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269 Cards in this Set

  • Front
  • Back
Risks of cardiac catheterization
hemorrhage fr entry site, low grade fever, nausea, vomiting, loss of pulse in the catherized extremity, (usually transient, resulting from a clot, hematoma, or intimal tear, transient dysrhythmias, rear risks include, stroke, seizures, tamponade and death.
In fetal circulation right & left atrium is connected by
the foramen avale
In fetal circulation the pulmonary artery and aortic artery is connected by
the ductus arteriosus
when does the forament ovale close
the fomamen ovale closes when the pressure in the let atrium exceeds the pressure in the right atrium
when does the ductus arteriosus close
starts to close in the presence of increased O2 concentration in the blood
Pedi: obstruction on the L side of the heart
results in CHF
Pedi: obstruction on the R side of the heart
results in cyanosis
Atrial Septal defect
abnormal opening between the atria, allowing blood from the higher pressure left atrium to flow into lower pressure right atrium
Ventricular septal defect
abnormal opening between the right and left ventricles,
Clinical manifestions of ASD (atrial septal defect)
can be asymptomatic, may develope CHF, there is a characteristic murmer, at risk for atrial dysrhythmias, pulmonary vascular obstructive disease and emboli formation later in life from chronic increase pulmonary flow
clinical manifestations of Ventricular septal defect
CHF is common, murmer, at risk for bacterial endocarditis, and pulmonary vascular obstructive disease, in severe cases eisenmenger syndrome may develope
patent ductus arteriosus
failure of the fetal ductus arteriosus to close within the first weeks of life. (causes left to right shunt)
Clinical manifestations of patent ductus arteriosus
may be asymptomatic, or show signs of CHF, murmer, widened pulse pressure and bounding pulses, at risk for bacterial endocarditis and pulmonary vascular obstructive disease later in life
Atrioventricular canal defect
incomplete fusion of endocardial cushions.
clinical manifestations of atrioventricular canal defect
moderate to severe CHF, there is characteristic of murmur, mild cyanosis that increases with crying. pts are at high risk for developing pulmonary vascular obstructive disease
aortic stenosis
narrowing or stricture of the aortic valve, causing resistance ot blood flow in the left ventricle, decreased cardiac ouput
pulmonic stenosis
narrowing at the entrance of the pulmonary artery
clinical manifestations of aortic stenosis
infants with severe defects demonstrate signs of decreased cardiac ouput with faint pulses, hypotension, tachycardia and poor feeding. children show signs of excersise intolerance, chest pain and dizziness when standing for a long period, murmer, at risk for bacterial endocarditis, coronary insufficiency and ventricular dsyfunction
Tetralogy of Fallot
includes ventricular defect, pulmonic stenosis, overriding aorta, and right ventricular hypertrophy
inability of the heart to pump an adequate amt. of blood to the systemic circulation at normal filling pressures to meet the metabolic demands of the body.
Tricuspid atresia
failure of the tricuspid valve to develop, consequently, ther is no communication frm the right atrium to the right ventricle
Clinical manifestations of tricuspid atresia
cyanosis, tachycardia and dyspnea, older children have signs of chronic hypoxemia with clubbing, at risk for bacterial endocarditis,
Heart failure is described in two ways
right-sided and left-sided heart failure
R-sided heart failure
inability of the of the right ventricle to pump blood effectively into the pulmonary artery, resulting in increased pressure in ther right atrium and systemic venous circulation
L-sided heart failure
the L ventricle is unable to pump blood in the the systemic circulation, resulting in increased pressure in the L atrium and pulmonary veins, the lungs become congested with blood, causing elevated pulmonary pressures and pulmonary edema
Impaired Myocardial function
tachycardia, sweating, decreased urine output, fatigue, weakness, restlessness, anorexia, pale, cool extremities, weak peripheral pulses, decreased blood presure, gallop rhythm, cardiomegaly
Pulmonary congestion
tachypnea, dyspnea, retractions, flaring nares, excercise intolerance, orthopnea, cough, hoarseness, cyanosis, wheezing, grunting
Systemic venous congestion
weight gain, hepatomegaly, peripheral edema, especially periorbital, ascites, neck vein distention
oxygen is a vasodilator that decreases pulmonary vascular resistance
Eisenmenger complex
refers to the clinical situation in which a left to right shunt becomes a right to left shung because of a progressive increase in pulmonary vascular resistance.
