Term
| What condition gives a 4th heart sound (end of atrial emptying after atrial contraction) |
|
Definition
| hypertrophic congestive heart failure, massive pulmonary embolism, tricuspid incompetence, or cor pulmonale. |
|
|
Term
| isovolumic phase of ventricular systole |
|
Definition
| the interval between the closing of the AV valves and the opening of the semilunar valves (aortic and pulmonary valves). |
|
|
Term
|
Definition
| due to the closing AV valves and associated blood turbulence. |
|
|
Term
| When do The semilunar (aortic and pulmonary) valves open? |
|
Definition
| at the beginning of this phase of ventricular systole. |
|
|
Term
|
Definition
| due to ventricular repolarization. The end of the T wave marks the end of ventricular systole electrically. |
|
|
Term
| The second heart sound (S2, "dup") occurs when? |
|
Definition
| The semilunar (aortic and pulmonary) valves close. S2 is normally split because the aortic valve closes slightly earlier than the pulmonary valve. |
|
|
Term
| A third heart sound (S3) is usually abnormal and is due to? |
|
Definition
| rapid passive ventricular filling. It occurs in dilated congestive heart failure, severe hypertension, myocardial infarction, or mitral incompetence. |
|
|
Term
| Ischemic heart disease is caused by |
|
Definition
| an imbalance between the myocardial blood flow and the metabolic demand of the myocardium. |
|
|
Term
| ACE Inhibitors (Angiotensin-Converting Enzyme) Inhibitors are drugs used to |
|
Definition
| treat high blood pressure and heart failure and may be prescribed after a heart attack.stop the body’s ability to produce angiotensin II. Angiotensin II is a natural substance that causes blood vessels to tighten (contract) when it binds with receptors on smooth muscle cells of an artery. |
|
|
Term
| ACE inhibitors allow arteries to |
|
Definition
| relax and expand (dilate), allowing blood to flow more easily. The dilation of the arteries decreases blood pressure, which decreases the workload of the heart. Dilation of the arteries also increases the supply of blood and |
|
|
Term
|
Definition
| pain, pressure, tightness and heaviness,may involve the chest, arms, neck, jaw and even the upper abdomen. sweating and shortness of breath may be associated with angina |
|
|
Term
|
Definition
| located between the left ventricle (pumping chamber) of the heart and the aorta, |
|
|
Term
|
Definition
| opens as oxygen-rich blood is pumped out of the left ventricle, and closes as the left ventricle fills with blood. This prevents the blood from flowing back into the heart as the left ventricle fills. |
|
|
Term
|
Definition
| aortic valve is deformed and narrowed. caused by valve leaflets that are thickened and fused. |
|
|
Term
|
Definition
| blood cannot flow easily into the aorta and pressure builds in the left ventricle. |
|
|
Term
|
Definition
| the heart beats too fast due to abnormal, extra electrical pathways between the heart’s upper and lower chambers. |
|
|
Term
|
Definition
| the heart is “strangled” by a buildup of fluid within the sac (the pericardium) that surrounds the heart |
|
|
Term
|
Definition
| the pressure caused by the fluid in the pericardial sac gets too high, it restricts the heart from filling up during its relaxation phase of the pumping cycle. When this happens, the heart is not an effective pump. |
|
|
Term
|
Definition
| one or more of the chambers of the heart enlarge, or dilate. |
|
|
Term
| Causes of dilated Cardiac mypoathy |
|
Definition
| coronary artery disease, valvular heart disease, metabolic diseases of the heart, infections and in some cases the cause is not determined. |
|
|
Term
| Hypertrpohic cardiomyopathy |
|
Definition
| heart muscle in which the wall of the heart, particularly the muscular pumping chambers, become abnormally thick |
|
|
Term
|
Definition
| the arteries that supply blood to your heart muscle become narrowed or blocked by fatty deposits called atherosclerotic plaque. |
|
|
Term
|
Definition
| sudden, temporary contraction of muscle fibers within the walls of the coronary artery. |
|
|
Term
|
Definition
| the percentage of blood that is pumped out with each heartbeat |
|
|
Term
| normal ejection fraction in a person at rest |
|
Definition
| between 55 and 70 percent. |
|
|
Term
|
Definition
