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244 Cards in this Set
- Front
- Back
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pitting edema is a sign of what?
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sign of DVT / post-thrombotic syndrome
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what kind of ulcerations (venous / arterial) have edema (what kind?)
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venous ulcerations have non-pitting edema in affected extremity
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eschar
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piece of dead tissue case off from surface of skin--> black, thick, dry, black necrotic tissue
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where is a gaiter likely to be
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lower 1/3 of calf
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WHAT TYPE OF ulcer is gaiter associat'ed w/?
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venous ulcer
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dependent rubor is a typical finding of someone w/?
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PAD
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describe arterial ulceration
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painful, on foerfoot/toes (distal from ischemic artery), deep, punch out, minimal granulation tissue, well demarcated edge
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describe venous ulceration
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in gaiter area, shallow, irregular borders, have granulation tissue and exudate.
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what is stasis
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pooling of blood
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where is stasis found
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lower extremities *
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why does stasis happen
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dysfxnal valves / muscles of extremities are inactive leads to what?
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who does stasis happen to
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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
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atresia
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condition where body orifice / passage in body is abnormally closed / absent
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risk factors for cellulitis
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diabetes mellitus, lymphedema, venous stasis/insufficiency, immune suppression, PVD, malnutrition, IV drug use
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what is cellulitis
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spreading bacterial infection of skin/sub Q tissue
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what causes cellulitis
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strep / staph infections
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where does cellulitis happen
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extreimties (lower legs) are common site *
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Asystole
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cardiac standstill -- flat line-- absence of electrical actviity / contractions
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describe A FIB
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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
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what is most common / clinically significant cardiac dysrhythmia
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atrial fib *
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paroxysmal afib is characterized by what kind of episodes?
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intermittent episodes *
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atrial flutter
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rapid, regular atrial tachydysrhtymia w/ regular ventricular response
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where is atrial flutter most common
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right atrium *
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what does atrial flutter look like?
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saw tooth
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how does atrial flutter present symptom wise
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asymptomatic, palpitations, dizziness, presyncope, syncope
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automaticity
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ability of cardiac muscle to spontaneously / continously contract w/o nervous stimulation
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what happens to the impulse during an AV block and where?
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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
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what causes AV block
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degenerative changes, drugs (digoxin, beta blockers, CA++ blocker, hyperkalemia, hypokalemia, increase vagus nerve activity, scarring from MI)
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conductivity
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ability to transmit impulse along a membrane in orderly manner
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contractility
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property of cardiac cells--> abilty to respond mechnically to an impulse
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DEFIB
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treatment of choice to end VFib or pulseless V Tachy -- rapid defib (2 mins) = impt to successful pt outcome
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how does defib work
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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
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escape rhythm
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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. |
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excitability
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ability to be electrically stimulated-- myocardial tissue is allowed to be depolarized by a stimulus
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infarction
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happens in myocardium when myocardial tissue starts to necrose after insufficient o2 from insufficnet blood flow
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JXNAL rhythm
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dysrhtymia originating in area of AV node--> b/c SA node fails to fire / signal is blocked
av node becomes pacemaker of heart |
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syncopy
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lapse in consciounses w/ fainting
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what causes syncopy
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cardioneurogenic / vasovagal (carotid sinus senstivities)
primary cardiac dyshrthymias |
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what's the diff b/w atrial flutter and afib?
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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. |
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what's VFIB?
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Lethal dysrhythmia characterized by chaotic electrical activity without organized QRS complexes detected. Ventricle is "quivering" - no effective contractions, no CO!
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what does VFIB look like on ECG?
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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.
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what is a patient like during VFIB
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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! |
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when does VFIB happen
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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.
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when does V flutter turn into V fibb?
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w/o treatment!
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what is ventricular flutter?
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the ventricles depolarize in a circular pattern, rapid, uniform, greater than 250bpm. Results in a minimal cardiac output and subsequent ischemia
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what is V Tach associated w/?
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. Associated with MI, CAD, significant electrolyte imbalances, cardiomyopathy, mitral valve prolapse, long QT syndrome, drug toxicity, CNS disorders.
