Advanced Nursing Exam 2: Key Terms & Definitions

regulation of the heart: sympathetic nervous system

increase HR, increases contraction force, increases BP

regulation of the heart: parasympathetic nervous system

activated with stimulation of vagus nerve; decreases HR

regulation of the heart: baroreceptors

o located in the aortic arch in the carotid

o ensures BP remains normalized

regulation of the heart: chemoreceptors

o in aortic arch in carotid bodies & medulla

o increases respiratory rate & BP in response to increase CO2

preload vs afterload

Preload is the force that stretches the cardiac muscles prior to contraction (filling, total body volume) - reduced via diuretics

Afterload is the load/force the heart pumps against - reduced via vasodilators & HTN meds

What is blood pressure's relationship with preload and afterload?

o Higher preloads and afterloads will lead to lowered cardiac output

o If BP is high, afterload is high

o If BP is low, preload is low

Where is the PMI? How does this change with ventricular hypertrophy?

o PMI = midclavicular 5th ICS

o may lower in patients with ventricular hypertrophy & become more lateral to the midclavicular line

What is troponin and how does it trend?

o biomarker of choice in the diagnosis of ACS

o detectable within 4 to 6 hours of MI, peak at 10 to 24 hours, and can be detected for up to 10 to 14 days

What is creatinine kinase and how does it trend?

o specific to cardiac muscle injury

o Rises within 3-6 hours, peaks at 12-24 hours, returns to baseline within 12-48 hours

What is CRP?

Inflammatory marker

What is homocysteine?

elevated levels indicate increased risk for CAD, PVD, and stroke

What is BNP?

marker of choice for distinguishing a cardiac or respiratory cause of dyspnea (high levels = heart)

Patient teaching for hypertension:

o symptoms/diagnosis do not usually onset until organs have been damaged

o Lifestyle changes should begin with prehypertension

o Simple 7: manage BP, control cholesterol, reduce BS, get active, eat better, lose weight, stop smoking

o Mediterranean diet (fish + chicken > red meat)

drugs for HTN: adrenergic inhibitors, ACE inhibitors, ARBs

o Adrenergic inhibiting agents — decrease SNS stimulus

o ACE Inhibitors — help with water & sodium retention

o A-II receptor blockers — act in the RAAS system

drugs for HTN: CCBs, direct vasodilators, diuretics

o Calcium channel blockers (CCB) — increase sodium excretion & help dilate the vessel

o Direct vasodilators — dilate vessel to decrease SVR

o Diuretics — decrease plasma volume

drugs for HTN crisis:

sodium nitroprusside (vasodilator), nitroglycerine, cardene (CCB)

If a patient is receiving a drug that reduces afterload, you should assess their:

blood pressure

Classification of HTN:

Normal: < 120/80

PreHTN: 120-129/> 80

Stage 1: 130-139/80-89

Stage 2: > 140/>90

Primary vs Secondary HTN:

o Primary: elevated BP of unknown cause

o Secondary: elevated BP with specific cause (only 5-10% of all cases)

What is cardiac output? How is it calculated?

o total blood flow through systemic or pulmonary circulation per minute (usually around 4-8L/min)

o CO = SV × HR

o SV= volume of blood pumped from L ventricle per beat

What is hypertensive crisis? (diagnostic level, risks, s/s, treatment)

o >180/>120

o Often seen in people with a history of HTN or with drug abuse

o s/s: HA, n/v, seizures, confusion, renal insufficiency, MI, HR, pulmonary edema, chest pain, dyspnea

o treated with hospitalization & IV drugs at a slow titration (goal MAP: 110-115)

What is a cardiac catheterization? Why is this test performed?

o Procedure: catheter inserted into arm, groin, upper thigh, or neck toward your heart

o Right-sided done to measure pressures, filling pressures, and lungs (Swan line purpose) - heart failure, hemodynamic issues

o Left-sided to done evaluate coronary arteries - STEMI & non-STEMI

After PCI and stent, thrombosis prevention includes...

o Dual therapy with aspirin + Plavix

o Effective if return of ST segment

o Monitor for s/s of bleeding

Modifiable & unmodifiable coronary artery disease risk factors:

Unmodifiable: age, gender (men), ethnicity (Caucasian), family history, genetics

Modifiable: Elevated serum lipid, HTN (>140/90), tobacco use & secondhand smoke – decreases estrogen in premenopausal women, physical inactivity, poor diet

