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232 Cards in this Set

  • Front
  • Back
half life of heparin
1 to 2 hours
Third degree AV block
Occurs when no atrial impulse is conducted through the AV node. In 3rd degree AV block 2 impulses stimulate the heart, one stimulate the ventricles and one the atria.
A decrease in the # of platelets in the circulating blood, major concern is bleeding
a defect resulting from the failure of the ductus (located between the aorta and the pulmonary artery) to close it is patent and shouldn't be, causing shunting of blood to the pulmonary artery
Patent ductus arteriosus
A pt has an abdominal aortic aneurysm what should be included immediately post op
severe back pain
a pat taking an ACE inhibitor may experience?
orthopnea and cough. Must be taken prior to meals
a pt with angina should avoid
extreme temperature
a successful cardioversion would indicate
conversion to sinus rhythm, adequate peripheral pulses and adequate blood pressure
a vasopressor is
a drug used to constrict the arteries and increase bp. These agents include dobutamine, dopamine, epinephrine, isoproterenol, norepinephrine, and ephedrine. They are most commonly used in intensive care and post op hospital settings for pts with critical hypotension ( low bp)
the removal of material form the surface of an object by vaporization, chipping, or other erosive processes
action of alpha 2
decreases the sympathetic activity, increases vagus activity, decreases serum epinephrine, norepinephrine and renin release the goal to reduce peripheral vascular resistance
action of alpha adrenergic blockers
block the alpha-adrenergic receptors resulting in vasodilation and decreased bp (arterioles and venules are dilated, decreasing peripheral resistance and lowering the bp
action of antiangina
decreased myocardial demand for oxygen, decrease preload by dilating veins thus indirectly decreasing afterload
action of anticoagulants-warfarin and heparin
prevents venous thrombosis (inhibit clot formation)
action of antiplatelet drugs
prevent arterial thrombosis
action of beta blockers
reduce cardiac output by diminishing the sympathetic nervous system response, they reduce HR, contractility and renin release
action of blocking beta 2 receptors
increase airway resistance
action of calcium channel blockers
calcium channel blockers decrease cardiac contractility and the workload of the heart thus decreasing O2
action of Lasix
inhibition of Na+ and water reabsorption from the loop of Henle and distal renal tubules; potassium, magnesium and calcium are excreted
action of loop diuretics
act on the ascending loop of Henle by inhibiting chloride transport of sodium
action of Milrinone (Primacor)
promotes vasodilation, decreasing preload and afterload, reducing the workload of the heart
action of nitrobid
acts by dilating the veins and in high doses, dilate arteries; prevents vasospasms
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
action of oral anticoagulants
oral anticoagulants inhibit hepatic synthesis of Vitamin K
action of osmotics
increase the osmolality (concentration) of the plasma and fluid in the renal tubules
actions of thiazides
act on the distal convoluted renal tubule, beyond the loop of Henle, to promote Na+ chloride and water excretion
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 bp (cardiac output and vascular resistance)
after stopping infusion for c/o tingling or burning what should be done by RN
check for blood return and, if present continue to administer drug
what is afterload
the tension produced by a chamber of the heart in order to contract usually the left venticle; also, the pressure that the chamber of the heart has to generate in order to contract usually the left ventricle
what are alpha adrenergic blockerrs used for
the tx HTN with individuals who have lipid abnormalities
is the rapid swelling (edema) of the skin, mucosa and submucosal tissues. Apart from the common form, mediated by allergy, it has been reported as a side effect of some medications, specifically ACE inhibitors
Angiotensin Antagonists (Angiotensin Converting Wnzyme Inhibitors) ACE
inhibits the formation of angiotensin II a vasoconstrictor and blocks the release of aldosterone
Angiotensin II blockers
prevent the release of aldosterone
antianginal drugs
used to tx 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
antidote for cardiac/digitalis glycosides
ovine and digibind
antidysrhythmic drugs
used to restore cardiac rhythm to normal
antiplatelet drugs
(Persantine) dipyridamole, (Tichil) ticolopidine, (Plavix) clopidogrel
Antithrombin III deficiency
ability to inhibit thrombin and certain coagulation factors. May cause DVTs
aortic stenosis
narrowing or stricture of the aortic valve, causing resistance of blood flow in the left ventricle decreased cardiac output
removal of blood from the individual apheresis is a medical technology in which the blood of a donor or pt is passed through an apparatus that seperates out one particular constituent and returns the remainder to the circulation. It is thus and extracorporeal therapy. Procedure which is carried outside the body
apical impulse
normal impulse that is distinct and located over the apex of the heart
aplastic anemia
low count of WBC, platelets, and RBC, severe anemia, significant neutropenia, thrombocytopenia. Bone marrow failure condition in which the formed elements of the blood are simultaneously depressed
aplastic crisis
diminished RBC production resulting in profound anemia
hardening that affects the small arterioles
is an abnormal inflammatory accululation of macrophage WBC within the walls of the arteries
disease affecting the arterial blood vessel. It is commonly referred to as a "hardening" or "furring" of the arteries. It is caused by the formation of multiple plaques within the arteries.
