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Cardiac final

Question	Answer
coronary sinus	delivers blood to the right atrium
tricuspid valve	separates the rt atrium from the rt ventricle during ventricular diastole
systole	contraction
systole contraction of the rt ventricle pushed blood	pulmonic valve, and propel blood into the pulmonary artery and the lungs
blood flows through the four pulmonary veins into the	left atrium
Lft atrium to	mitral valve to lft ventricle, diastole
Lft ventricle to	aortic valve to body
With systolic contraction, the left ventricle (LV) generates enough pressure to close the	mitral valve and open the aortic valve.
During ventricular diastole, these valves act as funnels and help move the flow of blood from the atria to the ventricles.	AV valves
During systole, the AV valves close to prevent	backflow (regurgitation) of blood into the atria.
The semilunar valves are the	pulmonic valve and the aortic valve that prevent blood from flowing back into the ventricles during diastole.
The pulmonic valve separates the right ventricle from the	pulmonary artery.
The aortic valve separates the left ventricle from the	aorta.
Coronary artery blood flow to the myocardium occurs primarily during	diastole, when coronary vascular resistance is minimized.
All of the coronary arteries feeding the left heart originate from the	left main coronary artery (LMCA).
The right coronary artery (RCA) branches from the	aorta to perfuse the right heart and inferior wall of the left heart.
The left main artery divides into two branches: the	left anterior descending (LAD) and the left circumflex coronary artery
It supplies blood to portions of the left ventricle, ventricular septum, chordae tendineae, papillary muscle, and, to a lesser extent, the right ventricle.	lft anterior descending artery
It supplies blood to the left atrium, the lateral and posterior surfaces of the left ventricle, and sometimes portions of the interventricular septum.	left circumflex coronary artery
The right coronary artery (RCA) originates from the right sinus of	Valsalva, encircles the heart, and descends toward the apex of the right ventricle.
The RCA supplies the	RA, RV, and inferior portion of the LV.
The electrophysiologic properties of heart muscle	regulating heart rate (HR) and rhythm.
Cardiac muscle cells possess the characteristics of	automaticity, excitability, conductivity, contractility, and refractoriness.
Myocardial contraction results from the release of large numbers of	calcium ions from the sarcoplasmic reticulum and from the blood. These ions diffuse into the myofibril sarcomere (the basic contractile unit of the myocardial cell).
Calcium ions promote the interaction of	actin and myosin protein filaments, causing these filaments to link and overlap.
Cardiac muscle relaxes when calcium ions are	pumped back into the sarcoplasmic reticulum, causing a decrease in the number of calcium ions around the myofibrils. This reduced number of ions causes the protein filaments to disengage, the sarcomere to lengthen, and the muscle to relax.
Cardiac Output	stroke volume x HR
Heart rate (HR) refers to the number of times the	ventricles contract each minute.
The normal resting HR for an adult is	60 and 100 beats/min.
The HR is extrinsically controlled by the	autonomic nervous system (ANS), which adjusts rapidly when necessary to regulate cardiac output.
The parasympathetic (vagus nerve) system	slows the HR
sympathetic stimulation (epinephrine and norepinephrine)	increases the heart rate and contractility
beta blockers, block	sympathetic (fight or flight) pattern by decreasing the HR.
Stroke volume (SV) is	the amount of blood ejected by the left ventricle during each contraction. Variables the effect stroke volume include
Preload refers to	the degree of myocardial fiber stretch at the end of diastole and just before contraction.
Preload is determined by	the amount of blood returning to the heart from both the venous system (right heart) and the pulmonary system (left heart) (left ventricular end-diastolic [LVED] volume).
Starling's law of the heart:	The more the heart is filled during diastole, the more forcefully it contracts.
Afterload, is	the pressure or resistance that the ventricles must overcome to eject blood through the semilunar valves and into the peripheral blood vessels.
Impedance, the peripheral component of afterload, is	the pressure that the heart must overcome to open the aortic valve.
The amount of impedance depends on	aortic compliance and total systemic vascular resistance, a combination of blood viscosity (thickness) and arteriolar constriction.
Myocardial contractility affects stroke volume and CO and is	the force of cardiac contraction independent of preload.
