Hemodynamics
 Pulmonary artery catheter (PA catheter) aka SWAN-GANZ
o Insertion pathway
 Internal jugular R atrium tricuspid R ventricle pulmonic valve pulmonary artery
 Gives pulmonary artery diastolic, systolic, and pulmonary capillary wedge pressure
 Measures how much blood pressure is in the pulmonary artery?
 Normal values quarter over dime (25/10)
o Pulmonary artery systolic measurement = 20-30 (measures right ventricular
pressure to push blood through pulmonic valve
o Pulmonary artery diastolic 8-15
o Capillary wedge pressure 6-12 mmHg
 It’s when you wedge the balloon at the end of the catheter (1.5cc air)
 Tamponades the vessel
 Measures the pressures on the left side of the heart (measures
everything ahead of the balloon)
 Measures central venous pressures (right atrial pressures)  2-6mmHg (below normal =
low intravascular volume)
 When placing the Swan Ganz
o Place patient in Trendelenburg
o Do it quickly too long can lead to lung infarction
 Adverse effects of Swan Ganz
o Arrhythmias
o Pneumothorax
o Balloon rupturing
o Heart blocks
o Lung infarction
o thrombosis
o Air embolism
o Ventricular turbulence –> can lead to naughting in catheter
o Valve damage
o Infection
 A-Line (arterial line)
o Get an A line in hypotensive patients
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o Sites radial brachial, and femoral arteries [umbilical for neonates]
o For direct, continuous bp measurement; blood sampling access, particularly ABG’s
 Distal BP has larger margin for error
 Newer A-lines calculate stroke volume and continuous CO
o Measures relative to atmospheric pressure
 SBP, DBP, MAP (MAP is most accurate)
 MAP >60 mandatory to maintain minimul perfusion of vital organs
 May be up to 10-15 mmHg > cuff pressure
o Components
 Transducer make sure it’s leveled at 0 pressure; have it at the flevostatic access (lines up
with R atrium)
 Make sure it’s leveled and zeroed before procedures
o Safety:
 Clench fist a couple times
 Look for blanched palm
 Occlude ulnar artery and radial artery
 Look at Allen’s test
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o It should be sutured in or will have a stat lock (specific to arterial lines) A-line NEEDS to be
secured into place
o Pressure bag in place infusion of NS @ 3ml/hr
 DO NOT INTERRUPT this line ever!
o Prevent air from entering the line do not disconnect A-line ever
o Check for distal circulation and possible thrombosis; change site every 72/96 hrs
o Prevent line separation and arterial hemorrhage
o Use sterile technique to prevent local and systemic infection/sepsis
o After removal, hold continuous pressure for at least 10 minutes if no bleeding, apply a
pressure dressing
 Insertion of central/a-lines
o Pt laid supine during insertion to minimize the possibility of air embolism
o Pt laid supine while removed
o Lidocaine is injected at the site pain coverage
o Site prepped like a surgical site to prevent infection at site and systemically
o If pt conscious turn head to opposite side from insertion and breathe out during insertion
(minimize possibility of air embolism; better access)
o Physician typically allows blood to flow from the catheter after insertion (minimize possibility of
clot and air embolism)
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o Then suture into place by MD and applies sterile dressing
 The nurse
 Secures all tapes and connections
 DO NOT INFUSE ANYTHING UNTIL CONFIRMATORY X-RAY of chest to confirm
placement
 Any signs of air embolism or pneumothorax after procedure
o Check lung sounds and for dyspnea (pneumothorax and air embolism to lung?)
o Checks for decreased LOC (air embolism to the brain)
 Check CXR check for placement and pneumothorax
 PICC line
o Maintain sterility
o Change dressing per hospital policy
o Measurement for swelling
o Measure external length
o Sign over the bed no blood draws or BP on that side!