atrial septal defect
abnormal opening b/n the atria, allowing blood from the higher pressure left atrium to flow into the lower pressure right atrium
atrioventricular canal defect
incomplete fusion of endocardial cushions
autoimmune hemolytic anemia
autoimmune hemolytic anemia (AIHA) is a type of hemolytic anemia where the body's immune system attacks its own RBCs, leading to their destruction (hemolysis)
AV block aka
complete heart block
avascular necrosis
Avascular necrosis is a disease resulting from the temporary or permanent loss of the blood supply to the bones. Without blood, the bone tissue dies and causes the bone to collapse. If the process involves the bones near a joint, it often leads to collapse of the joint surface. Tis disease also is known as osteonecrosis, aseptic (bone) necrosis, and ischemic bone necrosis.
beta 1
heart receptors
Beta 1 what caution should be considered when using these drugs
caution in pulmonary disorders, CHF, sinus bradycardia, 2nd/3rd degree AV block
Beta adrengergic- acebutolol HCL (Sectral)
management of ventricular dysrhythmias, used for anginal pectoris and HTN, primarily PVC
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 BP
beta blockers are used as
antianginals, antidysrhythmic, and antihypertensive
bretylium tosylate bretylol
for ventricular tachycardia and fibrillation to convert to a normal sinus rhythm
calcium channel blockers
block decrease calcium levels and promote vasodilation
can beta blockers be stopped abruptly
they should not be stopped abruptly
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-inotrophic action
increase myocardial contraction
cardiac output
the amount of blood pumped in one minute
cardiac output equation
CO = HR x SV
cardiac tamponade
medical emergency condition where liquid accumulates in the pericardium in a relatively short time. The elevated pericardial pressure prevents proper filling of heart cavities. Instead of reducing the filling of both ventricles equally, the septum of the heart will bend into either the left or right ventricle. The end result is low SV, shock and often death.