Contractility is increased by factors such as	sympathetic stimulation, calcium release, and positive inotropic drugs.
Contractililty is decreased by factors such as	hypoxia and acidemia.
The vascular system is divided into the	arterial system and the venous system.
In the arterial system, blood moves from the larger arteries to	arterioles, which meet the capillary bed.
In the venous system, blood travels from the capillaries to the
The exchange of nutrients across the capillary membrane occurs primarily by three processes:	osmosis, filtration, and diffusion.
BP is determined primarily by the	quantity of blood flow or cardiac output (CO), as well as by the resistance in the arterioles
Blood pressure	Cardiac output × Peripheral vascular resistance
chemoreceptors and baroreceptors	transmit signals to the sympathetic nervous system to control BP &HR via ANS
A change in blood flow is sensed by the kidney, they activate the	renin-angiotensin-aldosterone mechanism
The endocrine system stimulates the	sympathetic nervous system at the tissue level
Systolic BP is the amount of pressure/force generated by	the left ventricle to distribute blood into the aorta with each contraction of the heart. It is a measure of how effectively the heart pumps and is an indicator of vascular tone.
Diastolic BP is the amount of pressure/force against the	arterial walls during the relaxation phase of the heart.
Baroreceptors are in the	arch of the aorta and at the origin of the internal carotid arteries
Baroreceptors are stimulated when	the walls of BVare stretched by an increased BP.
Impulses from baroreceptors	inhibit the vasomotor center, which is located in the pons and the medulla. INHIBITION OF THIS CENTER RESULTS IN A DROP IN BP.
Peripheral chemoreceptors are located in the	carotid arteries and along the aortic arch
Chemoreceptors are sensitive primarily to	hypoxemia (a decrease in the partial pressure of arterial oxygen [PaO2]).
When stimulated, these chemoreceptors send impulses along the	vagus nerves to activate a VASOCONSTRICTOR RESPONSE AND RAISE BP.
The central chemoreceptors in the respiratory center of the brain are also stimulated by	hypercapnia (an increase in partial pressure of arterial carbon dioxide [PaCO2]) and ACIDOSIS.
Stretch receptors in the vena cava and the right atrium are sensitive to	pressure or volume changes.
When a patient is hypovolemic, stretch receptors in the blood vessels	stimulates the sympathetic nervous system to increase the heart rate (HR) and constrict the peripheral blood vessels.
When renal blood flow or pressure decreases, the kidneys retain	sodium and water. BP tends to rise because of fluid retention and activation of the renin-angiotensin-aldosterone mechanism
The renin-angiotensin-aldosterone mechanism results in	vasoconstriction and sodium retention (and thus fluid retention).
Vascular volume is also regulated by	antidiuretic hormone (vasopressin) from the posterior pituitary gland
In hyperthermia, the metabolic requirement of the tissues is	greater and BP and pulse rate rise
Veins have the ability to accommodate large	shifts in volume with minimal changes in venous pressure. This flexibility allows the venous system to accommodate the administration of IV fluids and blood transfusions, as well as to maintain pressure during blood loss and dehydration.
The force that pushes the blood forward in the veins is	skeletal muscle in the extremities. The superior and inferior vena cava are also valveless, which allows unimpeded blood flow return to the heart.
Age, gender, ethnic background, and family history of CVD are	nonmodifiable (uncontrollable) risk factors for CVD.
Modifiable (controllable) risk factors are	personal habits, including cigarette use, physical inactivity, obesity, and psychological variables. Ask the patient about each of these common modifiable risk factors.
Orthostatic (postural) and postprandial changes occur because of	ineffective baroreceptors.
Some patients, especially women, do not experience pain in the chest but instead feel discomfort or indigestion. Women often present with a “triad” of symptoms	indigestion or feeling of abdominal fullness, feelings of chronic fatigue despite adequate rest and feelings of “inability to catch one's breath”
The patient may also describe the sensation as (women’s heart attach signs)	aching, choking, strangling, tingling, squeezing, constricting, or viselike. Others with severe neuropathy may experience few or no traditional symptoms except shortness of breath, despite major ischemia.
