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Cardiac System Dys
cardiovascular system dysfunction, NSG 2010 Adult Nsg I Exam #4
| Question | Answer |
|---|---|
| afterload | the amount of resistance to ejection of blood from the ventricle |
| apical impulse (also called point of maximum impulse [PMI] | impulse normally palpated at the 5th intercostal space, left midclavicular line; caused by contraction of the left ventricle |
| baroreceptors | nerve fibers located in the aortic arch and carotid arteries that are responsible for reflex control of the blood pressure |
| cardiac conduction system | specialized heart cells strategically located throughout the heart that are responsible for methodically generating and coordinating the transmission of electrical impulses to the myocardial cells |
| cardiac output | amount of blood pumped by each ventricle in liters per minute; normal cardiac output is 5 L per minute in the resting adult heart |
| contractility | ability of the cardiac muscle to shorten in response to an electrical impulse |
| depolarization | electrical activation of a cell caused by the influx of Na into the cell while K+ exits the cell and the muscle contracts |
| diastole | period of ventricular relaxation resulting in ventricular filling |
| ejection fraction | percentage of the end-diastolic blood volume ejected from the ventricle with each heartbeat |
| hypertension | blood pressure greater than 140/90 mm Hg |
| hypotension | a decrease in blood pressure to less than 100/60 mm Hg |
| international normalized ratio (INR) | a standard method for reporting prothrombin levels, eliminating the variation in test results from lab to lab |
| murmurs | sounds created by abnormal, turbulent flow of blood in the heart |
| myocardial ischemia | condition in which heart muscle cells receive less O2 than needed |
| myocardium | muscle layer of the heart responsible for the pumping action of the heart |
| normal heart sounds | sounds produced when the valves close; normal heart sounds are S1 (atrioventricular valves) and S2 (semilunar valves) |
| postural (orthostatic) hypotension | a significant drop in blood pressure (usu. 10 mm Hg systolic or more) after an upright posture is assumed |
| preload | degree of stretch of the cardiac muscle fibers at the end of diastole |
| pulmonary vascular resistance | resistance to RIGHT ventricle ejection of blood |
| repolarization | return of the cell to resting state, caused by reentry of K+ into the cell while Na exits the cell |
| sinoatrial (SA) node | primary pacemaker of the heart, located in the right atrium |
| stroke volume | amount of blood ejected from the ventricle per heartbeat; normal stroke volume is 70 mL in the resting heart |
| systemic vascular resistance | resistance to LEFT ventricle ejection |
| systole | period of vascular contraction resulting in ejection of blood from the ventricles into the pulmonary artery and aorta |
| telemetry | the process of continuous electrocardiographic monitoring by the transmission of radiowaves from a battery-operated transmitter worn by the pt |
| systole | contraction of the heart muscle, when the chambers of the heart become smaller as the blood is ejected |
| diastole | relaxation of the heart muscle, when the heart chambers fill with blood in preparation for subsequent ejection |
| endocardium | inner layer of the heart; endothelial tissue that lines the inside of the heart and valves |
| myocardium | middle layer of the heart; made up of muscle fibers and is responsible for the pumping action |
| epicardium | exterior layer of the heart |
| right side of the heart | distributes venous blood (deoxygentated blood) to the lungs via the pulmonary artery for oxygenation |
| right atrium | receives blood returning from the superior vena cava, inferior vena cava and coronary sinus |
| left side of the heart | distributes oxygenated blood to the remainder of the body via the aorta |
| left atrium | receives oxygenated blood from the pulmonary circulation via the pulmonary veins |
| atrioventricular valves | separate the atria from the ventricles and are the TRICUSPID valve and the MITRAL (OR BICUSPID) valve |
| tricuspid valve | separates the right atrium from the right ventricle |
| mitral valve | lies between the left atrium and the left ventricle |
| semilunar valves | the PULMONIC valve and the AORTIC valve |
| pulmonic valve | valve between the right ventricle and the pulmonary artery |
| aortic valve | valve between the left ventricle and the aorta |
| myocardial ischemia | caused by inadequate O2 supply when the HR accelerates |
| arteries | carry OXYGENATED blood AWAY from the heart. EXCEPTION: pulmonary arteries take unoxygenated blood to lungs for O2 |
| pulmonary artery | carries unoxygenated blood to the lungs |
