NSG210 Week 06 Summary: Alterations in Perfusion - Valvular Heart Disorders and Dysrhythmias
Week 06 (September 28-October 2, 2026) carries the September 30 “Alterations in Perfusion” lecture. Exam 2 content runs through October 7. This falls inside Exam 2 (Weeks 04-07, perfusion continuation).
Note on naming: the source files for this content are raw/nsg210_wk04_VavularDisorders.md, raw/nsg210_wk04_Dyshythmias.md, raw/nsg210_wk04_CaseStudyValvularDisordersHinkleB.md, and raw/nsg210_wk04_UCSMtralRegurgitationB.md. The “wk04” prefix reflects when those files were added to raw/, not the course week - this content is Week 06 / September 30 per the Canvas layout.
Coverage gap: the September 30 lecture outline also includes cardiovascular assessment, heart failure, pulmonary edema, peripheral arterial disease, deep vein thrombosis, pulmonary embolism, and amputations. Heart failure and pulmonary edema already have raw source material and are summarized separately (see raw/nsg210_wk02_HeartFailure.md, raw/nsg210_wk02_LectureNotes04.md); cardiovascular assessment is in raw/nsg210_wk02_LectureNotes03.md. PAD, DVT, PE, and amputations have no raw source material yet and are not covered here. This file covers only valvular heart disorders and dysrhythmias/conduction problems.
Cardiac Valve Function
Cardiac valves control the direction of blood flow through the heart, opening and closing in response to pressure changes during systole and diastole. The atrioventricular valves separate atria from ventricles: the tricuspid valve (right atrium to right ventricle) and the mitral valve (left atrium to left ventricle). The semilunar valves sit between the ventricles and the great arteries: the pulmonic valve (right ventricle to pulmonary artery) and the aortic valve (left ventricle to aorta).
Mitral Valve Prolapse
Mitral valve prolapse is usually an asymptomatic deformity, affecting up to 3 percent of the population and associated with inherited connective tissue disorders; the annulus dilates and the chordae tendineae or papillary muscles may elongate or rupture. The leaflet balloons back into the atrium during systole, and rarely the ballooning is severe enough that the valve fails to close, letting blood regurgitate into the left atrium and, over time, causing mitral regurgitation, heart enlargement, atrial fibrillation, pulmonary hypertension, and heart failure. Most patients never have symptoms; a minority experience fatigue, dyspnea, lightheadedness, dizziness, syncope, palpitations, chest pain, or anxiety. The first sign is often an extra heart sound (a mitral click); a systolic click indicates leaflet ballooning, and a murmur may be heard if the valve opens during systole. Echocardiography is the primary diagnostic tool. Most patients need no medication; antiarrhythmics may be used for arrhythmia, prophylactic antibiotics before dental or invasive procedures are not recommended, and severe cases may need repair or replacement. Nursing management centers on educating the patient about the hereditary nature of the condition (first-degree relatives may need screening), encouraging avoidance of caffeine/alcohol/ephedrine/epinephrine, and reassuring patients without mitral regurgitation that pregnancy does not require close cardiac monitoring.
Mitral Regurgitation
Mitral regurgitation is backward blood flow from the left ventricle into the left atrium during systole, from thickened, fibrotic leaflets and chordae tendineae; causes include degenerative changes, ischemia, rheumatic heart disease, infective endocarditis, collagen vascular disease, and cardiomyopathy, and it can be chronic or acute. Abnormalities in the leaflets, chordae, annulus, or papillary muscles let blood flow backward into the atrium during systole; the excess volume stretches and thickens the left atrium, blocks normal flow from the lungs (causing pulmonary congestion and right ventricular strain), and eventually produces ventricular hypertrophy and systolic heart failure. Chronic mitral regurgitation is often asymptomatic; acute mitral regurgitation usually presents as severe congestive heart failure, with dyspnea, fatigue, weakness, palpitations, and cough from pulmonary congestion. The classic finding is a blowing systolic murmur best heard at the apex, possibly radiating to the left axilla; the pulse may be irregular from extrasystoles or atrial fibrillation. Echocardiography is the primary diagnostic tool (cardiac MRI may also be used). Medical management treats pulmonary congestion with heart failure medications and afterload reduction (ACE inhibitors, ARBs, direct arterial dilators, beta-blockers); surgical options are mitral valvuloplasty or valve replacement (mechanical or tissue). See raw/nsg210_wk04_UCSMtralRegurgitationB_answers.md for a worked unfolding case study (Maria R.) that walks this pathophysiology from an asymptomatic murmur through atrial fibrillation and pulmonary congestion to valve repair.
