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bvhhvhyhyhygyggfMed-surg exam 1

Chapter 31: HT

 HT
o High BP
o Most common chronic disease among US adults
o Systolic 140+ and diastolic 90+ or higher. Based on average of 2+ BP
measurements taken 1-4w apart by health care provider
o You cant diagnose based on 1 high BP
o Normal BP: 120/80
o Pre-HT: 120-139/ 80-89 (mainly diet and exercise to help) treat this earlier
and more often
o Stage 1 HT: 140-159/90-99
o Stage 2 HT: >160/>100
o To be considered hypertension 140/90+ for (2 reads)
o Hallmark definition of high blood pressure is persistent elevated systemic
vascular resistance
o Always take 2 blood pressure at different times to show consistency (she said
nerves, stress, and so on will effect these numbers)

 Incidence
o Primary HT: essential, older adults, 95% no/unidentifiable cause (fluke, think
get it just cause, they did nothing to cause it)
o When you age resistance goes up, the vessels are less compliant, so you are
“wearing out “ and pressure increases
o We see more with primary due to the aging process
o Secondary: 5%, renal disease, sleep apnea, pregnancy (caused from another
issue)
o Example of secondary pregnant women gets HBP due to pregnancy
o 33% of adult US pop have HT, 46% of those don’t have it under control,
highest in African American pop

 Factors influencing BP
o Excess sodium, fewer nephrons, stress, genetic alterations, obesity,
endothelial factors
o Risk factors: smoking, obesity, inactivity, dyslipidemia, diabetes, micro
albuminuria or GFR <60mL/min, older age, family history
o She said obesity is the main reason

 Patho
o BP= CO X HR
o HT results from increases in CO/peripheral resistance or both
o There must be a change in factors affecting peripheral resistance or CO
 o Abnormalities in body’s control mech to monitor/reg pressure

 Manifestations of HT
o Normally no symptoms other than elevated BP
o Symptoms r/t organ damage seen late/serious: retinal/eye changes, renal
damage, myocardial infarction, cardiac hypertrophy (thickened), stroke
o Elevated BUN, creatinine seen (this leads to end-organ damage)

 Assessment
o History, risk factors and physical exam (retinal exam have to dilate, not seen
w/ naked eye)
o Lab tests: urinalysis and blood chemistry, EKG, BUN, creatinine
o Assess potential symptoms of target organ damage: angina, SOB, altered
speech, altered vision, nosebleeds, headache, dizziness, balance problems,
nocturia
o CV assessment: apical and peripheral pulses
o Assess personal, social, financial factors that influence condition and
treatment process
o We know how to measure BP, proper cuff size, arm @ level of heart, feet flat
on ground, don’t measure right after activity, artery arrow @ brachial artery

 Medical management
o Maintain BP: <140/90, <150/90 for older adults, <130/80 for those with
diabetes/chronic kidney disease
o Lifestyle mods: weight reduction, DASH diet, increase activity, reduce
alcohol, reduce processed foods (canned food, red meat, high in sodium)
o Pharm therapy: decrease peripheral resistance/blood volume, dec
strength/rate of myocardial contraction,
o Diuretics, BB, alpha blockers, vasodilators, ACE inhibitors, ARBs, CCB,
dihydropyridines, direct renin inhibitors
o Normally once you are on HT meds you stay on for life
o WALKING******** 30 min daily exercise (going to be a question)

 Stage I HT
o AA and patients >60: CCB or thiazide diuretic
o Non AA and patient <60: ACE/ARB
o Low doses initiated, med dosage increased gradually if BP doesn’t reach
target
o Multiple meds may be needed to control

 Potential complications
o L ventricular hypertrophy (hard heart), MI, HF, TIA
o CVA, stroke, brain attack (idk what brain attack means)
o Renal insufficiency, chronic kidney disease, retinal hemorrhage
 Goals
o Understand disease process and treatment
o Diet, exercise, meds treatment process
o Absence of comp
o Lower/control BP without adverse effects/high costs

 Interventions
o Support and educate
o Reinforce/support lifestyle changes
o Take meds as prescribed
o Follow up care
o Do not overwhelm them, start with DASH diet avoiding high sodium foods,
canned, processed, and red meats are all high in sodium (teach them high
foods)
o You must teach them everything but not in one office visit

