Cardiac Exam 2

functions of the cardiovascular system

-transportation of oxygen, nutrients, and hormones to the tissues
-transportation of CO2 and wastes away from the tissues and to the lungs/kidneys
-urine formation

general cardiovascular responses to exercise

-activation of the sympathetic nervous system
-increased cardiac output
-increased blood flow to skeletal muscle and skin
-decreased blood flow to the viscera, including kidneys
-maintained blood flow to the brain

oxygen delivery

-if there is inadequate oxygen delivery to the tissues, anaerobic metabolism will be triggered
-this is detrimental because it limits protein and fat metabolism and increases production of lactic acid

oxygen extraction ratio

-this is the percentage of oxygen delivered that was actually CONSUMED

three surfaces of the heart

-the heart is rotated to the left and tilted posteriorly
-sternocostal surface is the right side of the heart
-diaphragmatic surface is mostly the left ventricle, some of the right ventricle
-posterior surface/base is mostly the left atrium, some of the r

apex of the heart

-tip of the left ventricle
-located at the level of the fifth rib at the midclavicular line

base of the heart

-located at the level of the third rib


-double-layered membrane surrounding the heart
-fibrous pericardium: outer layer
-serous pericardium: inner layer, made up of the partietal and visceral pericardium
-there is a small fluid-filled cavity between the parietal and visceral pericardium

layers of cardiac tissue

-epicardium: outermost layer, same structure as the visceral pericardium
-myocardium: middle layer, composed of cardiac muscle tissue
-endocardium: innermost layer, epithelium that lines the chambers and valves
-endocarditis: inflammation of the endocardi


-right ventricle: wall is very thin
-left ventricle: wall is very thick, needs more muscle to generate enough force to pump blood throughout the body
-the left ventricle is the workhorse, and most infarctions occur in the left

papillary muscle

-muscle that attaches to the ventricular wall and the chordae tendineae
-papillary muscles do NOT make the valves open and close, this is accomplished by pressure differences
-papillary muscles help to prevent the valve cusps from bulging upwards back int

four properties of cardiac muscle

-functional syncytium
-inherent spontaneous rhythmicity
-polarized irritability
-all or none law

functional syncytium

-the cells of the atria and ventricles contract simultaneously, functioning as if they were one cell
-this can be accomplished due to the branching of the muscle fibers and the intercalated disks, which allow for rapid transmission of the depolarization

inherent spontaneous rhythmicity

-the cells of the heart can depolarize on their own without outside nervous input
-this is why we can have heart transplants
-this is also why we can get arrhythmias

polarized irritability

-some parts of the heart are more excitable than others
-the most unstable resting potential is at the SA node
-sodium and potassium are very leaky here, so it's easy for depolarization to occur
-if the SA node is pacing the heart, HR will be around 60-90

all or none law

-there is no recruitment of motor units in cardiac muscle
-either all muscle fibers fire, or none do

filling of the ventricles

-about 70-80% of ventricular filling is PASSIVE
-the last 20-30% occurs when the atria go into systole and provide the atrial kick
-with atrial fibrillation, there is no active atrial output, so you only get about 70-80% of normal ventricular filling

atrial fibrillation

-most common abnormal heart rhythm in the older adult
-the cells of the atria do not depolarize together, so there is no atrial kick

opening and closing of the heart valves

-the valves open and close because of pressure differences, NOT because of papillary muscle or contraction

ventricular diastole

-during diastole, the ventricles relax and ventricular pressure starts to drop
-once the pressure in the ventricles is less than the pulmonary artery and aorta, those valves close
-some blood in the ascending aorta falls backwards and is caught by the cus

ventricular systole

-during systole, the ventircles contract and pressure starts to build up
-once the pressure in the ventricles is greater than the atria, the tricuspind and mitral valves are forced closed
-for just an instant, all 4 valves are closed
-pressure continues t