increased amount of RBC
characteristic of children with tetralogy of fallot, seen in toddlers and older children as an unconscious attempt to relieve chronic hypoxia, especially during excercise
hypercyanotic spells
aka blue spells, seen in infants with Tetralogy of Fallot, they are preceded by feeding, crying, defecation or any stressful procedures
right to left shunting and air
right to left shunting allows air in the venouse system to go directly to the brain, resulting in an air embolism, all lines should have filters, in place to prevent air from entering the system
median sternotomy
splits the sternum
lateral thoracotomy
extends from midaxillary line to the scaplula
opening the lower half of the sternum
signs of renal failure
elevated bun, creatinine, and decreased urine output of less than 1ml/kg/hr
recurrence of stenosis
nursing considerations for bacterial/infective endocarditis
prophylactic antibacterial /a dental procedures, pts must report any change in behavior, lethargy, malaise, anorexia
nursing considerations with Rheumatic fever
encourage compliance with meds, facilitate recovery from illness, provide emotional support, prevent the disease
manifestation of Rheumatoid fever
chorea (involuntary movements)
action of cholestyramine and colestipol
act by binding bile acids in the intestinal lumen
AV block aka
complete heart block
Reasons for bradycardia
influence of the autonomic nervous system, as with hypervagal tone, or in response to hypoxia and hypotension
Reasons for tachycardia
fever, anxiety, pain, anemia, dehydration
Non drug -Treatment for tachycardia in children
vagal maneuvers, s/a applying ice to the face, massaging the carotid artery, or having an older child perform a valsalva maneuver, eg exhaling agains a closed glottis, blowing on a thumb as if it was a trumpet for 30-60 seconds, if these fail other therapies are implemented
pulmonary artery pressure
group of disorders that result in an elevation of pulmonary artery pressure above 25mm Hg at rest
causes of pulmonary artery pressure
cardiac causes- rght to left shunt producing increased blood flow, hypoxic lung disease, thromboembolic disease, pulmonary vascular obstruction, collagen vascular diseases and exposure to toxic substances
clinical manifestations of Pulmonary artery hypertension
dyspnea with excercise, chest pain and syncope
kawaski disease
acute systemic vasculitis (inflammation of the vessel walls) of unknown cause
hallmark of kawasaki disease
aka circulatory failure
shock/circulatory failure
inadequate tissue perfusion to meet the metabolic demands of the body, resulting in cellular dysfunction and eventual organ failure
Treatment of shock
ventilation, fluid administration and improvement of the pumping action of the heart
early signs of shock in a child
apprehension, irritability, normal BP, narrowing pulse pressure (difference between diastolic and systolic Bp), thirst, pallor, diminished urine output, unexplained mild tachycardia, and a decrease in perfusion of the hands and feet
vaso-occlusive crisis
painful episode in sickle cell disease
sequestration crisis
a pooling of blood in the liver and spleen /c decreased blood volumen and shock
aplastic crisis
diminished RBC production resulting in profound anemia,
hyperhemolytic crisis
accelerated rate of RBC destruction characterized by anemia, jaundice and reticulocytosis
cooleys anemia
severe anemia that leads to cardiac failure and death
Chelation therapy
Chelation therapy is a process involving the use of chelating agents to remove heavy metals from the body
aka "Cooley's anemia", is an inherited disease of the RBCs, classified as a hemoglobinopathy. The genetic defect results in synthesis of an abnormal hemoglobin molecule. The blood cells are vulnerable to mechanical injury and die easily. To survive, many people /c thalassemia need blood transfusions at regular intervals.
Aplastic anemia
bone marrow failure condition in which the formed elements of the blood are sumultaneously depressed
Aplastic anemia
failure of the bone marrow to carry out its hematopoietic functions
the process that stops bleeding when a blood vessel is injured.
ensure clot formation only in the presence of blood vessel injury and to limit the clotting process the the site of vessel wall injury
group of bleeding disorders in which there is a deficiency of one of the factors necessary for coagulation of the blood
Hemarthrosis is a bleeding in joint spaces, often occurring in life-threatening cases such as hemophilia where the bleeding does not stop.
supportive measures for a hemophelia (RICE0
rice- rest, ice, compression and elevation
disseminated intravascular coagulation
Disseminated intravascular coagulation (DIC) is a pathological process in the body where the blood starts to coagulate throughout the whole body. This depletes the body of its platelets and coagulation factors, & there is a paradoxically increased r/o hemorrhage.