 Outcome goals
o Report knowledge of disease management
o Adhere to self-care program
o Exercise regularly, abstains from tobacco/excessive alcohol intake
o Adhere to dietary regimen, reduce Na/calories/fat intake
o Measure BP regularly
o Maintain BP less than 140/90 (150/90 for adults 60+) w/ lifestyle mods and
meds
o Demonstrate NO symptoms of angina, palpitations, vision changes
o NO changes in vision, no motor/speech/sensory deficits
o Reports NO headache, dizziness, weakness, changes in gait/falls, no
dyspnea/edema
o Maintain normal pulse R/R, respiratory rate w/in normal range
o Maintain normal urine output, renal function test w/in normal range
o Stable BUN and serum creatinine
o Has peripheral pulses
o Takes meds as prescribed
o Go to follow up apt.

 Gero considerations
o Med regimen may be difficult to remember, get pill organizer
o Expensive
o Mono-therapy may be simplest and cheapest
o Mono-therapy drugs with elderly people, help them with meds, write down
directions they do not understand/remember/or cannot hear you
o Ensure they understand, give them instructions, how and when to refill
o Include the family/caregiver in care
  HT crisis
o HT emergency: BP >180/120 and must be lowered immediately to prevent
damage to target organs
o ICU care, IV drip
o Reduce BP 20-25% in first hour
o Reduce to 160/100 over 6h, then gradual reduction to normal over days
o Exceptions: ischemic stroke and aortic dissection
o Meds: IV vasodilators such as; sodium nitroprusside, nicardipine,
fenoldopam mesylate, enalaprilat, nitro

o HT urgency: BP very elevated, no evidence of immediate/progressive organ

damage
o Pills, maybe IV push (think pt. on oncology floor, had high HT to begin with,
very high, nurse not super concerned but continued to take BP every hour
and nurse gave oral meds)
o Oral agents with goal to normalize BP in 24-48h
o Meds: labetalol, captopril, clonidine
o Close monitoring of BP/CV status and monitor for potential target organ
damage for both
*Emergency is worse than urgency: good quick assessments in both cases

Chapter 25: Assess CV function

 Anatomy
o Endocardium (for infections), myocardium (muscle), epicardium and encased
in fibrous sac the pericardium
o Pericardial sac surrounds the heart, 10-15mL of pericardial fluid, too much
fluid heart cant function
o ***Blood flows from R atrium- tricuspid valve- R ventricle- pulmonic valve-
lungs- L atrium- mitral valve- L ventricle- Aortic valve- aorta/body
 o Atrioventricular valves: T/M, semilunar valves: A/P

o R coronary, L coronary and circumflex artery are the major arteries to heart
(look at diagram of placement)
o I don’t think we need to know pressure levels within the heart but slide 9.
Just know higher pressure in ventricles, and higher on L side of heart
o The left ventricle pumps the entire body with high pressures
o The chordae tendinea stops back flowing

 Myocardium effects from CV event

o Infarction: cant return, muscle is dead
o Injury: getting bad, but can be reversed
 o Ischemia: loss of 02, can be fixed She could ask a question about
how EKG reflects these
conditions.

Ischemia: depressed T wave

Injury: wide QRS, dep T wave
Infarction: S wave off

 Cardiac conduction (electrophysiology)

o SA node: 60-100 in R atrium
o AV node: 40-60
o R/L bundle branch or purkinje fibers: 30-40

 Cardiac action potential

o Depol (systole/beating of heart): electrical activation of cell caused by influx of
Na into cell while K exits (Ejection of blood that produces the stroke volume)
o Repol (diastole/filling of heart): (relax/rest) return of cell to resting state caused
by reentry of K into cell while Na exits (filling of blood in the heart, hold your
hands out and make a cup, filling/resting)
o Refractory periods
-Effective refract period: phase in which cells are incapable of depol. Think
absolutely will NOT
-Relative refract period: phase in which cells require stronger than normal
stimulus to depol. Think a kid that needs to be bribed/forced to clean room
 o Systole: Na/Ca goes into cell
o Diastole: K/Na comes out of cell
o Don’t think we need to know phase 0-4 but slide 15