cardiogenic shock tx with
NTG and Dopamine
involves the delivery of a timed electrical current to terminate a tachydysrhythmia
catheter ablation therapy
destroys specific cells that are the cause of central conduction method of a tachydysrhythmia (performed after an EP study)
causes of pulmonary artery pressure
cardiac causes - right to left shunt producing increased blood flow, hypoxic lung disease, thromboembolic disease, pulmonary vascular obstruction, collagen vascular diseases and exposure to toxic substances
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
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
clammy or diaphoretic skin
stress, cardiogenic shock, and acute MI the skin becomes diaphoretic
clinical manifestations of aortic stenosis
infants with severe defects demonstrate signs of decreased cardiac output with faint pulses, hypotension, tachycardia and poor feeding, children show signs of excercise intolerance, chest pain and dizziness when standing for a long period, murmur, at risk for bacterial endocarditis, coronary insufficiency and ventricular dysfunction
clinical manifestation of atrioventricular
moderate to severe CHF, there is characteristics of murmur, mild cyanosis that increases with crying pts are at high risk for developing pulmonary vascular obstructive disease
clinical manifestations of patent ductus arteriosus
may be asymptomatic, or show signs of CHF, murmur, widened pulse pressure and bounding pulses, at risk for bacterial endocarditis and pulmonary vascular obstructive disease later in life
clinical manifestations of polycythemia vera
ruddy complexion, splenomegaly, increased blood volume evidenced by HA, dizziness tinnitus, fatigue, paresthesias and blurred vision/ increased blood viscosity evidenced by angina, claudication, dyspnea, and thrombophlebitis
clinical manifestation of pulmonary artery HTN
dyspnea with exercise, chest pain and syncope
clinical manifestation of tricuspid atresia
cyanosis, tachycardia and dyspnea, older children have signs of chronic hypoxemia with clubbing at risk for bacterial endocarditis
clinical manifestations of ventricular septal defect
CHF is common, murmur, at risk for bacterial endocarditis, and pulmonary vascular obstructive disease, in severe cases eisenmenger syndrome may developw
clinical manifestation of ASD (atrial septal defect)
can be asymptomatic, may develop CHF, there is a characteristic murmur, at risk for atrial dysrhythmias, pulmonary vascular obstructive disease and emboli formation later in life from chronic increase pulmonary flow
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
common side effects of digitalis
reduces edema, nausea
force generated by the heart muscle under any condition
cooleys anemia
severe anemia that leads to cardic failure and death
cough in relation to the heart
dry hacking cough from irritation of small airways is common in pts with pulmonary congestion from HF
creatinine kinase
lab test used to diagnose MI
cyanosis is indicative of what
impaired circulation or impaired airway patency
used in an emergency situation as teh tx of choice for v-fib and pulseless VT
electrical stimulation - mechanical contraction is called systole
difference between cardioversion and defibrillation
cardioversion is a planned procedure, defibrillation is and emergency procedure
digitalis toxicity
overdose or accululation of digoxin causes digitalis toxicity
digitalis use
disseminated intravascular coagulation
disseminated intravascular coagulation (DIC) is a pathological process in the body where the blood starts ot coagulate thoughout the whole body. This depletes the body of its platelets and coagulation factors and there is a paradoxically increased risk of hemorrhage
iv med given to pts /c significant L ventricular dysfunction
dobutamine (Dobutrex) action
increase cardiac contractility
drugs that block beta 1 receptors
Lopressor, atenelol, Zebeta, Kerlone, Sectral
early signs of shock in a child
apprehension, irritability, normal BP, narrowing pulse pressure (difference b/n diastolic and systolic BP), thirst, pallor, diminished urine output, unexplained mild tachycardia, and a decrease in perfusion of the hands and fett
effective HTN control in AA is better with
beta blockers and diuretics
eisenmenger complex
refers to the clinical situation in which a left to right shunt becomes a right to left shunt because of a progressive increase in pulmonary vascular resistance
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
electrophysiological studies
used to evaluate and tx various dysrhythmias that have caused arrest or significant symptoms
end diastolic
the volume of blood within a ventricle
endocardial isolation
involves making an incision into the endocardium that separates the area where the dysrhythmia originates from the surrounding endocardium. The edges of the incision are then sutured together. The incision and its resulting scar tissue prevent the dysrhthmia from affecting the whole heart
endocardial resection
the origin of the dysrhythmia is identified and that area of the endocardium is peeled away. No reconstruction or repair is necessary.
