Exam 1: NSG223/ NSG 223 (New 2024/ 2025 Update) Med Surg 2 Exam| Guide Questions and Verified Answers| 100% Correct| Graded A- Herzing

Exam 1: NSG223/ NSG 223 (New 2024/ 2025
Update) Med Surg 2 Exam| Guide Questions
and Verified Answers| 100% Correct|
Graded A- Herzing
QUESTION
Atherosclerosis pathology
Answer:

Narrowing (stenosis) of lumen, obstruction by thrombosis, aneurysm, ulceration, and rupture
cells die due to lack of blood flow
vulnerable where arteries bifurcate/branch
males have more below-the-knee pathology
QUESTION
Fatty streaks (atherosclerotic lesions)
Answer:
Yellow & smooth; composed of lipids and elongated smooth muscle cells; do not cause
symptoms
QUESTION
Fibrous plaques (atherosclerotic lesions)
Answer:
White to white-yellow; composed of smooth muscle cells, collagen fibers, plasma, and lipids;
found in main arteries and are progressive
QUESTION
Atherosclerosis prevention
Answer:
Statins – 1st line
Others: bile acid sequestrants (cholestyramine), fibric acid inhibitors (gemfibrozil), cholesterol
absorption inhibitors (ezetimibe), Niacin
Control hypertension which makes this worse (majority require 2 or more antihy- pertensives)
Eliminate nicotine
QUESTION
Atherosclerosis, nursing mgt
Answer:
Elevate HOB, feet down/dependent position
Walk to point of pain, rest, resume
Warm applications for arterial flow (bath, drink, pad, water bottle, etc.)
QUESTION
Acute coronary syndrome (ACS) pathophysiology
Answer:
Plaque rupture in MI with resulting thrombus formation that occludes artery, leading to
ischemia/necrosis of myocardium
QUESTION
Descriptions to identify an MI
Answer:
1.the type (NSTEMI, STEMI)
2.Location of injury to ventricular wall (anterior, inferior, posterior, or lateral)
3.Point in time within process of infarction (acute, evolving, or old)
QUESTION
ACS pharm mgt
Answer:
Go to the hospital
Get 12-lead ECG rhythm within 10 min
Obtain troponin labs
Routine interventions: MONAH (morphine, oxygen, nitro, aspirin, heparin), beta-blocker,
ACE-inhibitor, statin
Reperfusion therapy most helpful (restores blood flow to blocked arteries)
Fibrinolytic therapy – dissolves clots
-Secondary prevention of STEMI (Ace, BB, antiCoag)
QUESTION
ACS nursing mgt
Answer:
Elevate HOB
Oxygen 2-4 L/min @95%
Auscultate heart & lungs
12-ECG
Assess consciousness, urine output, skin, BP, activity tolerance
Reduce anxiety
QUESTION
Suspected MI
Answer:
MONA (morphine, oxygen, nitro, aspirin)
QUESTION
Patient with STEMI
Answer:
taken directly to cath lab for immediate PCI
QUESTION
Thrombolytics/Fibrinolytics
Answer:
-agents that dissolve blood clots
only used when primary PCI not available or transport to hospital is too long
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Cardiomyopathy diagnostic tests

Chest x-ray (cardiomegaly)
Echocardiography
ECG
Cardiac catheterization
Endomyocardial biopsy

Cardiomyopathy pharmacological mgt

beta blockers; potassium channel blockers, angiotensin-converting enzyme (ACE) inhibitors; digoxin, diuretics, and dysrhythmic agents.

Aortic or mitral valve débridement, excision, or replacement is required in what kind of patients?

– Develop congestive heart failure despite adequate medical treatment
– Have more than one serious systemic embolic episode
– Develop a valve obstruction
– Develop a periannular (heart valve), myocardial, or aortic abscess
– Have uncontrolled infection, persistent or recurrent infection, or fungal endocarditis
Surgical valve replacement
– Have prosthetic valve endocarditis

Endocarditis primary symptoms

fever & heart murmur

Additional are petechiae, Olsner nodes, Janeway lesions, Roth spots, headache, stroke, HF, tachycardia, cardio/splenomegaly

Endocarditis medical mgt

– NSAIDs as antipyretics
– Long-term IV microbial therapy

Endocarditis Pathophysiology

– Deformity or injury leads to clot formation
– Bacterial infections (Staph & Strep)
– Infection most frequently occurs from clustering vegetations

– Vegetations > 10mm = Left-sided heart endocarditis
– Pulmonary emboli = Right-sided heart endocarditis

Meds for Myocarditis

Penicillins, Amphotericin B

Myocarditis pathology

Viral infections or immune related (rheumatic fever, Crohn’s, Lupus)

Pericarditis – nursing mgt

Analgesics, forward-leaning or sitting position to relieve pain, gradual increases in acivity

Pericarditis assessment

– Evaluate patient in various positions
– presence of pericardial friction rub (hallmark sign) (creaky/scratch, louder at exhalation)
– pt has to sit, lean forward, and hold their breath for rub to be heard