 Cardiac cycle
o Events that occur in the heart from beginning of 1 heartbeat to the next
o Number of cycles depends on HR
o Each cycle has diastole, atrial systole (atrial kick, 15-25% of ven blood
volume is kicked out) and ven systole

 Cardiac output
o Stroke Volume, amount of blood ejected w/ each heartbeat
o Preload: degree of stretch of cardiac muscle fibers/amount of blood at end of
diastole
o Afterload: resistance of ejection of blood from ven (systemic vascular
resistance) if they have high BP afterload is high
o After load (allie): is the force that the hart is beating against
o Contractility: ability of cardiac muscle to shorten in response to electrical
impulse
o Ejection fraction: % of end diastolic volume ejected w/ each heartbeat.
Normal is 50-70mL, goes down with HF
o CO: amount of blood pumped by ven in L/min
o CO= SV X HR, normally 6-7L

 Influencing factors on CO
o Control of HR: ANS, baroreceptors
o Control of SV: Frank Starling law, increase SV from increased volume,
afterload is affected by systemic vascular resistance and pulmonary vascular
resistance
*Frank starling law: higher the preload the higher the SV
o More preload: volume expanders, fluids, blood
o Low preload: trauma, hemorrhage, diuretic, N/V, diarrhea

 Contractility
o Increased by Catecholamines, SNS (fight/flight), certain meds
o Increased contractility results in increased SV
o Decreased by hypoxemia, acidosis, certain meds

 Assessment
o Health history, family/genetic history
o Cultural/social factors
o Risk factors, modifiable or non-modifiable
o Modifiable: education, plans
o Non-modifiable: sex, genetics
 o Demographic info
o Cardiac nature, EKGs, heart attacks, caths?
o Common symptoms: chest pain/discomfort in upper body, SOB, dyspnea,
peripheral edema, wt. gain, abd distention, palpitations, unusual fatigue,
dizziness syncope, changes in LOC, N/V
o She said to add GI symptoms

 Chest pain
o Causes: angina pectoris, pericarditis (increase w/ deep breath, not as severe
as angina), pulmonary disorders, esophageal disorders, anxiety/panic
disorders, MS disorders

 Genetics in CV disease
o Familial hypercholesterolemia, hypertrophic cardiomyopathy, long QT
syndrome, hereditary hemochromatosis (hold onto iron), elevated
hemocysteine levels (red meat/genetic)

 Assess past health, family, social

o Meds, nutrition, elimination (do they have nocturia)
o Activity, exercise, sleep and rest
o Self-perception, roles and relationships, coping and stress

 Physical assessment of CV system

o General appearance, skin and extremities (cyanotic?)
o Pulse pressure, difference in sys/dia
o BP/orthostatic changes
o Arterial pulses, pulse dif in apical/radial pulses
o Jugular venous pulsations
o Heart inspection, palpation and auscultation

 Heart auscultation
o S1: tricuspid/mitral v close “lub”
o S2: pulmonic/aortic close “dub”
o S3/S4 gallops: all four = summation gallop
o S3 early diastole, think Kentucky lub-dub-DUB. (HF)
o S4 late diastole, think Tennessee LUB-lub-dub. (MI)
o Murmur hear turbulence
o Friction rub harsh and grating
 Normal
heart
sounds

Gallop sounds

 Other sounds
o Lungs: hemoptysis, cough, crackles, wheezes
o Abdomen: distension from ascites, liver/spleen enlargement
 o Hepatojugular reflex (HJR): HF

 Lab tests to eval heart function

o Cardiac biomarkers, blood chemistry, electrolytes, hematology, coagulation
o Lipid profile
o Brain naturetic peptide, C-reactive protein, homocysteine

 Electrocardiography
o 12-lead
o Continuous monitoring w/: hardwire at bedside monitor, telemetry (5 lead w/
box and seen on monitor at nurses station)

 Cardiac stress test

o Exercise stress test: pt. walks on treadmill w/ intensity progressing according
to protocols
o EKG/VS/symptoms monitored
o Terminated when target HR reached
o Also is pharm stress testing, vasodilating agent given to mimic exercise

