NC4 Cardiovascular Problems

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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
coarctation: narrowing
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
CHF: 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
True/False: 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
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.
polycythemia: increased amount of RBC
squatting: 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
ministernotomy: opening the lower half of the sternum
signs of renal failure: elevated bun, creatinine, and decreased urine output of less than 1ml/kg/hr
Restenosis: 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: irritability
shock: 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
Thalassemia: 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: failure of the bone marrow to carry out its hematopoietic functions
hemostasis: the process that stops bleeding when a blood vessel is injured.
finbrinolysis: ensure clot formation only in the presence of blood vessel injury and to limit the clotting process the the site of vessel wall injury
hemophilia: group of bleeding disorders in which there is a deficiency of one of the factors necessary for coagulation of the blood
hemarthrosis: 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: 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
apheresis: 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: CHF
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
preload: 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: afterload is the tension produced by a chamber of the heart in order to contract usually the left ventricle
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
paroxysmal: 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
propranolol: 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
(Bumex)bumetanide: 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
Sympatholytics: 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: BPH
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
Vasodilators: 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: angioedema
Calcium channel blockers: block decrease calcium levels and promote vasodilation
True/False Calcium channel blockers work better in AA: True they lower blood pressure in AA than any other regimen
platelet aggregation: clumping together of platelets to form a clot
Thrombosis: 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)
INR: 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: 2.0-3.0
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: coumadin
antiplatelet drugs: (Persantine) dipyridamole, ticolopidine (Tichil), clopidogrel (Plavix)
Eg of Thrombolytics: streptokinase, lenokinase, tissue plasminogen activator (t-PA, alteplase) reteplase (Ritavase)
fibinolysis: fibrin breakdown
Antilepemics: 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
contractility: force generated by the heart muscle under any condition
Creatinine kinase: lab test used to dignose MI
Troponin: a protein found in the myocardium, regulate the myocardial contractile process
Mygolobin: the heme protein that helps to transport oxygen
PTCA (percutaneous Transluminal Coronary Angioplasty): Improves blood flow to the myocardium breaks down atheroma
atheroma: is an abnormal inflammatory accumulation of macrophage white blood cells within the walls of arteries
stent: a woven mesh that provdes structural support to a vessel ar risk of acute closure
brachytherapy: involves the delivery of gamma or beta radiation by placing radioisotope close to the lesion
afterload also described as: the pressure that the chamber of the heart has to generate in order to eject blood out of the chamber.
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.
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
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
Xanthelesma: 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

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