Cardiovascular system Flashcards
heart tissues
Pericardium:
-fibrous protective sac enclosing the heart
Epicardium:
-inner ayer of pericardium
Myocardium:
-heart muscle, major portion of the heart
Endocardium:
-smooth lining of the inner surface and cavities of the heart
heart chambers
RA: receives blood from vena cava
Tricuspid valve
RV: receives blood from RA and pumps blood via pulmonary artery to lungs for O2
“low pressure pulmonary pump”
LA: receives oxygenated blood from lungs and 4 pulmonary veins
Bicuspid valve
LV: receives blood from LA and pumps via aorta t/o systemic circulation
“high pressure systemic pump”
Heart valves
Atrioventricular valces: prevent back flow during ventricular systole
- R tricuspid
- L bicuspid
Semilunar valves: prevent backflow from aorta and pulmonary A into ventricle during diastole
- Pulmonary valve: prevents R backflow
- Aortic valve: prevents L backflow
systole=
ventricular contraction
end systolic ventricle volume ~50 mL
diastole=
ventricular relaxation and filling
end diastolic ventricle volume ~ 120 mL
atrial contraction
“atrial kick”
occurs during the last 1/3 of diastole and completes ventricular filling
comprising last 20-30% of end diastolic volume
coronary circulation
arteries: arise directly from aorta near aortic valve; blood circulates to myocardium during diastole
- R coronary A
- L coronary A
- —L anterior descending
- —Circumflex
Veins: parallel arterial system; coronary sinus receives venous blood from the heart and empties into the RA
Conduction:
specialized conduction tissue: allows rapid transmissionof electrical impulses throughout the myocardium (NSR)
Normal sinus rhythm:
- Origin in SA node- impulse spreads t/o both atria, which contract together
- impulse stimulates AV node, is transmitted down bundle of His Purkinje fibers
- impulse spreads t/o the ventricles which contract together (atrial kick)
SA node
- located at junction of vena cava and RA
- **main pacemaker of the heart; initiates impulse rate of 60-100 bpm
- has sympathetic and parasympathetic innervation affecting both HR and strength of contraction
AV node
- located at junction of RA and RV
- has sympathetic and parasympathetic innervation
- merges with bundle of His
- intrinsic firing rate of 40-60 bpm
Purkinje tissue
- R and L bundle braces of the AV node are located on either side of intraventricular septum
- terminate in Purkinje fibers, specialized conducting tissue spread t/o ventricles
- intrinsic firing rate of 20-40 bpm
Stroke volume=
the amount of blood ejected with each myocardial contraction
normal range= 55-100 mL/beat
Influenced by:
1- L ventricular end diastolic volume: the amount of blood left in the ventricle at the end of diastole (AKA preload). The greater the preload, the greater the quantity of blood pumped– Frank starling law
2-contractility: ability of the ventricle to contract
3- Afterload: the force the LV must generate during systole to overcome aortic pressure to open the aortic valve
Cardiac output
the amount of blood discharged from the L or R ventricle per minute
average adult at rest= 4-5 L/min
determined by HR x SV
Left ventricular end diastolic pressure
pressure in the LV during diastole
normal range 5-12mm Hg
Ejection fraction
percentage of blood emptied from the ventricle during systole
clinically useful measure of LV function
EF= SV/LVEDV
SV= blood ejected with contraction LVEDV= blood left in ventricle at end of diastole (preload)
normal EF averages >55%
-lower EF= more impaired LV
atrial filling pressure
the difference between the venous and atrial pressures
R atrial filling pressure is decreased during strong ventricular contraction and atrial filling is enhanced
R atrial filling pressure is affected by changes in intrathoracic pressure; decreases during inspiration and increases during coughing or forced expiration
venous return increases when blood volume expands and decreases during hypovolemic shock
diastolic filling time decreases with:
increased HR and with heart disease
myocardial oxygen demand (MVO2)
represents the energy cost to the myocardium
clinically measured by the product of HR and SBP
AKA Rate pressure product (RPP)
MCO2 increases with activity and with HR and/or BP
R coronary artery supplies:
RA
most of RV
and in most individuals the inferior wall of LV, AV node and bundle of His
Supplies SA node 60% of the time