smooth muscle in blood vessels

-there is a lot MORE smooth muscle fibers in the arterial side than venous side, so the veins are more compliant
-the arterioles are really the GATE KEEPERS to the capillaries
-this is because arterioles have the MOST smooth muscle fibers
-when a patient

bulk flow

-blood pressure is what pushes fluid out of the capillaries and into the interstitial space for nutrient delivery
-this is why MAP and perfusion pressure are so critical
-osmotic pressure is what sucks fluid from tissues back into the capillaries for wast

collateral circulation

-coronary arteries have collateral branches that are typically closed
-when faced with tissue hypoxia, these collaterals will open up
-furthermore, chronic hypoxia can stimulate the formation of new anastomoses

right coronary artery

-branches off the aorta at the aortic valve
-supplies the right atrium, right ventricle, left ventricular inferior wall, and posterior 1/3 of interventricular septum
-in 90% of the population, the RCA also forms the posterior descending artery and supplie

left coronary artery

-branches off the aorta at the aortic valve
-only about an inch long
-branches into the left anterior descending and circumflex arteries

left anterior descending artery

-supplies the left ventricular anterolateral wall (more anterior than lateral) and anterior 2/3 of interventricular septum
-it does not contribute as much to the nodes as the RCA and left circumflex

left circumflex artery

-supplies the left atrium, left ventricular anterolateral wall (more lateral than anterior), and left ventricular posterolateral wall
-in 10% of the population, the left circumflex artery also forms the posterior descending artery and supplies the left ve

cardiac metabolism

-the heart is NOT a picky organ
-the heart can use glucose, fatty acids, amino acids, and lactate for fuel
-at rest, the heart mostly relies on fatty acids
-during moderate exercise, the heart equally relies on fatty acids, glucose, and lactate
-during he

oxygen consumption

-the amount of oxygen required by the body for a given activity
-VO2 = CO * A-VO2
-CO measures the heart's ability to pump blood
-A-VO2 difference measures the peripheral tissue's ability to extract O2
-the delivery system is what limits VO2 in people wit

heart rate

-max HR decreases with age
-increased HR means increased oxygen demand by the heart
-increased HR leads to decreased diastolic filling time

nervous system control of the heart

-the heart is dually innervated by the vagus nerve and sympathetic nerves (beta 1's)
-at rest, the vagus nerve is the MAIN thing controlling your heart by holding the SA node back (intrinsic rate of SA node is 110-118)
-MOST of the time in a 24-hour perio

vagus nerve

-decreases HR, contractility, and speed of conduction through AV node

sympathetic nerves (beta 1's)

-increase HR, contractility, and speed of conduction through AV node

sympathetic receptors

-alpha receptors are abundant in the peripheral vessels and cause VASOCONSTRICTION
-beta 1 receptors are located in the heart
-beta 2 receptors are outnumbered by alphas in the periphery, but they are dominant in the coronary arteries and cause VASODILATI

heart transplant

-when a heart is transplanted, the vagus nerve and sympathetic nerves are cut
-therefore, after receiving the heart, the patient's resting HR will be at the intrinsic rate of the SA node
-HR can still be modulated via hormones in the systemic circulation


-normal range in adults is 3.5-5.0 mEq/L
-hyperkalemia is > 5.1 mEq/L
-hypokalemia is < 3.2 mEq/L and is MORE concerning
-hypokalemia can cause dangerous ventricular arrhythmias, cardiac irritability, ST segment depression, dizziness, hypotension, and dec


-normal range in adults is 134-142 mEq/L
-hypernatremia is > 150 mEq/L
-CHF and hypovolemia are causes
-older adults have a faulty thirst mechanism and often don't hydrate well

stroke volume

-SV reflects the effectiveness of the heart as a pump
-3 components of SV: preload, contractility, and afterload
-preload is determined by venous return and distensibility
-contractility is determined by EDV and ejection fraction
-afterload is mostly dete

ejection fraction

-resting EF: 55-70% is normal
-resting EF < 55% is reduced
-should increase with exercise as SV increases beyond the increase in EDV due to sympathetic input

location of blood volume

-at any given moment, about 70% of your blood is located in your veins, available for quick return if needed
-10% is in the systemic arteries
-15% is in pulmonary circulation
-5% is in capillaries