Mitral Stenosis
Mitral stenosis reduces blood flow from the left atrium into the left ventricle, usually from rheumatic endocarditis causing progressive thickening of the leaflets and chordae tendineae (age-related calcification is a growing cause too). The narrowed orifice obstructs ventricular filling, causing left atrial hypertrophy and dilation, decreased cardiac output, pulmonary congestion, and eventual right ventricular hypertrophy and failure. The first symptom is typically dyspnea on exertion; progressive fatigue, decreased exercise tolerance, dry cough or wheezing from the enlarged left atrium follow, and severe cases show hemoptysis, palpitations, orthopnea, PND, and repeated respiratory infections, with atrial arrhythmias from the dilated, hypertrophied left atrium. The classic finding is a low-pitched, rumbling diastolic murmur best heard at the apex; echocardiography is primary, with ECG, exercise testing, and cardiac catheterization also used. Prevention centers on preventing rheumatic heart disease (effective antibiotic treatment of group A strep, prophylaxis for recurrent rheumatic fever with penicillin G IM every 4 weeks for 10+ years). Medical management treats heart failure and atrial fibrillation (cardioversion, anticoagulants, beta-blockers, digoxin, calcium channel blockers), advises avoiding strenuous activity, competitive sports, and pregnancy, and surgical options are valvuloplasty or valve replacement.
Aortic Regurgitation
Aortic regurgitation is backward flow of blood into the left ventricle from the aorta during diastole, from a congenital valve abnormality, inflammatory lesions, or aortic dilation; it can be chronic or acute (infection, dissecting aortic aneurysm, blunt chest trauma, or deterioration of a surgically replaced valve). The ventricle dilates to accommodate the extra volume and hypertrophies to expel it with more force, while reflex vasodilation lowers peripheral resistance and diastolic blood pressure. Chronic aortic regurgitation is usually asymptomatic until symptoms of pounding/forceful heartbeat (especially in the head or neck), visible or palpable carotid/temporal pulsations, dyspnea on exertion, fatigue, and progressive left ventricular failure appear; acute aortic regurgitation presents with rapid heart rate, cool extremities, and significant shortness of breath. Findings include a high-pitched, blowing diastolic murmur at the third or fourth left intercostal space, a widened pulse pressure, and a water-hammer (Corrigan) pulse; diagnosis is confirmed by echocardiography, cardiac MRI, or catheterization, with regular echocardiograms to monitor. Prevention is based on preventing and treating bacterial infection and rheumatic fever. Management avoids strenuous exertion and isometric exercise, treats arrhythmias and heart failure, controls blood pressure (ACE inhibitors and dihydropyridine calcium channel blockers), restricts sodium/fluid, and recommends valve replacement or valvuloplasty before left ventricular failure develops.