How does high lipid levels effect CAD?

o Hyperlipidemia leads to increased platelet aggregation

o LDLs contain more cholesterol and attract more to arterial walls

Nursing interventions decrease the oxygen demand of the heart:

o Enhanced breathing techniques (pursed-lip breathing)

o Incentive spirometry

o Limit activity to decrease heart rate

o Beta-blockers

What does stable angina feel like?

o Occurs when 70%+ of arteries are blocked

o Lasts the same length of time each time it happens, occurs from the same causes, happens regularly

o Usually lasts < 10 minutes

o Relieved with rest, position changes, or nitrate use

EKG finding of acute MI:

For STEMIs, an ECG will show elevations of the ST segment

medications for angina: nitroglycerine, morphine, beta blockers

o IV nitroglycerin (NTG) - vasodilator; first choice med; causes hypotension

o Morphine - choice for chest pain that is not relieved by nitro, also relieves anxiety

o β-adrenergic blockers - lowers HR, BP, and contractility; reduces the risk of a second heart attack

medications for angina: ACE inhibitors, antidysrhythmics, stool softeners

o ACE inhibitors - stabilize BP & prevent ventricular remodeling; use ARB if cough or edema occurs

o Antidysrhythmic drugs - used for life-threatening dysrhythmias

o Lipid-lowering drugs

o Stool softeners - bowel regimen to prevent bearing down or constipation

Why is nitroglycerine given?

o Can be given to relieve chest pain and prevent chest pain

o Helps to vasodilate to relieve strain on the heart

o Effectiveness is measured based on decreased chest pain

What is acute coronary syndrome (ACS)?

o Ischemia that is prolonged and not immediately reversible

o includes both NSTEMIs and STEMIs

o Interventions: ECG, upright positioning, supplemental oxygen, IV access, nitroglycerin, statins, morphine, bedrest for 12-24 hours

complications of myocardial infarction: cardiogenic shock

o heart suddenly cannot meet body's oxygen demand

o associated with a high death rate

o treated with decrease in oxygen demand

complications of myocardial infarction: papillary muscle dysfunction/rupture

o Causes mitral valve regurgitation

o Needs immediate heart surgery!

complications of myocardial infarction: left ventricular aneurysm

o Myocardial wall thins and bulges out during contraction

o Leads to heart failure, dysrhythmias, angina

complications of myocardial infarction: ventricular septal wall rupture

o s/s: loud systolic murmur, HF, cardiogenic shock

o requires emergency repair

o rare condition + high death rate

complications of myocardial infarction: acute pericarditis

o Inflammation of pericardium

o s/s: chest pain increases w/ inspiration or coughing + relieved by sitting forward

o diagnose with ECG

o treat with high-dose aspirin

complications of myocardial infarction: dressler syndrome

o Autoimmune reaction to necrotic heart muscle leads to pericarditis & fever 1-8 weeks after MI

o s/s: chest pain, MI, fever, malaise, pericardial friction rub, arthralgia

o treat with high-dose aspirin

o avoid NSAIDs & corticosteroids in the first four weeks after an MI

What is the most common complication of an MI?

arrhythmias

What is a STEMI? How is it immediately treated?

o occlusive thrombus creates ST elevation on ECG

o Treatment of choice: PCI

o Give IV thrombolytic within 30 minutes of arrival

What is an NSTEMI? How is it immediately treated?

o non-occlusive thrombus

o typically go to cath lab w/ PCI within 12-72 hrs; no thrombolytic therapy

o dual antiplatelet therapy & heparin

What is fibrinolytic therapy? Why is it used? What are complications/contraindications of the therapy?

o Used as a treatment for STEMI if they cannot go to cath lab

o Examples: tissue-type plasminogen activator

o Qualifications: no history of bleeding, chest pain must be occurring for < 12 hrs (preferably 3-4 hours after onset)

o Contraindications: bleeding, hypotension, kidney damage, LOC change

What is sudden cardiac death? (common causes, prodromal symptoms indication)

o Unexpected death from cardiac cause due to abrupt disruption in cardiac function resulting in loss of cardiac output and cerebral blood flow

o Commonly caused by ventricular dysrhythmias, structural heart disease, conduction disturbances

o If a patient has SCD but no prodromal symptoms, they did not have an MI (most likely due to an arrhythmia)

o If a patient has SCD and has prodromal symptoms, they probably had an MI

o Prodromal symptoms include chest pain, palpitations, dyspnea

o Death usually occurs within 1 hour of symptom onset

What is right HF? What are the symptoms?