end-systolic volume
the volume of blood left in a ventricle at the end of contraction
epinephrine used for
erb's point
third intercostal space to the left of the sternum
esmolol (Brevibloc)
to control atrial flutter and fibrillation, for short term use only, for clients who have dysrhythmias during surgery
excessive bruising on a pts skin receiving anticoagulant therapy
could be a sign of prolonged clotting times (dosage may be too high)
exchange transfusion
pts own blood is removed and replaced via transfusion
Fast (Na+) calcium blockers IB-mexiletine HCL (Mexitil)
analogue of lidocaine, tx for acute and chronic ventricular dyrhythmias, taken with food
Fast (Na+) calcium channel blockers IB, lidocaine (Xylocaine)
acute ventricular dysrhythmias following MI and cardiac surgery
Fast (NA+) calcium channel blockers flecainide (Tambocor)
for life threatening ventricular dyrhythmias prevention of paroxysmal supraventricular tachycardia and paroxysmal atrial fibrillation or flutter
febrile non-hemolytic transfusion
This is the most common adverse reaction to a blood transfusion. Symptoms include fever and dyspnea 1 to 6 hours after receiving the transfusion. Such reactions are clinically benign, causing no lasting side effects or problems, but are unpleasant for the patient
fibrin breakdown; ensure clot formation only in the presence of blood vessel injury and to limit the clotting process the site of vessel wall injury
food and warfarin
food delays absorption but does not inhibit
friction rub
pericarditis, harsh grating sound that can be heard in both systole and diastole
furomeside (Lasix)
tx fluid retention overload caused by CHF, renal dysfunction, cirrhosis, HTN, acute pulmonary edema
Furomeside works on which part of the kidney
hoop of Henle
heart failure is described in two ways
right and left sided
bleeding in joint spaces, often occurring in life-threathening cases such a a hemophilia where the bleeding does not stop
hemolytic anemia
anemia due to hemolysis, the abnormal breakdown of RBC either in the BV (intravascular hemolysis) or elsewhere in the body (extravascular). It has numerous possible causes, ranging form relatively harmless to life-threatening
group of bleeding disorders in which there is a deficiency of one of the factors necessary for coagulation of the blood
the process that stops bleeding when a BV in injured
High pulmonary pressure in PDA lead to ___ or ____?
CHF or pneumonia
how much blood is ejected from the right ventricle compared to inspiration and expiration
more is ejected from the right ventricle
how to obtain HR from a rhythm strip
count boxes in teh RR interval divide that number into 1500
How to distinguish a pericardial friction from a pleural friction rub?
If a pt is asked to hold their breath a pericardial friction rub will continue
hydralazine and isorbine used to tx
HF, and used when pts are not able to tolerate ACE inhibitors
hypercyanotic spells
aka blue spells, seen in infants with Tetralogy of Fallot, they are preceded by feeding, crying, defecation or any stressful procedure
hyperhemolytic crisis
accelerated rate of RBC destruction characterized by anemia, jaundice and reticulocytosis
increased plasma of homocystine, results from nutritional deficiency of folic acid and b6 and b13. Increased risk for thrombosis.
how does parasympathetic stimulation on the heart
slows down the heart
how does sympathetic stimulation on the heart and blood vessels
causes the heart to increase and BV to contract
effects of low or high blood volume influence blood volume
low blood volume signals the heart to increase the HR and high BV slows the HR
role of endothelial cells in maintaining cardiovascular function
derived hyperpolarizing factor: promotes vasodilation
role of nitric oxide in maintaining cardiovascular function
promotes vasodilation and anticoagulation
role of endothelium cells in maintaining cardiovascular function
promotes vasoconstriction and cellular growth
role of prostacyclin in maintaining cardiovascular function
promotes vasodilation and anticoagulation
what effect does dysfunction of the endothelial contribute to cardiovascular disorders
injury to the endothelial cell alters the normal regulatory forces and leads to vasospasm, thrombosis, growth of the intimal layer of the BV, rapture of atherosclerotic plaque, tissue ischemia and infarction, and dysrhythmias
hyperhemolytic crisis
accelerated rate of RBC destruction characterized by anemia, jaundice and reticulocytosis
increased plasma of homocystine, results from nutritional deficiency of folic acid and b6 and b13. Increased risk for thrombosis.