Pericardial effusion

abnormal accumulation of fluid b/w pericardial linings
– can accumulate and choke the heart (i.e., cardiac tamponade, impair v-filling & pumping)

Cardiac tamponade

– acute compression of the heart
– SOB, chest tightness, dizziness
– Beck triad is hallmark (hypotension, muffled heart sounds, elevated jugular venous pressure)
– heart sounds go from distant to imperceptible

Angina pectoris pathophysiology

– Atheroslerosis
– Associated w/angina pain: physical exertion, exposure to cold, eating a heavy meal, or stressful situation

Types of Angina

stable, unstable, intractable/refractory, variant, silent ischemia

Intractable or refractory angina

severe incapacitating chest pain

Variant angina

pain at rest with reversible ST-segment elevation; thought to be caused by coronary artery vasospasm

Silent ischemia

Objective evidence of ischemia (ECG changes w/stress test) but no pain

Angina nursing mgt

– Treat it: stop activities, semi-Fowler’s, 12-lead ECG, nitro, oxygen
– Reduce anxiety: guided imagery, music therapy, spiritual needs
– Promote care: education, symptoms, prevention

Angina pharmacological mgt

Atherosclerosis pathology

– Narrowing (stenosis) of lumen, obstruction by thrombosis, aneurysm, ulceration, and rupture
– cells die due to lack of blood flow
– vulnerable where arteries bifurcate/branch
– males have more below-the-knee pathology

Fatty streaks (atherosclerotic lesions)

Yellow & smooth; composed of lipids and elongated smooth muscle cells; do not cause symptoms

Fibrous plaques (atherosclerotic lesions)

White to white-yellow; composed of smooth muscle cells, collagen fibers, plasma, and lipids; found in main arteries and are progressive

Atherosclerosis prevention

– Statins – 1st line
– Others: bile acid sequestrants (cholestyramine), fibric acid inhibitors (gemfibrozil), cholesterol absorption inhibitors (ezetimibe), Niacin
– Control hypertension which makes this worse (majority require 2 or more antihypertensives)
– Eliminate nicotine

Atherosclerosis, nursing mgt

– Elevate HOB, feet down/dependent position
– Walk to point of pain, rest, resume
– Warm applications for arterial flow (bath, drink, pad, water bottle, etc.)

Acute coronary syndrome (ACS) pathophysiology

– Plaque rupture in MI with resulting thrombus formation that occludes artery, leading to ischemia/necrosis of myocardium

Descriptions to identify an MI

1. the type (NSTEMI, STEMI)
2. Location of injury to ventricular wall (anterior, inferior, posterior, or lateral)
3. Point in time within process of infarction (acute, evolving, or old)

ACS pharm mgt

– Go to the hospital
– Get 12-lead ECG rhythm within 10 min
– Obtain troponin labs
– Routine interventions: MONAH (morphine, oxygen, nitro, aspirin, heparin), beta-blocker, ACE-inhibitor, statin
– Reperfusion therapy most helpful (restores blood flow to blocked arteries)
– Fibrinolytic therapy – dissolves clots
-Secondary prevention of STEMI (Ace, BB, antiCoag)

ACS nursing mgt

– Elevate HOB
– Oxygen 2-4 L/min @95%
– Auscultate heart & lungs
– 12-ECG
– Assess consciousness, urine output, skin, BP, activity tolerance
– Reduce anxiety

Suspected MI

MONA (morphine, oxygen, nitro, aspirin)

Patient with STEMI

taken directly to cath lab for immediate PCI

Thrombolytics/Fibrinolytics

-agents that dissolve blood clots
– only used when primary PCI not available or transport to hospital is too long

Cardiac rehab phases

Phase 1: Inpatient – hospital admittance, diagnosis, education

Phase 2: Outpatient – discharged, supervised exercise

Phase 3: Community – self-directed exercise

Cardiac monitoring

– Hardwire – uses 1 or 2 ECG leads only

– Telemetry – transmits radio waves from battery-operated transmitter to central bank of monitors

– Lead systems – most selected are leads II and V1

– Ambulatory ECG – for home monitoring

– Continuous monitors – aka Holter monitors, uses blue-tooth technology

– Real-time monitors – automatically transmits ECG to monitoring center

– Implantable devices: pacemakers that automatically detect dysrhythmias for up to 3 years

Cardiac monitoring, nursing interventions

– Use proper skin prep to eliminate artifact (abnormal ECG pattern from other issues rather than heart) and change electrodes every 24 hours
– Best leads: lead II and lead V1

Stress test for cardiac monitoring

– Avoid eating or drinking for at least 3 hours before test
– Avoid chocolate or caffeine for 24 hours