 Diagnostic testing
o Radionuclide imaging (I think she would only ask like most often)
1. Myocardial perfusion imaging
2. Positron emission tomography
3. Test of ven function, wall motion
4. CT
5. MRI
6. X-ray (most often)

o Echocardiography: noninvasive ultrasound test used to measure ejection

fraction (normally 50-70%) and examine size, shape and motion of cardiac
structures. May be trans-thoracic or trans-esophageal (very common)

o Cardiac cath: invasive used to diagnose structural and functional diseases of

the heart and great vessels.
-R heart cath: pulmonary artery pressure and oxygen sat may be obtained; biopsy
of myocardial tissue may be obtained (central venous pressure)
-L heart cath: use on contrast agent, coronary artery blockages (we do left more
often)

 NSG interventions post cath

o Observe for bleeding and hematoma
o Assess peripheral pulses Q15min for 2-4 hours
o Evaluate temp, color, cap refill of affected extremity
o Screen for dysrhythmias
o Maintain bed rest for 2-6h
 o Instruct pt. to report chest pain, bleeding
o Monitor for contrast induced nephropathy
o Ensure pt. safety
o Student nurses cannot pull sheath (for clinical)

 Hemodynamic monitoring
o CVP, pulmonary artery pressure, intra-arterial BP monitoring, minimally
invasive CO monitoring devices

 Preventing cath-related bloodstream infections

o Hand hygiene
o Dressing, treat like central line
o Catheter site is sterile
o Pressure monitoring system changes every 4 days
o CHG bath
o Pt. Education

Chapter 26: dysrhythmia

 Dysrhythmia
o Disorders of formation or conduction of electrical impulses within heart
o Can cause disturbances of rate, rhythm or both
o Can alter blood flow and cause hemodynamic changes
o Diagnosis by analysis of electrographic waveform

 Normal electrical conduction

 o SA node- AV node- bundle of His- R/L bundle branches- purkinje fibers
o Depol= stimulation-systole
o Repol= relaxation- diastole

 Influences on HR/Contractility
o Sympathetic stimulation: increased w/ exercise, anxiety, fever, meds.
Decreased w/ rest, meditation, meds
o Parasympathetic: vagus nerve stimulation
o Compensation can only last so long
o Automaticity: heart cells can initiate impulses for themselves

 ECG
o Electrode placement (12 or 5 lead)
o P wave: atrial depol (emptying)
o QRS: ven depol (pulse/perfusion) atrial repol occurs during QRS
o T wave: ven repol
o U wave, not every pt. has, normally w/ electrolyte imbalances
o Isoelectric line is the baseline, should be straight horizontally across
o PR: 0.12-0.20
o QRS interval: <0.12
o ST segment: on isoelectric line
o Clip do not shave
o Soap and water/gauze to clean chest
o Use skin prep (benzocaine) as a last resort
o RN is responsible for clinical alarms, un-
licensed personnel can monitor

Artifact/interference
o Moving around, brushing
teeth, turning over, loose
leads, bad adhesive
o Check leads if there is
continual artifact
o AC inference: electrical
interference w/ equipment in
room
 HR determination
o R-R method x 10= HR (6 sec strip)
o 1500 method, count little boxes from R-R and then divide by 1500= HR
(more accurate)
o Can calculate most narrow and most wide R-R and average for more accurate
HR

 Analyzing rhythm
o Determine ventricular R/R
o QRS duration and shape
o P wave pairing, 1 P wave for every QRS is normal
o Atrial R/R
o PR interval and consistency
o Want a good rhythmic cadence, is it regular or irregular
o QRS interval/QT interval

 Normal sinus rhythm

 o From SA node
o HR 60-100, good cadence

 Sinus brady

o SLOW, HR 60-
o Everything else matches NSR

 Sinus tach

o FAST, HR 100+. Everything else matches NSR

 Premature Atrial Complex/contraction. PACs

o Not super serious, after a normal beat an early beat follows

 o May feel palpitations, more of an aggravation than life threating
o Comes early from the atria