L coronary artery supplies:
most of the LV
2 divisions:
1- L anterior descending: supplies LV and the inter ventricular septum
- in most individuals the inferior areas of the apex
- may also give off branches to RV
2- Circumflex: supplies blood to the lateral and inferior walls of the LV and portions of the LA
-supplies SA node 40% of the time
arteries
transport oxygenated blood from areas of high pressure to lower pressures in the body tissues
only exceptions:
- umbilican vein (in utero)
- pulmonary veins
arterial circulation is maintained by heart pump
influenced by elasticity and extensibility of vessel walls, and by peripheral resistance, amount of blood in the body
arterioles
terminal braces of arteries that attach to capillaries
primary site of vascular resistance
capillaries
include small blood vessels that connect the ends of arteries (arterioles) with the beginning of veins (venues)
form an anastomosing network
function for exchange of nutrients and fluids between blood and tissues
capillary walls are thin and permeable
veins
transport dark, unoxygenated blood from tissues back to the heart
larger capacity, thinner walls than arteries, greater number
1 way valves to prevent back flow
venous system includes both superficial and deep veins (deep veins accompany arteries while superficial ones don’t)
venous circulation is influenced by muscle contraction, gravity, respiration (increased return with inspiration), compliancy of R heart
lymphatic system
includes:
- lymphatics (superficial, intermediate, and deep)
- lymph fluid
- lymph tissues and organs (lymph nodes, tonsils, spleen, thymus, thoracic duct)
drains lymph from bodily tissues and returns it to venous circulation
major lymph nodes:
- submaxillary
- cervical
- axillary
- mesenteric
- iliac
- inguinal
- popliteal
- cubital
what order does lymph travel ?
lymph travels to lymphatic capillaries to lymphatic vessels to ducts to L subclavian vein
lymphatic contraction occurs by?
lymphatic contraction occurs by:
- parasympathetic, sympathetic and sensory nerve stimulation
- contraction of adjacent muscles
- abdominal and thoracic cavity pressure changes during normal breathing
- mechanical stimulation of dermal tissues
- volume changes within each lymphatic vessel
how does lymphatic system contribute to immune system function?
- lymph nodes collect cellular debris and bacteria
- remove excess fluid, blood waste and protein molecules
- produce antibodies
neurohumeral influences of cardiovascular system:
1- parasympathetic stimulation (cholinergic)
2- sympathetic stimulation (adrenergic)
3-additional control mechanisms
- baroreceptors (pressoreceptors) - control HR
- chemoreceptors -sensitive to changes in blood chemicals: O2, CO2, lactic acid
- body temperature
- ion concentration
4-peripheral resistance
parasympathetic stimulation
cholinergic
control located in medulla oblongata, cardioinhibitory center
via vagus nerve (CN X), cardiac plexus; innervates all myocardium; releases acetylcholine
slows rate and force of myocardial contraction; decreases myocardial metabolism
causes coronary artery vasoconstriction
sympathetic stimulation
adrenergic
control located in medulla oblongata, cardioacceleratory center
via cord segments T1-4, upper thoracic to superior cervical chain ganglia
- innervates all but ventricular myocardium
- releases epinephrine and norepinephrine
causes an increase in the rate and force of myocardial contraction and myocardial metabolism
causes coronary artery vasodilation
the skin and peripheral vasculature receive only postganglionic sympathetic innervation
-causes vasoconstriction of cutaneous arteries; -sympathetic inhibition must occur for vasodilation
drugs that increase sympathetic functioning= sympathomimetics
drugs that decrease sympathetic functioning= sympatholytics
baroreceptors
(pressoreceptors)
main mechanisms controlling HR
located in walls of aortic arch and carotid sinus; via vasomotor center
Circulatory reflex: respond to changes in BP
- increased BP results in parasympathetic stimulation, decreased rate and force of cardiac contraction; sympathetic inhibition, decreased peripheral resistance
- decreased BP results in sympathetic stimulation, increased HR and BP and vasoconstriction of peripheral blood vessels
- increased RA pressure causes reflex acceleration of HR
chemoreceptors
located in carotid body
