Selective beta blockers (Metoprolol succinate, Bisoprolol) are commonly used to protect
the heart.
Carvedilol (non-selective) is also used because it lowers heart workload and decreases
afterload through vasodilation.
Extra Notes
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People usually don’t need fluid restriction in early heart failure, but it’s often ordered in
later stages when fluid buildup or low sodium becomes a problem
Sodium looks low in heart failure because the body keeps holding on to water, diluting
the sodium, it’s not really lost, just watered down.”
Heparin is broken down in the liver, while Lovenox is cleared through the kidneys. So if
someone has kidney failure, they wouldn’t get Lovenox, even though it’s usually the
safer choice
Check BUN/creatinine/GFR before giving lovenox and check LFTs before giving heparin
With polycythemia, you want to increase fluids, but you have to be cautious in patients
with heart failure since it can lead to pulmonary edema.