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244 Cards in this Set

  • Front
  • Back
pitting edema is a sign of what?
sign of DVT / post-thrombotic syndrome
what kind of ulcerations (venous / arterial) have edema (what kind?)
venous ulcerations have non-pitting edema in affected extremity
piece of dead tissue case off from surface of skin--> black, thick, dry, black necrotic tissue
where is a gaiter likely to be
lower 1/3 of calf
WHAT TYPE OF ulcer is gaiter associat'ed w/?
venous ulcer
dependent rubor is a typical finding of someone w/?
describe arterial ulceration
painful, on foerfoot/toes (distal from ischemic artery), deep, punch out, minimal granulation tissue, well demarcated edge
describe venous ulceration
in gaiter area, shallow, irregular borders, have granulation tissue and exudate.
what is stasis
pooling of blood
where is stasis found
lower extremities *
why does stasis happen
dysfxnal valves / muscles of extremities are inactive leads to what?
who does stasis happen to
you'll find this condition with obese / pregnant people, chronic heart failure, afib, traveling on long trips w/o regular exercise, prolonged surgical procedure, immobile for long periods of time
condition where body orifice / passage in body is abnormally closed / absent
risk factors for cellulitis
diabetes mellitus, lymphedema, venous stasis/insufficiency, immune suppression, PVD, malnutrition, IV drug use
what is cellulitis
spreading bacterial infection of skin/sub Q tissue
what causes cellulitis
strep / staph infections
where does cellulitis happen
extreimties (lower legs) are common site *
cardiac standstill -- flat line-- absence of electrical actviity / contractions
describe A FIB
disorg in electrical acvitiy in atrea due to multiple ectopic foci--> ineffective contracton / ineffective ejection of blood into ventricles / irregular apical pulse rate. blood in atria might form clots that emoblize to brain
what is most common / clinically significant cardiac dysrhythmia
atrial fib *
paroxysmal afib is characterized by what kind of episodes?
intermittent episodes *
atrial flutter
rapid, regular atrial tachydysrhtymia w/ regular ventricular response
where is atrial flutter most common
right atrium *
what does atrial flutter look like?
saw tooth
how does atrial flutter present symptom wise
asymptomatic, palpitations, dizziness, presyncope, syncope
ability of cardiac muscle to spontaneously / continously contract w/o nervous stimulation
what happens to the impulse during an AV block and where?
depolarization impulse is delayed / blocked at AV node (or at AV bundle / bundle branches). ranges from prolonged av conduction (prolonged PR interval) to intermittent to no atrial impulses conducted to ventricles
what causes AV block
degenerative changes, drugs (digoxin, beta blockers, CA++ blocker, hyperkalemia, hypokalemia, increase vagus nerve activity, scarring from MI)
ability to transmit impulse along a membrane in orderly manner
property of cardiac cells--> abilty to respond mechnically to an impulse
treatment of choice to end VFib or pulseless V Tachy -- rapid defib (2 mins) = impt to successful pt outcome
how does defib work
by passage of a direct current electric shock through heart that is sufficient to depolarize the cells of the myocardium--> intent is that subsequent repolarization of myocardial cells will allow SA node to resume role of pacemaker
escape rhythm
when SA node discharges more slowly than a 2ndary pacemaker--> electrical discharge from 2ndary pacemaker might "escape"

---> 2ndary pacemaker wil discharge at its intrinsic rate

A junctional escape beat is a delayed heartbeat originating not from the atrium but from an ectopic focus somewhere in the AV junction. It occurs when the rate of depolarization of the sinoatrial node falls below the rate of the atrioventricular node. This dysrhythmia also may occur when the electrical impulses from the SA node fail to reach the AV node because of SA or AV block. It is a protective mechanism for the heart, to compensate for the SA node no longer handling the pacemaking activity, and is one of a series of backup sites that can take over pacemaker function when the SA node fails to do so.
• Excitability: ability to be electrically stimulated.
ability to be electrically stimulated-- myocardial tissue is allowed to be depolarized by a stimulus
happens in myocardium when myocardial tissue starts to necrose after insufficient o2 from insufficnet blood flow
JXNAL rhythm
dysrhtymia originating in area of AV node--> b/c SA node fails to fire / signal is blocked

av node becomes pacemaker of heart
lapse in consciounses w/ fainting
what causes syncopy
cardioneurogenic / vasovagal (carotid sinus senstivities)

primary cardiac dyshrthymias
what's the diff b/w atrial flutter and afib?
Atrial flutter is an organized regular rapid upper chamber rhythm that goes in almost all patients at about 300 beats a minute.

atrial fibrillation will cause an irregular heart beat.
what's VFIB?
Lethal dysrhythmia characterized by chaotic electrical activity without organized QRS complexes detected. Ventricle is "quivering" - no effective contractions, no CO!
what does VFIB look like on ECG?
Regularity: There is no regularity to the rhythm because there are no complexes or waves present that are able to be analyzed. Rate: There is no measurable rate. P WAVE: There are no P waves present.
what is a patient like during VFIB
A patient will be unconscious as blood is not pumped to the brain. Immediate treatment by defibrillation is indicated.