A-VO2 difference

-the body PREFERS to meet oxygen demand by increasing CO rather than oxygen extraction
-at rest, skeletal muscle pulls out about 25% of oxygen
-however, skeletal muscle can triple this amount if needed
-at rest, cardiac muscle pulls out about 70-80% of ox

nitric oxide

-endothelium can produce and store nitric oxide, which causes LOCAL VASODILATION
-it is released in response to drug stimulation, as well as flow-mediated
-nitric oxide release is an important mechanism of enhanced blood flow

metabolite release

-the chemical envirionment near a working muscle can trigger LOCAL VASODILATION
-metabolites include decreased pH, increasd CO2, increased calcium (vasoconstrictor), increased ADP, decreased O2, increased magnesium (vasodilator), and increased body temper

baroreceptor reflex

-baroreceptors are stretch receptors located in the walls of the aorta and carotid arteries that pay attention to blood flow going by them
-when there is an increase in SV and BP (supine), the baroreceptors respond by signalling for an increase in vagal t

atrial stretch reflex

-this reflex contributes to diuresis if the patient is lying flat
-atrial stretch receptors sense plenty of blood going by
-therefore, there is an increase in atrial natriuretic factor, decreased ADH, and decreased renin
-all of these contribute to an inc

myocardial oxygen consymption

-the amount of oxygen required by the heart for a given activity
-MVO2 = CBF * A-VO2
-remember that cardiac muscle fibers already extract 70-80% of the oxygen that is delivered at rest
-therefore, coronary blood flow is CRITICAL to ensure adequate oxygen

coronary blood flow

-blood flow to cardiac muscle
-determined by driving pressure and resistance to blood flow
-driving pressure = systemic DBP - LVEDP
-NORMAL left ventricular EDP is less than 12
-resistance to blood flow depends on metabolic factors (hypoxia, anemia), mech

myocardial oxygen supply vs demand

-HR and SBP are on the demand side
-RPP = peak HR * peak SBP, which is a good index of myocardial oxygen demand
-contractility is also on the demand side, meaning the stronger the contraction is, the more oxygen is required
-left ventricular wall tension

P wave

-atrial depolarization

PR interval

-from beginning of P wave to the beginning of the QRS complex
-should be 0.12-0.20 seconds
-this is the amount of time it takes the depolarization to transmit from the SA node, through the atria, through the AV node, and to the ventricles
-the 0.1 second

QRS complex

-ventricular depolarization
-should be 0.06-0.10 s

ST segment

-from the end of the QRS complex to the beginning of the T wave
-should be on baseline

J point

-point at the end of the QRS and beginning of the ST segment

T wave

-ventricular repolarization
-ST segment and T wave are sensitive indicators of myocardial oxygen supply and demand status
-inverted T wave doesn't mean that the patient definitely has ischemia/infarction, it can be due to hyperventilation

QT interval

-from the beginning of the QRS complex to the end of the T wave
-looks at the amount of time for the entire ventricular cycle
-normal QT interval should be less than half the distance of the R to R interval
-physicians are concerned about prolonged QT int

blood pressure

-BP = CO * TPR
-baroreceptors are extremely important for monitoring blood pressure when changing positions
-however, the baroreceptors accommodate quickly and are not as effective in older patients
-RAAS is an important control of both blood pressure and


