-
pericardium
fibrous protective sac enclosing the heart
-
epicardium
inner layer of pericardium
-
endocardium
smooth lining of the inner surface and cavities of the heart
-
tricuspid valve
right A-V valve, anchored by chordae tendineae
-
bicuspid/mitral valve
leff A-V valve
-
semilunar valve
pulmonary and aortic valves: prevent back flow
-
Right Coronary Artery
supplies atrium, R ventricle, infer wall of left ventricle, AV node, bundle of HIS, SA node
-
Left Coronary Artery
supplies the LAD (L anter descending)
LAD: supplies the L ventricle and interventricular septum, apex
-
Left Coronary Artery
Circumflex artery
supplies the later and infer walls of L ventricle and portions of L atrium, SA node
-
Coronary Sinus (vein)
goes straight to R atrium
-
conduction of heart beat
SA node --> impulse spreads to both atria and they contract together-->stim the AV node --> transmits down the bundle of HIS to purkinje fibers --> impulse spreads thruout ventricles and contract together
-
Purkinje fibers
conducting tissue of both ventricles; R and L branches of AV node; conducts the ventricles,
-
SA node
pacemaker of heart, initiates impulse; sympathetic and parasympathetic innervations affecting heart rate and strength of contraction
-
AV node
@ R atrium/ventricle junction; merges with bundle of HIS
-
Stroke Volume (SV)
amount of blood ejected with each HB. normal=55-100 mL/beat
-
Left Ventricular end diastolic volume or Preload
amount of blood left in the ventricle at the end of diastole. Greater the filling, greater the blood pumped (Frank-Starling Law)
-
Afterload
force the Left Ventricle must generate during systole to overcome aortic pressure to open the aortic valve
-
Cardiac Output
(CO=SV*HR)
amount of blood discharged from the left or R ventricle per min (4-5L per min)
-
Ejection Fraction
percentage of blood emptied from the ventricle during systole: clinically useful for measure of LV function
=SV / preload
normal = 60-70%, a lower EF = impaired
-
Diastolic filling time decreases with:
increased heart rate and heart dz
-
Myocardial oxygen demand (MVO2)
energy cost of myocardium
= HR*SBP
increases with activity and HR or BP
-
ateries and blood travels from
high pressure to low pressure
-
arteries and blood flow is influenced by
elasticiy of vessel walls, peripheral resistance, amount of blood in body
-
capillaries
connect arteriols and venules
-
lymphatic system includes
lymphatics, lymph fluid, lymph tissues, nodes, organs, (tonsils, nodes, spleen, thymus, thoarcic duct)
-
lymph travels...
from capillaries to vessels to ducts to L subclavian vein
-
parasympathetic control of heart (cholinergic)
in medulla oblongata: cardioinhib center
- vagus nerve (CN X)
- slows heart rate and force of contraction
- causes coronary vasoconstriction
-
sympathetic control of heart (adrenergic)
located in medulla oblongata: cardioacceleratory center
T1-T4 ganglia, releases epinenphern and nor-epinephrine
causes increase in rate and force of contraction
coronary vasodilation --> requires sympathetic inhibition
-
Baroreceptors
main mechanisms controlling heart rate
respond to changes in BP (circulatory reflex)
-
chemoreceptors
- sensitive to changes in blood chemicals (O2, CO2, lactic acid
- maintains pH
-
hyperkalemia and HR
increased potassium ions, decreases the rate and force of contraction, produces EKG changes
-
hypokalemia and HR
decreased potassium ions
causes arrythmias, ventricular fib (V-fib)
-
hypercalcemia and HR
increased calcium
increases heart actions
-
hyocalcemia and HR
decreased calcium
depresses heart actions
-
peripheral resistance - influenced by
viscosity of blood, diameter of arterioles/capillaries
-
increased peropheral resistance causes
increased blood volume and pressure
-
decreased preipheral resistance causes