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what does V Tach result in
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Causes severe decrease in CO - resulting in hypotension, pulmonary edema, decreased cerebral blood flow, and cardiopulmonary arrest.
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what does V tach look like
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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
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paroxysmal
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an abrupt onset and termination (of cardiac electrical activity)
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pacemaker
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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.
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telemetry
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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
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what does the foramen ovale connect? why?
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shunt connecting R and L atrium so maternal oxy blood can bypass fetus lungs
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what is flow of blood in foramen ovale?
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blood from: RA --> LA--> down to LV--> systemic circ
- small amnt goes into RV / pulm circuit to noursih lungs |
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what makes the foramen ovale close? when does it close
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in neonates: increased pressure in LA helps close the shunt and complete anatomical closure happens w/in first 30 days
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what does ductus arteriosus connect
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blood vessel connecting pulm artery to aortic arch
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what does ductus arteriosus allow blood to do?
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allows blood from RV to bypass fetus's fluid-filled non-fxning lungs
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what does ductus arteriorus becomes after it closes at birth
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ligamentum arteriosum
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what's a shunt
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hole / passage allowing fluid to move from 1 part of body to another
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endocardial cusion-- what is it?
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subset of cells in primordial heart that plays an impt role in proper heart septation
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where does endocardial cusion develop?
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on the atrioventricular canal
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what's the point of endocardial cusion
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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 |
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what is tachypnea a sign of w/ young children?
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fast breathing...>60 in infants...clinical manifestation of congenital heart disease in infants
manifestation of both pulmonary congestion and systemic venous congestion |
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what is grunting respiration
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sound heard each time person exhales
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why do we "grunt"
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body's way of trying to keep air in lungs so that they will stay open
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knee-chest position allows for what? why do kids do it?
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allows lungs to open up more
kids will crouch like this to enhance breathing is there is a physiological problem |
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Hypercyanotic spell is r/t to what conditioned, is triggered by what, lasts for how long, leads to what
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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.
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hypercyanotic spell interventions?
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interventions = give O2, and calm that baby down! give them morphine if you have to.
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afterload
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the tension or stress developed in the wall of the left ventricle during ejection
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anasarca
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by widespread swelling of the skin due to effusion of fluid into the extracellular space.
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what causes anasarca
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It is usually caused by liver failure (cirrhosis of the liver) or renal failure/disease and severe malnutrition/protein deficiency.
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what does anasarca lead to
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The increase in salt and water retention caused by low cardiac output can also result in anasarca as a long term maladaptive response.
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ascites
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excess fluid in the space between the tissues lining the abdomen and abdominal organs. Those
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what happen when ascites + HF? what are the sx?
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Those with ascites due to heart failure may also complain of shortness of breath as well as wheezing and exercise intolerance
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B-type natriuretic peptide (BNP) -- where is this synthesized?
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ventricles
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B-type natriuretic peptide (BNP) -- what is it released in response to? what does it correlate to? what does it cause?
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released in response to prolonged volume overload. elevated in HF. correlate well with LV pressure. causes arterial and venous dilation.
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cardiac biomarkers
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troponin (elevate in myocardial injury) and CK-MB
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why do we test for cardiac biomarker levels? and when?
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. 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. |
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cardiac output
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the volume of blood being pumped by the heart, in particular by a left or right ventricle in the time interval of one minute
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cardiac reserve
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The work that the heart is able to perform beyond that required of it under ordinary circumstances
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ejection fraction
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is the fraction of blood pumped out from the right ventricle of the heart to the pulmonary circulation
and left ventricle of the heart to the systemic circulation with each heart beat or cardiac cycle |
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hemoptysis - what is it / what cuases it?
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coughing up blood, or blood stained sputum. heart failure and mitral stenosis can cause this
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hepatomegaly
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when blood backs up into the liver from the IVC...from the heart. then the liver gets big
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hepatosplenomegaly
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enlargement of both the liver and the spleen from right sided heart failure.....r/t blood backing up
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what does an inverted T wave indicate?
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Coronary ischemia, hypokalemia, left ventricular hypertrophy, digoxin effect, some drugs
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left sided failure-- what are signs
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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
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what are sx of left sided failure?