o right ventricle pumps ineffectively; fluid backs up into the venous system

o s/s: jugular venous distention, hepatic congestion (hepatomegaly), lower extremity edema, renal failure

What is left HF? What are the symptoms?

o often occurs first; blood backs up into the lungs

o s/s: mild dyspnea, restlessness, agitation, slight tachycardia initially

What is biventricular failure?

Failure of both sides of heart, usually from when L sided has progressed to include R sided (symptoms of both sides will be present)

What are examples of general symptoms of heart failure?

edema, nocturia, cool skin, anxiety, chest pain, dysrhythmias

Systolic vs diastolic HF:

Systolic:

o HF + reduced left ventricle EF

o heart cannot pump blood forward; caused by impaired contractile function

Diastolic:

o HF with preserved EF

o impaired ability of the ventricles to relax and fill during diastole

What is acute decompensated heart failure (ADHF)? (early & late s/s)

o Sudden exacerbation of HF which requires urgent medical care

o Pulmonary & systemic congestion seen

o Early signs: increased RR, decreased PaO2

o Later signs: tachypnea, edema

o Further progression: respiratory acidosis, pulmonary edema

S/S of pulmonary edema:

Anxiety, dyspnea, frothy sputum, abnormal s3+s4

medications for CHF: diuretics, vasodilators, morphine, RAAS inhibitors

o Diuretics - decrease preload (loop diuretics - monitor potassium)

o Vasodilators - reduce circulating blood volume (nitroglycerine, sodium nitroprusside)

o Morphine - reduces preload & afterload, anxiety & dyspnea

o RAAS inhibitors - encourage fluid excretion

medications for CHF: positive inotropes

increase contractility

o β-agonists (dopamine, dobutamine, norepinephrine [Levophed])

o Phosphodiesterase inhibitor (milrinone)

o Digoxin - slows HR; do not give if HR < 60

What would be a primary assessment finding in a patient with CHF?

Sudden weight gain of >3 lb (1.4 kg) in 2 days may indicate ADHF, an exacerbation of chronic HF

Nursing interventions for CHF patient:

o High Fowler's position w/ feet in horizontal position in bed (promotes ventricular emptying)

o Low sodium diet (< 2g/day)

o DASH diet

o Daily weights

Meaning of the waves on an EKG strip:

o P- atrial depolarization (sinus vit)

o QRS - ventricular depolarization

o PR interval - the amount of time electrical impulse takes to travel from SA node to AV node

o T - ventricular repolarization

o U - repolarization of Purkinje fibers

o QT - start of ventricular depolarization to repolarization

How can you determine heart rate by looking at an EKG strip?

Count number of R waves in a 6-second strip, multiply by 10 - this is the heart rate

What is sinus rhythm?

normal rhythm where each wave and complex have a normal shape and rhythm w/ HR between 60-100BPM

What is sinus bradycardia? (s/s & treatment)

- sinus rhythm where the SA node fires at < 60 BPM

- S/S: hypotension, pale skin, weakness, angina, syncope, confusion, SOB

- Treatment: atropine (increases HR), pacemaker, d/c offending medications

What is sinus tachycardia? (s/s & treatment)

- sinus rhythm where the SA node fires at 101-200BPM

- S/S: dizziness, dyspnea, hypotension (due to decreased CO), angina with CAD (due to lack of ventricular filling during diastole)

- Treatment: treat cause, vagal maneuver, beta blockers

What is premature atrial contraction? (s/s & treatment)

- Irregular heart rhythm caused by an ectopic focus in atrium, distorting the P-wave

- Causes: stress, fatigue, caffeine, tobacco, alcohol, electrolyte issues

- S/S: heart “skips a beat”

- Treatment: withhold stimulants, administer beta blockers

- In patients with previous heart disease who are having PACs it could indicate electrical concerns in the ventricle that precipitates more serious issues!