how does parasympathetic stimulation on the heart
slows down the heart
how does sympathetic stimulation on the heart and blood vessels
causes the heart to increase and BV to contract
effects of low or high blood volume influence blood volume
low blood volume signals the heart to increase the HR and high BV slows the HR
role of endothelial cells in maintaining cardiovascular function
derived hyperpolarizing factor: promotes vasodilation
role of nitric oxide in maintaining cardiovascular function
promotes vasodilation and anticoagulation
role of endothelium cells in maintaining cardiovascular function
promotes vasoconstriction and cellular growth
role of prostacyclin in maintaining cardiovascular function
promotes vasodilation and anticoagulation
what effect does dysfunction of the endothelial contribute to cardiovascular disorders
injury to the endothelial cell alters the normal regulatory forces and leads to vasospasm, thrombosis, growth of the intimal layer of the BV, rapture of atherosclerotic plaque, tissue ischemia and infarction, and dysrhythmias
what s/s usually occur with HF. how are they assessed
Compensated HF may not have symptoms at rest. During activity, dyspnea and fatigue exist. Uncompensated HF is indicated by peripheral edema and acute HF is indicated by pulmonary edema. A physical examination assessing heart and lung sounds and observing for edema and JVD are keys to identifying HF.
what are the physiologic effects of digoxin on the heart
Exerts a cardiotonic inotropic effect that improves the pumping ability of the heart. Increases myocardial contractility allows the vventricles to empty more completely with each HR. With improved cardiac output, decreases in heart size, HR, end systolic and end diastolic pressure, vasoconstriction, sympathetic nerve stimulation, and venous congestion result
how does digoxin produce or assist diuresis
Improvement of cardiac output improves blood flow to the kidneys, which promotes diuresis
what is digitalization
When loading doses are given to quickly raise tissue concentrations of digoxin to a steady state
differentiate b/n a digitalizing dose of digoxin and a daily maintenance dose
They are larger
why do nurses need to check HR and rhythm before administering digoxin
Slows the rate of ventricular contraction; therefore, a slow HR will be slowed even further with the administration fo digoxin. Some dysthythmias may be indicative of digoxin toxicity.
when is it appropriate to withhold a dose of digoxin
If the HR is less than 60 beats per minute in adults or 100 beats per minute in a child, or if the client has symptoms of toxicity, the dose should be held and reported.
what are the adverse effects associated with digoxin and how might they be prevented or minimized
The main adverse effects that occur with toxicity include anorexia, nausea, vomiting, confusion and vision disturbances. Maintain daily dosing schedule and monitor electrolyte to help avoid digitalis toxicity.
for clients with renal failure who need digoxin, what are the options for safe, effective therapy?
Loading and maintenance doses should be reduced in clients with renal failure. These clients must be monitored closely for adverse effects and serum digoxin levels should be monitored periodically.
why is it important to maintain a therapeutic serum potassium level during digoxin therapy?
Potassium is a myocardial depressant that acts to decrease myocardial excitability. A proper serum level is required to prevent dysrhythmias.
what is the antidote for severe digoxin toxicity?
Digoxin immune tab (Digibind)
What tissues in the heart are able to generate an electric impulse and therefore serve as a pacemaker
SA is the pacemaker. Made of specialized tissues that can generate and conduct an electric impulse, but any part of the conduction system or atrial or ventricular muscle can spontaneously start an impulse.
What risk factors predispose a client to development of dysrhythmias?
Disturbances in electric impulse formation, conduction, or both. These may be activated by hypoxia, ischemia, or hypokalemia.
Name interventions that clients or health care providers can perform to decrease risks of dysrhythmias
Tx underlying disease first. Avoid cigarette smoking, overeating, and excessive intake of coffee and caffeinated drinks. Serum electrolytes and drug levels should be monitored.
Hemodynamic effects of sinus dysrhythmias?
Significant only if severe or prolonged.
Hemodynamic effects sinus tachycardia?
Increases the workload of the heart.
Hemodynamic effects sinus bradycardia?
Decrease CO
Hemodynamic effects atrial dysrhythmias?