-this system helps to regulate both blood pressure and blood volume
-it is triggered by firing of the sympathetic nervous system, which is MASS RESPONSE
-first, the kidney release renin into the bloodstream
-renin activates angiotensinogen into angiotensi

mean arterial pressure

-the average pressure pushing blood through the circulatory system
-MAP = DBP + 0.33(SBP - DBP)
-normal MAP is 70-110 mm Hg
-MAP < 60 means that there is INADEQUATE perfusion pressure
-the LOWER the MAP is, the more concerned you need to be about the vita

vascular area

-vascular area significantly goes up when you reach the arterioles, capillaries, and venules
-therefore, flow velocity is lower here to provide time for nutrient exchange

rate pressure product

-RPP is a great index of myocardial oxygen demand
-it increases with activity, but decreases at a given workload with training
-in cardiac rehab, we can't do a lot to increase blood supply
-however, we can LOWER the demand via exercise tra


-12-16 g/dL in females
-14-17 g/dL in males


-this is the best index of O2 carrying capacity in the blood
-36-47% in females
-41-51% in males


-percent of arterial hemoglobin oxygen saturation
-normal is greater than 94%
-patients with < 90% may require supplemental O2


-percent of venous hemoglobin oxygen saturation
-normal is 60-80%
-this value provides you with a sense of how much oxygen is being extracted by the tissues
-remember that the body likes to meet its oxygen demand by enhancing CO, not by pulling out a humo

normal cardiovascular changes with aging

-blood vessel walls get thicker and stiffer
-decreased elasticity of major blood vessels
-the ventricles of the heart are less distensible
-fibrotic changes occur in the valves
-enlarged left atrium due to the rigid left ventricle, often results in an aud

consequences of cardiovascular changes with aging

-increased SBP
-increased afterload
-decreased HR max and SV at max effort (no big impact on resting values)
-slowed myocardial tension development
-decreased inotropic response to catecholamines
-decreased max cardiac ouput
-decreased VO2 max

elderly vs young

-decreased HR at same %VO2 max in older patients, but similar at the same absolute work rate
-decreased CO at same relative and absolute work rates, so A-VO2 difference is higher
-decreased SV, increased BP, and increased TPR at the same relative and abso

orthostatic hypotension

-SBP decrease of greater than or equal to 20 or a DBP decrease of greater than or equal to 10 within 3 minutes of standing
-symptoms include dizziness, faintness, and lightheadedness

causes of orthostatic hypotension

-volume depletion (older patients are often on a diuretic and don't drink much)
-vasodilating drugs
-prolonged immobility
-slowed normal regulatory mechanisms (baroreceptor reflex)
-endocrine and metabolic disorders, such as diabetes
-nervous system disea

suggested interventions for orthostatic hypotension

-elastic stockings
-sleep with head of bed elevated about 15-20 degrees
-eat frequent small meals
-avoid valsalva maneuver
-avoid hot showers or excessive heat
-avoid sudden standing

arm vs leg exercise

-HR and BP are higher with arm exercise, at a GIVEN workload
-this is because a given workload is relatively higher for the arms than the legs
-therefore, there is no difference at the same RELATIVE workload
-we usually do about 40% of the work with the a

normal effects of dynamic exercise

-increased VO2
-increased CO
-increased HR
-increased SV, then levels off
-increased SBP
-no change in DBP
-decreased TPR
-left ventricular eccentric hypertrophy

effects of age, disease, and deconditioning

-decreased VO2 max
-increased VO2 at a given workload
-decreased CO
-decreased HR max
-decreased SV max
-decreased A-VO2
-increased BP
-increased TPR

normal effects of static exercise

-increased VO2
-increased CO
-increased HR that is greater than dynamics
-SV stays relatively the same
-huge increase in SBP
-increased DBP
-no change in TPR
-left ventricular concentric hypertrophy

general signs and symptoms of CVD

-weight change
-poor exercise tolerance

integumentary signs and symptoms of CVD

-pressure ulcers
-loss of body hair

CNS signs and symptoms of CVD

-impaired vision
-dizziness or syncope (especially in elderly)