The patient with advanced heart disease may experience orthopnea	dyspnea that appears when he or she lies flat
Paroxysmal nocturnal dyspnea (PND) develops after the patient has been	lying down for several hours.
Laying down, blood from the lower extremities is redistributed to the venous system, which	increases venous return to the heart. A diseased heart cannot compensate. Pulmonary congestion results.
A sudden weight increase of 2.2 pounds (1 kg) can result from excess fluid (1 L) in the interstitial spaces. Weight gain is the best indicator of	fluid retention.
Syncope refers to a	brief loss of consciousness. The most common cause is decreased perfusion to the brain.
Extremity pain may be caused by two conditions:	ischemia from atherosclerosis and venous insufficiency of the peripheral blood vessels
The New York Heart Association's Functional Classification	four classifications (I, II, III, and IV) depend on the degree to which ordinary physical activities (routine ADLs) are affected by heart disease.
Late signs of severe right-sided heart failure are	ascites, jaundice, and anasarca (generalized edema) as a result of prolonged congestion of the liver.
Pallor is characteristic of	anemia and can be seen in areas such as the nail beds, palms, and conjunctival mucous membranes in any patient.
Central cyanosis involves decreased oxygenation of the arterial blood in the lungs and appears as a	bluish tinge of the conjunctivae and the mucous membranes of the mouth and tongue or darkened discoloration of the nail beds, earlobes, lips, and toes.
Peripheral cyanosis occurs when blood flow to the peripheral vessels is decreased by peripheral vasoconstriction. Constriction results from a	low cardiac output or an increased extraction of oxygen from the peripheral tissues.
Rubor (dusky redness) that replaces pallor in a dependent foot suggests	arterial insufficiency.
Vascular changes in an affected extremity may include	paresthesia, muscle fatigue and discomfort, numbness, pain, coolness, and loss of hair distribution from a reduced blood supply. Poss clubbing
Clubbing is common in patients with	advanced chronic pulmonary disease, congenital heart defects, and cor pulmonale.
HTN BP	>140/90
Pre-HTN	120-139/80-89
Postural HTN is defined as a decrease of more than	20 mm Hg of the systolic pressure or more than 10 mm Hg of the diastolic pressure, as well as a 10% to 20% increase in heart rate.
The difference between the systolic and diastolic values is referred to as	pulse pressure.
Narrowed pulse pressure is rarely normal and results from	increased peripheral vascular resistance or decreased stroke volume in patients with heart failure, hypovolemia, or shock. It can also be seen in those with mitral stenosis or regurgitation.
An increased pulse pressure may occur in patients with	slow heart rates, aortic regurgitation, atherosclerosis, hypertension, and aging.
Normal values for the ABI are	1.00 or higher because BP in the legs is usually higher than BP in the arms.
ABI values less than 0.80 usually indicate moderate	vascular disease, whereas values less than 0.50 indicate severe vascular compromise.
A hypokinetic pulse is a weak pulse indicative of a narrow pulse pressure. It is seen in patients with	hypovolemia, aortic stenosis, and decreased cardiac output.
A hyperkinetic pulse is a large, “bounding” pulse caused by an increased ejection of blood. It occurs in patients with a	high cardiac output (with exercise, sepsis, or thyrotoxicosis) and in those with increased sympathetic system activity (with pain, fever, or anxiety).
Bruits are swishing sounds that may occur from	turbulent blood flow in narrowed or atherosclerotic arteries.
The order of cardiac assessment is	inspection, palpation, percussion, and auscultation
Movement over the aortic, pulmonic, and tricuspid areas is	abnormal.
Pulses in the mitral area (the apex of the heart) are considered normal and are referred to as the	apical impulse, or the point of maximal impulse (PMI).
The PMI should be located at the	left fifth intercostal space (ICS) in the midclavicular line.
S1 marks the beginning of	ventricular systole and occurs right after the QRS complex on the electrocardiogram (ECG).
The second heart sound (S2) is caused mainly by the	closing of the aortic and pulmonic valves
S2 is heard best at the	base of the heart at the end of ventricular systole.
Splitting of S1 and S2 can be accentuated by	inspiration (increased venous return), and it narrows during expiration.