Results in pulseless, unresponsive, apneic - start immediate CPR!
when does VFIB happen
Associated with acute MI, myocardial ischemia, heart failure, and cardiomyopathy, procedures related to stimulation of ventricle (cardiac catheterization), hyperkalemia, hypoxemia, acidosis, drug toxicity, accidental electrical shock.
when does V flutter turn into V fibb?
w/o treatment!
what is ventricular flutter?
the ventricles depolarize in a circular pattern, rapid, uniform, greater than 250bpm. Results in a minimal cardiac output and subsequent ischemia
what is V Tach associated w/?
. Associated with MI, CAD, significant electrolyte imbalances, cardiomyopathy, mitral valve prolapse, long QT syndrome, drug toxicity, CNS disorders.
what does V Tach result in
Causes severe decrease in CO - resulting in hypotension, pulmonary edema, decreased cerebral blood flow, and cardiopulmonary arrest.
what does V tach look like
a run of three or more PVCs (premature ventricular contraction) and the ventricle takes control as pacemaker, conduction is cell by cell; rhythm is usually regular, rate between 100-250 bpm, P wave may be seen - but usually buried in QRS complex, PR interval not measureable, QRS complex has bizarre shape, duration greater than 0.12 secs
an abrupt onset and termination (of cardiac electrical activity)
an electronic device used to pace the heart when the normal conduction pathway is damaged. The pacing circuit consists of a power source (battery-powered pulse generator), one or more conducting leads (pacing leads), and the myocardium. The electrical system (stimulus) travels from the pacemaker, through the leads, to the wall of the myocardium. The myocardium is "captured" and stimulated to contract.
the observation of a patient's HR and rhythm at a site distant from the patient. Helps to rapidly diagnose dysrhythmias, ischemia or infarction. There are two types: 1. Centralized monitoring system which requires a nurse or technician to continuously observe a group of patients' ECG's at a central location. 2. Does not require constant surveillance, the systems have have the capability or detecting and storing data. The system will alarm if it detects abnormailities depending on the severity of each
what does the foramen ovale connect? why?
shunt connecting R and L atrium so maternal oxy blood can bypass fetus lungs
what is flow of blood in foramen ovale?
blood from: RA --> LA--> down to LV--> systemic circ

- small amnt goes into RV / pulm circuit to noursih lungs
what makes the foramen ovale close? when does it close
in neonates: increased pressure in LA helps close the shunt and complete anatomical closure happens w/in first 30 days
what does ductus arteriosus connect
blood vessel connecting pulm artery to aortic arch
what does ductus arteriosus allow blood to do?
allows blood from RV to bypass fetus's fluid-filled non-fxning lungs
what does ductus arteriorus becomes after it closes at birth
ligamentum arteriosum
what's a shunt
hole / passage allowing fluid to move from 1 part of body to another
endocardial cusion-- what is it?
subset of cells in primordial heart that plays an impt role in proper heart septation
where does endocardial cusion develop?
on the atrioventricular canal
what's the point of endocardial cusion
during development, heart starts as tube--> as it develops, tubes goes through conformational changes--> remodels to form a 4-chambered heart

- endocardial cusions are VERY impt in helping developing heart tube form the heart's valves / septa to become a 4 chambered heart
what is tachypnea a sign of w/ young children?
fast breathing...>60 in infants...clinical manifestation of congenital heart disease in infants

manifestation of both pulmonary congestion and systemic venous congestion
what is grunting respiration
sound heard each time person exhales
why do we "grunt"
body's way of trying to keep air in lungs so that they will stay open
knee-chest position allows for what? why do kids do it?
allows lungs to open up more