respiratory signs and symptoms of CVD

-labored breathing
-productive cough

cardiovascular signs and symptoms of CVD

-chest pain

genitourinary signs and symptoms of CVD

-uringary frequency
-concentrated urine
-decreased urinary output

musculoskeletal signs and symptoms of CVD

-muscular fatigue

gastrointestinal signs and symptoms of CVD


NYHA classification

-classification of the severity of a patient's heart failure based on their function
-class 1: no limitation of activity
-class 2: slight limitation of activity
-class 3: moderate, marked limitations
-class 4: severe, symptoms at rest

pathogenesis of CAD

-the first step is injury to the endothelium
-fat deposition
-platelets adhere to damaged endothelium
-platelets release growth factors that stimulate production of connective tissue cells and attraction of smooth muscle cells
-sclerotic plaque forms


-injured endothelium lacks the normal formation and release of nitric oxide
-therefore, these diseased vessels are more prone to spasm and they lack the normal ability to dilate

risk factors for CAD

-modifiable: physical inactivity, smoking, high cholesterol, hypertension, systemic inflammation, homocysteine, and sleep apnea
-nonmodifialbe: age, family history, ethnicity
-contributing factors: obesity, diabetes, response to stress, personality type,

physical inactivity

-one of the top modifiable risk factors for CAD
-has been likened to smoking a pack of cigarettes/day in terms of risk
-there is a linear drop in risk of MI with increased frequency of exercise
-the exercise required does not need to be of vigorous intens


-one of the top modifiable risk factors for CAD
-triples risk

high cholesterol

-one of the top modifiable risk factors for CAD
-the best predictor or risk when looking at cholesterol is the TC/HDL ratio
-ratio > 4.5 indicates increased risk of developing atherosclerosis
-most doctors try to keep the TC < 200, LDL < 100, and HDL betw


-one of the top modifiable risk factors for CAD
-about 70% of patients over 65 have HTN
-HTN is NOT just a problem in the elderly
-high risk groups include African Americans, Hispanics, Pacific islanders, and Native Americans

systemic inflammation

-risk factor for CAD
-the liver puts out Crp in response to systemic inflammation
-excessively high levels of Crp indicate a tripled risk


-risk factor for CAD
-an amino acid that is produced from the breakdown of methionine, which is found in protein-rich foods such as red meat
-homocysteine appears to contribute to damage in the endothelium
-leafy greens can help to break apart homocystein

sleep apnea

-risk factor for CAD
-a disorder in which the person stops breathing for brief periods while asleep
-often seen in people with obesity

contributing factors for CAD

-obesity: particularly android
-response to stress: especially with HTN
-personality type: angry, hostile type A
-diabetes: number one cause of death in diabetics in MI
-hormonal status: premenopausal women are somewhat protected by estrogen, but HRT does

treating CAD

-most doctors won't intervene surgically until the vessel is occluced about 70%
-although it may take up to a year, the combination of moderate exercise, low fat diet, and stress management has proven to help reverse occlusion
-some studies show that exer

cardiopulmonary exam history

-medical diangosis
-risk factors
-diagnostic tests
-surgical history
-lab tests

cardiopulmonary exam subjective complaints

-chest pain: can be cardiac, pleural, or MSK (breathing won't impact ischemic pain)
-edema: could be R CHF (both legs). renal dysfunction, lymphedema
-fatigue: common but not specific
-lightheadedness and dizziness: make sure to check BP, could also be hy

cardiopulmonary exam inspection

-general appearance
-functional activity level (HUGE part of our job)

cardiopulmonary exam auscultation

-heart sounds should be auscultated in patients with heart failure, as they may have an S3
-end inspiratory crackles are also common in left CHF


-the first heart sound, heard when the atrioventricular (mitral and tricuspid) valves close and the ventricles go into systole
-systolic sound


-the second heart sound, heard when the semilunar (aortic and pulmonic) valves close and the ventricles go into diastole
-diastolic sound


