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Leading cause of death is... |
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Heart disease for both male and female women 10-15 years later than men |
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CO__SV__HR (possible answers: +, -, x, /, and =) |
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CO=SV x HR CO-cardiac output SV-stroke volume HR-heart rate -if CO goes down SV and HR will go up to compensate |
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personality types related to heart disease |
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type A-used to be related but not anymore type D-negative mood, pessimistic coupled with social inhibition-is more related to heart problems because it increases stress |
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dental care-related to CV |
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bacteria on teeth make their way to the vascular system and adhere to the valves and cause inflammation of the heart |
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Picture of a heart attack -Severe crushing substernal pain -Hand over chest-looking like they are in pain -Seen more often in men -Women-complain of indigestion, severe fatigue, SOB, and GI symptoms (postmenopausal or women with family history of heat attack) |
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aortic (goes to the body) pulmonic (goes to the lungs) |
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bottom-palpate at 5 ICS LMCL |
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-Superior vena cava→ Rt. Atria→ Tricuspid valve → Rt. Ventricle → Pulmonic valve → PA → lungs -PV → Lt. Atria → Mitral valve → Lt. ventricle → Aortic valve → Aorta → systemic circulation |
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-SA node (fires an impulse-pacemaker which controls our heart beat (50-90)) -AV node (takes over if SA node is not working--rate is 30-40) -Bundle of His --LBB & RBB --This allows you to study EKGs |
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-Semilunar valves open (A&P) -AV valves close (M&T) –hear this -Blood pumped from ventricles to pulmonary and systemic circulation -1/3 of cardiac cycle -ventricles become empty |
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-Semilunar valves close (A&P) –hear this -AV valves open (M&T) -Ventricles fill with blood -2/3 of cardiac cycle |
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hemodynamic events-aging (Jarvis p.465) |
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-increase in systolic pressure caused by stiffening of the large arteries which leads to arteriosclerosis (calcification of the vessel walls. -left ventricular wall thickness increases (does not make the heart bigger). this is an accommodation from the vascular stiffness. -no change in diastolic pressure causes an increase in pulse pressure. -no change in resting heart rate or cardiac output. -decreased ability of the heart to augment cardiac output with exercise. |
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which comes first, electrical event or mechanical event? |
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T or F right (T&P) side events precede left side events (M&A) |
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FALSE! left (M&A) side events precede right (T&P) side events |
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T or F right sounds are better heard during inspiration and left sounds are better heard during expiration |
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TRUE! -Right heart is engorged with blood and is in closer contact with the chest wall during inspiration -Volume of lung tissue confirming apex is smaller; left chambers are closer to chest wall during expiration |
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origin of heart sounds -sound 1&2 -sound 3 -sound 4 |
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-sound 1&2-valve closure -sound 3-blood movement within the heart (this is when murmurs are heard)-early in diastole -sound 4-muscle contraction-end of diastole |
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S4-S1-S2-S3 -S1→S2=systole -S2→S1=diastole |
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Seeing the client chest wall lift up when heart is pumping (abnormal) |
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Lifts and moves to a side (abnormal) |
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Distention when patient is setting up-bad-excessive fluid volume (only seen when laying down) |
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Palpable vibration on chest wall-usually accompanies a murmur (feels like cat purring) |
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all of systole, all of diastole |
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heart sound trasmission or radiation |
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do we hear it anywhere else? -murmurs transmitted to neck |
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M&T closing Corresponds with carotid pulse “high pitched” sounds-diaphragm Louder at apex S1 split-normal but rare -No relationship to respirations |
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A & P closing Higher pitched than S1 Louder at base Physiological split is nl. (more likely in S2 than S1) Both components of S2 heard during INSPIRATION at pulmonic area (left-2 ICS) Abnormal S2 Splitting -Fixed splitting --Throughout I & E ---Atrial septal defect -Paradoxical splitting --Heard on E ---Left Bundle Branch Block (LBBB) |
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Blood hitting ventricular wall creates vibrations heard in early diastole Low pitched-heard with bell over T to M areas Normal in children and young adults (the ventricles are so close to the chest wall) Abnormal -Called ventricular gallop rhythm, S3 gallop or pathological S3 -In older adults-after 35 or 40 (may mean heart is enlarged) -May persist in women until 40 |