The third heart sound (S3) is produced during the	rapid passive filling phase of ventricular diastole when blood flows from the atrium to a noncompliant ventricle.
The fourth heart sound (S4) occurs as	blood enters the ventricles during the active filling phase at the end of ventricular diastole.
S3 is called a	ventricular gallop
S4 is referred to as	atrial gallop.
An S3 heart sound is most likely to be a	normal finding in children or those younger than 30 years of age.
An S3 gallop in patients older than 35 years is considered	abnormal and represents a decrease in left ventricular compliance. It can be detected as an early sign of heart failure or as a ventricular septal defect.
An atrial gallop (S4) may be heard in patients with	HTN, anemia, ventricular hypertrophy, MI, aortic or pulmonic stenosis, and pulmonary emboli. It may be heard also with advancing age because of a stiffened ventricle.
The presence of both S3 and S4, called a	summation or a quadruple gallop,
summation or a quadruple gallop, is an indication of	severe heart failure, horse galloping.
Murmurs reflect	turbulent blood flow through normal or abnormal valves.
serum studies are commonly referred to as cardiac markers and include	troponin, creatine kinase–MB, and myoglobin.
Grading of Heart Murmurs	1-6
Total lipids	400-1000 mg/dL
CK MB	>1
Cholesterol	122-200 mg/dL
Older adult cholesterol	Older adult (> 70 yr): 144-280 mg/dL
Triglycerides	Females: 35-135 mg/dL, Males: 40-160 mg/dL, Older adult (>65 yr): 55-260 mg/dL
HDL’s	>40
LDLs	60-180 mg/dL, Older adult (>65 yr): 92-221 mg/dL
C-reactive proteins	<1.0 mg/dL higher levels indicate MI or tissue damage
Cardiac troponin T	<0.20 ng/mL higher levels indicate MI or tissue damage
Cardiac troponin I	<.03
Myoglobin	<90 mcg/L elevated indicate MI
Creatine kinase (CK) is an enzyme specific to cells of the	brain, myocardium, and skeletal muscle. They are not present in CBC unless an MI occurred
CK-MB activity is most specific for	MI and shows a predictable rise and fall during 3 days; a peak level occurs about 24 hours after the onset of chest pain.
Myoglobin, a low-molecular-weight heme protein found in cardiac and skeletal muscle, is the	earliest marker detected—as early as 2 hours after an MI with rapid decline after 7 hours
Desired level for total cholesterol	less than 200 mg/dL
Desired level for triglyceride	less than 150 mg/dL
Desired level for HDL	more than 40 mg/dL (“good” cholesterol)
Desired level for LDL	less than 100 mg/dL in patients with moderate risk factors
Desired LDL in high-risk cardiovascular patients	less than 70 mg/dL
Homocysteine is an	amino acid that is produced when proteins break down. A level less than 14 mmol/dL is considered optimal
Microalbuminuria, has been shown to be a clear marker of widespread	endothelial dysfunction in cardiovascular disease (along with elevated CRP) and renal disease
INR is the most reliable way to monitor anticoagulant status in	warfarin therapy
Normal INR levels	<20
Normal PT	11-13
PTT is assessed in patients who are receiving	heparin
The cardiac effects of hypokalemia are	increased electrical instability, ventricular dysrhythmias, and an increased risk of digitalis toxicity.
The effects of hyperkalemia on the myocardium include	slowed ventricular conduction, peaked T waves on the ECG, and contraction followed by asystole (cardiac standstill).
Cardiac manifestations of hypocalcemia are	ventricular dysrhythmias, a prolonged QT interval, and cardiac arrest.
Hypercalcemia (on the heart) shortens the	QT interval and causes AV block, digitalis hypersensitivity, and cardiac arrest.
Serum sodium values reflect fluid balance and may be	decreased, indicating a fluid excess in patients with heart failure (dilutional hyponatremia).
Indications for Cardiac Catheterization	to detect disease process, therapeutic determination or evaluation of prev medical treatment
Hypomagnesemia has been implicated in some forms of ventricular dysrhythmias known as	torsades de pointes. Ventricular tachycardia
Hypomagnesemia prolongs the	QT interval, causing this specific type of ventricular tachycardia.
