clinapps 2 exam 2

obstructive pulmonary disease

characterized by increased resistance airflow as a result of airway obstruction or narrowing

types of obstructive pulmonary diseases

cystic fibrosis


obstructive pulmonary disease with progressive limitation in airflow that is not reversible
preventable if treater early

chronic bronchitis

presence of cough and sputum production for at least 3 months in each of 2 consecutive years


destruction of alveoli and is a pathologic term that explains only one of several structural abnormalities in copd

copd pathophysiology

loss of elastic recoil
obstruction due to mucous hypersecretion, mucosal edema, and bronchospasm
air goes in easily but remains in the lungs (causing increased co2)
bronchioles collapse
result of chronic inflammation

risk factors for copd

cigarette smoking
occupational chemicals and dust
air pollution
severe reoccurring infections

geriatric changes (copd)

gradual loss of elastic recoil of the lung with stiffening of the chest wall
gas exchange

clinical manifestations of copd

chest breathing (use of accessory and intercostal muscles)
wheezing or chest tightness
chronic fatigue
coughing so severe is fractures ribs

physical examination findings of copd

barrel chest
decreased breath sounds
tripod position
pursed lip breathing
prolonged expiratory phase
right sided heart failure

copd diagnosis determined by

pulmonary function test (measures the amount of air you can inhale and exhale and whether your lungs deliver enough oxygen to your blood)

lower FEV1 indicates

a sicker patient

diagnostic studies for copd

chest x ray
sputum for culture and sensitivity

copd heart manifestations

hypertrophy of right side of heart as a result of pulmonary hypertension

copd heart symptoms

dyspnea (lung crackles)
distended neck veins
peripheral edema
weight gain

treatment for copd exacerbations

short acting bronchodilators (beta 2 agonists) and muscarinic antagonist
oral systemic corticosteroids
supplemental oxygen therapy


has drying effect on mucosa
supplied by nebulizers, vapotherm, and bubble-through humidifiers


large air sacs that form from destroyed alveoli that are removed to improve lung function


surgically created stoma used to
establish a patient airway
bypass airway obstruction
facilitate secretion removal
permit long-term mechanical ventilation
facilitate weaning from mechanical ventilation

advantages of tracheostomy

easier to keep clean
better oral and bronchial hygiene
patient comfort increased
less risk of long-term damage to vocal cords

speaking valves

thin diaphragm that opens on inspiration and closes on expiration
air flows over vocal cords during exhalation
must be deflated o use cuffless tube

removal of tracheostomy

patient must be hemodynamically stable
stable intact respiratory drive
can adequately exchange air and expectorate
monitor site for bleeding
splint stoma with fingers when coughing, swallowing, or speaking

risk factors for pneumonia

advanced age
underlying lung disease
altered consciousness
endotracheal intubation

community acquired pneumonia (cap)

infection occurs in community or within 2 days of hospitalization

hospital acquired pneumonia (nosocomial)

infection occurs 48 hours after hospitalization (5-10 cases per 1000 hospital admissions)
risk increased by intubation and mechanical ventilation


materials from mouth or stomach enter the lungs

health care associated pneumonia

hospitalized in acute care hospital for 2 or more days within 90 days of infection
usually in long-term facilities
received iv antibiotics, chemo, or wound care within 30 days of infection

ventilator associated pneumonia (vap)

airway infection that must have developed more than 48 hours after a patient is intubated
leading cause of death of hospital acquired infections

interventions for vap

elevation of head of bed
sedation vacations
peptic ulcer prophylaxis
deep venous thrombosis prophylaxis
oral care

aspiration of pneumonia

entry of substances from the mouth or stoma into the trachea and lower airway
associated with loss of consciousness and tube feeding

pneumoccal pneumonia manifestations

upper respiratory infection
pleuritic chest pain

mycoplasma pneumonia

younger people
working/living in crowded areas
chest pain
sore throat
dry cough

hospital acquired pneumonia manifestations

productive cough
looks sick

assessment of pneumonia

increased respiratory rate and fever
rhonchi/crackles and bronchial breath sounds
tactile fremitus
dullness to percussion
skin warm and dry
flushed and diaphoresis