kids will crouch like this to enhance breathing is there is a physiological problem
Hypercyanotic spell is r/t to what conditioned, is triggered by what, lasts for how long, leads to what
r/t teratolgy of fallot. can be triggered by tachycardia, crying, pooping, hypotension. these can last for 15-30minutes and can lead to seizures/ death.
hypercyanotic spell interventions?
interventions = give O2, and calm that baby down! give them morphine if you have to.
the tension or stress developed in the wall of the left ventricle during ejection
by widespread swelling of the skin due to effusion of fluid into the extracellular space.
what causes anasarca
It is usually caused by liver failure (cirrhosis of the liver) or renal failure/disease and severe malnutrition/protein deficiency.
what does anasarca lead to
The increase in salt and water retention caused by low cardiac output can also result in anasarca as a long term maladaptive response.
excess fluid in the space between the tissues lining the abdomen and abdominal organs. Those
what happen when ascites + HF? what are the sx?
Those with ascites due to heart failure may also complain of shortness of breath as well as wheezing and exercise intolerance
B-type natriuretic peptide (BNP) -- where is this synthesized?
B-type natriuretic peptide (BNP) -- what is it released in response to? what does it correlate to? what does it cause?
released in response to prolonged volume overload. elevated in HF. correlate well with LV pressure. causes arterial and venous dilation.
cardiac biomarkers
troponin (elevate in myocardial injury) and CK-MB
why do we test for cardiac biomarker levels? and when?
. These levels are tested after an ECG (if no elevated ST segment is noted) is performed to see if the pt is going through a NSTEMI or UA

elevated troponin will lead to interventions for an NSTEMI even though there are other (non MI) reasons troponin can be elevated.
cardiac output
the volume of blood being pumped by the heart, in particular by a left or right ventricle in the time interval of one minute
cardiac reserve
The work that the heart is able to perform beyond that required of it under ordinary circumstances
ejection fraction
is the fraction of blood pumped out from the right ventricle of the heart to the pulmonary circulation


left ventricle of the heart to the systemic circulation with each heart beat or cardiac cycle
hemoptysis - what is it / what cuases it?
coughing up blood, or blood stained sputum. heart failure and mitral stenosis can cause this
when blood backs up into the liver from the IVC...from the heart. then the liver gets big
enlargement of both the liver and the spleen from right sided heart failure.....r/t blood backing up
what does an inverted T wave indicate?
Coronary ischemia, hypokalemia, left ventricular hypertrophy, digoxin effect, some drugs
left sided failure-- what are signs
Signs: LV heaves, pulsus alterans, increase HR, PMI displaced inferiorly and posteriorly, decrease in PaO2, dyspnea on exertion, crackles (pulmonary edema), S3 and S4 heart sounds, pleaural effusion, changes in mental status, restlessness, confusion
what are sx of left sided failure?
Weakness, fatigue, anxiety, depression dyspnea, shallow respirations, paroxysmal nocturnal dyspnea, orthopnea, dry hacking cough, nocturia, frothy pink sputum.
nocturia-- what is it and what does it indicate?
symptom of R sided heart failure.

having to get up at night and pee.
needing to sleep with pillows
what does orthopnea indicate?
a later symptom of L sided heart failure / pulmonary edema
paroxysmal nocturnal dyspnea
In pts with HF fluid accumulates in their lower limbs throughout the day.. When they lay down this extra fluid is distributed throughout their body and the heart can't handle it which leads to pulmonary congestion..and then waking up in the middle of the night with SOB
polycythemia-- what is it, what can it cause
increase in red blood cells...can also cause cyanosis even when there is sufficient O2 in the blood.
initial stretch of the heart before contraction
pulmonary edema-- what does it indicate / what is it? what is primary sx?
S/Sx of L sided HF. abnormal buildup of fluid in the air sacs of the lungs, which leads to shortness of breath
right sided failure-- what are clinical manifestations?
- RV heaves
- murmurs
- jugular venous distension
- edema
- weight gain
- increased HR
- ascites
- anasarca
- hepatomegaly
sx of R sided heart failure
Fatigue, anxiety, depression, dependent-bilateral edema, RUQ pain, anorexia and GI bloating, nausea
ST elevation - what does it indicate? what kind of interventions are received?
a sign of cardiac tissue damage. An ECG is the first thing done in the ER with a pt presenting with chest pain. If ST elevation is noted, then the pt receives interventions for an infarct
Systemic Vascular resistence
resistance to blood flow offered by all of the systemic vasculature, excluding the pulmonary vasculature. SVR = (MAP - CVP) ÷ CO
most MI's are secondary to what?
thrombus formation
HTN: what does sustained high BP lead to ? what does it do to heart?
- increases cardiac worklad
- produces L Ventric hypertrophy (adaptive / compesnatory mechiansm)--> that strengthen cardiac contraction / increases o2

but when heart can't meet demands for myocard o2--> heart failure occurs
how does HTN affects contracility / stroke volume / co?
depresses contractility

depresses SV

CO is decreased
HTN is a major risk factor for what?
cerebral atheroscleoris

What happens to heart tissue with MI? why does MI happen?
- happens b/c of sustained ischemia
- causes irreversible myocardial necrosis
- contractile fxn of heart stops in necrotic area
MI: inferior wall infarction from what artery?
left anterior descending artery
MI: latera/posterior wall MI's from what vessel?
left circumflex artery
MI: clinical manifestations?
pain (20 min+)

more severe pain than angina

NOT releived by rest / position change / nitrates
what does MI feel like on skin?
ashen, clammy, cool to touch
what happens with output for MI
first, bp / hr is elevated, but BP may drop b/c of decreased CO