The erythrocyte [RBC]count is usually ________________ in heart diseases	increased, characterized by inadequate tissue oxygenation.
Hypovolemic shock and excessive diuresis results in ___________ hematocrit count	increased
WBC is typically ___________ after an MI	elevated and it is a strong indication of stroke & heart disease
Diagnostic tests for heart disease	X-rays, angiography, arteriography,
This is an invasive diagnostic procedure that involves fluoroscopy and the use of contrast media	arteiography. This procedure is performed when an arterial obstruction, narrowing, or aneurysm is suspected.
Complications of right sided catherization	Thrombophlebitis, Pulmonary embolism, Vagal response, Cardiac tamponade, Hypovolemia, Pulmonary edema, pulm edema, reaction & hemotm
Complications for lft sided catherization AND CORONARY ARTERIOGRAPHY	MI, stroke, arterial bleeding or thromboembolism, dysrhythmia
The most definitive but most invasive test in the diagnosis of heart disease is	cardiac catheterization.
For heart cath, standard preoperative tests are performed, which usually include a	chest x-ray, complete blood count, coagulation studies, and 12-lead ECG.
If the patient normally takes a digitalis preparation or diuretic, it is usually	withheld before the catheterization.
before and after the procedure, analysis of	electrolytes, blood urea nitrogen (BUN), creatinine, coagulation profile, and CBC is essential, and abnormalities are discussed with the physician.
After surgery, report any reports of	pain and discomfort at the insertion site, chest pain, nausea, or feelings of light-headedness.
The patient recovers in a specialty area where monitored beds are located. Because the contrast medium acts as an osmotic diuretic, monitor	urine output and ensure that the patient receives sufficient oral and IV fluids for adequate excretion of the medium.
If the patient experiences symptoms of cardiac ischemia such as chest pain, dysrhythmias, bleeding, hematoma formation, or a dramatic change in peripheral pulses in the affected extremity, contact	the Rapid Response Team or physician immediately to provide prompt intervention!
Neurologic changes, such as	visual disturbances, slurred speech, swallowing difficulties, and extremity weakness, should also be reported immediately.
The exercise electrocardiography test helps determine the	functional capacity of the heart and screens for asymptomatic coronary artery disease. Dysrhythmias that develop during exercise may be identified, and the effectiveness of antidysrhythmic drugs can be evaluated.
As a noninvasive, risk-free test,	echocardiography is easily performed at the bedside or on an ambulatory care basis.
Echocardiography uses	ultrasound waves to assess cardiac structure and mobility, particularly of the valves. It helps assess and diagnose cardiomyopathy, valvular disorders, pericardial effusion, left ventricular function, ventricular aneurysms, and cardiac tumors.
Transesophageal echocardiography (TEE) examines cardiac structure and function with an ultrasound transducer placed immediately behind the heart in the	esophagus or stomach. views of posterior cardiac structures such as the left atrium, mitral valve, and aortic arch.
The use of radionuclide techniques in cardiovascular assessment is called	myocardial nuclear perfusion imaging (MNPI). These studies are useful for detecting myocardial infarction (MI) and decreased myocardial blood flow and for evaluating left ventricular ejection
Positron emission tomography (PET) scans are used to	compare cardiac perfusion and metabolic function and differentiate normal from diseased myocardium
An image of the heart or great vessels is produced through the interaction of magnetic fields, radio waves, and atomic nuclei showing hydrogen density	MRI
This test helps determine whether calcifications are present in the arteries; calcifications are a common component of arterial plaque	EBCT
Specialized cardiac muscle cells possess unique properties:	automaticity, excitability, conductivity, and contractility.
The electrophysiologic properties of cardiac cells regulate	heart rate and rhythm.
____________ is the ability of cardiac cells to generate an electrical impulse spontaneously and repetitively.	Automaticity (the pacing mechanism)
_____________ is the ability of non-pacemaker heart cells to respond to an electrical impulse generated from pacemaker cells and to depolarize.	Excitability
_______________ is the ability to transmit an electrical stimulus from cell membrane to cell membrane. As a result, excitable cells depolarize in rapid succession from cell to cell until all cells have depolarized.	Conductivity . The wave of depolarization causes the deflections of the electrocardiogram (ECG) waveforms that are recognized as the P wave and the QRS complex.