Significant in the presence of underlying heart disease
Hemodynamic effects atrial fibrillation and flutter?
Impair ventricular filling, decrease CO and may lead to formation of thrombi.
Hemodynamic effects nodal dysrhythmias?
May involve tachycardia and an increased workload on the heart or bradycardia may form heart block.
Hemodynamic effects ventricular dysrhythmias?
May include brief episodes that are asymptomatic, or frequent or sustained dysrhythmias that result in hemodynamic collapse.
Hemodynamic effects ventricular fibrillation?
Produces no myocardial contraction and thus no CO and sudden cardiac death.
How do beta-adrenergic blocking agents act on the conduction system to slow HR?
Block sympathetic nervous system stimulation. Beta receptors in the SA node and ectopic pacemakers are slowed and therefore decrease automaticity. Blockade of receptors in the AV node increase the refractory.
Why are Class 1 drugs used less than class 2 or 3 drugs?
Less likely to promote longevity of life.
What are are common and potentially serious adverse effects of antidysrhythmic drugs?
New dysrhythmias may develop or the drugs may aggravate preexisting dysrhythmias.
What is angina pectoris?
Clinical syndrome characterized by episodes of chest pain that occurs when there is a deficit in myocardial oxygen supply in relation to myocardial oxygen demand.
What is the role of endothelial dysfunction in the development of coronary artery atherosclerosis and myocardial ischemia?
Atheroscerosis begins with the accumulation of lipid-filled macrophages onthe inner lining of coronary arteries. Intially, WBC become attached to the endothelium and move though the endothelial layer into the subendothelial spaces, where they ingest lipid and become foam cells. These lesions progress to fibrous plaques that alter blood flow in the vessels.
How do nitrates relieve angina?
Relax smooth vessel walls, producing vasodilation. This decreases preload, afterload, and cardiac workload.
Develop a teaching plan for a client who is beginning nitrate therapy.
Advise of the following:
Take meds as prescribed and avoid OTC meds.
Take on a regular schedule and do not discontinue without tapering.
Monitor BP and pulse daily. If systolic BP is lower than 90 mmHg, omit the dose and report the information.
Change positions slowly.
If sustained-released forms of medication, do not crush or chew.
Take medication by proper route.
Administer topical med to hairless parts of the body.
Make aware that they may require nitrate-free periods at night to prevent tolerance.
How do beta blockers relieve angina?
Prevent or inhibit sympathetic stimulation, thereby reducing HR and myocardial contractility
Why should beta blockers be tapered and discontinued slowly in clients with angina?
rapid removal of beta blockers can cause rebound angina and tachycardia
How do calcium channel blockers relieve angina?
Prevent the movement of extracellular calcium into the cell, thereby decreasing myocardial contractility and promoting coronary artery and peripheral artery vasodilation
Teaching plan for a client taking a calcium channel blocker.
Advise the pt:
Take med as prescribed and avoid OTC
Take med on a regular schedule and monitor BP and pulse daily. If systolic BP is lower than 90 mm Hg, omit the dose and report.
Change position slowly.
Do not crush of chew sustained-release.
How do adrenergic drugs improve circulation in hypotension and shock?
Increase PVR and raise BP. Increase myocardial contractility and HR, which in turn raises BP.
Which adrenergic should be readily available for management of anaphylactic shock?
Epinephrine is the drug of choice for anaphylaxis bc of its rapid onset and antiallergic effects.
What are the major adverse effects or adrenergic drugs?
Increase HR and BP, increasing workload on the heart.
How would you assess a client for therapeutic or adverse effects of an adrenergic drug being given by continuous IV infusion?
Monitoring of VS, skin color, temperature, urine output and mental status are indicators of therapeutic or adverse effects. In addition, hemodynamic monitoring and lab values are helpful indicators.
Why is it important to prevent extravasation of adrenergic drug infusions into tissues surrounding the vein?
Can cause significant tissue damage.
In hypovolemic shock, should fluid volume be replaced before or after an adrenergic drug is given and why?