Aortic Stenosis
Aortic stenosis narrows the orifice between the left ventricle and aorta, usually from degenerative calcification (congenital leaflet malformation and rheumatic adhesions/fusion are less common causes). It progresses gradually over years to decades: the left ventricle contracts more slowly and forcibly to overcome the obstruction, hypertrophying under the increased pressure until compensatory mechanisms fail and heart failure develops. Many patients are asymptomatic; the first symptom is typically dyspnea on exertion from increased pulmonary venous pressure, followed by orthopnea, PND, and pulmonary edema from left ventricular failure, dizziness and syncope from reduced cerebral blood flow, and angina from limited coronary flow against the oxygen demand of the hypertrophied ventricle. The classic finding is a loud, harsh systolic murmur over the aortic area that may radiate to the carotids and apex, described as crescendo-decrescendo, rough, rasping, and vibrating; an S4 may be heard. Cardiac imaging (echocardiography, MRI, or CT) diagnoses and monitors progression, and left-sided heart catheterization is needed before valve replacement is considered. Prevention focuses on controlling risk factors (diabetes, hypertension, hypercholesterolemia, elevated triglycerides, tobacco). Definitive treatment is aortic valve replacement, surgical or nonsurgical (transcatheter aortic valve replacement, TAVR); symptomatic patients who are not candidates for replacement may benefit from balloon percutaneous valvuloplasty. See raw/nsg210_wk04_CaseStudyValvularDisordersHinkleB_answers.md for a worked unfolding case study (Daniel R.) that walks this pathophysiology from a murmur with early decompensation, through exertional syncope and chest pain, to severe aortic stenosis and evaluation for TAVR.
Nursing Management: Valvular Heart Disorders
Across all four valve disorders, nursing management follows the same pattern: educate the patient about the diagnosis, its progressive nature, and the treatment plan; have the patient report new symptoms or changes to the provider; minimize infective endocarditis risk while avoiding routine antibiotic prophylaxis before dental work except in high-risk patients; and regularly measure heart rate, blood pressure, and respiratory rate, comparing against previous data and assessing for heart failure, arrhythmias, dizziness, syncope, weakness, or angina.
Normal Electrical Conduction and the ECG
The electrical impulse originates in the SA node (near the superior vena cava in the right atrium, firing 60-100 times a minute in adults), travels through the atria to the AV node (causing atrial contraction, called conduction), which slows the impulse to let the ventricles fill - the resulting atrial kick accounts for about one third of the volume ejected during ventricular contraction - and then travels through the bundle of His to the right and left bundle branches and Purkinje fibers in the ventricular muscle. Depolarization is electrical stimulation and systole is the resulting mechanical contraction; repolarization is electrical relaxation and diastole is the resulting mechanical relaxation.
The ECG waveform reflects this conduction system: the P wave is atrial depolarization, the QRS complex is ventricular depolarization, the T wave is ventricular repolarization, and the rare U wave is repolarization of the Purkinje fibers. The PR interval covers sinus node stimulation, atrial depolarization, and AV node conduction; the ST segment is early ventricular repolarization (analyzed for ischemia); the QT interval is total ventricular depolarization and repolarization (varies with rate, sex, and age); the PP interval determines atrial rate/rhythm and the RR interval determines ventricular rate/rhythm. On the graph, time and rate are measured on the horizontal axis and amplitude/voltage on the vertical axis; a positive deflection moves up, negative moves down.
Determining heart rate: count the small boxes within one RR interval and divide into 1,500 (a 1-minute strip has 300 large boxes and 1,500 small boxes) - for example 10 small boxes is 150 bpm and 25 small boxes is 60 bpm. For an irregular rhythm, count the RR intervals in a 6-second strip and multiply by 10; the same method works for atrial rate using the PP interval. Determining rhythm: use the RR interval for ventricular rhythm and the PP interval for atrial rhythm - a regular rhythm has intervals that are the same or differ by less than 0.8 seconds throughout the strip.
Normal sinus rhythm: ventricular and atrial rate 60-100 bpm, regular rhythm, normal QRS shape/duration, a normal and consistent P wave always in front of the QRS, PR interval 0.12-0.20 seconds, and a P:QRS ratio of 1:1.