| heart that cannot pump blood effectively enough to meet the demand of the body for oxygen and nutrition |
|
|
Term
|
Definition
| located between the left atrium and left ventricle of the heart |
|
|
Term
|
Definition
| The mitral valve The other AV valve is the tricuspid valve. |
|
|
Term
| valve does not close properly and some blood flows back into the left atrium; this is termed “regurgitation”. Small amounts of regurgitation are common |
|
Definition
|
|
Term
| fluid builds up in the pleural cavity around the lungs. |
|
Definition
|
|
Term
| abnormal blood flow from L heart to R, can cause pulmonary hypertension, increase right side pressures |
|
Definition
| R to L shift (atrial septal defects, ven septal defects) |
|
|
Term
| unoxygenated blood flows from R side of heart to L into arterial system |
|
Definition
| R to L shunt (tetralogy of fallot, transposition of great arteries |
|
|
Term
| Alteration in normal H rate/rhythm or distrubance of impulse contraction |
|
Definition
|
|
Term
|
Definition
|
|
Term
| Mechanisms of arrhythmias |
|
Definition
Altered automaticity
ectopic beats/electrical instability
spontaneous depol by a cell in the heart, re-entry or conduction blocks |
|
|
Term
| Impaired filling,(no preload to pump, so no O2), poor ejection (extra volume in heart), decreased CO, increased workload |
|
Definition
|
|
Term
| Types of conduction blocks |
|
Definition
|
|
Term
| Increased automaticity of sinus node |
|
Definition
|
|
Term
| Propagoator impulse fails to die out and persists to re-excite the heart after the refractory period has ended |
|
Definition
|
|
Term
| A-fib, a-flutter, WPW, extranodal bypass, v-tach |
|
Definition
| types of re-entry phenomenon |
|
|
Term
| Ischemia in the heart after surgery can cause |
|
Definition
|
|
Term
| imbalance between supply (perfusion) and demand of heart for O2blood, and causes reduced availability of nutrients and inadequate removal of metabolites |
|
Definition
| Ischemic heart disease, CAD |
|
|
Term
| An increase demand of the heart will do what to the rate and contractility? |
|
Definition
|
|
Term
| Etiology of Ischemic heart disease (one of two types) |
|
Definition
| Decreased blood supply: Valve disease, Coronary spasm, Thrombus, Others (hypotension, hi HR, congenital abnormalities, vasculities |
|
|
Term
| Etiology of Ischemic heart disease (one of two types) |
|
Definition
| Increased demand: hi BP, increased HR, increased blood volume, L vent hypertrophy, thyrotoxicosis |
|
|
Term
| Circulating adrenergic agonist, locally released platelet contents, impaiared secretion of endothelial cell realxing factors (like NO) relative to contracting factors (like endothelin) |
|
Definition
|
|
Term
| chest pain in 85%, other 15-25% no chest pain in older adults, diabetics, women |
|
Definition
| common symptom of ischemic heart disease |
|
|
Term
| chest pain in some, SOB, N/V, arrhythmias (brady, tachy or PVC's |
|
Definition
| common symptom of ischemic heart disease |
|
|
Term
|
Definition
|
|
Term
| Transient myocardial ischemia w/o cellular necrosis |
|
Definition
|
|
Term
|
Definition
| stable, unstable and varient (spasm) |
|
|
Term
| Increase in myocardial O2 demand that outstrips ability of stenosed coronary arteries to increase O2 delivery, no assoc with placque disruption |
|
Definition
|
|
Term
| Sx: not increased in severity, frequ or duration with no change in precipitating factors, pain short, 3 to 30 minutes, relieved by rest or nitro |
|
Definition
|
|
Term
| Associated with placque changes (fissuring or erosion), increased stenosis. |
|
Definition
|
|
Term
| Plaque fissuring/erosion: leads to? |
|
Definition
| exposure to subendothelial collagen and necrotic plaque contents: forms clot < 20 min., increased stenosis and further placque size |
|
|
Term
| clot < 20 min., sudden change in plaque morphology |
|
Definition
|
|
Term
| Sx: pain that occurs with progressive increasing frequency, precipitated with less exertion, and is more prolonged |
|
Definition
|
|
Term
| caused by coronary artery spasm; occurs at rest |
|
Definition
| Printzmetal's variant angina |
|
|
Term
| Necrosis of myocardial tissue from prolonged ischemia |
|
Definition
|
|
Term
|
Definition
Coronary Artery occlusion (thrombosis)
-plaque fissuring/erosion, clot lasts long enough to cause necrosis.
