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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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