What is paroxysmal supraventricular tachycardia? (s/s & treatment)

- ectopic focus above the bundle of his causes the ventricles to go too fast (rate of 120-220 BPM)

- Abrupt onset and termination of symptoms

- Associated with overexertion, stress, stimulants, and dig toxicity

- S/S: hypotension, dyspnea, angina

- Treatment: vagal nerve stimulation, adenosine, beta blockers, CCBs, amiodarone, cardioversion

administration of adenosine:

IV push should be administered undiluted and rapidly (over 1 to 2 sec). After administering , flush the line with 0.9% NaCl to prevent precipitation of particulate matter.

What is atrial flutter? (treatment)

- saw-tooth P-wave with a single ectopic focus in the atria and heart rate of 200-350 BPM

- "Flutters" shown indicate how many times the electrical current runs around the atrium before going to the ventricle

- Treatment: antidysrhythmic, cardioversion, radiofrequency ablation (high rates of energy focused at ectopic focus)

What is atrial fibrillation? (s/s & treatment)

- Most common dysrhythmia; usually seen with heart disease

- Atrial fibrillation "w/ RVR" means the ventricle rate is > 100

- Treatment: cardioversion, anticoagulation, radiofrequency ablation

If a patient has experienced Afib for longer than 48 hours, what changes about their care?

require 3-4 weeks of anticoagulation before cardioversion

What are premature ventricular contractions? (types & risk)

- ectopic foci in the ventricles cause an early QRS complex, which appears as wide, distorted QRS

- 3+ PVCs = VTACH

- Caused by stimulants, electrolyte imbalances, hypoxia, heart disease

- Only harmful if the patient already has heart disease

- Note: monitor for pulse deficit

- Treatment: correct cause, antidysrhythmic

What is ventricular tachycardia? (s/s & treatment)

- ectopic foci take over as the pacemaker of the heart leading to wide, distorted QRS intervals (3+ PVCs in a row)

- Lethal dysrhythmia!

- Can be pulsing or pulseless (stable or unstable)

- S/S: hypotension, pulmonary edema, cardiac arrest

- Treatment: treat underlying cause, stable VT is treated with antidysrhythmic or cardioversion, pulseless VT is treated with CPR and defibrillation

What is ventricular fibrillation? (causes & treatment)

- multiple ectopic foci in the ventricle leading to "quivering" with no effective contraction

- Lethal dysrhythmia!

- Heart rate is not measurable; patient is pulseless and apneic

- Caused by MI, ischemia, procedures

- Treatment: CPR, defibrillation, epinephrine, vasopressin

What is asystole and how is it treated?

- total absence of ventricular activity

- Not shockable!

- Must be assessed in more than one lead

- Treatment: CPR, epinephrine, vasopressin, intubation

What is Pulseless Electrical Activity and how is it treated?

- electrical activity observed on EKG but no mechanical cardiac activity is present

- Common causes - H's & T's

- Treatment: CPR, intubation, IV epinephrine

Common causes of PEA - H's & T's:

Hypovolemia, hypoxia, hydrogen ions (acidosis), hyper/hypokalemia, hypoglycemia, hypothermia

Toxins (drug OD), tamponade, thrombosis, tension pneumothorax, trauma

What instructions do you want to give a patient post-permanent pacemaker implantation?

Arm in sling on effected side, cannot raise arm for two weeks

What is defibrillation?

- Allows SA node to resume pacemaker role

- Treatment of choice for ventricular fibrillation and pulseless ventricular tachycardia

- Needs to be performed within 2 minutes of dysrhythmia onset

- Can be monophasic (delivers energy in one direction) or biphasic (delivers energy in two directions) – paddle placement is same

- Recommended energy for initial shocks in defibrillation

· Biphasic: 120 to 200 joules

· Monophasic: 360 joules

- Immediate CPR after shock (within 10 seconds)

What is synchronized cardioversion?

- Synchronized circuit delivers a countershock on the R-wave of the QRS complex of the ECG – SYNC button must be ON!!!