decreased arterial blood volume and pressure
-
Positive risk factors for coronary artery dz
- age (male >45, Female >55)
- family hx
- smoking hx
- sedentary
- obese
- HTN
- dyslipidemia
- pre-DM
-
Pallor skin
washed out, absence of pink, rosy color
-
grading scale for peripheral pulses
- 0 = absent pulses
- 1+ = pulse diminished
- 2+ = normal
- 3+ = full pulse, increased strength
- 4+ = bounding
-
Apical (apex) pulse/pulse at maximal impulse position
supine, palpate 5th interspace, midclavical vert. line (APEX) of heart
-
Normal HR
60-100, <60 in athletic/trained
-
HR for pediatric
115-140 bpm
-
-
-
irregular pulse
variations in force and frequency
d/t arrythmias, myocarditis
-
weak, thready pulse
d/t low SV or cardiogenic shock
-
bounding pulse
d/t shortened ventricular systole and decreased peripheral presure; aortic insufficiency
-
HEART SOUNDS
aoric valve - 2nd right intercostal space at sternal border
pulmonic valve - 2nd left intercostal space @ sternal border
Tricuspid valve - 4th left intercostal space @ sternal border
mitral valve - 5th left intercostal space at midclavical
-
HEART SOUNDS
- S1 - (lub) normal closure of mitral and tricuspid valves -- marks beginning of systole
- - decreased in 1st degree heart block
- S2 - (dub) normal closing of aortic and pulmonic valves, marks end of systole
- - decreased in aortic stenosis
-
Murmur - extra sounds
- 1. systolic - falls between S1 and S2
- - indicates valvular dz or can be normal
- 2. Diastolic - falls between S2 and S1
- - indicated valvular dz
-
grades of Murmurs
- grade 1 - softest audible murmur
- grade 6 - audible with stethoscope off chest
Thrill - abnormal tremor with a murmur felt
-
Bruit: HEART SOUNDS
- adventitious sound/murmur of arterial o venous origin
- common in carotid/femoral arteries
-
Gallop; HEART SOUNDS
- abnormal heart rhythm with 3 sounds each cycle
- 1. S3 - ventric. filling, occurs soon after S2
-
- - indicative of congestive (LV) heart failure
- 2. S4 - assoc with ventric filling and atrial contraction; occurs before S1;
- - indicative of pathology ie. coronary heart dz (CAD), MI, aortic stenosis, chronic HTN
-
EKG has how many leads
12 leads
-
EKG gives information about
heart rate, rhythm, conduction, areas of ischemia and infarct, hypertrophy, electrolye imbalance
-
-
EKG:P-R interval
time required for impulse to travel from atria thru conduction cycle to purkinje fibers
-
EKG: QRS wave
ventricular depol
-
EKG: ST segment
beginning of ventricular repol
-
EKG: QT interval
time for electrical systole
-
EKG: calculate HR
count number of QRS complexes in a 6-second strip and multiple by 10
-
Ventricular Fib
- pulse-less, emergency, adversely affects CO,
- requires CPR, medication, defib
chaotic activity of ventricle originating from multiple foci; unable to determine rate
EKG: bizzare/erratic activity without QRS complese
no effective CO, clinical death within 4-6 min
-
Premature ventric contraction (PVC)
premature heartbeat arising from ventricle -- no p wave, a wide QRS that is premature, followed by long compensatory pause
Serious PVC = >6 PVC in min, paired, or in sequential runs
-
ventricular tachycardia
a run of 3 or more PVCs occuring sequentially; very rapid rate (150-200 bpm), may occur paroxsymally (abruptly); usually d/t ischemic ventricle - seriously compromised CO
wide/bizzare QRS, no P waves
-
Supraventricular arrythmias
atrial arrythmias, rapid, repetitive firing of one or more ectopic foci in the atria (outside sinus node)
P waves are abnormal or absent, rhythm is irregular, chronic or paroxsymal, rapid rate
CO is usually maintained
-
Atrial flutter
250-300 bpm
-
-
atrial tachycardia
140-250 bpm
-
Atrioventricular blocks
if ventricular rate is slowed, CO is decreased
-
Third degree heart block