Leukemia is a cancer of the blood or bone marrow characterized by an abnormal proliferation of white blood cells (leukocytes).
combine immunodeficiency disease
Combined immunodeficiencies (or combined immunity deficiency) are immunodeficiency disorders that involve multiple components of the immune system, including both Humoral immunity and Cell-mediated immunity.
severe combined immunodeficiency disease- infection
susceptibility to infection occurs early in life, most often in the 1st month of life, suffers fr. chronic infection, fails to completely recover from an infection, is frequently infected with unusual agents, failure to thrive is a consequence of persistent illnesses
removal of blood from and individual Apheresis (Greek: "to take away") is a medical technology in which the blood of a donor or patient is passed through an apparatus that separates out one particular constituent and returns the remainder to the circulation. It is thus an extracorporeal therapy. (procedure which is carried outside the body)
digitalis use
cardiac glycosides
digitalis glycosides are a group of drugs that inhibit the sodium-potassium pump, thus they increase intracellular, which causes the cardiac muscle fibers to contract more efficiently
cardiac glycosides- positive-inotropic action
increases myocardial contracion
negative chronotropic action
decreases heart rate
negative dromotropic action
decreases conduction of the heart cells
other uses of cardiac glycosides
atrial fibriliation and atrial flutter
digitalis toxicity
overdose or accumulation of digoxin causes digitalis toxicity
Signs and symptoms of digitalis toxicity
anorexia, diarrhea, nausea and vomiting, bradycardia, pulse rate below 60, PVC, cardia dysrhythmias, headaches, malaise, blurred vision, visual illusions, confusion and delirium
antidote for cardiac/digitalis glycosides
ovine and digibind
Lanoxin- cardiac glycoside
treat CHF, atrial tachycardia, flutter or fibrillation
eg of rapid acting digitalis
digoxin (lanoxin)
eg of long-acting digitalis
digitoxin (Crystodigin0
antianginal drugs
used to treat angina pectoris, a condition of acute cardiac pain caused by inadequate blood flow to the myocardium resulting from either plaque occlusions within or spasms of the coronary arteries
Three types of angina
stable, unstable and variant
stable angina
occurs /c stress or excertion
unstable angina
occurs frequently over the course of a day with progressive severity
variant angina
occurs during rest
Three types of antianginals
nitrates, beta blockers and calcium channel blockers
action of antianginal
decrease myocardial demand for oxygen, decreasepreload by dilating veins thus indirectly decreasing afterload
the amt of blood in the ventricle at the end of diastole
peripheral vascular resistance
action of nitroglycerin
acts directly on the smooth muscle of blood vessels causing relaxation and dilation. It decreases cardiac preload and afterload and reduces myocardial oxygen demand. With dilation of the veins, there is less blood return to the heart and with dilation of the arteries there is less vasoconstriction and resistance
SE of nitroglycerin
headaches, hypotension, dizziness weakness, and faintness
beta blockers action
decrease the effects of the SNS by blocking the release of the catecholamines epinephrine and norepinephrine thereby decreasing the heart rate and blood pressure
beta blockers are used as
antianginals, antidysrhythmic and antihypertensive
eg of beta blockers
propranolol (Inderal), nadolol (Corgard) and pindolol (Vesken)
eg of calcium channel blockers
verapamil (Canal), nifedipine (Procardia), diltiazem (cardizem)
action of calcium channel blockers
calcium channel blockers decrease cardiac contractility and the workload of the heart thus decreasing O2
side effects of calcium channel blockers
headache, hypotension, dizziness and flushing of the skin
Antidysrhythmic drugs
used to restore cardiac rhythm to normal
Norpace- fast calcium channel blockers IA, Napamide, disopyramide
prevention suppression of unifocal and multifocal premature ventricular contractions, ventricular dysrythmias
procainamide,(Pronestyl, Procan) quinidine sulfate, polygalacturonate, gluconate (Quinidex, Cardioquin)
Atrial. ventricular and supraventricular dysrhythmias
Fast (Na+) calcium channel blockers IB, licocaine (Xylocaine)
acute ventricular dysrhythmias following MI and cardiac surgery