| right coronary artery | perfuses the right atria and ventricle |
| left coronary artery | branches into 1. left anterior descending artery and the 2. circumflex artery |
| left anterior descending artery | perfuses the left ventricle and septum |
| If an MI affects your _________ artery, it is called a “widow maker” | left anterior descending |
| The most important portion of the heart is the | left ventricle |
| veins | carry UNOXYGENATED blood back from the body to the heart. EXCEPTION: pulmonary veins bring oxygenated blood back from the lungs |
| right atrium | receives blood from the body |
| right ventricle | pumps blood to the lungs |
| left atrium | receives blood from the lungs |
| left ventricle | pumps blood to the whole body |
| The first arteries off the Aorta are the | coronary arteries which supply the heart itself |
| Order of the electrical charge is | 1. SA node, 2. AV node, 3. bundle of His, 4. right & left bundle branches, and 5. Purkinje fibers |
| SA node | primary pacemaker of the heart. Initiates the electrical impulse (60-100) |
| AV node | collects the impulses from the atria and delays them while the ventricles fill (40-60) |
| The AV node is the “back up” and can beat between | 40-60 bpm |
| Purkinje fibers can still beat _____ bpm when everything else stops working | 30 |
| Effective (or absolute) refractory period | the cell is completely unresponsive to any electrical stimulus |
| If electrical stimulus is stronger than normal | the cells may depolarize too early |
| If cells depolarize too early | heart has premature contractions |
| Premature contractions can cause | life-threatening dysrythmias (V-tach, V-fib) |
| V-tach and V-fib can be caused by | electrolyte disturbances (hypokalemia, hypomagnesemia), hypoxia, acidosis, MI, HF, hypothermia |
| cardiac output | heart rate X stroke volume |
| stroke volume affected by what 3 factors? | preload, afterload, contractility |
| increased contractility results in | increased stroke volume |
| vasoconstriction causes increases afterload which will | reduce the stroke volume |
| What diagnostic test measures contractility? | echocardiogram |
| Normal ejection fraction is | 55% - 65% |
| Nonmodifiable Risk Factors | Family Hx of CAD; increasing age; male gender (although POSTmenopausal women have 2 to 3 x the CAD rates of PREmenopausal women of the same age); race (higher incidence in African Americans than Caucasians due to greater risk of HTN) |
| Modifiable Risk Factors | hyperlipidemia, HTN, cigarette smoking; exposure to tobacco smoke; DM; obesity; physical inactivity; gingivitis |
| Assessment of the Cardiac System | Head, neck, nails, skin; eyes for arcus senilus (gray ring around iris) caused by cholesterol deposits and xanthomas (yellow raised plaques around the eye lids resulting from lipid deposits) |
| Assessment of cardiac system | skin: look for central and peripheral cyanosis; blue areas esp. by joints. Look for blotching of skins. Check capillary refill (3 secs or less) and for clubbing. Note pitting edema in lower extremities, upper extremities and in sacral area. |
| How to assess for neck jugular vein distension | place pt in supine position, turn their head to look away from you, shine a light source at an angle and see if their jugular vein is distended |
| Amount of jugular vein distension reflects pressure and volume changes in the | right atrium |
| Systole | S1 “lub”; the AV valves (mitral and tricuspid) shutting |
| Diastole | S2 “dub”; the semi lunar valves (aortic and pulmonic) shutting |
| 4 abnormal heart sounds | murmur, rub, bruit, S3 gallop |
| Best place to heart apical pulse | 5th intercostal space medial to left midclavicular line |
| S3 gallop | left ventricle is overfilled leaving blood in the ventricle after causing the valves and supporting structures to vibrate. Heard right after S2. |
| S3 gallop best heard how? | with bell of steth and pt laying on L side. Commonly heard in HF pts. |
| S4 gallop | heard when ventricle is resistant to filling. Heard right before S1. Assoc w/ CAD, HTN or stenosis of the aortic valve. |
| Snaps and clicks heart sounds | if heard, usu means stenosis of mitral valve or aortic valve. Could also be from a mechanical valve |
| Murmurs | blowing or swooshing sounds made by turbulent blood flow in a large vessel or valve b/c the valve is not shutting fully |
| Main job of a heart valve is to | close and seal |
| Friction rub | pericardial friction rub makes a “to and fro” sound as though you are rubbing your palms together, or the sound of rough leather rubbing together. Caused by pericardial surface rubbing against the heart |
| Friction rub best heard how? | with diaphragm of steth and pt sitting up and leaning forward |