complete heart block, life threatening, requires meds and pace-maker
-
ST segment depression caused by
ischemia or injury - impaired coronary perfusion
can be up-slopping, down-slopping or horizontal
-
EKG changes with MI are:
abnormal Q waves, ST elevation, T-wave inversion
-
-
-
-
Stage 1 HTN
130-140/90-100
-
stage 2 HTN
140-160/100-110
-
-
Primary HTN
no known cause
-
Secondary HTN
D/t atherosclerosis, vascular d/o, renal dz, endocrine d/o, pregnancy, drug related
-
hypotension
decrease in BP below normal, blood pressure not adequate for normal perfusion/oxygenation of tissues; may be related to bed rest, drugs, arrhythmias, blood loss/shock, MI
-
orthostatic hypotension
sudden drop in BP with change in position
- lightheadedness, dizziness, LOB
- drop in systolic more than 20mmHg or standing BP less than 100 should be reported and is significant
-
Pediatric BP
- Infant (<2 y/o) 106-110/59-63
- child (3-5 y/o) 113-116/67-74
-
Mean arterial pressure (MAP)
- arterial pressure within the larger arteries over time, dependent upon mean blood flow and arterial compliance
- =[SBP+(DBP*2)]/3
-
Dyspnea Scale
- +1 = mild, noticeable to pt only
- +2 = mild, some difficulty, noticeable to observer
- +3 = moderate difficulty, but pt can continue
- +4 = severe difficulty, patient cannot continue
-
Respiratory Rate
- New born = 30-40 bpm
- Adult = 12-20 bpm
-
Tachypnea
increase in RR >22 bpm
-
bradypnea
decreased in RR to <10 bpm
-
hyperpnea
increase in depth and rate of breathing
-
dyspnea (SOB)
- DOE - brought on by exertion
- Orthopnea - unable to breathe when in reclined position (supine)
- paroxysmal nocturnal dyspnea (PND) - sudden inability to breathe occuring during sleep
-
Breath sounds: crackles
(rales) rattling, bubbling sounds, d/t secretions in the lungs
-
Breath sounds: wheeze
whistling sounds
-
-
Hypoxemia
abnormally low amount of O2 in the blood
-
hypoxia
low O2 level in the tissues
-
anoxia
complete lack of O2
-
Anginal Scale
- 1+ = light, barely noticeable
- 2+ = moderate, bohtersome
- 3+ = severe, very uncomfortable
- 4+ = most severe pain ever experienced
-
-
Ischemic Cardiac Pain
diffuse, retrosternal pain, sensation of tightness, achiness, associated with sweating, dyspnea, indigestion, dizziness, syncope, and anxiety
-
Angina
sudden or gradual onset, occurs at rest or c activity, precipitated by physical or emotional factors, hot/cold temperatures, relieved by rest or nitroglyerine
-
MI pain
sudden onset, pain last for more than 30 min, may have no precipitating factors, not relieved by medications
-
Referred Pain
cardiac pain can be referred to shoulders, arms, neck, or jaw
pain referred to back can occur from dissecting aortic aneurysm
-
Edema Grading Scale
- 1+ = mild, barely perceptible indentation <1/4 inch pitting
- 2+ = moderate, easily identified depression, returns to normal within 15 seconds, 1/4-1/2 inch pitting
- 3+ = severe, depression takes 15-30 seconds to rebound, 1/2-1inch pitting
- 4+ = very severe, depression lasts for >30 seconds or more, >1 inch pitting
-
Rubor skin color
dependent redness with PVD
-
Digital clubbing
curvature of the fingernails with soft tissue enlargement at base of nail
associated with chronic O2 deficiency, heart failure
-
PVD (periph vascular dz) trophic changes
pale, shiny skin, dry skin, loss of hair
abnormal pigmentation, ulceration, dermatitis, gangrene
-
Fibrosis
tissues are thick, firm, and unyielding
-
Stemmer's Sign
dorsal skin of the toes and hands are resistant to lifting (lymphedema)
-
Decrease in skin temperature is associated with:
poor arterial perfusion
-
PVD Pain to look for (periph vascular dz)
intermittent claudication with pain, cramping, and fatigue during exercise and relieved by rest
-
SaO2 provides an estimate of which value?
