Test 1 Flashcards
devices for CHF
bi ventricular pacing ICD Intraaortic balloon pump left ventricular assistive device
STEMI indicates
occlusion in a large vessel and large at risk is a cardiac emergency
rarest form of cardiomyopathy hast the worst prognosis does not appear to be inherited characterized by diastolic dysfunction
restrictive cardiomyopathy
home care PT for CHF
flexibility, cycle ergometry and walking 20-60 min, 3-7 d/wk, 2-6 mo, 50-80 % of peak cycle heart rate or O2
sensitive to sense of movement in skeletal system
mechanical receptors
factors contributing to unstable angina
circadian variation in catecholamine levels increase platelet activation pathologic changes in atherosclerotic plaques
excessive accumulation of fluid, other than blood, within the pleural space congestive heart failure infection of the lung
hydrothorax
CHF ejection fraction
FRC=
RV+ERV
breathing exercises for CHF
inspiratory muscle training limited data for yoga
forced expiration
rectus abdominis external and internal oblique internal intercostal serratus posterior inferior
abnormal HR recovery after exercise
a decrese in HR of
respiratory alkalosis renal compensation
conserve amount of hydrogen ions and elimnate HCO3
marks site of the embryonic foramen ovale through which blood passes from right atrium to left atrium before birth
fossa ovalis
adrengeric
norepinephrine post ganglionic sympathetic
components of left ventricle
wall 2-3 times thicker than right mitral valve cusps papillary muscles chordae tendineae aortic valve
Large inferior opening int eh sinus venarum that brings poorly oxygenated blood (abdomen and lower limb)
Inferior vena cava
fibrous strands connecting papillary muscle to cusps of atrioventicular valves
chordae tendineae
site of venous blood that has passed through the cardiac muscle
opening of coronary sinus
contribute to inadequate oxygen supply in CHF
ventilatory muscle weakness abdominal ascities dyspnea
coincides with closure of atrioventricular valves at start of systole
first sound lub
restrictive cardiomyopathy in which and inflammatory disease that causes the formation of small lumps in organs (lungs)
sarcoidosis
metabolic acidosis
HCO3 decreases because of excess ketones (diabetes) chloride or acid ions vomiting, lactic acidosis
additional volume taken in
inspiratory reserve volume (IRV)
Formed largely by the left ventricle along with narrow portion of the right ventricle
diaphragmatic surface
additional volume let out
expiratory reserve volume (ERV)
when do the papillary muscles contract
during ventricular systole
diaphragm at upright
level
avg alveolar gas
3000 ml
structures involved in ventilation
bony thorax ribs
collapse compression (hydrothroax) obstruction (tumor)
atelectasis
stiffened walls of the ventricles with loss of flexibility due to infiltration by abnormal tissue
restrictive cardiomyopathy
atherosclerosis progression
fatty streaks (aorta, coronary arteries) Fibrous plaque (stable or unstable, progression is based on several factors)
bucket handle
inferior ribs
if the serous layer of the pericardium becomes rough, typically secondarily due to viral infections, then friction and vibrations may occur with each cardiac cycle may sound like squeaky leather and may be widespread
pericaridal (friction) rub
restrictive cardiomyopathy in which abnormal protein fibers accumulate int eh hearts muscle
amyloidosis
the bronchi have small arteries that supply oxygenated blood to the brochial tree
2 on left come off the descending aorta 1 on the right comes off the 3rd posterior intercostal artery
signs and symptoms of coronary artery disease
obstruction but doesn’t affect heart function may not demonstrate symptoms, depends on severity of obstruction per vessel and number of vessels
MI location anteroseptal
EKG V1-V3 Artery: LAD
cardiovascular disease risk factors
family history age diabetes hypercholesterolemia hypertension smoking obesity Inactivity/sedentary
most common type of valve prolapse
mitral valve
rehab center PT for CHF
aerobic exercise 20-60 min, 3-7 d/wk, 2-57 mo, 40-90% of peak cycle HR or VO2
how is prinzmetal angina treated
with a combination of nitrates and clacium channel blockers beta blockers are usually avoided
the heart muscle loses its ability to pump effectively. the heart becomes larger as it tries to compensate for its weakened condition
the heart in cardiomyopathy
abnormal BP response to exercise
a failure of systolic BP to rise in proportion to exercise intensity (without and meds)
prehypertension
120-139 80-89
Lobes of lungs
R: 3 oblique and horizontal fissure L: 2 oblique fissure
cortex can override the main centers for pulmonary ventilation
active expiration
what is the cause of angina and myocardial ishemia in CMD
inadequate O2 supply/demand to heart
precipitating factors foe IHD
cold exertion anxiety heavy meals tachycardia hypoglycemia
derived from incorporation of pulmonary veins
smooth walled part
VC=
IRV+tidal+ ERV
sudden SOB upon wake from sleep supine position increases venous return overloading the poorly functioning heart (increases pulmonary edema)
paroxysmal norturnal dyspnea and orthopnea
a slight depression in the interatrial wall
fossa ovale
Site of blood flow out of right atrium