| Most common clinical manifestations of cardiac issues | chest pain (#1), dyspnea, peripheral edema and wt gain, fatigue, dizziness, syncope, changes in LOC (disorientation), palpitations |
| Testing to assess cardiac function and dx cardiovascular diseases | cardiac biomarkers, CK and CK-MB, myoglobin, Troponin T and I, lipid profile, brain (B-type_ natriuretic peptide, C-reactive protein, homocysteine |
| Brain (B-type) natriuretic peptide | known as BNP. A lab used to dx CHF |
| C-reactive protein | measures inflammatory responses |
| 2 types of cardiac stress testing | exercise stress testing (on a tread mill) and pharmacologic stress testing (giving pt a drug to increase HR if they can’t get on a tread mill) |
| Chest x-ray done to | rule out CHF and enlarged heart |
| Cardiac catheterization – Nursing interventions | make sure pt has signed consent form; check pt’s allergy to dye or iodine; tell pt the dye may induce a feeling of flushing when injected or in women urinary urgency; tell pt they will be on a hard surface (stainless steel table) for an hour or so; NPO fo |
| Post cardiac catheterization – Nursing interventions | If femoral artery used, keep the limb immobilized for 2-6 hrs. Do not bend hip or leg! Log roll pt from side to side to bed pan, meals, and position changes for comfort. Inspect site and distal pulses q15 min. x 2 hrs. Keep IV’s going and expect large |
| Discharge instructions for pt going home after cardiac cath | do not bend at the waist (to lift anything) for the next 24 hrs, strain, or lift heavy objects. Avoid tub baths, but shower is fine. Can’t drive for 72 hours! |
| Be sure to tell your pt before an echocardiogram | that it is painless. Test will take about 30-45 mins |
| Nursing interventions before pt has a stress test | NPO or light breakfast, no caffeine for 24 hrs, give meds – but hold beta blockers |
| Nursing interventions for pt pre-TEE (transesophageal echocardiography) | Pt must fast for 6 hrs before the study |
| Nursing interventions for pt post-TEE | make sure pt continues to fast until fully alert and make sure their gag reflex has returned b/c they numb their throat before procedure |
| Nursing interventions for pt pre-MRI | make sure pt has no pacemaker, metal plates, prosthetic joints, or other metallic implants. Make sure pt removes any jewelry, watches or other metal items. Also transderm patches with heat-conducting aluminized layer and telemetry patches must be remove |
| Atherosclerosis | the abnormal accumulation of lipid deposits and fibrous tissue within arterial walls and lumen |
| In coronary atherosclerosis, blockages and narrowing of the coronary vessels reduce | blood flow to the myocardium |
| What is the #1 cause of death in the U.S.? | cardiovascular disease for men and women of all racial and ethnic groups |
| CAD (coronary artery disease) | the most prevalent cardiovascular disease in adults |
| Acute coronary syndrome (ACS) | S/S that indicate unstable angina and MI |
| Angina pectoris | chest pain brought about by myocardial ischemia |
| Atheroma | fibrous cap composed of smooth muscle cells that forms over lipid deposits within arterial vessels and that protrudes into the lumen of the vessel, narrowing the lumen and obstructing blood flow; also called plaque |
| Creatine kinase (CK) | an enzyme found in human tissue; one of the three types of CK is specific to heart muscle and may be used as an indicator of heart muscle injury |
| High-density lipoprotein (HDL) | a protein-bound lipid that transports cholesterol to the liver for excretion in the bile; composed of a higher proportion of protein to lipid than low-density lipoprotein; exerts a beneficial effect on the arterial wall |
| Ischemia | insufficient tissue oxygenation |
| Low-density lipoprotein (LDL)-a protein-bound lipid that transports cholesterol to tissues in the body; composed of a lower proportion of protein to lipid than high-density lipoprotein; exerts a harmful effect on the arterial wall | |
| Metabolic syndrome | a cluster of metabolic abnormalities including insulin resistance, obesity, dyslipidemia, and HTN that increase the risk of cardiovascular disease |
| Myocardial infarction (MI) | death of heart tissue caused by lack of oxygenated blood flow; if acute, abbreviated as AMI |
| Stent | a woven mesh that provides structural support to a coronary vessel, preventing its closure |
| Sudden cardiac death | immediate cessation of effective heart activity |
| Thrombolytic | an agent or process that breaks down blood clots |
| Troponin | myocardial protein that regulates contractility; measurement is used to assess heart muscle injury |
| Most common symptom of myocardial ischemia is | chest pain, but not always. Some indivs may be asymptomatic or have atypical symptoms such as weakness, dyspnea and nausea. |