 A-flutter

o QRS narrow, NO P waves, F waves in replacement

o Saw tooth
o Ratio (this picture is 2:1, 2 F waves for every 1 QRS)
o Goal: control rate and convert to sinus
o CCB, BB, adenosine, digoxin, anticoagulants (if in for 48h)

 A-fib

o The atria is quivering

o NO cadence, irregular and different rates, narrow QRS, NO P waves (f
waves)
o Average HR
o Uncontrolled: HR 100+
o Controlled: HR 60-100
o CCB, BB, Digoxin to control rate
o Amiodarone, diflitide to convert rhythm. Then maintenance w/ ACE
inhibitors
o If in A-fib for 48+ hours use anticoagulants
 Premature Junctional Complex/contraction
 o HR 40-60
o P wave is inverted (upside down), absent or hidden with QRS
o Monitor, may need to speed up rate, normally transient

 SVT or PSVT

o Often transient
o Cadence fast, QRS narrow, sometimes no P wave
o Starts out normal than all the sudden fast rhythm
o Comes early and goes away quickly

 Carotid sinus massage

o RN doesn’t do, attempt other vagal maneuvers (bear down/cough)

 Premature ven complex/contraction (PVC’s)

o Ugly, bizarre, weird beat

o Has NSR w/ the underlying PVC

 Ven tachy
o Cadence is regular, QRS wide and bizarre
o May be conscious or not, check pulse
o Lidocaine, amiodarone, procainamide
 PVCs and V-tach
o Bigeminy: every other beat
o Trigeminy: every 3 beats
o Couplet: 2 together
o V-tach is 3+

o Unifocal: all going in the same

direction
o Multifocal: going in different
directions

 Torsades de Pointes

o Polymorphic (multidirectional): normally unresponsive, no pulse, use de-fib

and start CPR
o DEFIB!!!!
o Isoproteronol, Mg/K IV
o Key is height in the amplitude

 V-fib
 o BAD, not receiving any blood flow to the heart, unresponsive and no pulse
o Give De-fib for v-fib. I always think WHAT THE FUCK for this pt.
o No QRS. Give epi, vasopressin, or amiodarone. Will be coding this pt.

 Asystole

o NO QRS, NO de-fib
o Unresponsive, no pulse, no CO, start CPR and give epi
o Treat the underlying cause

 Pulseless electrical activity

o Electrical activity can be observed but no mechanical activity of the ven is
present
o Pt. has NO pulse
o Prognosis poor unless underlying cause is treated quickly
o CPR, intubate, IV epi

 H/Ts
o To fix PEA or asystole fix these
o Hypovolemia, hypoxia, hydrogen ion (acidosis), hyper/hypokalemia,
hypoglycemia, hypothermia
o Toxins, tamponade, thrombosis (MI or pulmonary), tension pneumo, trauma

 Sudden cardiac death

o Death from cardiac cause
o Majority result form ven dysrhythmias (V tach/V fib)
o Think Jess neighbor

 1st degree AV block

o Cadence regular, has P wave, PR interval is greater than 0.20
 o Slowed conduction through AV node
o Normally benign

 2nd degree AV block Type I Wenckebach

o Longer, longer, longer and drop

o 1st PR is normal, 2nd longer, 3rd longer and then the 4th beat is
dropped/blocked

 2nd degree AV block type II

o NO prolonged PR interval, symptomatic

o Spontaneously QRS doesn’t conduct, wide QRS
o P wave cadence is good, random missing QRS
o Atropine
 3rd degree AV block/complete heart block

o Wide QRS, random P waves that do their own thing. No one is working
together
o No consistent PR interval
o Try atropine

 Care of pt. with dysrhythmia

o Causes/contributing factors
o Assess indicators of CO/oxygenation
o Health history: any coexisting condition indications of previous occurrence
o All meds, prescribed and OTC
o Psychosocial assessment: a patient’s perception of dysrhythmia
o Physical assessment: skin (pale/cool), signs of fluid retention (JVD, lung
auscultation), signs of dec CO (altered LOC), rate and rhythm of apical and
peripheral pulses, heart sounds, BP, pulse pressure

 Potential comp due to dysrhythmia

o Cardiac arrest, HF
o Thromboembolic event

 Goals for pt.