community acquired pneumonia (cap) treatment

start within 4-8 hours
antivirals supportive care

hospital acquired pneumonia (hap)


latent tb

granuloma intact
bacteria dormant
no further progression of active disease

active tb

compromised or inadequate immune system response
granuloma ulcerates
cheesy material into bronchi
bacili airborne
inflammatory response

symptoms of tb

bad cough lasting 3 weeks or longer
chest pain
coughing up blood or sputum
weakness and fatigue
weight loss
no appetite
sweating at night

medical treatment for tb


nursing management for tb

promote airway clearance
promote adherence to treatment regimen
promote activity and adequate hydration

cardiac output

the amount of blood pumped by the heart per minute
stroke volume x heart rate

systemic vascular resistance

the amount of force exerted on the circulating blood by the vasculature of the body
determined by length and diameter of blood vessels and viscosity of blood within vessels

hypertensive emergency

occurs over hours to days
bp greater than 220/140 with target organ disease

hypertensive urgency

occurs over days to weeks
bp greater than 180/110 with no clinical evidence of target organ disease

complications of hypertensive crisis

hypertensive encephalopathy (headache, seizures, n and v, and confusion)
renal insufficiency
cardiac decompensation (mi, hf, and pulmonary edema)
aortic dissection

mean arterial pressure equation

map = (co x svr) + cvp (central venous pressure)

treatment for hypertensive crisis

iv titrated to map
monitor cardiac and renal function
neurologic checks
determine cause
education to avoid future crisis

cardiac assessment for hypertensive crisis

assess for murmurs and gallops
assess for heart failure

lung assessment for hypertensive crisis

assess for evidence of pulmonary edema (wheezing and rales)

abdominal assessment of hypertensive crisis

assess for bruits (renal artery stenosis)
abdominal aortic aneurysm
auscultate for murmur (aortic dissection)

extremities assessment of hypertensive crisis

assess pulses (if different may suggest aortic dissection)

diagnostic testing for hypertensive crisis

chest x ray
chest computed tomography
transthoracic echocardiogram (distinguishes diastolic dysfunction, transient systolic dysfunction, and mitral regurgitation)

treatment for hypertensive urgency

oral administration of meds (nicardipine, captopril, and labetatol)
normalize blood pressure gradually for 24-48 hours
observe patient for several hours prior to discharge

nicardipine dosing

20-40 mg orally every 8 hours

captopril dosing

25 mg orally ever 8-12 hours

labetatol dosing

initial dose 200 mg orally then additional 200-400 mg dose after 6-12 hours

treatment for hypertensive emergency

admit patient to icu for iv medications and management of end-organ dysfunction
lower bp 10-15% over the first hour

nicardipine iv dosing

initial infusion 5 mg/hour increasing 2.5 mg/hour every 5 minutes to a max of 15 mg/hour

sodium nitroprusside iv dosing

0.3-0.5 mcg/kg/minute increase by 0.5 mcg/kg/minute every few minutes to a maximum dose of 10 mcg/mg/minute

labetatol iv dosing

10-20 mg iv followed by bolus doses of 20-80 mg at 10 minute intervals until target bp reached at 300 mg cumulative dose

esmolol iv dosing

initial loading dose 500 mcg/kg/minute over 1 minute then 50-100 mcg/kg/minute to max dose of 300 mcg/kg/minute

peripheral vascular disease

inadequate return of venous blood from the legs to the heart caused by damage to the valves allowing blood to leak backwards

peripheral arterial disease

progressive narrowing of arteries typically in pelvis and legs

leading cause of pad


risk factors for pvd and pad

family hx of premature mi or stroke
older than 50
overweight or obese
inactive lifestyle
high ldl and triglycerides

causes of pad

blood clot
diabetes (higher blood sugar = more damage to vessels)
inflammation of arteries (autoimmune)
structural defects