sensitive to changes in blood chemicals: O2, CO2, lactic acid
increased CO2 or decreased O2, or decreased pH (elevated lactic acid) results in an increase in HR
increased O2 levels result in a decreased HR
neurohumoral influences: ion concentrations
hyper/hypo kalemia
hypo/hyper calcemia
hypo/hyper magnesemia
Hyperkalemia
increased concentration of potassium ions:
- decreases the rate and force of contraction
- produces ECG changes – widened PR interval and QRS, tall T wave
Hypokalemia
decreased concentration of potassium ions:
- produces ECG changes – flattened T waves, prolonged PR and QT intervals
- arrhythmias may progress to ventricular fibrillation
Hypercalcemia
increased calcium concentration
increases heart actions
Hypocalcemia
decreased calcium concentration
depresses heart actions
Hypermagnesemia
increased magnesium is a calcium blocker which can lead to arrhythmias or cardiac arrest
Hypomagnesemia
decreased magnesium causes ventricular arrhythmias, coronary artery vasospasm and sudden death
peripheral resistance
increased peripheral resistance increases arterial blood volume and pressure
decreased peripheral resistance decreases arterial blood volume and pressure
influenced by arterial blood volume: viscocity of blood and diameter or arterioles and capillaries
patient interview
Presenting symptoms:
- chest pain, palpitations, SOB
- fatigue
- dizziness, syncope
- edema
Positive risk factors
Negative risk factors
- high serum
- HDL >60 mg/dL
PMH:
- other diagnoses, surgeries
- meds
social history:
quality of life issues
- functional mobility
- ADLs, sleep
observation and inspection of skin color for possible signs of decreased CO and low O2 saturation
- cyanosis
- pallor
- diaphoresis
cyanosis
bluish color of the skin, nail beds, lips and tongue
related to decreased CO
pallor
washed out, absence of pink, rosy color
associated with decreased peripheral blood flow, PAD
diaphoresis
excess sweating and cool, clammy skin
non-modifiable risk factors for cardiovascular disease
Age:
- men >45
- women >55
Family history:
-cardiac event in 1st degree male relative pre-menopausal women
Modifiable risk factors for cardiovascular disease (goals to reduce risk)
Cholesterol:
- total: 40 mg/dL (men); >50 (women)
- Triglycerides:
physical exam for cardiovascular system
pulse
heart sounds
heart rhythm
blood pressure
respiration
oxygen saturation
pain
grading scale for peripheral pulses
0= absent pulse, not palpable
1+= pulse diminished, barely perceptible
2+= easily palpable, normal
3+= full pulse, increased strength
4+= bounding pulse
HR norms
adult and teens: 60-100 bpm
-40-60 in aerobically trained
children: 60-140 bpm
newborn: 90-164 bpm
tachycardia
HR >100 bpm
compensatory tachycardia can be seen with volume loss (surgery, dehydration)
positional tachycardia syndrome:
-sustained HR increase >30 bpm per minute within 10 minutes of standing (>40 bpm in teens)
bradycardia
HR
pulse abnormalities
irregular pulse: variations in force and frequency; may be due to arrhythmias, myocarditis
weak, thready pulse: may be due to low SV, cardiogenic shock
bounding, full pulse: may be due to shortened ventricular systole and decreased peripheral pressure; aortic insufficiency
auscultation landmarks
aortic valve:
2nd R intercostal space at sternal border
pulmonic valve:
2nd L intercostal space at sternal border
tricuspid valve:
4th L intercostal space at sternal border
bicuspid valve:
5th L intercostal space at midclavicular area
Normal heart sounds
S1 “lub”
- normal closure of mitral and tricuspid valves
- marks beginning of systole
- decreased in 1st degree heart block
S2 “dub”
- normal closure of aortic and pulmonary valves
- marks end of systole
- decreased in aortic stenosis
murmurs
extra sounds
systolic: falls between S1 and S2
- may indicate valvular disease (mitral valve prolapse) or may be normal
diastolic: falls between S2 and S1
- usually indicates valvular disease
grades of heart murmurs:
1- softest audible murmur
6- audible with stethoscope off the chest
thrill: an abnormal tremor accompanying a vascular or cardiac murmur
- felt on palpation
bruit
an adventitious sound or murmur (blowing sound) or arterial or venous origin
common in carotid or femoral arteries
indicative of atherosclerosis
gallop rhythm
an abnormal heart rhythm with 3 sounds in each cycle; resembles the gallop of a horse