Adequate fluid therapy is necessary for the maximal pressor effect; therefore, fluid volume should be replaced before the administration of an adrenergic drug
What are clinical indications for the use of diuretics?
Used to manage edema and nonedema conditions. They are used most frequently in edema, heart failure, and HTN. They are helpful in preventing renal failure.
What is the general mech by which diuretics act?
Diuretic drugs act on the kidneys to decrease reabsorption of sodium, chloride, water, and other substances. In edematous states, diuretics mobilize tissue fluids by decreasing plasma volume.
How are diuretic effects assessed?
Daily wight, I and O, and assessing breath sounds and peripheral edema.
Side effects of thiazides
Contraindicated in clients with allergies to sulfonamides. Hyperglycemia, hyperuricemia and hypercalcemia.
Side effects of Loop diuretics
Can cause large fluid volume deficits and hypokalemia.
Side effects of potassium- sparing diuretics
Side effects of osmotic diuretics
Can cause large fluid losses and electrolyte imbalance.
Why should serum potassium levels be monitored during therapy?
Hypokalemia can occur with many diuretics that may cause cardiac dysrhythmias. Hyperkalemia caused by potassium-sparing diuretics or overuse of potassium supplements can cause cardiac depression.
Flow of blood through the heart
L heart > systemic arteries > systemic veins > R heart > pulmonary artery > L heart
What is P = Q x R
Blood Pressure = Quantity of Blood flowing through vessels per minute x Resistance of the vessel walls; where Q = cardiac output
How is cardiac output determined?
CO = HR x SV; HR= number of beats per minute; SV= the amount of blood that leaves the L ventricle through the aorta with each heart beat.
Causes for generalized decrease in blood flow
orthostatic hypotension, shock
Cause of orthostatic hypotension
Body gets vertical before baro-reflex can compensate for change
What are the signs of shock?
Decreased BP; Altered mental status; Increased HR, which strains the heart; Increased respiratory rate; Vasoconstriction in peripheral vessels/kidneys; Decompensation.
What are the signs of vasoconstiction in the peripherals?
Decreased peripheral pulse strength, cool, pale skin, decreased urine output, peripheral cyanosis
Cause of hypovolemic shock?
Low blood volume
Cause of cardiogenic shock?
Due to decreased cardiac output
Cause of septic shock?
Due to loss of vascular resistance, bacterial endotoxin triggers vasodilation
Cause of anaphylatic shock?
Due to loss of vascular resistance; Histamine triggers vasodilation, increased capillary permeability
Cause of Neurogenic shock?
Due to loss of vascular resistance; Loss of sympathetic adrengeric stimulation to vasocontriction
How to leaks lead to system failure?
Loss of RBCs; Loss of circulating volume; Compression of tissues in the area (cardiac tamponade, compartment syndrome);
Antecedents that lead to leaks.
Increased vascular permeability; Damage to the vessel wall or to the wall of the heart.
What is HTN?
a BP > 140/90 in adults
Mild = 140-159/90-99
Moderate = 160/100-120
Severe = /120
Borderline = between 120/80 and 140/90
What causes HTN?
Increase blood volume or to much resistance
What are the types of HTN?
Primary=Idiopathic (increased resistance, genetic, dietary, chronic high stress, smoking, obesity, chronic lead exposure)
Secondary=Most due to obstructed renal blood flow
Describe the how renal flow obstruction effects BP
Obstructed renal flow increases renin secretion. Renin acts on angiotensinogen and converts it to angiotensin 1 in the blood. Angiotensin 1 circulates and is converted to angiotensin 2 in the lung by angiotensin converting enzyme (ACE). Angiotensin 2 is a potent vasoconstrictor, increases R=increases BP. Angiotensin 2 also stimulates adrenal secretion of aldosterone, which acts on kidney tubules to reabsorb sodium (and water). This increases blood volume, which increases BP.
S/S of HTN
Increased BP reading. No other symptoms unless severe. Can have HA and blurred vision in HTN crisis.