-prolonged vasospasm
decreases O2 carrying in blood and hypotension on arteries |
|
|
Term
| Myocardial cell response within 20 min |
|
Definition
|
|
Term
| myocardial cell response in 20-40 min |
|
Definition
| irreversible myocyte injury, area of necrosis |
|
|
Term
| mycardial cell response in 3-6 hours after MI |
|
Definition
| extent of necrosis is complete |
|
|
Term
| Three factors of irreversible injury in MI |
|
Definition
Subendocardial (Non Q wave)inschemic necrosis to inner 1/3 to 1/2 of vent wall)
Intramural=within the wall
Transmural=full thickness is most frequent (Q wave) |
|
|
Term
| Least well perfused region of myocardium |
|
Definition
|
|
Term
| Where is left vent myocardial pressure the greatest? |
|
Definition
|
|
Term
| Factors associated with size of necrosis of myocardium |
|
Definition
| location and duration of occlusion, size of vascular bed perfused by artery, extent of collateral vessels, quantity of O2 free radicals generated, reperfusion |
|
|
Term
| vessel re-opened and blood flows back into ischemic area |
|
Definition
| reperfusion, may decrease area of injury |
|
|
Term
|
Definition
| injury to cells and apoptosis, O2 utilized by cell is impaired, and the O2 being delivered may form ROS, ROS damage from leukocyte infiltration |
|
|
Term
| may leave cells stunned for a few hours to days |
|
Definition
| reperfusion: cardiac contractility affected, inflammation caused by hypoxia will release myocardial depressant factors from TNFa and IL-1 |
|
|
Term
| Clinical manis: EKG changes, CK, CK-MB, CK, MB isoforms, Troponin I and T levels, systemic response of catecholiamines and angiotensin II |
|
Definition
| MI, diagnosed by clinical sx, EKG and labs |
|
|
Term
| What are elevated cardiac enzymes of MI? |
|
Definition
| CK, CK-MB, CK, MB isoforms, Troponin I and T, |
|
|
Term
| Where and when is troponin released |
|
Definition
| from myoctes due to cardiac damage, MI |
|
|
Term
| How long does Troponin stay elevated? |
|
Definition
| 7-10 days, so can't reflect new injury |
|
|
Term
| Sx of release of catecholamines and Angiotensin II release during MI? |
|
Definition
| anxious, fearful, weak, cold clammy skin, acute confusion/stroke 85+, hypotensive or hypertensive |
|
|
Term
| impaired cardiac function that renders the heart unable to maintain CO for metabolic requirements of tissues/organs |
|
Definition
|
|
Term
| Two kinds of heart failure |
|
Definition
|
|
Term
| Which heart failure is the most common |
|
Definition
|
|
Term
| In left sided heart failure, what is systolic dysfuction |
|
Definition
| ability of ventricle to contract and eject sufficient blood |
|
|
Term
| impairment in the ability of the ventricle to contract and eject enough blood (LVSD) |
|
Definition
| Left sided heart failure, most common |
|
|
Term
| Etiology of?: volume overload (preload), pressure overload (afterload), myocyte ischemia/loss (low O2), less myocyte contractility |
|
Definition
|
|
Term
| In left sided heart failure, what is diastolic dysfuction |
|
Definition
| impairment in ability of ventricle to relax and fill with blood |
|
|
Term
| Etiology of diastolic dysfunction in left sided heart failure |
|
Definition
| diseases that decrease relaxation, decrease elastic recoil or increase stiffness: LV hypertropy, myocardial fibrosis, amyloid, constrictive pericadities, mitral stenosis |
|
|
Term
| Diseases that decrease relaxation, elastic recoil or increase stiffness of L vent |
|
Definition
| LV hypertropy, myocardial fibrosis, amyloid, constrictive pericadities, mitral stenosis |
|
|
Term
| These cause what? Left heart failure, R vent infarction, pulmonary disease, cor pulmonale, congenital heart disease, pulmonic or tricuspic valve disease |
|
Definition
| Right sided heart failure |
|
|
Term
| Causes of Right sided heart failure |
|
Definition
| Left heart failure, R vent infarction, pulmonary disease, cor pulmonale, congenital heart disease, pulmonic or tricuspic valve disease |
|
|
Term
| Compensatory mechanisms of heart failure |
|
Definition
Activation of Neurohormonal systems
Myocardial hypertrophy |
|
|
Term
| 4 parts of neurohormonal system for heart failure |
|
Definition
Activation of sympathetic NS
Vasopressin secretion
Activation of renin-angiotensin-aldosterone