Sinus Node Arrhythmias
Sinus bradycardia is a slower-than-normal SA node rate (under 60 bpm, otherwise normal characteristics), from lower metabolic needs, vagal stimulation, medications, sinus node dysfunction, increased ICP, or coronary artery disease; unstable, symptomatic bradycardia is frequently due to hypoxemia. Treatment depends on cause and symptoms: atropine 0.5 mg IV bolus (repeated every 3-5 minutes up to 3 mg), emergency transcutaneous pacing if unresponsive, or dopamine/isoproterenol/epinephrine; resolving the underlying cause may be the only treatment needed.
Sinus tachycardia is a faster-than-normal SA node rate (over 100 bpm, otherwise normal characteristics), from physiologic or psychological stress, medications, stimulants, enhanced automaticity, or autonomic dysfunction; a rapid rate can reduce cardiac output and cause syncope and low blood pressure. Treatment targets the cause: vagal maneuvers (carotid sinus massage, gagging, bearing down, forceful coughing, cold stimulus), adenosine, synchronized cardioversion if hemodynamically unstable, beta-blockers or calcium channel blockers, catheter ablation for persistent inappropriate sinus tachycardia, and increased fluid/sodium intake for POTS.
Sinus arrhythmia is an irregular SA node rhythm (rate increases with inspiration, decreases with expiration); nonrespiratory causes include heart disease and rare valvular disease. It has no significant hemodynamic effect and is not typically treated.
Atrial Arrhythmias
Premature atrial complexes (PACs) are a single ECG complex starting in the atrium before the next normal impulse, from caffeine, alcohol, nicotine, a stretched atrial myocardium, anxiety, hypokalemia, hypermetabolic states, or atrial ischemia/injury/infarction - an irregular rhythm from the early P wave, with a shorter-than-normal PR interval. Infrequent PACs need no treatment; frequent PACs may herald a worsening disease state or more serious arrhythmias and are treated by addressing the underlying cause (reducing caffeine, correcting hypokalemia).
Atrial fibrillation is a common arrhythmia from abnormal impulse formation causing rapid, disorganized, uncoordinated atrial twitching, with impulses initiated from the pulmonary veins and conducted through the AV node; it is classified as paroxysmal, persistent, or permanent. Characteristics: atrial rate 300-600 bpm, ventricular rate 120-200 bpm, highly irregular rhythm, no discernible P waves (irregular undulating waves instead), an unmeasurable PR interval, and a many:1 P:QRS ratio. Management depends on cause, pattern, duration, ventricular response, and structural/valvular disease: prevent embolic events with anticoagulants (warfarin, direct thrombin inhibitors, Factor Xa inhibitors, guided by the CHA2DS2-VASc stroke risk score), control ventricular rate with antiarrhythmics, and consider converting to sinus rhythm, with regular monitoring of hemoglobin, hematocrit, liver, and renal function. This is the same arrhythmia that develops from left atrial enlargement in the mitral regurgitation case study above - the enlarged, stretched atrium from chronic valve disease is a direct substrate for atrial fibrillation.
Ventricular Arrhythmias
Premature ventricular complexes (PVCs) start in the ventricle before the next normal sinus impulse, from caffeine, nicotine, alcohol, cardiac ischemia, increased workload, digitalis toxicity, hypoxia, acidosis, or electrolyte imbalance - an irregular rhythm from the early, bizarre QRS, PR interval under 0.12 seconds, and a P:QRS ratio of 0:1 or 1:1. They are common and may increase with age; initial treatment corrects the cause, frequent/persistent PVCs are treated with amiodarone or beta-blockers, and long-term pharmacotherapy usually isn’t indicated, though an association with adverse outcomes warrants evaluating for underlying causes.
Ventricular tachycardia (VT) is three or more PVCs in a row at over 100 bpm, with similar causes to PVCs but higher risk after larger MIs and with lower ejection fractions; the patient is nearly always unresponsive and pulseless. A stable patient gets continuing assessment, a 12-lead ECG, antiarrhythmics, antitachycardia pacing, or cardioversion/defibrillation (procainamide, amiodarone, sotalol, and lidocaine are the medications); cardioversion is the treatment of choice for symptomatic monomorphic VT and defibrillation for pulseless VT, and an ICD is considered long-term for an ejection fraction under 35 percent.