- this --> decreased renal perfusion , decreased urine output
what lungs sounds do you hear with MI? what does it suggest
crackles suggesting LV dysfxn
what signs might indicate RV dysfxn
JVD, hepatic engorgement, peripheral edema
Sudden cardiac death is what and leads to what?
abrupt disruption in cardiac function

leads to loss of CO and cerebral blood flow
how fast does death occur with Sudden cardiac death
1 hour of onset of acute sx (angina, palpitations)
what heart condition is most commonly assocaited with Sudden cardiac death
acute ventricular dysrhythmia

ven tachy

vent fib (very lethal)
what to prevent a recurrence of Sudden cardiac death
implantable cardioverter-defib
what is the most common clinical manifestation of reversible myocardial ishcmiea
angina pectoris (stable)
myocardium becomes hypoxic w/in first ____ secs of ______
first 10 secs of coronary occulsion
w/ total occlusion of coronary arteries, myocardial cells are deprived of ___ and ___, so ____ begins and ____ accumulates
- o2 / glucose
- lactic acid
HTN is associated w/ what heart probs?
- left sided failure
- a Fib
- L ventricular afterload increases
angina pectoris leads to ___ bloodflow r/t _____ of ______ afteries by _______
- decreased
- narrowing of coronary arteries
- athersclerosis
what kind of meds for angina pectoris?
- anti platelets
- anti coags
unstable angina-- what happens?
- rupture of thickened plaaque--> exposing to thrombogenic surface
what accts for referred pain to left shoudler/arms during angina?
buildup of lactic acid --> irritates myocardial nerve vibers--> tranmits a pain msg to cardiac nerves
what is chronic stable angina characterized by
- chest pain occuring intermittently over long period of time /w same pttern of onset, duration, intesnity of sx
for chronic stable angina: T/F: angina is sharp or stabbing
false -- it is rarely sharp / stabbing and doesnt change w/ psition / breathing
how long to wait for stable angina to go away? what to do?
5-15 mins, subsides when preciptating factor = relieved

pain at rest = unusual
T Wave inversion indicates what?
what is Virchows triad? what does it contribute to?
venous stasis

damage of endothelium (inner lining of vein)

hypercoagulabiltiy of blood

contributes to thrombosis
varicosity. where is this found? what is it?
varicose veins are dilated, tortuous subq veins found in saphenous vein system
varicosity-- what is it due to
1) due to congential weakness of veins-- more common in women

superficial veins in LE's become dilated/tortuous in response to increased venous pressure

- valves don't fit together properly anymore
what makes varicosity worse / why? leads to what?
standing for long periods of time due to increased venous pressure and further venous distnetion?
why does HF occur in someone with DCM
b/c heart cant perfuse what volume is in him- so whatever fluid we’re putting in him, he still has big prob with contractility

big boggy heart, cannot provide pumping power
what heart condition is associated w/ DCM and why?
AARTHYMIA!—very common b/c electroconduction of heart is altered when heart is big and boggy
how do aarthymias affect flow?
fwd flow can be sginficaitnly decreased
normal ejection fraction
what is endocarditis? who do we see this in?
o Inflammation of inner lining of heart / valves

o Occurs in drug users, valve replacments, or mitral valve proplapse /strcutral defects (congenital)
what is pathophys of endocarditis
• Vegeatation (fibrin, leukoscytes, platelets, micrboes)—are the primary lesgion of infective endocarditis

o These things will adhre to valve / endocardium

 When these portions of vegetations get lost into circulation--> embolization
what is part of your asseessment with someone wiht endocarditis?
o Look for fever
o Anorexia
o Weight loss
o Fatigue
o Cardiac murmurs
o Heart failure
o Embolic complications from vegetation fragments traveling thru circulation
o Petechiaie