S3:
- associated with ventricular filling
- occurs soon after S2
- in older individuals may indicate CHF (LV)
S4:
-associated with ventricular filling and atrial contraction
-occurs just before S1
indicative of pathology (CAD, MI, aortic stenosis, or chronic HTN)
P wave
atrial depolarization
PR interval
time required for impulse to travel from atria through conduction system to Purkinje fibers
normal 0.12-0.20 seconds
QRS wave
ventricular depolarization
ST segment
beginning of ventricular repolarization
ST segment changes:
- with impaired coronary perfusion (ischemia or injury), the ST segment becomes depressed
- depression can be upsweeping, horizontal or downsloping
- ST depression or elevation >1mm measured at the J point in 2 consecutive leads is considered abnormal
T wave
ventricular repolarization
QT interval
time for electrical systole
ventricular arrhythmias
originate from an ectopic focus in the ventricles (outside normal conduction system)
significant in adversely affecting CO
1-premature ventricular contractions (PVCs)
2- Ventricular tachycardia
3- Ventricular fibrillation
Premature ventricular contractions
a premature beat arising from the ventricle
occurs occasionally in the majority of the normal population
on ECG:
- no P wave
- bizarre and wide premature QRS
- followed by a long compensatory pause
serious PVCs: >6/min, paired or in sequential runs, multifocal, very early PVC
Ventricular tachycardia
a run of 3 or more consistent PVCs
very rapid rate (150-200 bpm)
may occur paroxysmally (abrupt onset)
usually the result of an ischemic ventricle
ECG:
- wide, bizarre QRS waves
- no P wave
Seriously compromised CO
Non-sustained ventricular tachycardia (NSVT): 3 or more consecutive beats in duration, terminating spontaneously in 30 seconds in duration and/or requiring termination due to hemodynamic compromise in
Ventricular fibrillation
a pulseless, emergency situation requiring emergency medical services; cardiopulmonary resuscitation (CPR), defibrillation, meds.
characterized by chaotic activity of ventricle originating from multiple foci; unable to determine rate
ECG:
-bizarre, erratic activity without QRS complex
no effective CO
clinical death within 4-6 min
Atrial arrhythmias
(supraventricular)
rapid and repetitive firing of one or more ectopic foci in the atria (outside the sinus node)
on ECG: P waves are abnormal (variable in shape) or not identifiable (Afib)
rhythm may be irregular: chronic or occurring paroxysmally
Rate:
- rapid with atrial tachycardia (140-250 bpm)
- atrial flutter (250-350 bpm)
- atrial fibrillation (>300 bpm)
CO is usually maintained if rate is controlled; may precipitate ventricular failure in an abnormal heart
Atrioventricular blocks
abnormal delays or failure to conduct through normal conducting system
1st, 2nd or 3rd (complete) degree AV blocks; bundle branch blocks
if ventricular rate is slowed, CO decreased
3rd degree, complete heart block is life threatening; requires meds (atropine), surgical implantation of pacemaker
Potassium level influence on ECG
hyperkalemia: decreases rate and force of contraction
- widens QRS
- flattens P wave
- T wave peaks
Hypokalemia:
- flattens T wave (or inverts)
- produces U wave
Calcium level influence on ECG
Hypercalcemia: increases heart actions
- widens QRS
- shortens QT interval
Hypocalcemia:
-prolongs QT interval
Hypothermia influence on ECG
elevates ST segment
slows rhythm
decreased body temp causes HR to decrease
Digitalis influence on ECG
depresses ST segment
flattens T wave (or inverts)
QT shortens
Quinidine influence on ECG
antiarrhythmia
QT lengthens
T wave flattens (or inverts)
QRS lengthens
beta blockers influence on ECG
(propanolol, inderal)
decreases HR, blunts HR response to exercise
nitrates influence on ECG
nitroglycerin
increases HR
holter monitoring
continuous ambulatory ECG monitoring via tape recording of cardiac rhythm for up to 24 hours
-used to evaluate cardiac rhythm, transient symptoms, pacemaker function, effect of meds
allows correlation of symptoms with activities
Normal BP
Adult:
-SBP
orthostatic hypotension
drop in BP that accompanies change from supine to standing position
initial BP and HR with patient in supine, at rest for >5 min
repeat measures at immediate standing and again at 3 minutes
orthostaic= SBP drops >20, DBP >10
common symptoms: lightheadedness, dizzy, LOB and leg weakness