_________________ is the ability of atrial and ventricular muscle cells to shorten their fiber length in response to electrical stimulation, generating sufficient pressure to propel blood forward. Contractility is the mechanical activity of the heart.	Contractility
It is responsible for the generation and conduction of electrical impulses that cause atrial and ventricular depolarization	The cardiac conduction system
The conduction system consists of the	sinoatrial node, atrioventricular junctional area, and bundle branch system.
Hearts primary pacemaker	SA node
The SA Node generates between	60 to 100 beats per minute and therefore has the greatest degree of automaticity.
P wave on the ECG	atrial depolarization
This delay is reflected in the PR segment on the ECG	impulses from the T-cells slow down or speed up contractions of the AV node. Allows the ventricles to fill
At the ends of both the right and the left bundle branch systems are the	Purkinje fibers.
Purkinje cells make up the	bundle of His, bundle branches, and terminal Purkinje fibers
These cells are responsible for the rapid conduction of electrical impulses throughout the ventricles, leading to ventricular depolarization and the subsequent ventricular muscle contraction	Purkinje cels
The P wave is a deflection representing	atrial depolarization
Change in the shape of a P wave can indicate	alternate tissue firing
It represents the time required for atrial depolarization as well as the impulse delay in the AV node and the travel time to the Purkinje fibers	PR interval
PR interval time	.12-.20 seconds
The QRS complex represents	ventricular depolarization.
The QRS duration represents the time required for	depolarization of both ventricles
QRS duration time	.04-.10 secs
The ST segment is normally an isoelectric line and represents	early ventricular repolarization. It occurs from the J point to the beginning of the T wave. Its length varies with changes in the heart rate, the administration of medications, and electrolyte disturbances.
The T wave follows the ST segment and represents	ventricular repolarization
The U wave represents	late ventricular repolarization
The QT interval represents the total time required for	ventricular depolarization and repolarization.
NORMAL RHYTHMS	Rate: Atrial and ventricular rates of 60 to 100 beats/min, reg rhythms, P waves -present, PR interval .12-.20, QRS duration .04-.10
Premature complexes are	early rhythm complexes
Sympathetic nervous system stimulation or vagal inhibition results in an	increased rate of SA node discharge, which increases the heart rate.
When the rate of SA node discharge is more than 100 beats per minute, the rhythm is called	sinus tachycardia
Increased sympathetic stimulation is a normal response to physical activity but may also be caused by	anxiety, pain, stress, fear, fever, anemia, hypoxemia, hyperthyroidism, and pulmonary embolism.
In some cases, sinus tachycardia is a compensatory response to decreased cardiac output or blood pressure, as occurs in	hypovolemic shock, myocardial infarction (MI), infection, and heart failure.
Procainamide	antiarrhythmic • Decreases myocardial excitability, diarrhea, N/V
Normal HR	60-100 bpm
In pulsus alternans,	a weak pulse alternates with a strong pulse despite a regular heart rhythm
Hepatojugular reflux is the distension of the neck veins precipitated by the maneuver of	firm pressure over the liver.
Hepatojugular refux is seen in	tricuspid regurgitation, heart failure due to other non-valvular causes, and other conditions including constrictive pericarditis, cardia tamponade, and inferior vena cava obstruction.
BNP is produced and released by the	ventricles when the patient has fluid overload as a result of HF
Significance of BNP in a CBC	proof of HF
high homocysteine levels from	eating red meat, hypertension, elevated low-density lipoprotein and depressed high-density lipoprotein levels, and diabetes mellitus RISK factor for metabolic syndrome
Hypertension is a systolic blood pressure at or above	140 mm Hg and/or a diastolic blood pressure at or above 90 mm Hg in people who do not have diabetes mellitus.
Patients with diabetes and heart disease should have a blood pressure below	130/90
Four control systems play a major role in maintaining blood pressure:	the arterial baroreceptor system, regulation of body fluid volume, the renin-angiotensin/aldosterone system, and vascular autoregulation.
Malignant hypertension is a severe type of elevated blood pressure that	rapidly progresses.