o Splinter hemorahges in nail beds
o Clubbing!
o Splenomegaly  SPLEEN ENLARGES
o Splinter hemmoraghes BLACK LONGITUDINAL STREAKS in anil beds
o Osler’s nodes: PIANFUL, TENDER, RED, PURPLE pea size lesions on fingertips, toes
o Janeway’s lesion (flat, painless, small red spots)—palms/soles
o Emboli might lodge in small periph blood vessels of arms/legs ischemia / gangrene
o Emboli to brain neurological damage
o Could cause dyspnea / Respiratory arrest
interventions for endocarditis
o Provide adequate rest w/ activity to prevent thrombus
o Antiembolism stocking
o Monitor CV status
o Monitor for signs of heart failure
o Monitor for splenic emboli (aeb sudden abdominal pain--. Radiating to left shoulder / rebound abd tenderness)
o Monitor for renal emboli (flank pain  to groin, hematuria)
o Monitor for confusion, aphaisa, dysphagisa  central nervous system emboli (CNS damage,)—changes in LOC
o Pulmonary emboli (dyspnea / cough)
o Assess skin, mucous membranes, conjnictve for pethacie
o Assess for nodes / lesion, clubbing
o GIVES AB’S penicillin
endocarditis nursing dx's:
o Decreased cardiac output R/T altered rhythm / valv insufficinency, fluid overload
o Activity intolerance r/t generalized weakness
primary intervention w/ endocarditis?
how to treat varicose veins?
o Leg elevation / pressure stocking / exercise
o Sclerotherapy
o Surgical removal
for HTN: what could chest pain mean?
could be a pulmonary embolus secondary to DEEP VEIN THROMBOSIS
what drugs would you use for HTN and why
- ACE inhibitors are use for htn prevent converstion of Angiio I to angio II prevenst vasoconstriction  prevents sodium / water rention
intermittent claud = classic sx of ?
arterial occlusive diases
s/sx of DVT
calf tendereness, calf edeam, + Homan’s
dependent rubor = sign of what? what does it look like?
 Legs = pale when elevated (eleavation pallor), but DARK RED when in dependent position
pericarditis is what?
inflammation of pericardial sac
what does pericarditis lead to
cardiac compression, decreased ventricular filling / emptying, heart failure
when does pericarditis happen / why?
1) infection causes--> are idiopathic and suspected to be viral

2) non infectious causes: 2-3 dyas after acute MI as complication of infarction

3) hypersensitivity/autoimmune reaction (dressler syndrome-- 4-6 wks post MI, rheumatic fever, drug rxns)
what does someone feel like w/ pericarditis?
progressive, frequently severe chest pain that is sharp / pleuritic in nautre

worse w/ deep inspriation / when lying supine

pain may radiate to neck, arms, left shoulder (making it hard to differentiate b/w that and angina)
how to relieve pericarditis (feeling)
sitt up / lean fwd (dyspnea associated is r/t pt's need to breathe in rapid/shallow breaths to avoid chest pain)
what is hallmark finding in acute pericarditis
pericardial friction rub

scratching / grating high-ptched sounds from friction b/w roughened pericardial / epicardial surfaces
what are 2 major complicattion from pericarditis
- pericardial effusion
(accumulation of excess fluid in pericardium)

- cardiac tamponade
(deveops as pericardial effusion increases in volume--> causes increase in intrapericardial pressure)

results in compression of heart

leads to decreased left atrial filling (causing decreased CO), muffled heart sounds, narrow pulse pressure
pericarditis-> what will pt develop (s, sx)

decreased CO


pulsus paradoxus
pericarditis nursing interveiton
mgmt of pt's pain / anxiety



ibuprofen to control pain / inflammation
myocarditis: what is it?
focal / diffuse inflammation of myocardium
what cuases myocarditis
virsuses, bacteria, fungi, radiaton tx
what does myocarditis look like?
ranges from SCD to benign

when dose myocarditis happen
7-10 days after viral infection
what accompanies myocarditis ?
pericarditis--> thus, will have pericardial friction rub / effusion ... as well as pleuritic chest pain
medical mgmt of myocarditis?
digoxin--> to imrpove myocardial contracitlity / reduce ventric rate

ACE inibhitor / beta blocker (if heart is enlarged) / treat HF

diruetics to reduce fluid volume / decresae preload
what is the ongoing nursing dx in care of pt with myocarditis
nursing intervetntion for myocarditis
- assessment for s/sx of HF

- decrease cardiac worklad (use of semi-fowler's position)

- spacing of activity / rest periods
- quiet enviornemtn

meds to
- increase hearts contraciltity
- decrease preload / afterload -- will need careful monitroting

pt will be anxious so help w/ that
what are the primary manifestations of systolic fialure?
decreased ejection fraction and increased pulmonary artery wedge pressure

: Systolic heart failure results in left ventricle (LV) systolic dysfunction. The LV loses its ability to generate enough pressure to eject blood forward through the aorta. This results in increased pulmonary artery wedge pressure (PAWP). The hallmark of systolic dysfunction is a decrease in the left ventricular ejection fraction (EF).
Systolic heart failure results in ?
left ventricle (LV) systolic dysfunction.
a compesnatory mechiasm invovled in HF that leads to inappropriate fluid retention / additional worklaod of the heart is :
neurohormonal response

The following mechanisms in heart failure lead to inappropriate fluid retention and additional workload of the heart: activation of the renin-angiotensin-aldosterone system (RAAS) cascade and release of antidiuretic hormone from the posterior pituitary gland in response to low cerebral perfusion pressure from low cardiac output.
pateints w/ a heart trasnplanation are at risk for which complications the 1st year after transplantation?
- infection


sudden cardiac death
which signs/symptoms would you find with myocarditis?