Ventricular fibrillation is rapid, disorganized ventricular quivering with no effective contraction, from acute coronary disease/MI, untreated VT, cardiomyopathy, valvular heart disease, Brugada syndrome, proarrhythmic medications, acid-base/electrolyte abnormalities, or electrical shock; the rate exceeds 300 bpm with no recognizable QRS complexes. Immediate defibrillation and CPR are essential for survival.
Ventricular asystole shows absent QRS complexes confirmed in two leads (P waves may briefly persist), with no heartbeat, pulse, or respiration - it requires immediate high-quality CPR, rapid assessment for the reversible causes (the Hs and Ts), intubation, and IV access.
Conduction Abnormalities (AV Blocks)
AV blocks occur when conduction through the AV node or bundle of His is decreased or stopped, from medications, Lyme disease, myocardial ischemia/infarction, hypothyroidism, or increased vagal tone; types are first-degree, second-degree (type I and type II), and third-degree. First-degree AV block conducts every atrial impulse but at a slower-than-normal rate through the AV node (PR interval over 0.20 seconds, otherwise a 1:1 P:QRS ratio) and rarely causes a hemodynamic effect. Third-degree AV block conducts no atrial impulses into the ventricles, producing AV dissociation - the ventricular rate is lower than the atrial rate, more P waves appear than QRS complexes, and it may require permanent pacing. Management targets maintaining adequate cardiac output: no treatment or removing the cause in a stable patient, a permanent pacemaker for a medication-related block, and temporary pacing for severe symptomatic bradycardia or tachycardia.
Arrhythmia Assessment and Nursing Care
Priority assessment identifies the possible cause and the arrhythmia’s effect on the heart’s ability to maintain perfusion, through health history (previous occurrences, decreased cardiac output symptoms, possible causes), medication review, labs (medication levels, contributing factors), psychosocial assessment (effect on the patient, their understanding, anxiety), and physical assessment (signs of diminished cardiac output, skin, fluid retention, pulse rate/rhythm, extra heart sounds, blood pressure, pulse pressure). Collaborative problems/potential complications are cardiac arrest, heart failure, and thromboembolic events (especially with atrial fibrillation).
Goals are to eliminate or decrease the arrhythmia to maintain cardiac output, reduce anxiety, build understanding of the arrhythmia/diagnostics/treatment, and develop self-management skills. Monitoring includes blood pressure, pulse, respirations, breath sounds, 12-lead and continuous ECG, antiarrhythmic medications, and a 6-minute walk test to assess ventricular rate response to exercise. Reducing anxiety means staying with the patient during episodes, maintaining a calm and reassuring attitude, and helping the patient identify causative, influencing, and alleviating factors. Patient education covers the arrhythmia’s cause and treatment options, maintaining therapeutic antiarrhythmic drug levels, taking a pulse before each dose and notifying the provider if it’s outside set parameters, the relationship between arrhythmia and cardiac output, recurrence-reduction measures, an emergency action plan, and CPR training for family members.
Cardioversion, Defibrillation, Pacemakers, and ICDs
Cardioversion and defibrillation both deliver an electrical current to depolarize myocardial cells so the SA node can recapture pacemaker control after repolarization; higher defibrillation voltage can cause more myocardial damage, and biphasic defibrillators deliver the charge in both directions. Electrical cardioversion is a timed shock synchronized to the QRS complex (to avoid discharging during the T wave and triggering VT/VF), used electively for tachyarrhythmias: anticoagulation is needed for arrhythmias lasting over 48 hours, antiarrhythmics are withheld for 48 hours before, and the patient should not eat or drink for at least 4 hours prior; postprocedure care maintains the airway and monitors vital signs, SpO2, and ECG. Defibrillation is an emergency treatment for ventricular fibrillation and pulseless VT (the most common cause of sudden cardiac death) - not used on a conscious patient or one with a pulse; early defibrillation, including by lay people using public AEDs, improves survival, and epinephrine or antiarrhythmics (amiodarone, lidocaine, magnesium) may be given if the arrhythmia persists after an unsuccessful shock.