SS of malignant hypertension	morning HA, blurred vision, dyspnea and/or symptoms of uremia (accumulation in the blood of substances ordinarily eliminated in the urine)
Malignant HTN BP	>200 systolic >150 diastolic
Essential (primary) HTN	No known cause• Associated risk factors:•Family history of hypertension•High sodium intake•Excessive calorie consumption•Physical inactivity•Excessive alcohol intake•Low potassium intake
SECONDARY HTN	Renal vascular and renal parenchymal disease, Primary aldosteronism• Cushing's disease• Lipidemia• Brain tumors• Encephalitis• Psychiatric disturbances• Pregnancy, smoking, obesity
Drugs associated with secondary HTN	estrogen, •Glucocorticoids •Mineralocorticoids •Sympathomimetics
Diuretics	Thiazides- prototype: hydrochlorothiazide, Loop diuretics- prototype: furosemide, Potassium sparing diuretics- prototype: spironolactone
Thiazide: hydrochlorothiazide	for use in mild to moderate HTN. Increases excretion of sodium and water by inhibiting sodium reabsorption in the distal tubule. SE: hypokalemia
Loop diuretics	furosemide (Lasix), • Diuresis and subsequent mobilization of excess fluid (edema, pleural effusions)SE: fluid imbalances.
Potassium sparing diuretics	spironolactone (Aldactone). Causes loss of sodium bicarbonate and calcium while saving potassium and hydrogen ions by antagonizing aldosterone. For sever HTN. Weak diuretic. SE:hyperkalemia, Na loss
Calcium Channel Blockers:	diltiazem, amlodipine, nacardipine, nifedipine
Calcium Channel blockers action:	increase myocardial oxygen supply, therefore lowering the heart rate. Calcium channel blockers cause the coronary arteries to dilate (NO CALCIUM
ACE Inhibitors:	enalapril, enalaprilat, captopril, fosinopril, moexopril, ramipril, trandolapril
Angiotensin-converting enzyme (ACE) inhibitors action:	block conversion of angiotensin I to the vasoconstrictor angiotensin II. ACE inhibitors also prevents degradation of bradykinin & other vasodilatory prostaglandins. ACE inhibitors also ↑ plasma renin levels. Net result -systemic vasodilation (enalapril)
Nitrates:	Nitroglycerin, amyl nitrite, isosorbide dinitrate
Nitrates action:	^ coronary blood flow by dilating cor.arteries & improving flow to ischemic regions, Produces vasodilation Decreases left ventricular end-diastolic pressure and left ventricular end-diastolic volume (preload); Reduces myocardial oxygen consumption
Beta Blockers	atenolol, carvedilol, metoprolol tartrate, propranolol
Beta blockers action:	Blocks stimulation of beta1(myocardial)-adrenergic receptors. Does not usually affect beta2(pulmonary, vascular, uterine)-receptor sites ( atenolol)
Cardiac glycosides:	digoxin
Cardiac glycosides Action	Increases the force of myocardial contraction; Prolongs refractory period of the AV node; Decreases conduction through the SA and AV nodes
Centrally acting antiadrenergics:	guanfacine, methyldopa
Centrally acting antiadrenergics action	Stimulates CNS alpha2-adrenergic receptors, producing a decrease in sympathetic outflow to heart, kidneys, and blood vessels. Result is decreased blood pressure and peripheral resistance, decrease in heart rate, & no change in cardiac output. (methyldopa)
Loup diuretics:	furosemide, bumetanide, torsemide
Loup diuretics Action	Inhibits the reabsorption of Na & Cl from the loop of Henle and distal renal tubule; Increases renal excretion of H2O, Na, Cl, Mg, K & Ca; Effectiveness persists in impaired renal function ( furosemide/ lasix)
Thizide & thiazide like diuretics:	Hydrochlorothiazide, chlorothiazide, methyclothiazide
Thizide & thiazide like diuretics Action	Increases excretion of Na & H2O by inhibiting Na reabsorption in the distal tubule; Promotes excretion of Cl, K, H, Mg, Ph, Ca, HCO3. ( Hydrochlorothiazide)
Vasodilators:	diazoxide, epoprostenol, fenoldopam, hydrALAZINE, hydralazine/isosorbide dinitrate, minoxidil (systemic), nitroprusside, papaverine
Vasodilator action	Directly relaxes vascular smooth muscle in peripheral arterioles. Produces ↓ in BP, reflex tachycardia and increased cardiac output; Inhibits insulin release from the pancreas and decreases peripheral utilization of glucose
lipid-lowering agents/ hmg coa reductase inhibitors/ statin:	atorvastatin, cerivastatin, fluvastatin, lovastatin, pitavastatin, pravastatin, rosuvastatin, simvastatin
lipid-lowering agents/ hmg coa reductase inhibitors/ statin action:	Inhibits 3-hydroxy-3-methylglutaryl-coenzyme A (HMG-CoA) reductase, an enzyme which is responsible for catalyzing an early step in the synthesis of cholesterol (lovastatin)
PR interval	0.12-0.20 sec (up to 5 small blocks) (represents the time required for atrial depolarization)
P wave
PR segment	segment from end of p wave to beginning of QRS complex. Electrical impulse is traveling through AV node.