clinical manifestations of pad

buttock pain
numbness/tingling of leg and foot
changes in skin color
changes in skin temp
sores that do not heal
uncontrolled hypertension
renal insufficiency/failure
thin shiny skin
hair loss on lower legs
pallor of foot w elevation

complications of pad

atrophy of skin and underlying muscles
delayed healing
wound infection
tissue necrosis
arterial ulcers

how pad is diagnosed

ankle brachial plexus
ultrasound doppler test

treatment of pad

angioplasty and stents (invasive)
atherectomy (invasive)
peripheral artery bypass surgery

medications for pad

ramipril (ace inhibitor)
aspirin (antiplatelet agent)
clopidogril (plavix)

medications for intermittent claudication (symptom of pad)

cilostazol (inhibits platelet aggregation and vasodilates)
pentoxifylline (lowers blood viscosity and increases rbc flexibility)

nursing interventions for pad

assess pulses
cap refill
hair distribution
open areas
and pain assessment

nursing education for pad

exercise improves oxygen extraction in legs and skeletal metabolism
walking is the most effective exercise

pvd risk factors

varicose veins or family hx of varicose veins
extended periods of sitting or standing
over 50

symptoms of pvd

swelling in lower legs and ankles
aching or tiredness in the legs
new varicose veins
leathery looking skin on legs
flaking or itching skin
stasis ulcers

diagnosis of pvd

vascular ultrasound

nursing education for pvd

avoid sitting or standing for long periods of time
exercise regularly
lose weight if overweight
elevate legs
wear compression stockings
good skin care

treatment of pvd

ligation and stripping
ambulatory phlebectomy
vein bypass

heart failure

complex clinical syndrome that can result from any structural or functional cardiac disorder that impairs the ability of the ventricle to fill and eject blood

heart failure results in

ventricular dysfunction
decreased cardiac output
decreased tissue perfusion
fluid retention


volume in ventricles awaiting delivery


pressure in aorta to overcome

myocardial contractility

intrinsic ability to shorten and develop muscle tension

renin angiotensin aldosterone system responds to

decreased co2
decreased renal blood flow
increased renin from kidneys

aldosterone is for

sodium retention


secreted by posterior pituitary and increases water absorption with increases in blood volume

sympathetic nervous system involvement in hf

increases catecholamines (increases epinephrine and norepinephrine leading to vasoconstriction)
leads to increased bp, afterload, and hr

ventricular remodeling

process of changing shape and mass of ventricles

ventricular dilation

enlargement of chambers
muscle fibers stretch to increase contractility

ventricular hypertrophy

increase in cardiac wall thickness
initially serves to increase contractility
decrease inside volume

systolic hf

ef less than 40%

diastolic hf

ef greater than 50%

hf causes

left ventricular dysfunction
uncontrolled htn
volume overload due to excess dietary sodium, excess dietary fluid, and hepatic dysfunction
renal insufficiency (fluid retention)
high output state
hormonal disturbances
medication related
substance abuse

left sided hf symptoms

cough (dry hacking)
s3 heart sounds
pulmonary edema (crackles)

right sided hf symptoms

increased weight gain

labs to monitor with hf

coagulation panel

management of hf

loop diuretics
inotropic support
iv morphine

ace inhibitors (for hf treatment)


ace inhibitors (for hf treatment) function

reduction in mortality
improvement in exercise tolerance
improves symptom control

ace inhibitors (for hf treatment) adrs

taste disturbance

angio 2 receptor blockes (hf)

used in patients who are ace 1 intolerance
can be added to beta blockers, digoxin, and diuretics

beta blockers (hf) cardioselective


beta blockers (hf) nonselective

start with hemodynamically stable patient with no fluid retention
watch for hyperglycemia
symptoms may worsen in 3-6 months

nursing assessments for patients with hf

daily weights
fluid restriction
labs (creatinine and electrolytes)