-abnormal heart sound known as ventricular gallop that is associated with a dilated ventricle (eccentric hypertrophy)
-this sound follows S2
-it can be an early sign of CHF
-it may be present at rest, but it could also be brought on if the workload is too


-abnormal heart sound known as atrial gallop
-associated with a rigid ventricle

aortic valve

-located at the second rib space, to the right of the sternum

pulmonic valve

-located at the second rib space, to the left of the sternum

tricuspid valve

-located at the 4th-5th rib space, at the lower left sternal border

mitral valve

-located at the 5th rib space, medial to the midclavicular line

activity assessment

-it is important to monitor a patient's HR, rhythm, BP, and symptoms in supine, sitting, standing, and during activity
-this is because you want to make sure that you correctly interpret the heart's response to a positional change or activity

resting heart rate

-normal RHR is 60-100 bpm
-bradycardia: could be due to training effects, medications, severe CAD, or not in sinus rhythm
-tachycardia: could be due to deconditioning, medications, CHF, anemia, hypoxia, or arrhythmia
-RHR < 50 or > 110, check with MD or R


-without ECG monitoring equipment, you can only determine if the rhythm is regular or irregular
-regularly irregular: includes early beats and pauses
-irregularly irregular: only an average HR can be determined, A-fib is a common cause
-when a patient has


-a strong pulse indicates a good SV or decreased peripheral resistance
-a weak pulse indicates a low SV or increased peripheral resistance

heart rate response during exercise

-HR should increase about 10 beats/MET unless patient is on a beta blocker
-HR increase during exercise can give you an idea of heart health (smaller increase in trained, greater increase in untrained)
-bradycardic response: > 10 bpm drop in HR with incre


-RPE can be used as an alternative to HR as a measure of exercise intensity
-rating should be based on total feeling of exertion and fatigue
-this is especially usefl for patients on beta blockers
-we usually want patients around an RPE of 13, which is st

heart rate recovery post exercise

-heart rate recovery reflects parasympathetic reactivation
-normally, HR should drop by more than 12 bpm after the first minute post-exercise
-a drop of 12 or fewer is abnormal, even in most patients with beta blockers

resting blood pressure

-normal resting blood pressure is less than 120/80
-hypertension is defined as SBP > 130 and/or DBP > 80
-SBP < 90 should be cautious with exercise, but SBP < 80 is often a contraindication to exercise
-SBP > 180 is a contraindication to exercise
-DBP < 6

blood pressure response during exercise

-SBP should increase about 7-10/MET, with no change in DBP
-hypotensive response: SBP drop of 10-20 with increased workload or DBP drop > 10 below resting, patient can continue exercise with drop of 10 if asymptomatic, but patient should be stopped with d

pulse pressure

-normal is greater than 20
-should increase with exercise
-if it decreases with exercise to < 20, notify MD or RN
-the lower the pulse pressure is, the more concerned you need to be about tissue perfusion
-at the same time, you don't want the p

exercise recommendations based on hemoglobin and hematocrit

-the lower the hemoglobin is, the more concerned you need to be about exercise intolerance
-use a symptoms-based approach when determining appropriateness for activity
-most hemodynamically stable and asymptomatic patients will not receive a blood transfu


-the higher the INR is, the more conservative you need to be
-normal is 0.9-1.1
-many patients post-op will have an INR of 2-3 to decrease risk of DVT and PE
-with INR < 4, you can do regular exercise without progression
-with INR 4-5, avoid resistive exe

modified chair step test

-this test is often used for the frail elderly who can't walk far enough for a 2-minute test to be useful
-this can be used as an exercise test, as well as a tool to guide exercise prescription
-four-stage test, with each stage lasting 3 minutes

immediate signs and symptoms of exercise intolerance

-if any of these signs occur, you should lower the working HR to about 10 bpm lower than the HR at which the abnormal response occurred
-appearance of distress
-abnormal BP response
-unusual fatigue

delayed signs and symptoms of exercise intolerance

-slow recovery post exercise, especially a delayed drop in HR beyond 5-10 minutes
-excessive fatigue lasting longer than 1-2 hours post activity
-weight gain due to fluid retention

chest x-ray

-cardiac enlargement: heart should be < 50% of the diameter of the whole chest
-localized chamber enlargement
-calcification in valves or coronary arteries
-pulmonary venous congestion
-alveolar edema
-enlargement of the pulmonary artery or dilatation of