Release of antrial natriuretic peptide and brain natriuretic peptide |
|
|
Term
Activation of sympathetic NS
Vasopressin secretion
Activation of renin-angiotensin-aldosterone
Release of antrial natriuretic peptide and brain natriuretic peptide |
|
Definition
| Neurohormonal system activated in heart failure |
|
|
Term
| Increased release of catecholamines (norepi and epi) |
|
Definition
| Activation of sympathetic NS: part of Neurohormonal system activated in heart failure |
|
|
Term
| Initally compensates for decreased CO by: increasing HR, peripheral resistance and contractility |
|
Definition
| Increased release of catecholamines (norepi and epi) Neurohorm system for HF |
|
|
Term
| Adverse effects of norepi/epi from sympathetic NS |
|
Definition
| Increased work, increased O2 demand, facilitates arrhytmias |
|
|
Term
| Vasopression secretion in HF does what? |
|
Definition
| Vasoconstriction causes reabsorption of water in renal tubules (Vasopressin secretion: part of NH system activated in heart failure) |
|
|
Term
| Vasoconstriction that reabsorbs water in renal tubules: increased preload (LVEDP), increased stretch and forcible contraction (Frank Starling), increased CO |
|
Definition
| Vasopressin secretion in activation of NH system of HF, Also ALDOSTERONE |
|
|
Term
| Adverse effects of Vasopressin (NH activation of heart failure) And Aldosterone |
|
Definition
Too much stretch then decreased CO due to actin/myocin do not connect.
Pulmonary edema, then low O2 supply, myocellular hypoxia |
|
|
Term
| A decreased CO will lead to high or low resistance? |
|
Definition
|
|
Term
| What NH system is activated during heart failure that involves the renal blood pressure? |
|
Definition
| Renin-angiotensin-aldosterone system |
|
|
Term
| What NH system is activated during HF that involves the reabsorption of water in renal tubules |
|
Definition
| Vasopressin-leads to vasoconstriction |
|
|
Term
| Results of aldolsterone secretion? |
|
Definition
| Na reabsorption and water retention: increased preload (LVEDP), then stretch, then forcible contraction (frank starling), then increase CO. SAME from vasporessin |
|
|
Term
| Angiotensin II is released during what condition and what reaction does it have? |
|
Definition
| Produces smooth myo vasoconstriction during NH system release during HF |
|
|
Term
| Adverse effects of Angiotensin II |
|
Definition
| increased afterload, inhibits NO release, stimulates fibroblast proliferation |
|
|
Term
| Nitric oxide does what to muscles |
|
Definition
| smooth muscle vasodilation |
|
|
Term
| What drugs stops angiotensin system (therefore stops vasoconstriction, promotes Vasodilation)? |
|
Definition
| Beta blockers, ACE inhibitors |
|
|
Term
| NH response to Heart failure that inhibits secretion of renin, aldosterone, relaxes smooth muscle and inhibits Na and water absorption |
|
Definition
| Release of Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) |
|
|
Term
| Where/how is ANP stored and secreted? |
|
Definition
| Stored in granules in atrial cytoplasm and secreted from atrium in response to NH activation during HF |
|
|
Term
| Where/How is BNP stored/secreted? |
|
Definition
| stored in granules in ventricular cytoplasm, secreted from ventricle with stretch |
|
|
Term
| What is BNP used to monitor? |
|
Definition
| progress of Heart failure |
|
|
Term
| What inhibits the secretion of renin, aldosterone, and relaxes smooth muscle and inhibits Na and water retention? |
|
Definition
| ANP and BNP release from atrium and ventricles during stretch during heart failure. |
|
|
Term
| What happens to cardiac muscle during heart failure, as a compensatory measure? |
|
Definition
| myocardial hypertophy, with or w/o cardiac chamber dilation |
|
|
Term
| What initiates myocardiac hypertrophy |
|
Definition
-wall stress and cell stretch that induces contractile protein synthesis, # of sarcomeres and mitochondria
-endothelial injury-endothelin release (VC)
-myocyte injury-inflammatory response
-death of myocytes-apoptosis
-end: myocardial contractile failure |
|
|
Term
| What does increased wall stress and cell stretch do to cardiac myocytes? |
|
Definition
| increases protein synthesis, # of sarcomeres, and mitochondira: leads to increased size of myocytes |
