chapater 11 heart Flashcards
parasympathetic stimulation of hrt
- can be artificial-acetylcholine
- slows HR and decreases contractility
barroreceptors
- stretch receptors located in aortic arch and carotid sinus monitoring bp
- send signals to medullary cardiovascular center which regulates neural output to sympathetic and parasympathetic fibers
i. e. decrease in bp decreases signals to medullary cardiovascular center and thus increases sympathetic efferent activity and decreases parasympathetic efferent activity–resulting in increase HR and contractility
Erb’s point
-area at which pulmonic/aortic sounds are best heard
sympathetic stimulation of heart
- can be artificial-norepi
- produces increase HR and contractility
valves heard during S1
-AV valves, tricuspid, and mitral
valves heard during S2
-semilunar, aortic, pulmonic valves
opening snap
- usually opening of valve can’t be heard–only when damaged
- if AV valved is narrowed/stenotic can be heard-during diastole
ejection click
- not normal to hear
- stenotic semilunar valve during systole
cardiac cycle
sequence of valve openings/closure:
MVc TVc PVo AVo AVc TVo MVo
M1
- during S1
- from closure of mitral valve when left ventricle pressure rises to more than lt atrial pressure
T1
- tricuspid component of S1
- from closure of tricuspid valve when rt ventricle pressure> rt atrium pressure
isovolumetric contraction
- time btwn closure of AV valve and opening of semilunar valve
- pressure in rt ventricle>pulmonary artery–pulmonic valve opens
- pressure in lt ventricle>aortic artery–aortic valve opens
dicrotic notch
- point at which ejection is completed and aortic and left ventricular curves separate
- simultaneous to S2
A2
- part of S2
- aortic valve closes
- simultaneous with dicrotic notch
P2
- pulmonic component of S2
- point when rt ventricle pressure
isovolumetric relaxation
- time between closure of semilunar valves and opening of AV
- rt atrium pressure>rt ventricle –tricuspid valve opening
- lt atrium pressure>lt ventricle–mitral valve opening
S3
-after S2
-normal in children
-if occurs in pt>30 yoa-volume overload of ventricle
-could be from regurgitant valvular lesion and CHF
“kentucky”
atrial contraction (kick)
- end of diastole
- additional 20% of ventricle filling
S4
- normal for pt 30 yoa indicative of noncompliant/stiff ventricle
- caused by pressure overload on ventricle
atrial pulse
- produced by ejection of blood into aorta
- anacrotic notch-atrial pulsation during end of rapid ejection period
- contour and volume effected by:lt ventricular stoke volume, ejection velocity, relative compliance/capacity of arteries
arterial bp
- measures lateral pressure exerted against arterial wall
- result of CO and peripheral vascular resistance
systolic bp
- peak pressure in arteries
- regulated by stroke volume and compliance of blood vessels
diastolic bp
- lowest pressure in arteries
- effected by peripheral resistance
jugular venous pulse
-direct info about pressures in rt side of hrt because direct continuation of rt atrium
“a” wave of jugular venous pulse
-rt atrial contraction
“x” descent wave of jugular venous pulse
-cause by atrial relaxation just before ventricle contraction
“c” wave in jugular venous pulse
-drop rt atrial pressure
-
“x prime” descent on jugular venous pulse
-free wall of rt ventricle approaches septum during contraction and AV rings descend toward apex increasing size of atrium causing a fall in pressure
“v” wave of jugular venous pulse
-during ventricular systole rt atrium begins to fill with blood–increasing rt atrium pressure
“y” descent wave in jugular pulse
-end of ventricular systole, rt ventricular pressure falls rapidly–tricuspid valve opens
Chest pain
-common causes:
Cardiac: CAD, aortic valve dz, pulmonary HTN, mitral valve prolapse, pericarditis, idiopathic hypertrophic sub aortic stenosis
Vascular: dissection of aorta
Pulmonary: PE, pneumonia, pleuritic, pneumothorax
Musculoskeletal: costochondritis, arthritis, muscular spasm, bone tumor
Neural: herpes zoster
GI: ulcer dz, bowel dz, hiatal hernia, pancreatitis, cholecystitis
Emotional: anxiety, depression
Palpatations
- most common cardiovascular causes
- other causes: thyroidtoxicosis, hypoglycemia, fever, anemia, pheochromocytoma, anxiety
- caffeine, tobacco, drugs may can cause
Dyspnea
-common causes
CV: lt ventricle heart failure, mitral stenosis
Pulmonary: COPD, asthma, restrictive lung dz, PE, pulmonary HTN
Emotional:anxiety
anemia
paroxymal nocturnal dyspnea (PND)
- supine position increases intrathoracic blood volume–weakened hrt may not be able to compensate resulting in CHF
- specific to CHF
- usually assoc. with orthopnea (use of more pillow to sleep)
dyspnea on exertion (DOE)
- caused by chronic CHF or severe pulmonary disease
- compare to distance able to walk before experiencing dyspnea compared to 6 months or 1 year ago
trepopnea
- rare form of positional dyspnea
- pt less dyspnea while lying on lt than right side
syncope
-may have cardiac and non-cardiac causes
-assess activity prior to event, chest pain/palpitation, position
-common causes:
cardiac:decreased cerebral perfusion due to hr disturbance; lt ventricular output obstruction
metabolic: hypoglycemia; hypoxia; hyperventilation
psychiatric: hysteria
neurologic: epilepsy; cerebral vascular dz
orthostatic hypotension: volume depletion; antihypertensives, antidepressants
vasovagal: vasodepression
micturition: visceral reflex
cough: chronic lung disease
carotid sinus: vasopressor response to carotid sinus sensitivity
fatigue
- not specific for cardiac issues (i.e. anxiety/dpn, chronic dz, anemia)
- common for CHF and mitral valve dz
dependent edema
- if symmetric lower extremity edema assoc. with CHF with worsening as day progresses
- usually dyspnea precedes edema with pt. who have CHF
differential cyanosis
- right to left shunting of blood through patent ductus arteriosus (PDA) due to pulmonary hypertension
- deoxygenated blood is pumped out only to lower extremities cyanosis there only
- upper extremities normal color
abnormalities of first heart sounds
- factors responsible for intensity of S1:
- rate of rise of ventricular pressure-faster the rise the louder the mitral component
- condition of valve-AV stiffens closure is louder; mitral stenosis-louder/accentuated S1
- position of valve-at time of ventricular contraction affects intensity of sound; longer the PR interval the softer the S1(i.e. wenckebach-until drop)
- distance of hrt from chest wall-obese, COPD, large pleural effusion all soft S1
abnormalities of second hrt sound
- conditions changing intensity of S2:
- changes in systolic pressure-i.e hypertension
- condition of valve: calcification/fibrosis of semilunar valve softens closure
ejection click
- systolic click
- high-pitched sounds occurring early at onset of ejection produced by deformed semilunar valves
- pulmonary or aortic stenosis may cause as well
- as calcification progresses click no longer can be heard
midsystolic click
- occurs in the middle of systole
- may be single or multiple
- commonly with mitral or tricuspid prolapse
murmurs
- can be from turbulent energy in walls of hrt
- turbulent energy: obstruction to flow or flow from narrow vessel to wide vessel
- eddies strike walls to produce vibration that is heard
- can be due to large volume of blood through normal opening