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atrial muscle contraction: Low pitched sound heard with bell over T to M area Normal -In well trained athletes -In persons over age 50 Abnormal -In people who aren’t well conditioned -Under age 50 -Called pathological S4, atrial gallop, or S4 gallop |
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Heart sound loudness decreased by |
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Dec. force of contraction-CHF Increased thickness of chest wall-Obesity Increased air in chest cavity-COPD (emphysema) Increased fluid around the heart-plural effusion (cardiac empanada) Electrical problems-arrhythmias |
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tissues alter conduction of heart sounds (liquid, bone, muscle, etc...) |
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Liquid: may increase audibility; large amount will decrease Bone: good conductor Muscles, fat and air: large amount will interfere |
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-Blowing, swooshing sound with turbulent blood flow in heart or great vessels -blood having trouble getting through valves (because the valves are too small, too much blood going through, or backward flow of blood) |
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1-6 1: Softest audible 2: Medium intensity 3: Loud, no thrill 4: Loud, associated with palpable thrill 5: Heard with stethoscope ½ off chest wall 6: Heard with stethoscope off of chest wal 3+ grade can usually come with other symptoms |
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no evidence of physiological or structural alteration |
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associated with physiological alterations -anemia, pregnancy, increased blood vol. |
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always caused by structural abnormalities of the heart |
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-Continuous, low-pitched, soft hum, heard throughout the cardiac cycle-loudest in diastole -Due to turbulence of blood flow in the jugular venous system -Normal in children and has no pathologic significance |
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Apical Pulse what site? how long do you auscultate? when to check? what do you check? |
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-At M site or at apical impulse if heart is enlarged -ALWAYS auscultate for one full minute whether regular or not -ALWAYS check AP if the peripheral pulse is irregular -Rate, rhythm, and regularity |
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Pulse rate increases slightly on inspiration and decreases slightly on expiration. |
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Fetal to pulmonic circulation occurs in immediate newborn period-ductus arteriosus & foramen ovale close & blood goes to the lungs |
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pregnant-what it does to your heart |
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systolic murmurs blood volume increase 30-40% |
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systolic murmurs over 50% |
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don't have good circulation hair loss |
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Abnormal: 0: Not Palpable 1+: Thready, weak, fades easily, easily obliterated Normal: 2+: May be somewhat difficult to palpate, obliterated with pressure 3+: Easily palpable, doesn’t fade, takes sufficient pressure to obliterate 4+: Strong, easily palpated, cannot obliterate, ―bounding |
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Checks patency of radial and ulnar arteries -Occlude both arteries in one hand -Client pump hand -Release one artery (first radial and then repeat steps 1 & 2 and do ulnar) at a time and check for color to return |
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-one examiner check apical and one check radial pulse for the same one minute -compare rates and check for A/R deficit (signals weak ventricular contraction) -example --Apical rate=118 --Radial rate=78 --A/R deficit=40 |
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Blood pressure differences |
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Check both arms -Difference of more than 10-15 mm Hg may indicate arterial obstruction in side with lower reading |
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Intermittent claudication |
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leg pain following exertion; ischemic pain rest -shows arterial insufficiency |
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# of blocks walked or stairs climbed to produce pain |
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signs of arterial insufficiency |
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Pain with exertion Pallor Cool temperature Changes in skin, hair and nails -Thin, fragile skin -Hair loss-lower extremity-line of demarcation -Thickened, claw-like toenails -Ulcers lateral malleoli & tips of toes Parasthesias: sensation of tingling Diminished or absent pulses No Edema |
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Ankle-brachial index (ABI) |
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-Objective, noninvasive measurement of arterial disease -Use of a Doppler stethoscope to determine the extent of peripheral disease -Systolic ankle pressure/systolic brachial pressure -Normal is 1-1.2 -.9=PVD |
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pain in calf & popliteal area on passive dorsiflexion of foot occurs in about 35% of deep vein thrombosis! |
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signs of venus insufficiency |
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Pain-aching, tiredness Pulses present, but difficult to palpate Skin coarse, thick and brown Edema present Ulcers at medial malleoli Varicose veins |
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