PaO2 - partial pressure of O2. based on the oxyhemoglobin desaturation curve
-
hypoxemia
O2 below 90% in blood
-
hypoxia
low O2 levels in the tissues
-
anoxia
complete lack of O2
-
cardiac pain referral
shoulders, arms, neck, jaw
-
dissectiong aortic aneurysm referal pain:
back
-
PVD Pulses are:
absent/diminished
-
check LE pulses in supine - femoral, popliteal, dorsalis pedis, poster tib
-
UE pulses: check brachial, radial, and carotid
-
clubbing of fingers/toes
curvature of the fingernails with soft tissue enlargement at base of nail -- associated with chronic O2 deficiency and heart failure
-
Fibrosis
skin is thick, firm, unyielding, positive stemmers sign (lymphedema)
-
PVD is associated with
abnormal pigmentation, ulceration, dermatitis, gangrene
-
poor arterial perfusion and skin temp=
decrease in superficial skin temp
-
Edema examiniation
measure girth, pitting edema, caused by venous insufficiency or lymphedema, B edema = CHF
-
always examine venous system before arterial
venous insufficiency can invalidate arterial tests
-
Greater Saphenous Vein : Percussion test
in standing - palpate one segment of the vein while tapping the vein 20 cm higher - if pulse wave felt in lower hand, valves are insufficient
-
venous filling time test -- examine time to refill veins after emptying
in supine, elevate one leg for 1 min to 45 degrees, then place in dependent position, delayed filling (>15 s) is indicative of venous insufficiency
-
doppler Ultrasound
measuring systolic BP in non-palpable pulses for both venous and arterial insufficiency
-
ABI - ankle brachial index -- ratio of LE pressure divided by UE pressure
- Scale:
- >1 = normal
- .8-1 = mild PAD
- .5-.8 = moderate PAD, intermittent claudication
- <.5 = severe PAD; ischemia of limb, rest pain
-
rubor of dependency - examine color of foot during elevation followed by dependency
- insufficiency = pallor with elevation, rubor of dependency with dependent postion -- reactive hyperemia
- changes that take longer than 30s is indicative of PAD
-
intermittent claudication
exercise-induced pain or cramoing in the legs that is absent at rest - typically calf pain but can also occur in the butt hip thigh or foot
-
intermittent claudication test
have pt ambulate until pain is felt, have pt sit and rest - note the time of walking. examine for numbness, coldness, pallor or loss of hair over tib anter
-
lymphatic system
- palpate nodes = cervical, axilla, epitrochlear, superficial inguinal
- examine for edema - visual swelling, ROM, loss of funct mobility
- measure girth
- examine skin changes - texture, fibrotic changes
- presence of papules, leakage, wounds
- changes in function (ADL, funct mob, sleep)
- paresthesias?