begins as soft deposits of fat that harden with age
major cause of cad

c-reactive protein

nonspecific marker of inflammation
elevated in patients with cad
chronic exposure associated with unstable plaques and oxidation of ldl cholesterol

collateral circulation

arterial anastomoses within the coronary circulation
increased with chronic ischemia

nonmodifiable risk factors for cad

family hx
genetic predisposition

modifiable risk factors for cad

elevated serum lipids (cholesterol, triglycerides, hdl, and ldl)
tobacco use and second hand smoke exposure
physical inactivity
metabolic syndrome
psychologic states
homocysteine level
substance abuse

statin (treatment for cad)

inhibit cholesterol synthesis decreasing ldl and increasing hdl
must monitor for liver damage and myopathy

niacin (treatment for cad)

lowers ldl and triglyceride by inhibiting synthesis
increases hdl
flushing, pruritis, GI side effects and orthostatic hypotension are all side effects

fibric acid derivatives (lopid)

decrease triglycerides and increase hdl
has GI side effects

bile acid sequestrants (welchol)

increase conversion of cholesterol to bile acids
GI side effects and can bind with other drugs

ezetimibe (zetia)

decrease absorption of dietary and biliary cholesterol

modifications for physical activity for older adults

longer warm up
longer periods of low level activity
longer rest periods
avoid extremes of temperature
30 minutes most days minimum

cad angina

reversible ischemia
occurs when arteries are blocked 75% or more
hypoxic within 10 seconds of occlusion
viable for 20 minutes

clinical manifestations of cad angina

squeezing, heavy, choking, or suffocating sensation
indigestion or burning
various locations

clinical manifestations of cad chronic stable angina

intermittent chest pain that occurs over long period with the same pattern of onset duration and intensity of symptoms
5-15 minute duration
ST segment depression
control w drugs

silent ischemia

ischemia that occurs in the absence of any subjective symptoms
associated with diabetic neuropathy
confirmed by ECG changes

nocturnal angina

occurs only at night but not necessarily during sleep

angina decubitus

chest pain that occurs only while lying down
relieved by standing or sitting

prinzmetal's (variant) angina

occurs at rest usually in response to spasm of major coronary artery
seen in patients with a history of migraine headaches and Raynaud's
spasm may occur in the absence of cad

microvascular angina

chest pain occurs in the absence of significant coronary atherosclerosis or coronary spasm
myocardial ischemia associated with abnormalities of the coronary microcirculation
affects small distal coronary arteries

short acting nitrates

dilate peripheral and coronary blood vessels
give sublingually tablet or by spray
if no relief in 5 minutes call ems
can use prophylactically

long acting nitrates

reduce angina incidence
side effect are headache and orthostatic hypotension
can be given orally, nitroglycerin ointment, or transdermal release

collaborate care for chronic stable angina

angiotensin converting enzyme inhibitors
beta adrenergic blockers
calcium channel blockers
sodium current inhibitor (ranexa)

diagnostics for chronic stable angina

chest x ray
12 lead ekg
calcium score screening heart screen
exercise stress test
pharmacologic nuclear imaging


ability to initiate an impulse


ability to respond to an impulse


ability to transmit an impulse


ability to response with pumping action

how does the cardiac cell work?

cardiac cells contract (depolarization) and depolarization spreads through gap junctions

cardiac conduction system

refers to system of electrical signaling that instructs these muscle cells to contract

three ion channels of the cardiac action potential

fast sodium channels
slow calcium channels
potassium channels


contraction of the heart
causes membrane to become permeable to sodium and potassium (sodium flows in potassium flows out)
positive electrical potential outside the cells


resting state of the heart
sodium channels close and potassium flows outside cells until the end
outside of cell returns to negative electrical potential

sa node

sets up pace of the heart
inherent rate of 60-100

junctional fibers

designed to carry action potential rather slowly so that atria to contract and force blood into the ventricles

av node

relays impulses from sa node to ventricles
located in wall between right atrium and right ventricle
inherent rate 40-60

av bundle

group of fast conducting fibers carry the av node activity to the intraventricular septum really quickly
inherent rate 20-40