Right atrioventricular valve
pulmonary sensors in the joint and muscle detect
physical activity increased breathing rate
Left coronary artery supplies
left atrium most of left ventricle Anterior 2/3 of AV septum (including AV bundles) SA node in 40% of people
alpha 2 adrenergic
parasympathetic, help with decreasing sympathetic activity discharge
lies beside anterior interventricular artery
great cardiac vein
right and left coronary arteries open into (after aortic valve)
right and left aortic sinuses
stage 4 hypertension
>210 >120
forced inspiration
quiet muscles sternodleidomastoid scalene muscles leator costarum serratus posterior superior
runs along acute margin of right ventricle, paralleling right marginal artery
small cardiac vein
preganglionic cardiac and pulmonary sympathetic fibers originat
in the spinal cord at T1-5
avg tidal volume
500ml
main coronary arteries
left circumflex left anterior descending right coronary
cardiac disease marked limitation OK at rest, less than ordinary activity causes symptoms above
Class III
Well established onset when characteristics remain unchanged for 60 days characterized by chest pain (transient hypoxia, relieved with change in activity or SLNG)
Stable angina
stage 2 hypertension
160-179 100-109
sympathetic nervous systems
preganglionic and postganglionic
metabolic alkalosis compensation
increase PaCO2 through decreasing respiration to hold on to CO2
produced by closure of aortic and pulmonary valves at end of systole
second sound dub
symptoms of CHF
dyspnea (paroxysmal nocturnal or orthopenea)
components of the left atria
pulmonary veins smooth-walled part fossa ovale atrioventricular valve
Blunt descending projection formed by left ventricle
apex
diaphragm at sidelying
uppermost side is lower lowermost side is higher
proper diagnosis of hypertension
3 visits with high BP in 3 months
SNS postganglionic reach
viscera run along the surface of the great vessels bronchi and vascular muscle
increase levels of collagen, destruction of the medial elastin, changes in composition of fibrous protiens
fibrous plaque
strength training for CHF
10 reps for 2-4 mo OR 60-80% of max voluntary contraction progression is slow with weight training
Signs of CHF
chest xray (large cardiac silhouetted) EF Cold pale cyanotic extremities (increased sympathetic activity) abnormal heart sounds (S3) sinus tachycardia abnormal breathing peripheral edema crackles/rales Jugular vein distension decreased exercise tolerance
failure to reach 85% of APMHR in the absence of beta blockers or other medication with similar effects
chronotropic incompetence
volume of air that remains in the lungs after a forceful expiratory effort
residual volume (RV)
corresponds to primitive atrium of embryonic heart; contains pectinate muscles
auricle
characteristics of CMD
ejection fraction angina and myocardial ischemia cardiac arrhythmias MI hypertension renal insufficiency
neurotransmitters
achetylcholine norepinephrine
Hallmark sign of CHF occurs when the LV is non-compliant and poor relaxation during systole
S3
the product of tidal volume and respiratory rate
Minute ventilation (Ve)
expiration pressure
pressure in lungs increases
Right marginal artery origin and distribution
right coronary artery right ventricle and apex of heart
blood flows into the coronary arteries after
the valves (aortic) have closed as a result of the elastic recoil of the aorta and great vessels
chronic elevation in BP most powerful contributor to cardiovascular disease
hypertension
what is prinzmetal angina secondary to
increase coronary vasomotor tone or vasospasm
ejection fraction of CMD
30-40%
dilated left ventricle and left atrium bulging interventricular septum from left to right thin ventricular walls myocardial mitochondria dysfunction
dilated cardiomyopathy
signs and symptoms of Ischemic heart disease in men
radiating pain (jaw or left side) crushing pain (elephant on chest) sweating skin color
stage 1 hypertension
140-159 90-99
layers of the pericardiaum
fibrous serous visceral
cholenergic receptors
muscarinic nicotinic cardiac and smooth muscle of lung and bronchioles tissue
S&S with SPO2 80, PaO2 45
as above
pathophysiologics of CHF
neurohormonal (sympathetic system) muscle wasting pulmonary/edema renal
Where the bronchus and pulmonary vessels enter and leave the lung
hilum
Pace maker of the heart controlled at level of
SA node brainstem
result of traumatic injury to the wall of the lung or infection which allows air to be pulled into the pleural space collapse towards hilum
pheumothorax
pericardium that secretes (20-30 ml)
serous
peripheral edema with CHF
weight gain >3 lbs
you hear clear whisperq
whispering pectoriloquy
receives all cardiac veins except anterior cardiac veins and smallest cardiac veins
coronary sinus
criteria for modification or termination of exercise in CHF
marked dyspnea or fatigue RR > 40 breath/min development of S3 heart sound increase in pulmonary crackles decrease in HR or BP or >10 bpm/mmHg Diaphoresis, pallor or confusion
composed largely of the right atrium and right ventricle along with narrow portion of the left vntricle
sternocostal surface
treatment for MI in CMD
fix the underlying cause of infarction