| Atypical symptoms of coronary atherosclerosis are more common in | women and in persons who are older and have a hx of HF or diabetes |
| Is ischemia reversible? | Yes |
| Is infarcted tissue reversible? | No |
| Angina can be caused by any condition that inhibits blood flow or increases O2 demand to the heart such as | cold, digestion, stress, HTN, smoking |
| Anginal pain varies from mild to severe and can be described as | tightness, choking, heavy sensation, “elephant sitting on my chest”, retrosternal pain that may radiate to neck, jaw, shoulders, back or arms (usually L arm). Anxiety frequently accompanies the pain. A feeling of impending doom. Other symptoms may occu |
| Stable angina | angina that subsides with rest or NTG (nitroglycerin) |
| Unstable angina | characterized by increased frequency and severity and is not relieved by rest and NTG. Requires medical intervention! |
| Treatment for angina | seeks to decrease myocardial O2 demand and increase O2 supply; medications; reduce and control risk factors. Reperfusion therapy may be done by stents, PTCA, CABG, angioplasty |
| Priority Nursing concern in treatment of anginal pain | controlling the pain! |
| Treatment of anginal pain | pt is to stop all activity and sit or rest in bed. Get new set of vitals, call telemetry, observe for respiratory distress and assess pain. Administer O2! Administer meds as ordered or by protocol, usually NTG (sublingual usually); use calm manner, tur |
| Tell pt that with NTG | they will get a headache |
| Pt teaching with angina | lifestyle changes and reduction of risk factors; teach to keep diary of anginal pain; teach regarding disease process; meds; stress reduction; when to go to the hospital and when not to go |
| Myocardial infarction | an area of the myocardium is permanently destroyed. Usually caused by reduced blood flow in a coronary artery due to rupture of an atherosclerotic plaque and subsequent occlusion of the artery by a thrombus. |
| S/S of MI | pain (may radiate, crushing), HTN or hypotension, SOB, N/V, cool, clammy, pale skin, anxiety, denial, fear of impending doom. Females may present with atypical symptoms. MD’s often misdiagnose as indigestion. Be aware! |
| Used to dx MI | presenting symptoms, EKG changes (look for ST elevations on an EKG strip), heart enzymes (troponin) |
| CK-MB | the only enzyme on a CK panel that is specific for heart muscle. Starts to increase a few hours after MI, peaks at 18 hrs, and returns to normal in 3 days |
| Normal CK-MB | 0-3 ng/ml |
| Troponin | levels starts to rise in 3-4 hrs, and peaks by 24 hrs, and elevated levels can still be seen weeks after the event. |
| Normal troponin level | < .4 ng/ml |
| Treatment of Acute MI | Obtain dx tests incl ECG w/I 10 mins of admission to the ED; O2; aspirin, NTG, morphine, beta-blcokers, ACE inhibitor within 24 hours; evaluate for percutaneous coronary intervention or thrombolytic therapy. As indicated heparin or LMWH, clopidogrel or t |
| NTG relieves pain by | dilating arteries; increases blood supply and therefore O2 |
| Complications of AMI | arrhythmias (major cause of death in the first hour), cardiogenic shock (prevented with tx of pain and IV fluid therapy), heart failure (pump failure, pulmonary edema, can be predicted by HBD levels, pulmonary embolism (result of arrhythmias and prolonged |
| Nursing management if your pt has an MI while they are on the floor | ABC’s (airway, breathing, circulation), O2, EKG, call MD, sl NTG, make sure they have a patent IV and telemetry (even if they don’t have an order for telemetry. Get order later!), and get them off your floor!!! |
| All of the valves have 3 leaflets except | the bicuspid valve (also called the mitral valve) |
| Mitral valve prolapse | part of the valve balloons back into the atrium causing blood to regurgitate from the left ventricle into the left atrium |
| Medical management of mitral valve prolapse | controlling symptoms (preventing smoking, caffeine, and ETOH). Sometimes anti-arrhythmic meds. Nursing imps: educate pt about it being hereditary and encourage relatives to check for it. Encourage frequent MD visits. Educate about need for prophylacti |
| Mitral regurgitation | blood flows back into left atrium from the left ventricle, due to valve not being able to close properly. Patho- tears, calcification, muscle not able to contract property |
| Mitral stenosis | obstruction of blood flowing from left atrium into left ventricle. Patho- this causes left atrium to increase more blood volume than it’s used to. Pulmonary circulation becomes backed up or congested. This causes the right ventricle to have to contract |
| Mitral stenosis | different s/s are hemoptysis, dry cough and repeated respiratory infections |