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Weakness, fatigue, anxiety, depression dyspnea, shallow respirations, paroxysmal nocturnal dyspnea, orthopnea, dry hacking cough, nocturia, frothy pink sputum.
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nocturia-- what is it and what does it indicate?
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symptom of R sided heart failure.
having to get up at night and pee. |
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orthopnea
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needing to sleep with pillows
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what does orthopnea indicate?
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a later symptom of L sided heart failure / pulmonary edema
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paroxysmal nocturnal dyspnea
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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
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polycythemia-- what is it, what can it cause
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increase in red blood cells...can also cause cyanosis even when there is sufficient O2 in the blood.
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preload
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initial stretch of the heart before contraction
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pulmonary edema-- what does it indicate / what is it? what is primary sx?
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S/Sx of L sided HF. abnormal buildup of fluid in the air sacs of the lungs, which leads to shortness of breath
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right sided failure-- what are clinical manifestations?
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- RV heaves
- murmurs - jugular venous distension - edema - weight gain - increased HR - ascites - anasarca - hepatomegaly |
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sx of R sided heart failure
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Fatigue, anxiety, depression, dependent-bilateral edema, RUQ pain, anorexia and GI bloating, nausea
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ST elevation - what does it indicate? what kind of interventions are received?
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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
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Systemic Vascular resistence
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resistance to blood flow offered by all of the systemic vasculature, excluding the pulmonary vasculature. SVR = (MAP - CVP) ÷ CO
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most MI's are secondary to what?
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thrombus formation
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HTN: what does sustained high BP lead to ? what does it do to heart?
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- 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 |
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how does HTN affects contracility / stroke volume / co?
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depresses contractility
depresses SV CO is decreased |
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HTN is a major risk factor for what?
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cerebral atheroscleoris
stroke |
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What happens to heart tissue with MI? why does MI happen?
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- happens b/c of sustained ischemia
- causes irreversible myocardial necrosis - contractile fxn of heart stops in necrotic area |
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MI: inferior wall infarction from what artery?
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left anterior descending artery
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MI: latera/posterior wall MI's from what vessel?
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left circumflex artery
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MI: clinical manifestations?
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pain (20 min+)
more severe pain than angina NOT releived by rest / position change / nitrates |
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what does MI feel like on skin?
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ashen, clammy, cool to touch
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what happens with output for MI
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first, bp / hr is elevated, but BP may drop b/c of decreased CO
- this --> decreased renal perfusion , decreased urine output |
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what lungs sounds do you hear with MI? what does it suggest
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crackles suggesting LV dysfxn
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what signs might indicate RV dysfxn
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JVD, hepatic engorgement, peripheral edema
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Sudden cardiac death is what and leads to what?
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abrupt disruption in cardiac function
leads to loss of CO and cerebral blood flow |
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how fast does death occur with Sudden cardiac death
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1 hour of onset of acute sx (angina, palpitations)
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what heart condition is most commonly assocaited with Sudden cardiac death
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acute ventricular dysrhythmia
ven tachy vent fib (very lethal) |
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what to prevent a recurrence of Sudden cardiac death
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implantable cardioverter-defib
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what is the most common clinical manifestation of reversible myocardial ishcmiea
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angina pectoris (stable)
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myocardium becomes hypoxic w/in first ____ secs of ______
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first 10 secs of coronary occulsion
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w/ total occlusion of coronary arteries, myocardial cells are deprived of ___ and ___, so ____ begins and ____ accumulates
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- o2 / glucose
- lactic acid |
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HTN is associated w/ what heart probs?
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- left sided failure
- a Fib - L ventricular afterload increases |
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angina pectoris leads to ___ bloodflow r/t _____ of ______ afteries by _______
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- decreased
- narrowing of coronary arteries - athersclerosis |
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what kind of meds for angina pectoris?
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- anti platelets
- anti coags |
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unstable angina-- what happens?
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- rupture of thickened plaaque--> exposing to thrombogenic surface
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what accts for referred pain to left shoudler/arms during angina?
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buildup of lactic acid --> irritates myocardial nerve vibers--> tranmits a pain msg to cardiac nerves
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what is chronic stable angina characterized by
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- chest pain occuring intermittently over long period of time /w same pttern of onset, duration, intesnity of sx
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for chronic stable angina: T/F: angina is sharp or stabbing
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false -- it is rarely sharp / stabbing and doesnt change w/ psition / breathing
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how long to wait for stable angina to go away? what to do?