- lymohangiography - x-ray of lymph nodes
-
chest x-ray
reveal abnormalities of lung fluids, overall cardiac shape and size (cardiomegaly), aneurysm
-
myocardial perfusion imaging
- Dx and eval ischemic heart dz, MI
- identify myocardial blood flow, areas of stress induced ischemia (exercise test), old infarct
- thallium - injected into blood and will show up in normal tissue but not ischemic/infarct tissue -- can be used with exercise test
-
echocardiogram
non-invasive; ultrasound to visualize internal structures - size of chambers, movement of valves, septum, abnormal wall movement
-
cardiac catheterization
passage of tiny tube thru heart into blood vessels with contrast medium into coronary arteries and x-ray
-
cardiac catherization
provides info about anamtomy of the heart and great vessels, ventricular function, abnormal wall movements - allows determination of EF (eject fraction)
-
central line (swan-ganz cath)
- into the R side of heart
- measures central venous pressure, pulm artery pressure, pulm capillary wedge pressure
-
enzyme changes associated with MI - CK or CPK
elevation of CK or CPK (serum creatine kinase or creatine phosphokinase) - peaks at 24 hours; released after tissue injury
-
enzyme changes associated with MI - CK-MB
CK-MB (serum creatine kinase MB) - peaks at 12-24 hours; better isolates the source to the myocardium, high sensitivity
-
enzyme changes associated with MI - proteins
elevations in tropinin I, troponin T: high sensitivity 10 hours after injury
-
enzyme changes associated with MI - myoglobin
elevation of myoglobin
-
serum lipids
lipid panel - mg/dL -- used to determine coronary risk
-
SpO2 values
Normal: SpO2 95%-100%; Clinical sig: SaO2 below 88% - supplemental O2 required
-
PaOs values
Normal: PaO2 80-100 mm HgClinical sig: increased in hypervent, decreas in cardiac decompensation, COPD, some NM d/o
-
pH values
- Normal: pH 7.35 - 7.45Clinical sig: <7.35 = acidotic, >7.45 is alkalotic increase in: -respitory alkalosis: hypervent, sepsis, liver dz, fever-metabolic alkalosis: vomiting, potassium depletion, diuretics, volume depletiondecrease in:-respiratory acidosis: COPD, respit depressants, myasthenia-metabolic
- acidosis (bicarbonate deficit): increased acids (DM, ETOH, starvation),
- renal failure, increased acid intake and loss of alkaline body fluids
-
PaCO2 values
Normal: PaCO2 35-45 mm HgClinical sig: increas in COPD; decreas in pregnancy, PE, and anxiety
-
normal values - ABG
clinical significance
- Normal: SpO2 95%-100%;
- Clinical sig: SaO2 below 88% - supplemental O2 required
- Normal: PaO2 80-100 mm Hg
- Clinical sig: increased in hypervent, decreas in cardiac decompensation, COPD, some NM d/o
- Normal: PaCO2 35-45 mm Hg
- Clinical sig: increas in COPD; decreas in pregnancy, PE, and anxiety
- Normal: pH 7.35 - 7.45
- Clinical sig: <7.35 = acidotic, >7.45 is alkalotic
- increase in:
- -respitory alkalosis: hypervent, sepsis, liver dz, fever
- -metabolic alkalosis: vomiting, potassium depletion, diuretics, volume depletion
- decrease in:
- -respiratory acidosis: COPD, respit depressants, myasthenia
- -metabolic acidosis (bicarbonate deficit): increased acids (DM, ETOH, starvation), renal failure, increased acid intake and loss of alkaline body fluids
-
PTT partial thromboplastin time values
- Normal: partial thromboplastin time (PTT) 25-40sec
- Clinical sig: increased in factor VII, IX, and X deficiency
-
PT - prothrombin time values
- Normal: prothrombin time (PT) 11-15secClinical sig: increased in
- factor x deficiency, hemorrhagic dz, cirrhosis, hepatitis drugs
- (warfarin), if clotting time is 2.5 + more than normal, PT is contraind
-
INR values
- Normal: INR (international normalized ratio) - ratio of individual's PT to reference range 0.9-1.1