Fast (Na+) calcium channel blockers IB- mexiletine HCL (Mexitil)
Analogue of lidocaine, treatment for acute and chronic ventricular dysrhythmias, taken with food
Fast (Na+) calcium channel blockers IC- flecainide (Tambocor)
for life-threatening ventricular dysrhythmias prevention of paroxysmal supraventricular tachycardia and paroxysmal atrial fibrilation or fluttter
outburst of symptom: a sudden onset or intensification of a pathological symptom or symptoms, especially when recurrent
propafedone HCL (Rythmol)
treatment of life-threatening ventricular dysrhythmias
tocainide HCL (Tonocard)
for ventricular dysrhythmias, especially PVC similar to lidocaine except in oral form
moricine (Ethmozine)
to treat life-threatning ventricular dysthythmias, blocks sodium channels decreases conduction velocity in atria and ventricles and prolongs reffractory period in the AV node
Beta adrengergic- acebutolol HCL (Sectral)
management of ventricular dysrhythmias, used for anginal pectoris and hypertension, primarily PVC,
esmolol (Brevibloc)
to conrol atrial flutter and fibrilllation, for short term use only, for clients who have dysrhthmias during surgery
ventricular dysrhythmias, PAT and atrial and ventricular ectopic beats
sotalol HCl (betapace)
for life threatening ventricular dysrhthmias, initially dosage is greater and then decreases over time
bretylium tosylate bretylol
for ventricular tachycardia and fibrillation to convert to a normal sinus rhythm
phenytoin (Dilantin)
treatment of digitalis-induced dysrhythmias
SE of Quinidine
nausea, vomiting, diarrhea, confusion and hypotension, can cause heart block and neurologic psychiatric symptoms
SE of lidocaine
cardiovascular depressin, bardycardia, hypotension, seizures, blurred vision and double vision
SE of beta-blockers
bradycardia and hypotension and neurologic prlomes
SE of calcium channel blockers
nausea, vomiting, hypotension and bradycardia
Furomeside works on which part of the kidney
loop of henle
thiazides affect what part of the kidney
they affect the distal tubule
potassium sparing diuretics act on what part of the body
acts on the collecting tubule in the kidney
what part of the kidney does the osmotics affect
they affect the proximal tubule
Action of thiazides
Act on the distal convoluted renal tubule, beyond the loop of Henle, to promote Na+, chloride and water excretion.
SE of thiazides
electrolyte imbalance,(hypokalemia, hypercalcemia, hypomagnesemia, and bicarbonate loss) hyperglycemia, hyperuricemia (elevated serum uric acid level and hyperlipidemia
Action of loop diuretics
act on the ascending loop of Henle by inhibiting chloride transport of sodium
furomeside (Lasix)
treat fluid retention/fluid overload caused by CHF, renal dysfuntion, cirrhosis, hypertension, acute pulmonary edema
Action of Lasix
inhibition of Na+ and water reabsorption from the loop of Henle and distal renal tubules; potassium, magnesium and calcium are excreted
SE of Lasix
Nausea, diarrhea, electrolyte imbalances, vertigo, cramping, rash, headache, weakness, ECG changes, blurred vision, photosentivity
treatment of renal disease and hypertension and edema assoc. with CHF, similar to Lasix
ethacrynic acid (Edecrin)
for severe edema (pulmonary and peripheral. It is a potent diuretic and has rapid action, also use for hypercalcemia. Moderate to high doses may cause ototoxicity
Osmotic - Mannitol
for oliguria and decreasing ICP, to prevent acute renal failure, used in narrow angle glaucoma reducing ICP
Osmotic- (Ureaphil)
for oliguria and decreasing ICP, to prevent acute renal failure, used in narrow angle glaucoma, reducing IOP
Action of Osmotics
increase the osmolality (concentration) of the plasma and fluid in the renal tubules
SE of osmotics
fluid and electrolyte imbalance, pulmonary edema, from rapid shift of fluids, nausea, vomiting, tachycardia from rapid fluid loss and acidosis
Carbonic Anhydrase Inhibitors
used primarily to decrease IOP in clients with open-angle (chronic glaucoma, used also for diureses, mgmnt of epilepsy, and treatment of high altitude or acute mountain sickness, may be used for a client in metabolic alkalosis whi needs a diuretic
SE of Carbonic Anhydrase Inhibitors
electrolyte imbalance, metabolic acidosis, nausea, vomiting, norexia, confusion, orthostatic hypotension and crystaluria, hemolyutic anemia and renal calculi
Carbonic Anhydrase Inhibitors- acetazolamide (Diamox)