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5-15 mins, subsides when preciptating factor = relieved
pain at rest = unusual |
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T Wave inversion indicates what?
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ischemia
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what is Virchows triad? what does it contribute to?
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venous stasis
damage of endothelium (inner lining of vein) hypercoagulabiltiy of blood contributes to thrombosis |
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varicosity. where is this found? what is it?
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varicose veins are dilated, tortuous subq veins found in saphenous vein system
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varicosity-- what is it due to
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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 |
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what makes varicosity worse / why? leads to what?
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standing for long periods of time due to increased venous pressure and further venous distnetion?
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why does HF occur in someone with DCM
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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 |
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what heart condition is associated w/ DCM and why?
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AARTHYMIA!—very common b/c electroconduction of heart is altered when heart is big and boggy
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how do aarthymias affect flow?
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fwd flow can be sginficaitnly decreased
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normal ejection fraction
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55-60%
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what is endocarditis? who do we see this in?
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o Inflammation of inner lining of heart / valves
o Occurs in drug users, valve replacments, or mitral valve proplapse /strcutral defects (congenital) |
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what is pathophys of endocarditis
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• 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 |
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what is part of your asseessment with someone wiht endocarditis?
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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 |
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interventions for endocarditis
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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 |
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endocarditis nursing dx's:
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o Decreased cardiac output R/T altered rhythm / valv insufficinency, fluid overload
o Activity intolerance r/t generalized weakness |
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primary intervention w/ endocarditis?
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Prevent EMBOLI / PULM EDEMA / HEART FILARE
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how to treat varicose veins?
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o Leg elevation / pressure stocking / exercise
o Sclerotherapy o Surgical removal |
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for HTN: what could chest pain mean?
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could be a pulmonary embolus secondary to DEEP VEIN THROMBOSIS
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what drugs would you use for HTN and why
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- ACE inhibitors are use for htn prevent converstion of Angiio I to angio II prevenst vasoconstriction prevents sodium / water rention
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intermittent claud = classic sx of ?
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arterial occlusive diases
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s/sx of DVT
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calf tendereness, calf edeam, + Homan’s
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dependent rubor = sign of what? what does it look like?
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Legs = pale when elevated (eleavation pallor), but DARK RED when in dependent position
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pericarditis is what?
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inflammation of pericardial sac
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what does pericarditis lead to
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cardiac compression, decreased ventricular filling / emptying, heart failure
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when does pericarditis happen / why?
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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) |
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what does someone feel like w/ pericarditis?
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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) |
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how to relieve pericarditis (feeling)
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sitt up / lean fwd (dyspnea associated is r/t pt's need to breathe in rapid/shallow breaths to avoid chest pain)
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what is hallmark finding in acute pericarditis
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pericardial friction rub
scratching / grating high-ptched sounds from friction b/w roughened pericardial / epicardial surfaces |
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what are 2 major complicattion from pericarditis
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- 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 |
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pericarditis-> what will pt develop (s, sx)
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tachypnea
tachycardia decreased CO JVD pulsus paradoxus |
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pericarditis nursing interveiton
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mgmt of pt's pain / anxiety
antibotics NSAIDS ibuprofen to control pain / inflammation |
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myocarditis: what is it?
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focal / diffuse inflammation of myocardium
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what cuases myocarditis
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virsuses, bacteria, fungi, radiaton tx
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what does myocarditis look like?
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ranges from SCD to benign
fever fatigue malaise myalgia dyspnea nausea vomiting |
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when dose myocarditis happen
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7-10 days after viral infection
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what accompanies myocarditis ?
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pericarditis--> thus, will have pericardial friction rub / effusion ... as well as pleuritic chest pain
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medical mgmt of myocarditis?
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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 |
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what is the ongoing nursing dx in care of pt with myocarditis
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DECREASED CO
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nursing intervetntion for myocarditis
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- 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 |
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what are the primary manifestations of systolic fialure?
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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). |
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Systolic heart failure results in ?
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left ventricle (LV) systolic dysfunction.