Patients who may require cardiac monitoring

· Chest pain
· Palpitations
· Acute Coronary Syndrome – STEMI, NSTEMI, unstable angina
· Following major surgery – ITU, HDU, cardiac surgery
· Major trauma
· Post cardiac/respiratory arrest
· Acute medical conditions –
· Pulmonary embolus, drug overdose, electrolyte imbalance
· Unexplained syncope episodes
· Shock
· Undergoing a specific treatment

positive deflection

When an ECG waveform moves toward the top of the paper

negative deflection

When an ECG waveform moves toward the bottom of the paper

P wave

– atrial depolarization
– up to 0.11 seconds

QRS complex

– ventricular depolarization
– up to 0.12 seconds

T wave

– ventricular repolarization
– aka resting state

U wave

– repolarization of the Purkinje fibers
– sometimes appears in those w/hypokalemia, HTN, or heart disease

PR interval

– atrial depolarization
– 0.12 to 0.20 seconds

ST segment

ventricular repolarization

QT interval

– ventricular depolarization and repolarization
– usually 0.32 to 0.40 seconds

Torsades de pointes

– A lethal ventricular dysrhythmia
– Associated with long QT interval
– Treated with magnesium

TP interval

isoelectric period where line remains flat

PP interval

measured from one P wave to the next to determine atrial rate & rhythm

Determining Heart Rate from the Electrocardiogram

– Count the number of small boxes within an RR interval and divide 1,500 by that number

– Ex: there are 10 small boxes between two R waves, the heart rate is 1,500/10, or 150 bpm; if there are 25 small boxes, the heart rate is 1,500/25, or 60 bpm

– If the intervals are the same or if the difference between the intervals is less than 0.8 seconds throughout the strip, the rhythm is called regular. If the intervals are different, the rhythm is called irregular.

Image: Determining Heart Rate from the Electrocardiogram

Sinus Bradycardia

· Ventricular and atrial rate: < 60 bpm
– Tx: Atropine

*intervals are spaced out

Sinus tachycardia

· Ventricular and atrial rate: > 100 bpm, < 120 bpm

*intervals are shortened
– Treat with beta-blockers
– If wide QRS: CCB, adenosine, procainamide, amiodarone, sotalol
– If persistent: Catheter ablation

Sinus Arrhythmia

· Ventricular and atrial rhythm: Irregular
– creates an impulse at an irregular rhythm; the rate usually increases with inspiration and decreases with expiration

*not typically treated

Premature Atrial Complex (PAC)

– Ventricular and atrial rhythm: Irregular due to early P waves, non-compensatory pause

– PR interval: The early P wave has a shorter-than-normal PR interval (but still 0.12-0.20 seconds)

– are ectopic beats that originate from the atria and are not rhythms (palpitations)

– Treatment only necessary when >6/min, reduce caffeine, correct hypokalemia

Atrial flutter

– 250 to 400 beats/minute
– abnormal rhythm from atria
– saw tooth P configuration
– Tx: IV adenosine

Atrial fibrillation

– rate is 350-600 bpm

Watchman Device

Used when patient has a-fib but is contraindicated for anti-thrombotics

Ventricular fibrillation

Ventricular tachycardia

Treatment: cardioversion, defibrillation

Atropine

Drug of choice to treat symptomatic sinus bradycardia

Heparin-induced thrombocytopenia (HIT) (type II)

a potentially life-threatening complication of heparin administration, leading to a decrease in platelet count and detectable HIT antibodies

Heparin

– normal control value is 25 to 35 seconds;
– the therapeutic values of adequate anticoagulation are approximately 45 to 70 seconds.

Warfarin

– the most commonly used oral anticoagulant and is the prototype vitamin K antagonist
– acts in the liver to prevent the synthesis of vitamin K-dependent clotting factors (i.e., factors II, VII, IX, and X)

Rivaroxaban

– Prototype for direct factor Xa inhibitor
– inactivates circulating and clot-bound factor Xa
– inhibits platelet activation and fibrin clotting formation by inhibiting actor Xa in both intrinsic and extrinsic coagulation pathways
– used in the treatment and secondary prevention of venous thromboembolism and in stroke prevention in patients with nonvalvular atrial fibrillation.

Digoxin

– cardiac glycoside to treat HF in patients with left ventricular dysfunction
– also treats a-fib
– slows HR, decreases fatigue

Digitalization

the administration of a loading dose (a dose larger than the regular prescribed daily dosage) of digoxin to reach the therapeutic index

Propranolol

– Prototype class II antiarrhythmic (beta-blockers)
– to slow the ventricular rate of contraction in atrial flutter and atrial fibrillation
– decrease HR & BP

Diltiazem (Cardizem)

– prototype class IV drug (CCB)
– decrease HR
– only effective in supraventricular tachycardia

Amiodarone (Cordarone)

– Potassium channel blocker
– For life-threatening ventricular & atrial dysrhythmias
– Vasodilating effects, decreases HR, and decreases the contractility of the left ventricle

CHA2DS2-VASC score

– Stroke Risk Assessment for the Patient With Atrial Fibrillation
– Score 0 = no therapy or aspirin 75-325 mg daily
– Score 1 or higher = Warfarin or factor Xa inhibitor (rivaroxiban [Xarelto])