for edema, treating abscence (petit mal) seizures, and open-angle glaucoma
dichlorphenamide (Daranide, Oratrol)
Treatment of open-angle glaucoma by reducing the IOP and for narrow-angle glaucoma befoe surgery
methazolimide (Neptazane)
treatment of open-angle glaucoma by reducing the IOP and for narrow-angle glaucoma before surgery
K+ sparing diuretics,
weaker than thiazides and loop diuretics, also used as mild diuretics or in combination with another diuretic
spironolactone (Aldactone)
used for hypertension, edema K+ sparing
triamterene (Dyrenium)
increae urine output to treat fluid retension/overload associated with CHF, hepatic cirrhosis and nephrotic syndrome
SE of triamterene (Dyrenium)
nausea, vomiting, diarrhea, rash dizziness, headache, weakness, dry mouth photosensitivity
SE of k+ sparing diuretic
the main SE of these drugs is hyperkalemia
What are the five sympatholytic drug classification (sympathetic depressants)
five groups 1:beta-adrenergic blockers, 2, centrally acting sympatholytics (adrenergic blockers), 3. alpha-adrenergic blockers, 4. adrenergic neuron blockers (peripherally acting sympatholytics) and 5. alpha 1 and beta 1 adrenergic blockers.
beta adrenergic blockers aka
beta blockers
action of beta blockers
reduce cardiac output by diminishing the sympathethic nervous system response, they reduce HR, contractility and renin release
know that African Americans do not respond to this type of antihypertensive
beta blockers
Effective HTN control in AA is better with
beta blockers and diuretics
beta 1
heart receptors
beta 2
bronchial receptors
Drugs that block beta 1 receptors
Lopressor, atenelol, Zebeta, Kerlone, Sectral
Beta 1 what caution should be considered when using these drugs
caution in pulmonary disorders, CHF, sinus brady cardia, 2nr /3rd degree AV block
Can beta blockers be stopped abruptly?
They should not be stopped abruptly
SE of beta blockers
rebound hypertension, angina, dysrhythmias, and MI, insomnia, depressin, nightmares, sexual dysfunction
decrease the sympathetic response from the brainstem to the peripheral vesels
Sympatholytics stimulate which alpha
Alpha 2
action by Alpha 2
decreases sympathetic activity, increases vagus activity, decreases serum epinephrine, norepinephrine and renin release the goal to reduce peripheral vascular resistance
Sympatholytic drugs
Methyldopa (Aldomet), clonidine, Guababenz and guanfacine
SE of Sympatholytics
drowsiness, dry mouth, dizziness and slow heart rate
Alpha adrenergic blockers
used to treat HTN with indivuduals who have lipid abnormalities
Drug of choice for diabetics
Alpha-adrenergic blockers, prazosin, terazosin and doxazosin
Other uses of Prazosin
Action of Alpha adrenergic blockers
block the alpha-adrenergic receptors resulting in vasodilation and decreased blood pressure (arterioles and venules are dilated, decreasing peripheral resistance and lowering the blood pressure
SE of Alpha adrenergic blockers- prazosin, terazosin and doxazosin
dizziness, faintness, lightheadedness, increased HR, (can occur with first dose)
Adrenergic Neuron Blockers aka
Peripherally acting sympatholytics
Adrenergic Neuron Blockers are used for
they are a potent antihypertensive drug that block norepinephrine release from the sympathetic nerve ending, causing a decrease in norepinephrine release that results in lowering of blood pressure (cardiac output and vascular resistance
SE of Adrenergic neuron blockers
hypotension, suicidal ideation, nightmares
Alpha 1 and Beta 1 Adrenergic blockers
blocks alpha 1 and beta 1 receptors
action of blocking beta 2 receptors
increases airway resistance
Eg of alpha 1 and beta 1 adrenergic blockers
Labetalol (Normodyne) nad carteolol (Cartrol)
Common SE of alpha 1 and beta 1 adrenergic blockers
orthostatic (postural) hypotension, GI disturbances, nervousness, dry mouth and fatigue, large doses may cause AV block
potent HTN drugs, they act by relaxing smooth muscle of the blood vessels, mainly the arteries causing vasodilation, promotes blood flow to brain and kidneys
True/False diuretics are given with vasodilators
true- vasodilators decreases BP, NA+ and H20 is retained resulting in peripheral edema
eg of vasodilators
hydralazine and minoxidil, Nitroprusside is used to treat severe HTN
SE of hydralazine
tachycardia, palpitations, edema, nasal congestion, headache, dizziness, GI bleeding, lupuslike symptoms, and neurologic symptoms (tingling numbness).