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a compesnatory mechiasm invovled in HF that leads to inappropriate fluid retention / additional worklaod of the heart is :
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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. |
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pateints w/ a heart trasnplanation are at risk for which complications the 1st year after transplantation?
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- infection
rejection sudden cardiac death |
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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 |
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atrial flutter
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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
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a fib overivew
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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 "...like 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.
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what is pericardial effusion
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accumulation of excess fluid in pericardium
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what is cardiac tamponade
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develops as pericardial effusion develops in volume--> causes increasse in pericardial pressure
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PATENT ductus arteriosus
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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 |
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PATENT ductus arteriosus
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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 |
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what is the characteristic response found with acute pericarditis?
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an inflammatory response-- influx of neutrophils, increased pericardial vascularity, and fibrin deposition on epicardium
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what are the target organs that HTN affects and in what way?
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heart (hypertensive heart disease), brain(cerebrovascular disease), peripheral vasculature (peripheral vascular disease), kidney(nephrosclerosis), and eyes (retinal damage).
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what is valvular stenosis?
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constriction or narrowing of the valve opening
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Valvular regurgitation (also called valvular incompetence or insufficiency)
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occurs withincomplete closure of the valve leaflets and results in the backward flow of blood
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Adult mitral valve stenosis results from ?
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rheumatic heart disease. Less commonly, itcan occur congenitally, from rheumatoid arthritis and from systemic lupuserythematosus
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what happens to the heart/valves with mitral valve stenosis?
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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 |
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clinical manifestations of mitral valve stenosis?
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- exertional dyspnea due to reduced lung compliance
- fatigue / palpitations from AFIB are poss - diastolic murmur |
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what is mitral stenosis (simply)
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valvular tissue thickens / narrows valve opening--> prevents blood from flowing from left atrium to left ventricle
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what does venous insufficiency result in
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edema, venous stasis (causing venous stasis ulcers), swelling, and celllulitis
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what does venous insufficiency look like?
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stasis dermatitis or brown discoloration along ankles, extending up calf
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what do venous insufficiency ulcers look like
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edges are uneve, ulcer bed is pink, grannulation present
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raynaud's- what causes it?
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vasospasm of arterioles / arteries of lower/uppre extremities--> vasoconstriction
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what does raynaud's look like
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blanching of extremity --> followed by cyanosis during vasocontriction
reddened tissue when vasospasm is relieved numbnes,s tingling, swelling, cold temp |
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raynaud's interventions
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monitor pulses
give vasodilators avoid core / stress avoid smoking wear warm clothing avoid injury to hands/fingers |
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aortic aneurysm
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aortic aneurysm
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what is the process/pathophys behind ACS
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1) plaque ruptures (spontaneous / induced)
2) platelet adhesion 3) platelet activation 4) platelet aggregation |
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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 |
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what are troponins
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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) |
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how to treat ACS? interventions?
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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 |
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what to do if ACS present with STEMI?
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-- st elevation--> immediate re-perfusion
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NSTEMI (t-wave inversion)
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- antiplatelet tx
- beta blockers / CA blockers |
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ABC's of ACS pt education
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A = aspirin / anti-platelets / antianginals
B = beta blockers / blood pressure C= cholesterol / cigs D = diet / diabetes E = exercise / education |
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what is HF
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- abnormal ventricular filling / ejection ---> leads to low cardiac output
impairment of ventricle to fill / eject blood |
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manifestations of HF?
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dyspnea / fatigue
PND / Orthopnea fluid retention--> pulm / periph edema |
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risk factros for HF
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- age
- HTN - MI - Diabetes (esp in women) - obesity - Valvular heart disease |
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what happens in HF (backward failure)
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- ventricular pressure rises
- high LV pressure goes baackwards into lungs - high RV pressure goes backwards into venous system |
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what happens in HF (fwd failure)
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- ventricle fail to pump will in fwd direction
LV fwd fail--> peripheral hypoperfusion RV fwd fail--> failure to adequatliy fill LV |
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what is Systolic Dysfxn (HF?) what does it lead to? what happens to the ventricle?