- angina
- pleuritic chest pain
- splinter hemorrahge
- peicardial friction rub
- presence of osler's nodes
- angina
- plerutici chest pain
- pericardial friction rub
atrial flutter
Some people have Atrial Flutter along with their A-Fib, or rarely by itself without A-Fib. In Atrial Flutter the atria don't fibrillate but rather beat faster than the ventricles but in a coordinated, regular rhythm. You can consider Atrial Flutter as a more regular, milder variety of A-Fib. A-Flutter often, though not always, originates in the right atrium, whereas A-Fib usually comes from the left atrium. A-Flutter rarely occurs by itself; it is usually associated with A-Fib.265
a fib overivew
In Atrial Fibrillation (A-Fib) the upper part of your heart beats (quivers) faster than the rest of your heart. If you could look inside your chest, the top part of your heart would be shaking like Jell-O or beating more rapidly than the lower section of your heart. You feel an uncomfortable flutter in your chest or like your heart is going to jump out of your ribs or that your heart is "flip-flopping around." Your pulse is irregular and/or more rapid than normal. Someone described their A-Fib as " a motor idling too fast in my chest." Or "like I had a maniacal bass drummer hidden away in my chest." You may feel lightheaded (fainting), very tired, have shortness of breath, sweating and chest pain, swelling in your legs, and sometimes a distressing need for frequent urination (probably because of the release of atrial natriuretic peptide [ANP])211.
what is pericardial effusion
accumulation of excess fluid in pericardium
what is cardiac tamponade
develops as pericardial effusion develops in volume--> causes increasse in pericardial pressure
PATENT ductus arteriosus
when fetal ductus arteriosus (artery connecting aorta / pulm artery ) fail to close w/in 1st few wks of life

- the patency --> allows blood to flow from higher-pressure aorta --> lower-pressure pulmonary artery--> left - to - right shunt
PATENT ductus arteriosus
when fetal ductus arteriosus (artery connecting aorta / pulm artery ) fail to close w/in 1st few wks of life

- the patency --> allows blood to flow from higher-pressure aorta --> lower-pressure pulmonary artery--> left - to - right shunt
what is the characteristic response found with acute pericarditis?
an inflammatory response-- influx of neutrophils, increased pericardial vascularity, and fibrin deposition on epicardium
what are the target organs that HTN affects and in what way?
heart (hypertensive heart disease), brain(cerebrovascular disease), peripheral vasculature (peripheral vascular disease), kidney(nephrosclerosis), and eyes (retinal damage).
what is valvular stenosis?
constriction or narrowing of the valve opening
Valvular regurgitation (also called valvular incompetence or insufficiency)
occurs withincomplete closure of the valve leaflets and results in the backward flow of blood
Adult mitral valve stenosis results from ?
rheumatic heart disease. Less commonly, itcan occur congenitally, from rheumatoid arthritis and from systemic lupuserythematosus
what happens to the heart/valves with mitral valve stenosis?
stenotic mitral valve--> takes on a fish mouth shape b/c of thickening/shortening of mitral valves

this causes obstruction of blood flow---> creates a pressure difference b/w left atrium and left ventricle during diastole

left atrial pressure and volume increase

leads to higher pulmonary vasculatrure pressure--> then hypertrophy of pulmonary vessels

pressure overload occurs in left atrium, pulmonary bed, and right ventricle
clinical manifestations of mitral valve stenosis?
- exertional dyspnea due to reduced lung compliance
- fatigue / palpitations from AFIB are poss
- diastolic murmur
what is mitral stenosis (simply)
valvular tissue thickens / narrows valve opening--> prevents blood from flowing from left atrium to left ventricle
what does venous insufficiency result in
edema, venous stasis (causing venous stasis ulcers), swelling, and celllulitis
what does venous insufficiency look like?
stasis dermatitis or brown discoloration along ankles, extending up calf
what do venous insufficiency ulcers look like
edges are uneve, ulcer bed is pink, grannulation present
raynaud's- what causes it?
vasospasm of arterioles / arteries of lower/uppre extremities--> vasoconstriction
what does raynaud's look like
blanching of extremity --> followed by cyanosis during vasocontriction

reddened tissue when vasospasm is relieved

numbnes,s tingling, swelling, cold temp
raynaud's interventions
monitor pulses

give vasodilators

avoid core / stress

avoid smoking

wear warm clothing

avoid injury to hands/fingers
aortic aneurysm
aortic aneurysm
what is the process/pathophys behind ACS
1) plaque ruptures (spontaneous / induced)