What are the effects of HTN.
Increased stress on the vessel wall (aneurysm formation, rupture, or dissection, CVA, retinal damage, coronary vessel damage, potentially reversible kidney damage, irreversible brain damage
Increased afterload of heart leads to more work and MI and CHF
How is HTN tx?
Reduce force of the pump: sympathetic adrenergic beta blockers, aerobic fitness training
Reduce blood volume: Diuretics, low Na diet
Reduce peripheral resistance: Drugs: Vasodilator, blockers of A 2, ACE, Ca-channels, sympathetic adrenergic alpha blockers. Diet: Low Na, good Ca and Mg, low alcohol. Decrease body weight
Conditions that lead to atherosclerosis
Genetic, HTN, DM, High blood cholesterol, low exercise, smoking, turbulent flow, social stress, high levels of TNF-alpha and IL-1beta
How is atherosclerosis prevented?
Drugs: lower cholesterol, lower BP
Diet: low in sat fat and trans fat, small frequent meals, increased anti-oxidants, estrogen, niacin, aerobic exercise, strength training, lose weight, stop smoking
What leads to vessel obstruction (thrombus)?
Nick on vessel wall, atheroma (platelet aggregation over plaque), turbulent blood flow, slow blood flow, inappropriate clotting/ hypercoagulability
S/S of peripheral vessel obstruction
Decreased peripheral pulse strength, cool extremity, turbulence of flow, pallor when elevated, rubor/cyanosis when dependent, pain, paresthesia/paralysis, tissue necrosis
S/S of venous blockage
Increases CHP (edema, tenderness); Lack of fresh blood flowing into congested area (stasis ulcers, stasis dermatitis)
How is peripheral vessel obstruction diagnosed?
X-ray, ultrasonic doppler, temperature changes, MRI, volume changes
Tx of peripheral vessel obstruction
Get blood flowing through the area, surgery (angioplasty, endarterectomy, bypass grafting, laser surgery, mild exercise), prevent tissue trauma, prevent clots of emboli, lyse existing clots or emboli, reduce risk factors (cholesterol level, smoking, stress, sedentary lifestyle)
S/S of AV valve stenosis
Noisy when pushing blood through narrow valve to ventricle during ventricular filling (diastole).
X-ray/echocardiogram shows atrial hypertrophy.
Tall P wave when atrium is hypertrophied.
Forceful ejection of blood causes turbulent flow through the valve.
Congestion upstream.
S/S of tricuspid valve stenosis
Jugular venous distension; ascites; peripheral edema; may also see liver enlargement
S/S of mitral valve stenosis
pulmonary edema; heard as crackles and wheezes; dyspnea (esp. on exertion)
S/S of atrium insufficiency
Dilation of atrium, then hypertrophy of both atrium and ventricle; Blood moves easily but is turbulent as it flows back; X-ray and elecrocardiogram show hypertrophy of atrium and ventricle; ECG show increased P wave; Congestion upstream
S/S of aortic valve stenosis
Difficultly pushing blood from left ventricle through narrow valve into aorta during systole causes LV to hypertrophy; X-ray, ECG shows LV hypertrophy; Turbulent flow heard as systolic ejection murmur; Congestion upstream (pulmonary congestion)
S/S of aortic valve insufficiency
Great amount of blood forcefully ejected in systole; In diastole runs backward through insufficient valve into LV or forward through systemic arteries; X-ray; Echocardiogram shows LV dilation; hypertrophy; ECG shows hypertrophy of LV as large QRS wave; Forceful ejection = systolic ejection murmur; Regurgitation of blood returning to LV causes pandiastolic murmur; Congestion upstream; Decreased LV output
Tx for valve disorders
Prevent major antecedents (immediate antiobiotic tx of Strep infections and bacterial infection of heart; prophylactic use of antibiotic for persons with Hx of rheumatic heart disease when dental woek is done); Control HR to get max SV; Decreased blood volume to decrease pulmonary congestion; Surgical repair