- Clinical sig:
- INR below 2=desirable
- INR above 2: consult with MD for increas risk of bleeding
- INR above 3 = risk of hemarthrosis
-
bleeding time values
- Normal: bleeding time: 2-10 min; c-reactive protein CRP <10 mg/L
- Clinical sig: increased in platelet d/o, thrombocytopenia
- increased in levels associated with increased risk of athrosclerosis>100 mg/L associated with inflammation and infection
-
normal values of hemostasis (clotting/bleeding times)
clinical significance
- Normal: prothrombin time (PT) 11-15sec
- Clinical sig: increased in factor x deficiency, hemorrhagic dz, cirrhosis, hepatitis drugs (warfarin), if clotting time is 2.5 + more than normal, PT is contraind
- Normal: partial thromboplastin time (PTT) 25-40sec
- Clinical sig: increased in factor VII, IX, and X deficiency
- Normal: INR (international normalized ratio) - ratio of individual's PT to reference range 0.9-1.1
- Clinical sig: INR below 2=desirable
- INR above 2: consult with MD for increas risk of bleeding
- INR above 3 = risk of hemarthrosis
- Normal: bleeding time: 2-10 min; c-reactive protein CRP <10 mg/L
- Clinical sig: increased in platelet d/o, thrombocytopenia
- increaed in levels associated with increased risk of athrosclerosis
- >100 mg/L associated with inflammation and infection
-
WBC values
- Normal: WBC (white) 4,300 - 10,800
- Clinical sig: indicative of immune
- status; increased value in infection: bacterial and viral;
- inflammation, hematologic malignancy, leukemia, lymphoma, drugs
- (corticosteroids)
- decreased in aplastic anemia, B12 or folate deficiency with immunosuppression: increas risk of infect
- EXERCISE CONSIDERATIONS:
- - above 5000: light ex only
- - below 5000 with fever: exercise contraind
- - below 1000: use mask, standard precautions
-
RBC values
- Normal: RBC (red):
- female 4.2-5.9 10^6/uL;
- male = 4.6-6.2 10^6/uL
- Clinical sig: increased = polycythemiadecreased = anemia
-
ESR (erythrocyte sedimentation rate) values
- Normal: ESR (erythrocyte sedimentation rate) -
- female=below 20 mm/hr;
- male = below 15 mm/hr
- Clinical sig: increased sedimentation rate in infection and inflammation:
- rheumatic or pelvic inflamm dz, osteomylitis used to monitor effects of
- tx; RA, SLE, Hodgkins dz
-
Hct values
- Normal: Hct (hematocrit) % of RBC of the whole blood
- male = 45%-52%
- female= 37%-48%
- Clinical Sig: increased in erythrocytosis, dehydration, shockdecreased in severe anemias, acute hemorrhage
- EXERCISE CONSIDERATIONS:
- -more than 25% but less than normal = light ex only
- -less than 25% = exercise is contraind
-
Hgb values
- Normal: Hgb (hemoglobin)
- males: 13-18 g/dL
- females: 12-16 g/dL
- Clinical Sig: increased in polycythemia, dehydration, shock
- decreased in anemia, prolonged hemmhorage, RBC destruction (cancer or sickle cell dz)
- EXERCISE CONSIDERATIONS:
- - 8-10 g/dL: results in decreased ex tolderance, increased fatigue, and tachycardia; light ex only
- - below 8g/dL: ex contraind
-
Normal values for CBC
Clinical significance
- Normal: WBC (white) 4,300 - 10,800
- Clinical sig: indicative of immune status; increased value in infection: bacterial and viral; inflammation, hematologic malignancy, leukemia, lymphoma, drugs (corticosteroids)
- decreased in aplastic anemia, B12 or folate deficiency
- with immunosuppression: increas risk of infect
- EXERCISE CONSIDERATIONS:
- - above 5000: light ex only
- - below 5000: with fever, exercise contraind
- - below 1000: use mask, standard precautions
- Normal: RBC (red): female 4.2-5.9 10^6/uL; male = 4.6-6.2 10^6/uL
- Clinical sig: increased = polycythemia
- decreased = anemia
- Normal: ESR (erythrocyte sedimentation rate) - female=below 20 mm/hr; male = below 15 mm/hr