2) platelet adhesion

3) platelet activation

4) platelet aggregation
presentation of ACS

how does it present difftly and in who?
1) typical chest discomfort (pressure, tight, squeezing, heaviness, burning)

2) women-- may feel extreme fatigue, diaphoriseis, SOB (atypical

3) diabetics may not feel the pain

4) elderly may get passed off for being confused
what are troponins
they are biomarkers that can be elevated in blood levels due to any of kind of cardiac injury

- ischemia due to coronary occlusion/spasm
- secondary due to supply/demand mismatch
- nonischemic cardiac injruy (HF, cardiomyopathy, etc)
how to treat ACS? interventions?
1) cardiac montior

2) ECG w/in 10 mins

3) BP in both arms

4) O2 Sat

5) IV

6) Pain relief

7) ASA

8) Labs
what to do if ACS present with STEMI?
-- st elevation--> immediate re-perfusion
NSTEMI (t-wave inversion)
- antiplatelet tx
- beta blockers / CA blockers
ABC's of ACS pt education
A = aspirin / anti-platelets / antianginals

B = beta blockers / blood pressure

C= cholesterol / cigs

D = diet / diabetes

E = exercise / education
what is HF
- abnormal ventricular filling / ejection ---> leads to low cardiac output

impairment of ventricle to fill / eject blood
manifestations of HF?
dyspnea / fatigue

PND / Orthopnea

fluid retention--> pulm / periph edema
risk factros for HF
- age


- MI

- Diabetes (esp in women)

- obesity

- Valvular heart disease
what happens in HF (backward failure)
- ventricular pressure rises

- high LV pressure goes baackwards into lungs

- high RV pressure goes backwards into venous system
what happens in HF (fwd failure)
- ventricle fail to pump will in fwd direction

LV fwd fail--> peripheral hypoperfusion

RV fwd fail--> failure to adequatliy fill LV
what is Systolic Dysfxn (HF?) what does it lead to? what happens to the ventricle?
LV contracitility impared--> leads to reduced ejection fraction

ventricle is dilated / thin walled / hypertrophied?
what is Diastolic Dysfxn (HF?) what does it lead to? what happens to the ventricle?
- normal systolic fxn impaired -- ventricle cannot relax / fill w/ blood

- results in increased filling pressure due to stiff, noncompliant ventricle

- ventricle = thickened / hypertrophied
what are causes of diastolic dysfxn?
- htn
- cad
- aortic stenosis
what is the classic triad of left ventricular failure? what heart condition is this r/t ?


exertional dyspnea

r/t aortic valve stenosis

valve becomes 1/3'rd its normal size
what happens in aortic valve stenosis
- obstrution of flow from LV to aorta during systole

- this causes left ventric hypertrophy

---> increased myocardic o2 consumption b/c of incrased myocardial mass

- compensatory mechanisms eventaully fail

- reduced co--> decreased tissue perfusion, pulm htn, HF
what is coarctation of aorta?
narrowing of aorta right around ductus arterioris
what kind of probs would you see with coarctation of aorta?
afterload probs

fluid backing up b/c of high pressure on aorta --> could lead to heart failure, fluid pooling in L V--> backing up in pulm circ
assessment for coarc of aorta?
- lung sounds (crackles / coarseness)

- chest xray

- pulse ox

- chest o2 sat

- peripheral BP (lower vs upper)