- Treatment of choice for pulsing VT or supraventricular tachydysrhythmias

- Patient is sedated if stable prior to treatment

- Lower initial energies than defibrillation

- If patient were to become pulseless, turn SYNC off and defibrillate

What is infective endocarditis? (causes, risk factors, s/s)

o Caused by bacteria (Staphylococcus, Streptococcus) viruses and fungi

o Valves and endocardium are infected through the blood; parts of vegetation can break off and enter circulation

o Risk Factors: older adults, IV drug users; patients with prosthetic valves, intravascular devices, or on renal dialysis

o S/S: fever, chills, weakness, muscle aches, fatigue, anorexia, new or worsening systolic murmur; if embolization into limbs – splinter hemorrhages in nail beds, petechiae, Osler’s nodes, Janeway’s lesions, Roth’s spots

Osler's nodes:

painful nodules on finger and toe pads

Janeway's lesions:

flat, painless, small, red spots that may be found on the palms and soles in patients with infective endocarditis

Roth's spots:

hemorrhagic retinal lesions

Symptoms to monitor for with IE that could indicate embolization to the spleen, kidneys, brain, or lungs:

- Spleen: pain in LUQ, tender rigid abdomen

- Kidneys: flank pain, hematuria, renal failure

- Brain: change in neuro status, visual changes, balance changes

- Lungs: dyspnea, chest pain, hemoptysis

What are the major criteria used to diagnose IE?

at least two of the following: two positive blood cultures 12 hours apart, nonvalvular regurgitation, or intracardiac mass or vegetation noted on echocardiography

Purpose of tests for IE (blood cultures, echo, chest x-ray, ECG, catheterization):

o Ask about recent dental or surgical procedures

o Two blood cultures drawn 1 hour apart from 2 different sites - will show infection & ESR + CRP levels elevated

o Echocardiogram done to detect vegetation

o Chest X-Ray will show cardiomegaly

o ECG will show AV block

o Catheterization used to assess valve function and coronary arteries before surgery

To prevent Infectious Endocarditis, prophylactic antibiotics given to select patients having:

- Certain dental procedures

- Respiratory tract incisions

- Tonsillectomy and adenoidectomy

- Surgical procedures involving infected skin, skin structures, or musculoskeletal tissue

- Patients with prosthetic material in the heart, history of IE, CHD, or heart transplants

Priority actions/parameters to monitor when caring for patients with endocarditis:

o Monitor neuro status for embolization

o IV long-term antibiotics - ensure IV drug users have access to PIV treatments; no central lines!

o Antipyretics, fluids, rest

List order of completion: ECG, blood cultures, IV antibiotic, Tylenol

ECG, blood cultures, IV antibiotic, Tylenol

How to prevent rheumatic fever:

Prevention & treatment of strep with antibiotics, proper IV-related technique

Mitral valve stenosis: (cause, s/s)

- Majority caused by rheumatic fever

- Results in decreased blood flow from left atrium to left ventricle

- Leads to increased left atrial pressure and increased pulmonary pressure; risk for atrial fibrillation

- S/S: exertional dyspnea, loud S1, fatigue, palpitations, hoarseness, hemoptysis, chest pain, stroke

Mitral valve regurgitation: (acute vs chronic)

Acute: causes pulmonary edema -> cardiogenic shock

· S/S: thready peripheral pulses, cool extremities

Chronic: causes hypertrophy -> decreased CO

· S/S: weakness, palpitations, progressive dyspnea, peripheral edema, S3

Aortic valve stenosis: (cause, s/s, treatment, caution)

- Often congenital

- Obstruction of blood flow from left ventricle to aorta leads to ventricular hypertrophy, decreased CO, pulmonary hypertension, and HF

- S/S: angina, syncope, dyspnea (symptoms do not present until valve is 1/3 original size), diminished S2, prominent S4

- Require valve replacement

- Use nitro cautiously because it can reduce preload & BP, can worsen chest pain

Aortic valve regurgitation: (acute vs chronic)

Acute: caused by infective endocarditis, trauma, or aortic dissection (life threatening!)

· S/S: dyspnea, chest pain, hypotension, cardiogenic shock

Chronic: caused by rheumatic heart disease, syphilis

· S/S: asymptomatic for years, exertional dyspnea, orthopnea, angina, S3, S4, "water-hammer" pulse

Regurgitation from aorta into left ventricle leads to dilation and hypertrophy, decreased contractility, and pulmonary HTN

What are predisposing factors for endocarditis in a patient with a prosthetic valve?

o Occurs due to the foreign nature of the prosthesis

o Patients with mechanical valve replacements require life-long anticoagulation