- Clinical sig:increased sedimentation rate in infection and inflammation: rheumatic or pelvic inflamm dz, osteomylitis used to monitor effects of tx; RA, SLE, Hodgkins dz
- Normal: Hct (hematocrit) % of RBC of the whole blood
- male = 45%-52%
- female= 37%-48%
- Clinical Sig: increased in erythrocytosis, dehydration, shock
- decreased in severe anemias, acute hemorrhage
- EXERCISE CONSIDERATIONS:
- -more than 25% but less than normal = light ex only
- -less than 25% = exercise is contraind
- Normal: Hgb (hemoglobin)
- males: 13-18 g/dL
- females: 12-16 g/dL
- Clinical Sig: increased in polycythemia, dehydration, shock
- decreased in anemia, prolonged hemmorage, RBC destruction (cancer or sickle cell dz)
- EXERCISE CONSIDERATIONS:
- - 8-10 g/dL: results in decreased ex tolderance, increased fatigue, and tachycardia; light ex only
- - below 8g/dL: ex contraind
-
platelet count values
- normal: 150,000-450,000 cells/mm^3
- clinical sig: increaesed in leukemia, hemoconcentration
- decreased in thrombocytopenia, acute leukemia, aplastic anemia, cancer chemo
- EXERCISE CONSIDERATIONS:
- - below 20,00: AROM, ADLs only
- - 20,000-30,000: light ex only
- - 30,000-50,000: moderate ex
-
fibrinogen plasma values
- normal: 175-433 mg/dL
- clinical sig: increased in inflamm states, pregnancy, oral contracept
- decreased in cirrhosis, hereditary dz
-
atherosclerosis
- lipid plaques affecting moderate to large sized arteries
- thickening and narrowing of intimal layer of blood vessel wall from focal accumulation of lipids, platelets, monocytes, plaque, and other debris
- risk fx:
- -age, sex, race, familial hx of CAD
- - smoking, HTN, yperlipidemia, elevated cholestrol and LDL levels, elevated blood homocystine, emotional stress
- - obesity, sedentary lifestyle, DM, elevated fibrogen levels
- - 2 or more risk fx multiples the risk of CAD
-
ACS acute coronary syndrome characteristics
- ranges from angina to infarction to sudden cardiac death
- imbalance of myocardial O2 supply and demand resulting in ischemic chest pain
- subacute occlusions may produce no symptoms
- symptoms present when lumen is at least 70% occluded
-
ACS acute coronary syndrome - angina pectoralis
- chest pain or pressure due to ischemia, may be accompanied by levines sign (pt clenches fist over sternum)
- represents imbalance in myocardial O2 supply and demand;
- brought on by:
- 1. increased demands on heart: exertion, emo stress, smoking, extremes of temperature (cold), over eating, tachyarrhythmias
- 2. vasospasm: symptoms may be present at rest
- There are 3 types of angina:
- 1. stable: classica exertional angina occuring during ex or ativity; occurs at a predictable rate-pressure product, RPP (HRxBP), relieved with rest and/or nitroglycerin
- 2. unstable: (preinfarction, crescendo angina); coronary insufficiency at rest without any precipitating factors or exertion. chest pain increases in severity, frequency, and duration; refractory to treatment. increases risk for MI or lethal arrhythmia; pain is difficult to control
- 3. variant: (prinzmetal's angina): caused by vasospasm of coronary arteries in the absence of occulsive dz. responds well to nitroglycerin or calcium channel blocker long-term
-
ACS acute coronary syndrome - MI
- prolonged ischemia, injury, and death of an area of the myocardium caused by occlusion of one or more of the coronary arteries
- precipitating factors: atherosclerosis with thrombus formation, coronary vasospasm or embolism, cocaine toxicity
- zones of infarct:
- 1. central zone: consists of necrotic non-contractile tissue; electrically inert; on EKG - see pathological q-waves
- 2. zone of injury: area immed adjacent to central zone; non-contractile tissue, cells undergo metabolic changes, electrically unstable, EKG shows elevated ST segment in leads over damaged area