|
|
Term
| Increased wall stretch/stress in heart failure leads to parallel addition of new sarcomeres, does what? |
|
Definition
|
|
Term
| Increased wall stretch/stress in heart failure leads to lengthwise addition of new sarcomeres, does what? |
|
Definition
|
|
Term
| increased size of cardiomyocytes leads to? |
|
Definition
|
|
Term
| altered Ca delivery (altered contractility), ischemia, apoptosis due to? |
|
Definition
| Increased cardiomyocte size during heart failure |
|
|
Term
| Increased cardiomyocyte cell wall stress/stretch after hypertrophy during heart failure leads to what? |
|
Definition
| gene expression altered, re-expression of embryonic forms of myosin and troponin, less contraction |
|
|
Term
| Endothelial injury during myocardial hypertrophy leads to? |
|
Definition
| endothelin release, then vasoconstriction, so get decreased O2 supply |
|
|
Term
| Myocyte injury during myocardial hypertrophy in heart failure leads to? |
|
Definition
Inflammatory response: cytokine release of TNFa: cardiac hypertrophy and apoptosis, and IL: cardiac remodeling, then contractile dysfunctin AND
-deposits fibrous tissue and interstitial collagen, then stiffness |
|
|
Term
| What causes cytokine release and deposition of fibrous tissue in myocardial hypertrophy? |
|
Definition
myocyte injury
TNFa: cardiac hypertrophy/apoptosis
IL: remodeling-contractile dysfunction |
|
|
Term
| TNFa leads to what cardiac changes, and who releases it? |
|
Definition
| cardiac hypertrophy/apoptosis, myocyte injury starts inflamm response |
|
|
Term
| IL causes what in myocardial hypertrophy and what stimulates it? |
|
Definition
| Cardiac remodeling (contractility dysfuntion), released by cytokines during myocyte injury |
|
|
Term
| What drugs prevents cardiac remodeling? |
|
Definition
|
|
Term
| How do myoctes die during cardiac hypertrophy? |
|
Definition
| apoptosis, leads to more stress on remaining myocytes |
|
|
Term
| What is the ultimate failure in myocytes during hypertrophy? |
|
Definition
|
|
Term
| What clinical manifestation does activating sympathetic NS do? |
|
Definition
| increased heart rate (activated in L sided failure) |
|
|
Term
| What clinical manifestations does decreased CO do? |
|
Definition
| dyspnea, orthopnea, crackles and wheezes, fatigue, S3 and S4 heart sounds, displaced lateral apical impulse |
|
|
Term
| dyspnea, orthopnea, crackles and wheezes, fatigue, S3 and S4 heart sounds, displaced lateral apical impulse |
|
Definition
| Left sided heart failure due to decreased CO (backed up into L atrium, pulmonary ciruc, then pulm congestion) |
|
|
Term
| Lung hypoperfusion in left sided heart failure is due to what? |
|
Definition
| decreased CO from backed up blood to left atrium, leads to pulm edema. |
|
|
Term
| In left sided failure, decreased CO does what to arterial BP? |
|
Definition
| decreased BP and perfusion |
|
|
Term
| CNS syncope, restlessness; muscle weakness, fatigue, activity intolerance; angina, valvular displacement, decreased urine output, cyanosis |
|
Definition
| decreased CO during left heart failure |
|
|
Term
| What causes papillary muscles to displace causing valve disease? |
|
Definition
| left heart failure, cardiomyopathy |
|
|
Term
| echo: left vent hypertrophy/dilation, low EF, high BNF, |
|
Definition
| some clinical signs of left failure |
|
|
Term
| Alteration in pressure/vol curve in systolic dysfunction? |
|
Definition
| isovolumic pressure-volume shifts to right |
|
|
Term
| Alteration in pressure-vol curve in diastolic dysfunction? |
|
Definition
| shifts of isovolumic pressure-volume curve to the left in clinical manifestation of left heart failure. |
|
|
Term
| Sx: poor EF, blood back into right atrium, vena cava and leads to systemic venous congestion, Jucular vein distension, ascites, large spleen and liver |
|
Definition
| Right sided heart failure clinical symptoms |
|
|
Term
| Right vent hypertrophy, dilation, and poss failure due to disorders of the lung or pulm vasculature that produces pulm hypertension |
|
Definition
|
|
Term
| R vent hypertrophy due to lung disorder |
|
Definition
|
|
Term
| Hearts response to pulmonary hypertension |
|
Definition
| R vent hypertrophy, causes inc pressure. |
|
|
Term
| normal right atrial pressure |