Pacemaker therapy supplies electrical stimuli for slower-than-normal impulse formation or symptomatic AV/ventricular conduction disturbances, and biventricular pacing (CRT) treats advanced heart failure; pacemakers can be permanent or temporary, with a pulse generator (sets rate and stimulus strength) and leads placed endocardially (threaded through a vein) or epicardially (sutured on during open heart surgery), with the permanent generator implanted subcutaneously in the pectoral region. Nursing monitors device function and battery status and educates the patient on self-care. Early complications include electrode dislodgment (minimize activity); leadless pacemakers avoid a surgical pocket and transvenous leads; electromagnetic interference can inhibit pacing or cause reversion to asynchronous pacing, so patients should avoid strong electromagnetic fields (household appliances are generally safe), wear medical identification, avoid prolonged exposure to magnets, and request a hand search at security gates. Remote monitoring (transtelephonic, inductive, or wandless) transmits ECG and pacemaker data to the provider, simplifying diagnosis of a failing generator and reassuring the patient.
The implantable cardioverter defibrillator (ICD) detects and terminates life-threatening tachycardia or fibrillation, indicated for patients who survived sudden cardiac death or symptomatic VT, post-acute-MI patients with LV dysfunction, and nonischemic dilated cardiomyopathy with heart failure; a wearable version bridges high-risk patients waiting for implantation. The generator is implanted subcutaneously with an RV lead that senses intrinsic activity and delivers an impulse when the rate exceeds a programmed threshold; battery life is typically at least 10 years, and antiarrhythmic medication can reduce tachyarrhythmia occurrence and shock frequency. Nursing care after any device insertion monitors rhythm and device settings, assesses cardiac output and hemodynamic stability, watches the incision site for bleeding/hematoma/infection, gets a chest x-ray to confirm lead position and rule out pneumothorax, and addresses patient anxiety, depression, or anger while including family in education and support; infection prevention means changing dressings as prescribed and reporting redness, swelling, drainage, fever, or an elevated white count.
Case Studies
Two unfolding case studies pair with this content. Daniel R. (72, raw/nsg210_wk04_CaseStudyValvularDisordersHinkleB.md) tracks worsening aortic stenosis - from a harsh systolic murmur and mild crackles, through syncope and chest pain requiring emergency evaluation, to a diagnosis of severe aortic stenosis and evaluation for TAVR - illustrating the aortic stenosis pathophysiology and management above. Maria R. (68, raw/nsg210_wk04_UCSMtralRegurgitationB.md) tracks worsening mitral regurgitation from an incidental murmur through new atrial fibrillation and pulmonary congestion to a discussion of valve repair; a full worked answer sheet is at raw/nsg210_wk04_UCSMtralRegurgitationB_answers.md.
Memory Anchors
Mitral valve problems (prolapse, regurgitation, stenosis) murmur at the apex; aortic valve problems (regurgitation, stenosis) murmur at the sternal border/aortic area and can radiate to the carotids. Regurgitation murmurs happen when the valve should be closed but leaks (mitral regurgitation and aortic regurgitation are both backward-flow problems); stenosis murmurs happen when the valve should be open but is too narrow. Echocardiography is the primary diagnostic test across every valve disorder. For dysrhythmias: count small boxes in the RR interval and divide into 1,500 for rate; PR interval over 0.20 seconds is first-degree block; a wide, bizarre QRS is ventricular in origin; atrial fibrillation has no discernible P waves and needs a CHA2DS2-VASc score to guide anticoagulation; cardioversion is synchronized and elective, defibrillation is unsynchronized and emergent for a pulseless patient.