- 3. zone of ischmia: outer area, cells also under-going metabolic changes, electrically unstable, EKG shows T-wave inversion
-
ACS acute coronary syndrome - MI
Infarct sites
- 1. transmural: q-wave infarct -- full thickness myocardium
- 2. nontransmural: (non-Q-wave infarct) -- subendocardial, subepicardial, intramural infarcts
- 3. sites of coronary artery occlusion: A. infer MI, R ventr infarct, distrubances of upper conduction system; R coronary artery; B. lateral MI, ventricular ectopy: circumflex artery; C. Anterior MI, distrubances of lower conduction system: left anterior descending artery
- impaired ventricular function results in:
- 1. decreased SV, CO, and EF
- 2. increased end diastolic ventricular pressure
- Electrical instability: arrythmias, present in injured and ischemic areas
-
ACS acute coronary syndrome - Heart Failure
- clinical syndrome in which the heart is unable to maintain adequate circulation of the blood to meet the metabolic demands of the body
- Types of heart failure:
- 1. left-sided heart failure: (CHF) characterized by pulmonary congestion, edema, low cardiac output due to backup of blood from L Ventricle to L atrium and lungs; occurs with insult to L ventricle from myocardial dz, excessive workload of the heart (HTN, valve dz, congenital defect), cardiac arrhythmias, heart damage.
- 2. right-sided heart failure: characterized by increased pressure load on right ventricle with higher pulm. vascular pressures; occurs with insult to R ventricle from LV failure, mitral valve dz, or chronic lung dz (cor pulmonale). produces hallmark signs of jugular vein distention and peripheral edema.
- 3. biventricular failure: severe LV pathology producing back-up in the lungs, increase PA pressure, and RV signs of HF
- Associated symptoms: Mm wasting, myopathies, osteoporosis
- clinical manifestations of heart failure
- compensated HF: heart returns to functional status with reduced CO and ex tolerance. Control achieved thru 1. physiological compensatory mechanisms; SNS stimulation, LV hypertrophy, anaerobic metabolism, cardiac dilation, aterial vasoconstriction and 2. medical therapy
-
Clinical manifestations of LV cardiac failure
- LV failure:
- S/S of pulm congestion: dyspnea, dry cough, orthopnea, paroxysmal nocturnal dyspnea, pulmonary rales/wheezing
- S/S of low CO: hypotension, tachycardia, lightheadedness, dizziness, cerebral hypoxia: irritability, restlessness, confusion, impaired memory, sleep disturbances; fatigue/weakness, poor ex tolerance, enlarged heart on chest x-ray, murmur(extra heart sounds), murmur of mitral or tricuspid regurgiation
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Clinical manifestations of RV cardiac failure
- RV Failure:
- S/S of pulm congestion: dependent edema, wt gain, ascities, liver engorgement (heptomegaly)
- S/S of low CO: anorexia, nausea, bloating, cyanosis, R upper quadrant pain, jugular vein distension, cyanosis at nail beds, R sided S3 sounds, murmurs of pulm or tricuspid infficiency
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MET: metabolic equivalent
- amount of O2 consumed at rest (sitting) = 3.5mL/kg per min
- MET levels: multiples of resting VO2; can be directly determined during ex tolerance tests (ETT) but not commonly done
- MET levels are estimated during ETT
- can be used to predict energy expenditure during certain activities
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Sternal precautions
- Sternal precautions include:
- Do not lift more than 5-8 pounds.
- No pushing or pulling with your arms.
- Do not reach behind your back or reach both arms out to the side.
- Do not reach both arms above shoulder height.
- All for 6-8 wks post-surgery
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