- look at legs / feet - check for warmth, musles
emergency care for someone with chest pain?
The American Heart Association's guidelines for emergency care of the patient with chest pain includes the administration of aspirin, nitroglycerin, morphine, and oxygen. These interventions serve to relieve chest pain, improve oxygenation, decrease myocardial workload, and prevent further platelet aggregation.
pulsus pardoxus (decrease in systolic bp) is associated w/?
cardiac tamponade
regurgitant murmur indicates waht?
a valvular disease (i.e., endocartitis)
47. The nurse would assess a patient with complaints of chest pain for which of the following clinical manifestations associated with a myocardial infarction (MI)? (Select all that apply.)
A. Flushing
B. Diaphoresis
C. Nausea and vomiting
D. S3 or S4 heart sounds
47. B, C, D. During the initial phase of an MI, catecholamines are released from the ischemic myocardial cells, causing an increased sympathetic nervous system (SNS) stimulation. This results in the release of glycogen, diaphoresis, and vasoconstriction of peripheral blood vessels. The patient's skin may be ashen, cool, and clammy (not flushed) secondary to this response. Nausea and vomiting may result from reflex stimulation of the vomiting center by severe pain. Ventricular dysfunction resulting from the MI may lead to the presence of the abnormal S3 and S4 heart sounds.
how to posiiton someone with heart failure?
characterisitcs of arterial disease
- parethesia
- ulcers over bony prominences on toes / feet
- decreased periph pulses
- thick brittle nails
- pallor on elevation of legs
characteristics of venous disease
- heavy ulcer drainage
- edema around ankles
- brown pigmenetation of legs
- ulceration around medial malleolus
- dull ache in calf / thigh
- pruritis
which cardiac enzyme is first elevated in someone with MI?
what psoition is best for MI?
what does S3 sound indicated (MI)
left ventricular failure
MI: if a pt's BP is low-- do you want to give a ca++ blocker?
no-- it could cause the PT'S BP TO BOTTOM OUT
AFTER MI: how long does it take heart tissue to heal?
4-6 wks
what leg position to be in post cardiac cath?
nitroglycerin usage
client should tkae 1 tablet q 5 mins and if no relief after 3rd tablet, then go to ER
what is congestive heart failure?
heart muscle cannot pump effectively to perfuse the body
what is chest pain from (CAD)
ischemia to myocardium as result of hypoxemia
CAD - after cath-- how many degrees shoudl HOB be?
10 degrees (no more)
should someone with CAD have salt intake?
yes-- it's ok-- salt only affects HTN
32. The nurse is discussing the importance of exercise with the client diagnosed with coronary
artery disease. Which intervention should the nurse implement?
1. Perform isometric exercises daily.
2. Walk for 15 minutes three (3) times a week.
3. Do not walk if it is less than 40F.
4. Wear open-toed shoes when ambulating.
3- when cold outisde, VASOCONSTRCITION HAPPEN--> this decrease o2 to the heart muscle-- so, clinet shouldnt exercise outside when cold

client should do isotonic (not isometric) exercises
what is an early manifestation of mitral valve stenosis?
DYSPNEA on exertion

- chest pain rarely occurs
what are some signs of R sided failure
- 3+ pedal edema
- enalrged liver
- edematous abdomen
Which assessment data would the nurse expect to auscultate in the client diagnosed
with mitral valve insufficiency?
1. A loud S1, S2 split, and a mitral opening snap.
2. A holosystolic murmur heard best at cardiac apex.
3. A mid-systolic ejection click or murmur heard at the base.
4. A high-pitched sound heard at the 3rd left intercostal space.
2- murmur = associated w/ mitral valve insufficiencey is LOUD, high-pitched, rumbling, holosystolic (occuring throughout systole) and is heard best at cardiac apex

39. The client has just received a mechanical valve replacement. Which behavior by the
client indicates the client needs more teaching?
1. The client takes prophylactic antibiotics.
2. The client uses a soft-bristle toothbrush.
3. The client takes an enteric-coated aspirin daily.
4. The client alternates rest with activity.
3) -- ASA/nsaids -- might interfere w/ clotting / potentaite effects of anticog tx-- dont take asa daily

- use a soft-bristle toothbrush to prevent gum trauma / bleeding (b/c pt is already on anti-coags)-- must assume
biological valves
- need to be repalced often b/c they deteroiate

- but DONT need anticoag tx

anticoag tx with MECHNICAL valve
42. Which signs/symptoms should the nurse assess in any client who has a long-term
valvular heart disease? Select all that apply.
1. Paroxysmal nocturnal dyspnea.
2. Orthopnea.
3. Cough.
4. Pericardial friction rub.
5. Pulsus paradoxus.
- PND- occurs w/ valvular disordres
- client must sti / stand nomrally to breathe -=-
- coughing will occur with long-term valv disease--> difficutly walking / performing activity
rheumatic heart disease causess....?
valvular heart disease
client w/ A FIB is on what kind of meds?
anti coag
what does digoxin do?
slows down HR

increases crdic contradctiltiy

drug of choice for atrial fib
what does atropine do?
decreases vagal stimulation--> increases HR
69. Which nursing diagnosis would be priority for the client diagnosed with myocarditis?
1. Anxiety related to possible long-term complications.
2. High risk for injury related to antibiotic therapy.
3. Increased cardiac output related to valve regurgitation.
4. Activity intolerance related to impaired cardiac muscle function.
4- actvitiy intolerance = priority with a client w/ myocarditis--> an inflammation of the heart muscle. nursing care is aimed at decreasing myoscirdial work and maintaining cardiac output
who is at greatest risk from dying from a MI
AA females
what is the only treatement for someone w/ dilated cardiomyotphay?
HEART TRASNPLANT-- or else client will end up in end-stage heart failure
MYocardial ischemia
depresion in st segment / t wave inversion happen in response to inaedquate supply of blood and o2--> casuing electrical distrubane in myocardial cells
MYocardial ischemia
depresion in st segment / t wave inversion happen in response to inaedquate supply of blood and o2--> casuing electrical distrubane in myocardial cells