o Eradicating/dec occurrence of dysrhythmia to maintain CO
o Minimize anxiety
o Acquire knowledge about dysrhythmia and its treatment

 NSG interventions
o Monitor/manage dysrhythmia
o Minimize anxiety (stay w/ them, maintain safety, discuss emotional state,
maximize pt. control, help them to identify factors contributing to episodes)
o Educate pt. and continuing care
o Promote home/community based care
o Assess VS, light-headed, dizziness, fainting
o Obtain 12-lead, continuous monitoring
o Anti-arrhythmic meds, “6 min walk test”, check HR, vitals
 Education
o Treatment options
o Therapeutic medication levels
o How to take pulse/BP before medications
o How to recognize s/s of dysrhythmia
o Measures to reduce reoccurrence
o Plan of action of an emergency
o CPR (family teaching)

 Continuing care
o Referral for home care if they display
1. Hemodynamically unstable w/ signs of dec CO
2. Significant comorbidities, socioeconomic issues
3. Limited self-management skills
4. Electronic device recently implanted

 Evaluation of pt.
o Maintain CO: stable VS, no signs of dysrhythmia
o Experience dec anxiety: positive attitude, confidence in abilities to act in
emergency
o Express understanding of dysrhythmia and treatment

 Adjunctive modalities and management

o Used when meds alone are ineffective
o Pacemakers, cardioversion, de-fib
o Nurse is responsible for assessment of pt. understanding regarding
mechanical therapy

 Cardioversion and defib

o Treat tachy-dysrythmias by delivering electrical currents that depol critical
mass of myocardial cells
o When cells repol sinus nose usually able to recapture role as heart pacemaker
o In cardioversion, current delivery synchronizes w/ pt. EKG
o In defib current delivery is unsynchronized
o De-fib paddles are either posterior and anterior or right above heart and right
below L nipple

 Safety measures
o Ensure good contact between skin, pads and paddles
o Use conduction medium 20-25 pounds of pressure
o Place paddles so they don’t touch bedding, clothing or near med patches or
o2
o If cardioverting turn synchronizer on
o If de-fib turn synchronizer off
 o Do not charge device until ready to shock
o Call “clear” 3x, make sure no one is in contact with pt. bed or equipment

 Pacemaker
o Electronic device that provides electrical stimuli to heart muscle
o Permanent: Implanted trans-venous
o Temporary: transcutaneous pacemaker, transvenous, epicardial

 Complications of pacemaker use

o Infection, bleeding, hematoma, dislocation of lead, skeletal muscle or
phrenic nerve stimulation, cardiac tamponade, pacemaker malfunction

 Pacemaker for resynchronization therapy (CRT)

o Resynchronizes the cardiac cycle by pacing both ven
o Biventricular pacing
o Used to treat pt. w/ HF
o Can be combined w/ ICD for max therapy

 ICD
o Detects and terminates life threatening episodes of tachy/fib
o Anti-tachycardia pacing

 Automatic cardioverter de-fib vest

o Rare
o External, literally a vest

 NSG management after permanent electronic device insertion

o EKG assessment
o CXR
o CO and hemodynamic stability
o Incision site
o Signs of ineffective coping
o Level of knowledge and education needs of family and pt.
o Pt. teaching: site care/observation, loose clothing, restrict arm movement
until healed (2w), no heavy lifting or driving, avoid heavy magnetic fields
and security scanners, place cell phone away from device, medic alert
bracelet, carry device/provider info in wallet

 ECG pacing
 o 1st and last beat is the patient own
o You want a ratio capture
o 1:1 in this picture
o For every 1 spike there is 1 ventricle capture

 Assess pacemaker malfunction

o Loss of capture **
o Under sensing
o Over sensing **
o Loss of pacing
o Change in pacing QRS shape
o Rhythmic, diaphragmatic or chest wall twitching/hiccupping
Pacemaker rhythms

Arrows are the

spikes, spike should
indicate a heartbeat
called a capture

When you have a

spike w/out a
heartbeat that’s loss
of capture

Over sensing we have

too many spikes
 Invasive methods to diagnose/treat recurrent dys
o Electrophysiological studies: ablation
o Cardiac conduction surgery: maze procedure, catheter ablation therapy