|
Definition
|
|
Term
| Right atrial pressure that will stop blood |
|
Definition
|
|
Term
| What happens if pressure in right ventricle is allowed to build slowly? |
|
Definition
| Hypertrophy, increased sarcomeres |
|
|
Term
| Massive pulmonary embolization can lead to? |
|
Definition
|
|
Term
| Most common cause of chronic cor pulmonale? |
|
Definition
| COPD (emphysema), pulmonary hypertension RT L vent failure |
|
|
Term
| Patho of ?: increased pulmonary hypertension that inc right vent afterload, then right vent hypertrophy and dilation, then right atrial dilation |
|
Definition
|
|
Term
| Sx: EKG/echo: right vent hypertrophy/dilation. Split S2. pulmonic valve murmer, tricuspid murmur, edema, JVD, liver congestin, inc. RVEDP, RV, RA pressure |
|
Definition
| Clinical man of cor pulmonale |
|
|
Term
| Why does cor pulmonale have split S2 and pulmonic and tricuspid valve murmurs? |
|
Definition
|
|
Term
| L heart failure affects what valvular disease? |
|
Definition
|
|
Term
| what do these cause? rheumatic heart disease, congenital defects, degenerative aging (in age 60-70) |
|
Definition
aortic stenosis
rheumatic fever (strep) type III hypersensitivity response) |
|
|
Term
| Patho: gradual obstruction of blood flow (increase gradient of 100-150 mm), increased afterload, LV hypertrophy, LV ischemia and failure (stiff, fatigued, dilates) |
|
Definition
|
|
Term
| Sx: LV hypertrophy, failure, decreased LV output, increased LVEDP, decreased EF, S4 murmur, pressure vol curve to right |
|
Definition
| Aortic stenosis clinical manifestations |
|
|
Term
| What causes Mid-systolic murmur, S4 |
|
Definition
| aortic stenosis,from trying to squeeze blood through. |
|
|
Term
| LV has to generate more pressure to get the blood out past what valve during what condition |
|
Definition
| Aortic valve during stenosis |
|
|
Term
| Etiology of ?: rhematic fever, bacterial endocarditis, syphillus, autoimmune or connective tissue disorders, aortic/cardiac enlargment, trauma |
|
Definition
| aortic regurgitation. Hypertrophy dilates valve ring |
|
|
Term
| Patho: regurg of blood from aorta to LV during diastole, volume ejected both directions, LV hypertrophy/dilation, S3 |
|
Definition
|
|
Term
| sx: Diastolic murmur, S3. increase pulse pressure, hyperdynamic pulses, increased LVEDP (congestion), LV hypertrophy/dilation, Press-vol curve to right and up |
|
Definition
|
|
Term
| What is the most common valve disease and what causes it? |
|
Definition
| Mitral stenosis, rheumatic fever, calcification |
|
|
Term
| Patho: progressive fibrosis, bacterial endocarditis, incr left atrial pressure, atrial hypertrophy and dilation |
|
Definition
|
|
Term
|
Definition
|
|
Term
|
Definition
| pulmonary congestion, perfusion sx: fatigue, neuro |
|
|
Term
| Sx: congestion (dyspnea, pulm edema), diastolic murmur, opening snap, decreased CO, thrombus formation chances inc., atrial hypertrophy, Tall _ waves and a-fib, pressure-vol shifted to left |
|
Definition
|
|
Term
| what is the only mital issue that shift pressure volume curve to the LEFT |
|
Definition
| Mitral Stenosis : TOP LEFT valve |
|
|
Term
| What produces a diastolic murmur, possible snap? |
|
Definition
| Mitral stenosis, opens stiffly to let blood into ventricle |
|
|
Term
| Etiology: chronic: prolapse of leaflets from L vent dilation due to CAD, post inflamm scarring from rheumatic, Acute: papillary muscle or chordae tendinae rupture/dysfunction |
|
Definition
|
|
Term
| Patho: regurg of blood from LV to LA during vent systole, LA dilation, LV dilation if not there already |
|
Definition
|
|
Term
| Sx: in acute state: sudden onset of failure, S3 in failure, pansystolic regurg murmur, (in both dias and syst) |
|
Definition
|
|
Term
| Sx: chronic: asx over time, then pansystolic murmur S3 in failure, incr LVEDP with congestion, dilated atrium and ven and LV hyper, atrial fib, pres-vol shifted to right |
|
Definition
|
|
Term
| What valvular disorder causes a-fib |
|
Definition
|
|
Term
| What valvular disorder causes a systolic murmur? |
|
Definition
|
|
Term
| What valvular disorders causes diastolic murmers? |
|
Definition
| Aortic Insuff and Mitral stenosis |
|
|
Term
| What valvular disorder causes s3 murmur in failure? |
|
Definition
|
|
Term