purkinje fibers

fibers that run along the outer edge of ventricles

map of electrical impulse in heart

sa node
atrial syncytium
junctional fibers
sa node
av bundle
bundle branches
pukinje fibers
ventricular syncytium

sns influence

supplies atria and ventricles
epinephrine is the mediator
increases rate of sa node, av node, excitability, and force of contractility

pns (vagus nerve) influence

affects primarily atria
acetylcholine is mediator
decreases sa node, rate of av conduction, and excitability


measures the direction of electrical impulses from cardiac cells

as electrical current travels toward negative pole

wave form deflects downward from isoelectric line

as electrical current travels toward positive electrode

wave form deflects upward from isoelectric line

proper skin prep before placing electrodes

soap and water NO ALCOHOL
get rid of excess body hair

ekg paper 5 large boxes is

1 second

ekg paper 15 large boxes

3 seconds

calculating heart rate rule of 10

regular or irregular rhythm
count number of r waves in 6 second strip x 10 = hr

p wave

atrial depolarization

qrs complex

ventricular depolarization

t wave

ventricular repolarization

u wave

final phase of repolarization

normal pr interval

0.12-0.20 seconds

normal qrs complex interval


normal qt interval

less than 0.4 seconds
can be affected by age and gender
also affect my medications (zofran and anesthetics) and electrolyte imbalances (magnesium and potassium)

ekg paper small boxes

0.04 second

ekg paper large boxes

0.20 second

sinus rhythm

rate 60-100 bpm
regular rhythm
p waves = 1 to each qrs complex
qrs = all the same (less than 0.12)

sinus bradycardia

hr less than 60 bpm
regular rhythm
p waves = 1 to each qrs complex all the same shape and size
qrs all the same (less than 0.12)
may impact cardiac output
normal in conditioned athlete
treatment based off symptoms in cardiac patients
can be caused by vaso

sinus tachycardia

hr 101-150
regular rhythm
p waves = 1 to each qrs; same shape and size
qrs all the same (less than 0.12)
decreased ventricular and coronary artery filling time
may cause cardiac ischemia
may lead to increased OR decreased bp
caused by sympathetic stimulat

sinus pause

irregular during pause
underlying sinus rhythm
sudden decrease in rate (may cause syncope or dizziness)
no p wave or qrs complex during pause or arrest
diseased sa node, vagal stimulation, mi
treatment depends on length of pause (atropine and pacer at the

types of atrial dysrhythmias

a flutter
a fib

premature atrial contraction (pac)

early beat in normal rhythm
p wave early and differs in size and shape from other p waves
normal qrs
may have short pause after pac
may arise from bigeminal, trigeminal, or couplets
precursor of afib
can signal hf, pericarditis, hormones, caffeine, electr

supraventricular tachycardia

a rapid tachyarrhythmia that originates above the ventricle (also called PSVT paroxysmal supraventricular tachycardia)

svt causes

heart failure
thyroid disease
heart disease
chronic lung disease
too much alcohol
too much caffeine
drug use
asthma meds and certain otc meds

atrial flutter

sawtooth pattern
rapid atrial rate (250-350)
abnormal electrical circuit in the atria
ventricular rhythm usually regular
s/s of decreased cardiac output
shortness or breath
chest pain
fluttering heartbeat
swelling in you

causes of atrial flutter

high blood pressure
coronary artery disease
heart failure
congenital heart disease
past heart surgery
alcohol consumption
lung disease
overactive thyroid
sleep apnea
over exercising
family history

atrial fibrillation (afib)

disorganized ineffective quivering of the atria
no p waves
ventricular rate is totally irregular and varied
no pri
uncontrolled a fib = greater than 100 ventricular bpm
controlled a fib = less than 100 ventricular bpm
apical/radial pulse deficit

causes of afib

heart valve disorders
copd/lung diseases
sick sinus functioning
congenital heart disease
overactive thyroid
high bp
previous heart surgery
stress due to surgery, pneumonia, or other illness
sleep apnea