QRS complex	0.04- 0.10 (up to 3 small blocks) ventricle depolarization. From beginning of qrs to the J point.
ST segment	from j point to beginning of t-wave. Represents early ventricular repolarization.
T wave represents	ventricular repolarization
U wave represents	late repolarization.
QT interval represents	the total time required for depolarization and repolarization.
calcium channel blockers Indications	Hypertension; Angina ; SVT & rapid ventricular rates in a-flutter or a-fibrillation (ex.diltiazem, amlodipine)
thiazide diuretics Indications	Management of mild to moderate hypertension; Treatment of edema associated with Congestive heart failure; Renal dysfunction; Cirrhosis; Glucocorticoid therapy; Estrogen therapy (ex. Hydrochlorothiazide)
Nitrates Indications	Indications management of angina pectoris; treatment of CHF; treatment of acute MI; Treatment of CHF associated with acute MI (ex. Nitroglycerin)
hmg coa reductase inhibitors (statin) Indications	Primary prevention of CAD in asymptomatic pts. with increased total & (LDL) cholesterol and decreased (HDL) cholesterol; Slows the progression of coronary atherosclerosis (ex. lovastatin)
ace inhibitors Indications	management of hypertension; Management of symptomatic heart failure; Slowed progression of asymptomatic left ventricular dysfunction to overt heart failure (ex. enalapril)
loop diuretics Indications	Edema due to heart failure; Hypertension; hepatic impairment or renal disease (ex.furosemide/Lasix)
beta blockers Indications	Management of hypertension; Management of angina pectoris; Prevention of MI (ex. atenolol)
centrally acting antiadrenergics Indications	Management of moderate to severe hypertension (with other agents) (ex. methyldopa)
Coronary arteries	Right main; Left main; Left anterior descending (LAD); circumflex
Total lipids	400-1000
LDL	60-80 ----geri 92-221
HDL	>40 increased with geri patients
Triglycerides Male	40-160
Triglycerides Female	35-135
Triglycerides Geri	55-260
Cholesterol	122-200----geri 144-280
HDL/ LDL ratio	3:1
angiotensin ii receptor antagonists Indications	Hypertension (alone or with other agents) (EX. olmesartan)
angiotensin ii receptor antagonists Action	Blocks vasoconstrictor and aldosterone-secreting effects of angiotensin II at various receptor sites including vascular smooth muscle and the adrenal glands (EX. olmesartan)
angiotensin ii receptor antagonists	olmesartan, candesartan, eprosartan, irbesartan, losartan, telmisartan, valsartan
Potassium Sparing Diuretics:	spironolactone, triamterene
potassium sparing diuretics Indications	Management of primary hyperaldosteronism; Management of edema associated with CHF, cirrhosis and nephrotic syndrome; Management of essential hypertension; Treatment of hypokalemia (ex. spironolactone,)
Potassium Sparing Diuretics Action	Causes loss of sodium bicarbonate and calcium while saving potassium and hydrogen ions by antagonizing aldosterone (spironolactone,)

Created by: Jillzs

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