mean arterial pressure (MAP)
the arterial pressure within the large arteries over time; dependent upon mean blood flow and arterial compliance
MAP= (SBP + DBPx2) / 3
important clinical measure in critical care
normal MAP 70-110 mmHg
respiratory rate
normal adult= 12-20 bpm
normal child= 20-30 bpm
normal newborn= 30-40 bpm
tachypnea= RR>22 bpm
bradypnea = RR
dyspnea
=SOB
dyspnea on exertion (DOE)
borg dyspnea scale:
0= nothing
10=maximal
orthopnea
inability breathe when in a reclining or supine position
paroxysmal nocturnal dyspnea
sudden inability to breathe occurring during sleep
Blood pressure levels
Normal/optimal
180 / >110
adventitious lung sounds
crackles (rales): rattling, bubbling sounds; may be due to decorations in the lungs
wheezes (rhonchi): whistling sounds
Anginal scale
1+ = light, barely noticeable
2+ = moderate, bothersome
3+ = severe, very uncomfortable
4+ = most severe pain ever experienced
pulse oximetry
an electronic device that measures the degree of saturation of hemoglobin with oxygen (SaO2)
normal 95-100% oxygen
provides an estimate of PaO2 (partial pressure of oxygen) based on oxyhemoglobin desaturation curve
hypoxemia
abnormally low amount of oxygen in the blood (SaO2
hypoxia
low oxygen level in the tissues
anoxia
complete lack of oxygen
ischemic cardiac pain
(angina or myocardial infarction)
diffuse, retrosternal pain; or a sensation of tightness, ashiness, in the chest
associated with dyspnea, sweating, indigestion, dizziness, syncope, anxiety
referred cardiac pain
cardiac pain can refer to shoulders, back, arms, neck or jaw
pain referred to the back can occur from dissecting AAA
examining the peripheral vascular system
Condition of extremities
- diaphoresis: associated with decreased CO
- arterial pulses: decreased/absent pulses associated with PAD; examine bilaterally distal>proximal
- skin color: cyanosis, pallor, rubor
- skin temperature
- skin changes
- pain: intermittent claudication
- edema:
tests for peripheral venous and arterial circulation
examine lymphatic system
rubor
dependent redness with PAD
skin changes
clubbing:
- curvature of the fingernails with soft tissue enlargement at base of nail
- associated with chronic oxygen deficiency, chronic pulmonary disease or heart failure
trophic changes
-pale, shiny, dry skin, with loss of hair is associated with PAD
fibrosis
- tissues are tick, firm and unyielding
- Stemmer’s sign: dorsal skin folds of the toes and fingers are resistant to lifting
- indicative of fibrotic changes and lymphedema
abnormal pigmentation, ulceration, dermatitis, gangrene: all associated with PAD
temperature: decrease in superficial skin temp is associated with poor arterial perfusion
Intermittent claudication
pain, cramping and LE fatigue occurring during exercise and relieved by rest
-associated with PAD
typically in calf; may also be in thigh, hips or buttocks
patient may experience pain at rest with severe decrease in arterial blood supply; typically in forefoot, worse at night
peripheral causes of edema:
chronic venous insufficiency and lymphedema
bilateral edema is associated with CHF
grading scale for pitting edema
1+ mild, barely perceptible indentation
30 seconds or more
>1 in pitting
tests for peripheral venous circulation
examine venous circulation before arterial (venous insufficiency can invalidate some arterial tests)
1- Percussion test- greater saphenous vein
2-Trendelenburg test (retrograde filling test) - communicating veins and saphenous system
3- Venous filing time
4- doppler US
5- air plethysmography (APG)
tests of peripheral arterial circulation
1- ankle brachial index (ABI)
2- rubor of dependency
3- intermittent claudication
- have patient walk on level grade, stop with pain
- note time, subjective rating of pain
- examine for coldness, numbness or pallor, loss of hair over anterior tib
- leg cramps may also result from diuretic use with hypokalemia
ABI
the ratio of LE pressure divided by UE pressure
pt in supine and at rest for 5 min
BP at brachial artery and at posterior tibial or doornails media arteries
ABI assists in risk stratification for cardiovascular disease
> 1.40 indicates non-compliant arteries
1 - 1.4 = normal
0.91 -0.99 = borderline
rubor of dependency
examine color changes in skin during elevation of foot followed by dependency (seated, hanging position)