bradycardia treatment

observe for symptoms
if symptomatic atropine 0.5 mg-1 mg iv pacemaker on standby

tachycardia treatment

treat cause (rhythm can be compensatory)
beta blockers or calcium channel blockers

holter monitor

small wearable device that keeps track of heart rhythm
can detect irregularities of rhythm that ekg cannot

implantable loop recorder

type of heart-monitoring device that records heart rhythm continuously for up to 3 years
records electrical signals of your heart and allows remote monitoring by small device inserted beneath the skin

treatment of svt

vagal maneuvers
synchronized cardioversion if severe symptoms
cardizem (1 choice of calcium channel blockers)
beta blockers
digoxin (will not lower bp)


synchronous defibrillation with less use of energy
patient is usually awake and hemodynamically unstable
painful! medicate before

treatment of afib

want to reset rhythm
electric cardioversion
pharmacological cardioversion (calcium channel blockers, amiodarone, digoxin)
left atrial appendage closure (watchman device)

warfarin (coumadin)

blocks liver from using vitamin K to make clotting factors (vitamin K is antidote)
5-7 days to be effective

international normalized ratio (INR)

tests how much time it takes for a patient's blood to clot
range is 2-3
avoid foods with high vitamin K

non vitamin k oral anticoagulants

pradaxa (dabigatran) thrombin inhibitor
xarelto (rivaroxaban)
eliquis (apixaban)

causes of premature ventricular contarctions

electrolyte imbalance
hypoxia fever
emotional stress

treating the cause of pvc

assess patient (hemodynamically stable)
electrolyte therapy
oxygen therapy
further diagnostics


condition which makes it harder for heart to pump and supply blood to the other parts of the body

dilated cardiomyopathy

pumping dysfunction (mostly l ventricle) chamber enlargement
typically presents between 30-60 y/o
most common in african american males
third leading cause of heart failure
most common form of cardiomyopathy

ischemic dilated cardiomyopathy

coronary artery disease
myocardial infarction

non-ischemic dilated cardiomyopathy

familial (genetics) Duchenne muscular dystrophy
structural heart (valves, pressure or volume overload, l to r shunt)
drugs (chemo, cocaine, toxins ex) co2, lead, mercury)
immune (autoimmune, hypersensitivity, transplant rejection, infect

cardiomyopathy evaluation

stress test or coronary angiography
lab tests (genetic mutation)
cardiac biopsy
troponin and bnp

treatment of dilated cardiomyopathy

ace inhibitors/arbs
beta blockers
treat underlying cause
implantable cardioverter defibrillator
LVAD (does not have a pulse)

hypertrophic cardiomyopathy

commonly inherited cv disease
largely caused by gene mutations
complication include syncope, hf, and sudden death

signs and symptoms of hypertrophic cardiomyopathy

may be asymptomatic
chest pain
systolic murmur

treatment of hypertrophic cardiomyopathy

no intensive sports (low intensity workouts)
beta blockers
verapamil (ca channel blocker)
diltiazem (for those intolerant to verapamil)
implantable cardioverter devices
permanent pacemakers
septal ablation
heart transplant

restrictive cardiomyopathy

heart muscle characterized by impaired ventricular filling with typically preserved systolic function and normal or mildly increased ventricular wall thickness

causes of restrictive cardiomyopathy

cardiac sarcoidosis

management of restrictive cardiomyopathy

diuretics and aldosterone antagonists
pacer for av block
corticosteroids, melphan, autologous stem (for amyloidosis)
iron depletion (treatment for hemochromatosis)
cardiac transplant
implantable cardioverter-defibrillator

takotsubo broken heart syndrome

acute cardiac syndrome
left ventricular ballooning
often precipitated by acute emotional or physical stress

symptoms of broken heart syndrome

cheat pain and st elevations

management of broken heart syndrome

spontaneous recovery
ef guides treatment (ef less than 45% and complications are considered high risk)
beta blockers and ace inhibitors
follow up care is a must