| Heart disease due to intrinsic myocardical dysfunction |
|
Definition
|
|
Term
| Heart disease acquired by disease |
|
Definition
| secondary cardiomyopathies |
|
|
Term
| Three types of cardiomyopathies |
|
Definition
| Dilated (90%), hypertrophic, restrictive |
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Term
| Most common type of cardiomyopathy |
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Definition
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Term
| Etiology of primary form: idiopathic, genetic mutation to sarcomere and mitochondrial genes and skeletal proteins; alcohol, pregnancy, viral, bacterial |
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Definition
| Primary DILATED cardiomyopathy |
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Term
| Etiology: secondary form: ischemic, valvular, hypertensive and/or congenital heart disease |
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Definition
| Secondary DILATED cardiomyopathies |
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Term
| Patho: progressive cardiac dilation and wall thinning, contractile systolic dysfunction, concurrent hypertrophy |
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Definition
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Term
| Sx: large, flabby heart, hi weight, slowly progressing HF, decreased EF, inc EDV, dec SV, all chamber dilated, poor prognosis (50% death in 2 years) |
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Definition
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Term
Etiology: primary-genetic mutation to proteins encoding sarcomere (90%)
Secondary-hypertensive HD, aortic stenosis |
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Definition
| HYPERTROPHIC cardiomyopathy |
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Term
| Patho: sacrcomere proliferation and myocyte hypertrophy, fibroblast production with collagen deposition. L vent w/o vent dilation, thickening of septum vs LV wall (25%) |
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Definition
| HYPERTROPHIC cardiomyopahy |
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Term
| sx: diastolic dysfunction: decreased LV compliance, accepting less blood into vent and lower SV, decreased diastolic relaxation |
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Definition
| HYPERTROPHIC cardiomyopathy |
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Term
| What does a thickened septum vs LV free wall do in Hypertrophic cardiomyopathy? |
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Definition
| compressed LV cavity so gets outflow obstruction |
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Term
| Sx: heavy, muscles and hypercontracting heart, Harsh systolic murmur from effort to move blood into LV, increas contractility, and LVP (atrial dilation, dyspnea, inc pulm pressure) |
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Definition
| HYPErTROPHIC cardiomyopathy |
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Term
| SX: disorganization of septal myo cells (in primary), abnormal collagen deposits/interstitial fibrosis, anginea and HF due to blood supply not being met, a-fib, sudden death |
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Definition
| HYPERTROPHIC cardiomyopathy: LV outflow can be obstructed. Power behind cycle will be >120. can't relax due to fibrosis |
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Term
| Etiology: primary: idiopathic, infiltrative disease amyloidosis, sarcoidosis, tumor, radiation; secondary: preicardial constriction |
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Definition
| RESTRICTIVE cardiomyopathy |
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Term
| Patho: primary decrease in vent compliance results in impaired vent filling during diastole, DIASTOLIC DISORDER |
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Definition
| RESTRICTIVE cardiomyopathy |
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Term
| Sx: normal sized vent, interstitial fibrosis, decreased CO, increased LVEDP |
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Definition
| RESTRICTIVE cardiomyopathy |
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Term