SE of minoxidil
same as hydralazine including edema, excess hair growth, can pricipitate and anginal attack
Angiotensin Antagonists (Angiotensin Converting Enyme Inhibitors) ACE
inhibits the formation of angiotensin II a vasoconstrictor and blocks the release of aldosterone
Hormone aldosterone
promotes sodium retension and potassium excretion, when aldosterone is blocked, sodium is excreted water and potassium is retained
Eg of ACE inhibitors
Captopril (Capoten), benazepril (Lotensin), enalapril maleate (Vasotec), fosinopril (Monopril), lisonpril (Prinivil, Zestril), moexpril (Univasc), perindopril (Aceon), quinapril (Accupril), ramipril (Altace), and trandolapril (Mavik)
True/False African Americans respond better when an Ace Inhibitor is combined with a diuretic
True- AA do not respond well to ACE inhibitors, when combined with a diuretic, therapeutic levels are reached
SE of ACE inhibitors
cough, nausea, vomiting, diarrhea, HA, dizzines, fatigue, insomnia, serum potassium excess (hyperkalemia, and tachycardia
Angiotensin II blockers (new drugs)
prevent the release of aldosterone
Eg of Angiotensin II blockers
Losartan (Cozaar), valsartan (Diovan), irbesartan (Avapro), candesartan cilexitil (Atacand), eprosartan (Teveten) and telmisartan (Micardis)
SE of Angiotensin II blockers
Calcium channel blockers
block decrease calcium levels and promote vasodilation
Eg of calcium channel blockers
Verapamil (Calan), Diltiazem (cardizem) Nefedipine (Procardia)
True/False Calcium channel blockers work better in AA
True they lower blood pressure in AA than any other regimen
SE of Calcium channel blockers
flush, headache, dizziness, ankle edema, bradycardia and AV block
platelet aggregation
clumping together of platelets to form a clot
formation of a clot at the arterial or venous level
Action of anticoagulants-warfarin and heparin
prevents venous thrombosis (inhibit clot formation)
Action of antiplatelet drugs
prevent arterial thrombosis
Eg of low molecular weight heaparin
enoxaprin sodium (lovenox)
international normalized ratio
oral anticoagulants
coumadin, licomano & anisindoine (Miradon)
Action of oral anticoagulants
oral anticoagulants inhibit hepatic synthesis of vitakmin K+
normal INR
1.3 - 2.0
Therapeutic warfarin
Food and warfarin
food delays absorption but does not inhibit
what is the half life of coumadin
.5- 3 days
1/2 life of heparin
1-2 hours
warfarin is contraindicated in
pregnancy can cause the placental barrier
Vit K counteracts the effect of
antiplatelet drugs
(Persantine) dipyridamole, ticolopidine (Tichil), clopidogrel (Plavix)
Eg of Thrombolytics
streptokinase, lenokinase, tissue plasminogen activator (t-PA, alteplase) reteplase (Ritavase)
fibrin breakdown
closetipol (Colestid), Clofibrate (Atromid S), genfibrozil (Lopid)
Eg Vastatins/Statins
Artovastatin calcium (Lipitor), Lovastatin (Mevacor), fluvastastin (Liscol)
Action of nitrobid
acts by dilating the veins and in high doses, dilate arteries, prevents vasospasms
force of contraction
Creatinine kinase
lab test used to dignose MI
a protein found in the myocardium, regulate the myocardial contractile process
the heme protein that helps to transport oxygen
Eg of thrombolytics
PTCA (percutaneous Transluminal Coronary Angioplasty)
Improves blood flow to the myocardium breaks down atheroma
is an abnormal inflammatory accumulation of macrophage white blood cells within the walls of arteries
a woven mesh that provdes structural support to a vessel ar risk of acute closure
involves the delivery of gamma or beta radiation by placing radioisotope close to the lesion
In cardiac physiology, preload is the volume of blood present in a ventricle of the heart, after passive filling and atrial contraction, usually the left ventricle.