| Aortic regurgitation | flow of blood back into the left ventricle from the aorta. Patho-defect in the aortic valve prevents it form closing all the way, and the aorta pumps blood back into the left ventricle so that the ventricle is getting blood from there and the left atrium |
| Aortic regurgitation | different s/s are “bobbing head” or visible pulsations at temporal and carotid arteries, widened pulse pressure and Corrigan’s pule (a pulse that disappears) |
| Aortic stenosis | narrowing of the space between the left ventricle and the aorta. Patho- usually due to calcifications, adhesions, abnormality of leaflets |
| Aortic stenosis | different s/s: chest pain, vibration upon palpation (best to have pt sit up and lean forward to hear murmur and when palpating) |
| Advantages of mechanical valves | do not deteriorate or become infected as easily, but are thrombogenic and require life-long anticoagulation therapy |
| Tissue (biologic) valves | Xenograft (heterograft): pig or cow valve; homograft (allograft): human valve; autograft: patient’s own valve |
| Important patient teaching with valve disorders | educating pt on antibiotic prophylactic treatment. Teach families CPR. |
| Cardiomyopathy | acquired muscular disorders of the muscles of the heart. Primarily these involve enlargement of the chambers of the heart and put the pt at risk for cardiac decompensation or CHF. Patho: idiopathic, viral infections, metabolic, connective tissue and neu |
| Cardiomyopathy – S/Sx | early stages there may not be any, dyspnea on exertion and fatigue, coughing on exertion, edema, nausea, chest pain, syncope. Tachycardia, S3 and S4 sounds. May show up on CXR or Echo. Often in younger people the first S/Sx is sudden cardiac death |
| Medical Management of Cardiomyopathy | inotropic agents (make heart squeeze harder), NTG, diuretics, anticoagulants, treatment of arrhythmias, pacemaker, severe cases may need a heart transplant |
| Cardiomyopathy – Nursing Management | rest (avoidance of poorly tolerated activites and alternating activity with rest, avoid stress, abstain from alcohol, medication compliance esp once home |
| Rheumatic endocarditis | occurs most often in school-age children, after group A beta-hemolytic streptococcal pharyngitis. Many cases go undetected, then show up later in life. Spread by direct contact w/ oral or resp. secretions. Malnutrition, overcrowding and lower socioecon |
| Rheumatic endocarditis – Patho | injury to heart tissue is caused by inflammatory or sensitivity rx to the streptococci (not a true infection). Myocardial and pericardial tissue is also affected by endocarditis results in permanent changes in the valves. Weakens the myocardium and gets |
| Rheumatic endocarditis – S/Sx | fever, chills, sudden sore threat, sinusitis/otitis media, abd pain, positive strep test (throat culture), rash on extremities and torso, rapid, uncontrolled, jerky movements, newly developed heart murmur – this is a sign that the condition is worsening. |
| Endocarditis – Nursing Management | teach about need to promptly recognize and treat strep throat to prevent rheumatic fever. Teach about need to take prophylactic Abx before invasive procedures (including dentist) |
| Infective endocarditis | a microbial infection of the endothelial surface of the heart. Vegetative growths occurs and may embolize to tissues throughout the body. Usu. Develops in ppl w/ prosthetic heart valves or structural cardiac defects. Also occurs in pts who are IV drug |
| Infective endocarditis – S/Sx | fever, murmur (may get worse over time), clusters of petechia, sores on fingers or toes, hemorrhages in eyes and under fingernails, positive blood cultures |
| Infective endocarditis – Medical management | Abx tx, frequent blood cultures, surgery (debridement, valve replacement) |
| Infective endocarditis – Nursing management | monitor temp and heart sounds frequently (listen for murmurs). Assess all invasive lines meticulously. Teaching. |
| Pericarditis | inflammation of the pericardium (membrane sac surrounding the heart). Can be classified as adhesive or due to what kind of fluid is accumulating in the sac (serum, pus, blood, etc.) Patho – fluid build-up or adhesions increase pressure on the heart, rest |
| Pericarditis – S/Sx | Most characteristic symptom is chest pain when laying, turning, deep inspirations. May be asymptomatic. Creaky or scratchy sounding friction rub heard upon auscultation – louder at the end of exhalation, best heard when pt is sitting and leaning forward |
| Pericarditis – Medical Management | Tx of symptoms, find and treat the cause – may require a pericardiocentesis, or window |
| Pericarditis – Nursing Management | Teach pt pain may be relieved when forward leaning position, or sitting up. Treat pain. Reassure pt that they are not having MI. Activity restrictions. Monitor for HF. |
Created by:
mlewellen
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