Holter monitor

-continuous 24 hour ECG
-this is indicated for patients who report syncope, dizziness, dyspnea, and arrhythmias, but the signs disappear when seeing the doctor
-it is importnat for teh patient to document when they performed activities, what they, and if

electrophysiologic mapping studies

-patient is awake and the doctor tries to bring on the dysrhythmia by applying electrical stimulation
-when aberrant pathways are found, they are ablated


-ultrasound transducer shows dimensions and motions of cardiac structures, such as ventricular wall and valve motion
-it can also be used to estimate SV and EF
-if the doctor suspects a valve problem, echo is usually the first test because it is non-invas


-non-invasive scan that is used to calculate EF
-radiolabeled blood is injected into the heart chamber
-LV EF is highly predictive of 1-year survival
-exercise LV EF is the strongest EF predictor of outcomes


-detect coronary artery obstruction
-sense wall motion abnormalities
-look for valve disease
-measure cardiac blood flow
-MRI is NOT good enough to replace cardiac catheterization

radionuclide studies

-these are often performed in conjunction with an exercise test
-whenever the test is about done, Thallium is injected via IV
-the doctor will look for an area where the Thallium wasn't picked up, which indicates poor perfusion to that area, called a cold

exercise stress test

-can be very helpful for determining exercise capacity
-can also help to aid in the diagnosis of cardiopulmonary issues

cardiac catheterization

-invasive diagnostic procedure in which a catheter is passed into a vein or artery and then guided into the heart
-every patient who is going to have cardiac surgery will have a cardiac cathether
-this way, the surgeon knows EXACTLY which coronary arterie

arterial line

-monitoring device consisting of a catheter that is inserted into an artery and attached to an electronic monitoring system
-provides continuous BP monitoring
-the transducer needs to be level with the right atrium for the measurements to be accurate

pulmonary artery catheter

-catheter that is usually inserted through the subclavian or internal jugular veins
-used to monitor right atrial and pulmonary arterial pressures, fluid balance, CO, SVO2, and vascular resistance

pulmonary artery catheter with balloon inflated

-pulmonary artery catheter has balloon inflated and is migrated until it wedges into a capillary
-because the pulmonary veins do not have valves, the pressure in the left side of the heart should be the same as the pressure picked up in the balloon

normal heart pressures

-right atrial pressure: 0-8 mm Hg
-right ventricular pressures: diastolic is 0-8, systolic is 15-30
-pulmonary artery pressures: diastolic is 5-15, systolic is 15-30
-pulmonary artery wedge pressure: 4-12, should be the same as the diastolic pressure on t


-MAP = DBP + 1/3(pulse pressure)
-normal MAP = 70-110
-MAP < 60 indicates inadequate perfusion pressure and is frequently a contraindication to exercise

thermodilution method

-temperature change of the blood can be used to measure cardiac output

cardiac index

-cardiac output per square meter (height)
-3.5 is normal
-< 2.2 indicates cardiogenic shock

cardiogenic shock

-shock caused by inadequate function of the heart, or pump failure

intra-aortic balloon pump

-used for unstable patients to assist the left ventricle to increase diastolic pressure and coronary blood flow
-the balloon inflates during diastole, and it's timed with the QRS
-the balloon deflates during systole to prevent high afterload
-inserted via


-fairly new internal assistive device for the left ventricle
-it sucks blood through the port and pushes it into the aorta
-can deliver up to 5 L/min forward flow
-helps to unload the left ventricle