afterload is the tension produced by a chamber of the heart in order to contract usually the left ventricle
afterload also described as
the pressure that the chamber of the heart has to generate in order to eject blood out of the chamber.
force generated by the heart muscle under any condition
stroke volume
amt of blood ejected per heartbeat
ejection fraction
the fraction of blood pumped out of a ventricle with each heart beat. the term ejection fraction refers specifically to that of the left ventricle.
ejection fraction decreases if contractility is depressed
end diastolic
the volume of blood within a ventricle
end-systolic volume
the volume of blood left in a ventricle at the end of contraction
left ventricle ejection time
prolonged systole
noturia is a sign of heart failure (true) fluid collected in the dependent tissues (extremities) during the day redistributes into the circulatory system once the patient is recumbent at night, the increased circulatory volume is excreted by the kidneys
Signs of worsening heart failure
can be revealed by sleep related events, sleeping upright in a chair instead of bed, increasing the number of pillows used, awakening SOB at night, or awakening with angina
Reasons for pallor
lack of oxy hemoglobi, result of anemia or decreased arterial perfusion
peripheral cyanosis
bluish tinge, most often of the nail beds
central cyanosis
bluish tinge on the tongue and buccal mucosa, sign of cardiac disorders (pulmonary edema and congenital anamolies,) (venous blood passes through the circulation /s being oxygenated
yellowish raised areas on the skin, or noted on the eyelids (denotes increased cholesterol)
Clammy or diaphoretic skin
stress, cardiogenic shock, and acute MI the skin becomes diaphoretic
excessive bruising on a patients skin receiving anticoagulant therapy
could be a sign of prolonged clotting times (dosage may be too high)
thinning of the skin around the area of a pace maker would be a sign of
erosion of the device through the skin
pulse pressure
difference between systolica and diastolic
what is the meaning of pulse pressure in regards to the work of the heart
it is a reflection of stroke volume, ejection velocity and systemic vascular resistance.
What is the normal measurement of pulse pressure
30-40mg Hg
What causes pulse pressure to increase
anwity, exercise, brady cardia, fever, atherosclerosis, aging hypertension, shock, HF, hypovolemia, mitral regurgitation, mitral stenosis
Significance of pulse pressure below 30mm Hg
sign of serious reduction in cardiac output which requires further assessment
Reasons for postural hypotension
reduced volume of blood/fluid, inadequate vasoconstrictor mechanism, insufficient autonomic action on vasoconstriction
Pulse quality measurements
absent pulse- 0, weak, thready pulse, difficult to palpate, +1, diminished pulse +2, easy to palpate, +3, strong, bounding, +4 (may be abnormal)
erb's point
third intercostal space to the left of the sternum
apical impulse
normal impulse that is distinct and located over th eapex of the heart
S1 ans S2
normal heart sounds produced by the closing of the heart valves
closing of the mitral and tricuspid valve- heard best at the apex
produded by the closing of the aortic and pulnonic valves and is loudest at the base of the heart
how much blood is ejected fron the right ventricle compared to inspiration and expiration
more is ejected from the right ventricle
gallop sounds
like that of horses
S3- during rapid ventrivular filling
gallop sounds heard best when pt lying on the left side
gallop sounds heard in atrial contraction, heard when the ventricle is enlarged and there is resistance to filling
friction rub
pericarditis, harsh grating sound that can be heard in both systole and diastole
cheny stokes respiration
severe left ventricular failure
signs of hemptysis
pink frothy sputum, indicative of acute pulmonary edema
cough in relation to the heart
dry hacking cough from irritation of small airways is common in patients with pulmonary congestion from HF
where are crackles heard first
in the bases, and may progress to other fields
what enzymes are screened for in an acute MI
Ck, and CK-MB they are the first enzyme levels to rise
What enzymes peak 2-3 days after an MI
lactic dehydrpgenase and its isoenzymes
What is the best blood test to detect MI up to three weeks after
test for troponin