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LV contracitility impared--> leads to reduced ejection fraction
ventricle is dilated / thin walled / hypertrophied? |
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what is Diastolic Dysfxn (HF?) what does it lead to? what happens to the ventricle?
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- normal systolic fxn impaired -- ventricle cannot relax / fill w/ blood
- results in increased filling pressure due to stiff, noncompliant ventricle - ventricle = thickened / hypertrophied |
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what are causes of diastolic dysfxn?
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- htn
- cad - aortic stenosis |
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what is the classic triad of left ventricular failure? what heart condition is this r/t ?
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angina
syncope exertional dyspnea r/t aortic valve stenosis valve becomes 1/3'rd its normal size |
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what happens in aortic valve stenosis
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- 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 |
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what is coarctation of aorta?
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narrowing of aorta right around ductus arterioris
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what kind of probs would you see with coarctation of aorta?
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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 |
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assessment for coarc of aorta?
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- lung sounds (crackles / coarseness)
- chest xray - pulse ox - chest o2 sat - peripheral BP (lower vs upper) - look at legs / feet - check for warmth, musles |
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emergency care for someone with chest pain?
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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.
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pulsus pardoxus (decrease in systolic bp) is associated w/?
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cardiac tamponade
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regurgitant murmur indicates waht?
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a valvular disease (i.e., endocartitis)
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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.
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how to posiiton someone with heart failure?
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semi-fowers
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characterisitcs of arterial disease
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- parethesia
- ulcers over bony prominences on toes / feet - decreased periph pulses - thick brittle nails - pallor on elevation of legs |
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characteristics of venous disease
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- heavy ulcer drainage
- edema around ankles - brown pigmenetation of legs - ulceration around medial malleolus - dull ache in calf / thigh - pruritis |
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which cardiac enzyme is first elevated in someone with MI?
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troponin
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what psoition is best for MI?
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semi-folwers
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what does S3 sound indicated (MI)
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left ventricular failure
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MI: if a pt's BP is low-- do you want to give a ca++ blocker?
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no-- it could cause the PT'S BP TO BOTTOM OUT
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AFTER MI: how long does it take heart tissue to heal?
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4-6 wks
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what leg position to be in post cardiac cath?
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STRAIGHT !
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nitroglycerin usage
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client should tkae 1 tablet q 5 mins and if no relief after 3rd tablet, then go to ER
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what is congestive heart failure?
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heart muscle cannot pump effectively to perfuse the body
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what is chest pain from (CAD)
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ischemia to myocardium as result of hypoxemia
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CAD - after cath-- how many degrees shoudl HOB be?
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10 degrees (no more)
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should someone with CAD have salt intake?
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yes-- it's ok-- salt only affects HTN
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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 |
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what is an early manifestation of mitral valve stenosis?
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DYSPNEA on exertion
- chest pain rarely occurs |
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what are some signs of R sided failure
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- JVD
- 3+ pedal edema - enalrged liver - edematous abdomen |
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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
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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 |
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biological valves
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- need to be repalced often b/c they deteroiate
- but DONT need anticoag tx anticoag tx with MECHNICAL valve |
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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 |
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rheumatic heart disease causess....?
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valvular heart disease
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client w/ A FIB is on what kind of meds?
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anti coag
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what does digoxin do?
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slows down HR
increases crdic contradctiltiy drug of choice for atrial fib |
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what does atropine do?
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decreases vagal stimulation--> increases HR
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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
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who is at greatest risk from dying from a MI
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AA females
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what is the only treatement for someone w/ dilated cardiomyotphay?
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HEART TRASNPLANT-- or else client will end up in end-stage heart failure
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ST SEGMENT DEPRESSION / t WAVE INTERVESION =
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MYocardial ischemia
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whhy does ST SEGMENT DEPRESSION / t WAVE INTERVESION = ?
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depresion in st segment / t wave inversion happen in response to inaedquate supply of blood and o2--> casuing electrical distrubane in myocardial cells
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ST SEGMENT DEPRESSION / t WAVE INTERVESION =
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MYocardial ischemia
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whhy does ST SEGMENT DEPRESSION / t WAVE INTERVESION = ?
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depresion in st segment / t wave inversion happen in response to inaedquate supply of blood and o2--> casuing electrical distrubane in myocardial cells
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