with insufficiency, pallor develops in elevated position; reactive hyperemia (rubber of dependency) develops in dependent position
changes that take >30 seconds are also indicative of arterial insuffienciency
examining the lymphatic system
palpate superficial lymph nodes: cervical, axillary, epitrochlear, superficial inguinal
examine for edema
examine skin
- changes in texture, fibrotic tissue changes
- presence of papules, leakage, wounds
changes in function
paresthesias might be present
lymphangiography and lymphoscintigraphy using radioactive agents (X-ray of lymph vessels)
subjective rating of pain with intermittent claudication
I: min discomfort or pain
II: moderate discomfort/pain; patient’s attention can be diverted
III: intense pain; patient’s attention can’t be diverted
IV: excruciating and unbearable pain
chest xray
will reveal abnormalities of lung fluids, overall cardiac shape and size (cardiomegaly), aneurysm
myocardial perfusion imaging
used to diagnose and evaluate ischemic heart disease, myocardial infarction
Thallium-radioisotope injected into blood
used to identify myocardial blood flow, areas of stress induced ischemia (exercise test), old infarcts
positron emission tomography (PET)- radioactive marker
echocardiogram
non-invasive
US to assess internal structures: size of chambers, wall thickness, EF, movement of valves, septum, abnormal wall movement
cardiac catheterization
passage of a tiny tube from brachial or femoral artery through aorta into blood vessels with introduction of a contrast medium into coronary arteries and subsequent x-ray
provides info about anatomy of heart and great vessels, ventricular and valve function, abnormal wall movements
allows determination of EF
central line (swan ganz catheter)
catheter inserted through vessels into R side of heart
measures central venous pressure, pulmonary artery pressure, pulmonary capillary wedge pressures
cardiac MRI
creates 3D images of the heart to investigate coronary arteries, aorta, pericardium and myocardium
arterial blood gases
SpO2:
PaO2:
PaCO2:
pH:
SpO2
normal: 98-100%
PaO2
90-100 mmHg
partial pressure of oxygen
PaCO2
35-45 mmHg
increased in COPD, hypoventilation
decreased in hyperventilation, pregnancy, PE and anxiety
pH
7.35 - 7.45
- 45 = alkalosis
- respiratory alkalosis: hyperventilation, sepsis, liver disease, fever
- metabolic alkalosis: vomiting, potassium depletion, diuretics, volume depletion
hemostasis (clotting/bleeding times)
prothrombin time (PT): 11-15 seconds
partial thromboplastin time (PTT): 25-40 seconds
international normalized ratio (INR): ratio of one’s PT to reference range: 0.9-1.1
-patients with DVT, PE100 mg/L associated with inflammation and infection
White blood cells
4300-10,800 cells/mm3
indicative of status of immune system
increased in infection: bacterial, viral; inflammation, hematologic malignancy, leukemia, lymphoma, drugs (corticosteroids)
decreased in aplastic anemia, B12 or folate deficiency
with immunosuppression: increased risk of infection
PT considerations:
-consider metabolic demands in presence of fever and use mask when WBCs
Red blood cell
“erythrocyte” - transports O2 and CO2 to and from tissues
male: 4.6-6.2
female 4.2-5.9
increased in polycythemia
decreased in anemia
Erytherocyte sedimentation rate
ESR
the speed at which the RBCs settle after an anticoagulant has been added to a blood sample
- the rate increases with infection or inflammation (RA, pelvic inflammatory disease)
- osteomyelitis- used to monitor effects of treatment
male:
hematocrit (Hct)
% of RBC in whole blood
males: 45-52%
females: 37-48%
* age dependent
increased in erythrocytosis, dehydration, shock
decreased in severe anemias, acute hemorrhage
PT considerations: can cause decreased exercise tolerance, increased fatigue and tachycardia
hemoglobin (Hgb)
male: 13-18 g/dL
female: 12-16 g/dL
age dependent
increased in polycythemia, dehydration, shock
decreased ni anemias, prolonged hemorrhage, RBC destruction (cancer, sickle cell)
PT considerations: can cause decreased exercise tolerance, increased fatigue and tachycardia
platelet count
150,00 - 450,000 cells/mm3
increased in chronic leukemia, hemoconcentration
decreased in thrombocytopenia, acute leukemia, aplastic anemia, cancer chemotherapy
PT considerations:
-increased risk of bleeding with low levels so monitor for hematuria, petechiae, and other signs of active bleeding