| What types of diseases are these? acute pericarditis, pericardial effusion, constrictive pericarditis? |
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Definition
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Term
| pericardial membranes are inflamed and roughened and may have exudate |
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Definition
| acute pericarditis: from infections, noninfect inflamm, radiation |
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Term
| SX: chest pain that can mimic MI, worse with deep breaths, CREAKY leather friction rub |
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Definition
| Acute pericarditis (pericardial effusion on echo) |
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Term
| accumulation of serous, inflamm exudate or blood in pericardial cavity |
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Definition
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Term
| Acute pericardial effusion adds how much fluid, and chronic adds before sx: |
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Definition
acute 100-200
chronic 500+ |
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Term
| SX: SOB, JVD, hepatomegaly, ascites, MUFFLED heart sounds, cardiac tamponade, |
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Definition
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Term
| Pulsus paradoxus (BP during exp exceeds during insp x 10), increases right sided H pressure due to compression of thin walled atria hypotension due to decreased SV and CO due to restricted filling (can be late sign) |
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Definition
| Cardiac tamponade in pericardial effusion |
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Term
| Normal pericardial tissue replaced by fibrous tissue, scars or calcification |
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Definition
| CONSTRICTIVE pericarditis |
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Term
| What type of pericarditis causes remodeling? |
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Definition
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Term
| Sx: fibrotic lesions encase heart in heard shell, progresses slowly, |
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Definition
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Term
| colonization of endocardium/heart valves by a microbe that leads to formation of vegetations and destruction of underlying cardiac tissues. |
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Definition
| Infective endocarditis--most common to mitral and aortic valves. (blood pools) |
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Term
| Patho: 1 Damaged endocardial tissue 2 seeding of blood with microbes and attachment 3 bacterial proliferation and vegetative formation |
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Definition
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Term
| How does blood seed during infective endocarditis |
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Definition
| Valves get soft-tissue matrix and vascular supply so leukocytes can kick in (not normal), damage endocardial tissue allows microbes to attach). Bacterial colonies form tight fibrin networks. protected by self-defense and keeps growing |
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Term
| What happens during infective carditis after blood seeding on valves? |
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Definition
| Destruction of underlying cardiac tissue due to inflamm process, systemic emboli, tissue fibrosis and calcification. |
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Term
| Subacute infective endocarditis disease process |
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Definition
| mild for months, less virulent, most recover |
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Term
| Sx: + blood culture, echo shows vegetation, fever, faatigeu weight loss (IL1 and TNFa), 90% have murmur, cardiac complications, embolitic, glomerulonephritis due to Ab/Ag antibodies) |
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Definition
| Clinical of infective endocarditis |
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