 Hemodynamic monitoring
o Non-invasive
 BP, HR, P
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 Mental Status
 Skin temp, cap refill
 Urinary output
o Direct measurement A-line
 Titration of gtts
 Unstable BP
 Frequent ABGs/lab monitoring
o Invasive monitoring: CVP, PA
o Indications
 Dehyradration/ hemorrhage/ GI bleeds/ burns
 Surgery
 Shock (all types): septic, cardiogenic, neurogenic, anaphylactic shock
 Acute MI/cardiomyopathy/ decompensated HF
 Cardiac performance
 PRELOAD
o Stretch created by volume in the ventricles just before they contract
 Volume in the ventricles at the end of diastole (filling pressure)
o The volume of blood ejected with each beat is a stroke volume (SV)
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o Preload is the most important factor determining SV  CO
o Effects instantaneous and beat to beat
 Frank-Starling Law of the Heart
o As end-diastolic volume (EDV) is increased, the stroke volume is increased
o Strength of ventricular contraction varies directly with EDV
 Intrinsic properties of myocardium
 As EDV increased, myocardium is stretched more
 Greater contraction and SV
 Factors affecting preload
o Circulating blood volume
o Venous return
 Atrial kick
 Filling time
 Intrathoracic pressure
 Vascular tone (“squeeze” factor)
 Ventricular compliance
 Contractility
o Measurement: central venous pressure
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 AFTERLOAD
o Resistance against which the ventricles must pump to eject the volume (systemic vascular
resistance  SVR) (800/1400 d/sec)
o Aka resistance to flow or “clamped” blood vessels
o This resistance is created by vasodilation/vasoconstriction of systemic arteries and arterioles
 Factors affecting afterload
o Valve function
o Vascular tone
 Vascular health/condition
 ANS (neurohormonal stimulation)
 Medications
 Pulmonary vascular resistance (PVR)
o Pulmonary hypertension
o COPD
o Pulmonary embolism
o Acidosis (pulmonary vasoconstriction)
o Hypoxemia
o Drugs
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 Systemic vascular resistance (SVR)
o Arterial resistance (vasoconstriction, SNS stimulation, aortic impedance-aortic stenosis)
o Cardiac failure
o Increased blood viscosity
o Pain/anxiety
o Hemorrhage (early)
o Drugs
o Distributive shocks
 Agents that affect afterload
o To decrease afterload
 Vasodilators nipride, nitro
 Ace inhibitors
o To increase afterload
 Vasoconstrictors  norepi, epi, phenylephrine, dopamine
 Contractility
o Force of muscular contraction inotropy
o Factors affecting contractility
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 Positive inotropes: dopamine (pure CO med); Digoxin (improve contractility but decreases
HR)
 Negative inotropes: beta blockers
 Pre-load
 Afterload
 Muscular ability
 Viable muscle mass
 Oxygen supply/demand
 Myocardial metabolic state
 Neurohormonal influence
 Contractility
o Direct measurement of ejection fraction (EF)
 Percentage of blood ejected from left ventricle with each contraction
 The ratio of how much blood ejected to the volume at the end of diastole (left ventricular
end-diastolic volume)
 Determined by echocardiogram or during left heart catheterization
 Normal 
 Effects of afterload on the heart
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o Factor  increased afterload
 Causes
 Hypovolemia
 Vasoconstriction
 Effects on heart
 Decreases stroke volume
 Increases ventricular work
 Increases myocardial oxygen requirements
 Increases stroke volume
o Factors  decreased afterload
 Causes
 Vasodilation
 Effects on heart
 Decreases ventricular work
 Decreases myocardial oxygen requirements

 Cardiac output
o The amount of blood ejected from the left ventricle in one minute
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o CO = HR x SV
o Determined by volume returning to left heart (preload), SVR (afterload), and contractility
 Cardiac index cardiac output factoring patient’s surface body area
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Hypovolemic
Cardiogenic
CO/CI (sv x hr)
CO  4-6 L/min
CI  2.5 – 4.0 L/min
Preload  stretch/fluid status
CVP/RAP 2-6 mmHg
Afterload  resistance SVR 
800-1400 Dynes/sec
PVR <350 Dynes/sec
Contractility 
squeeze/contractions
EF 60%
HR 60-100
Decreased  loss of fluid
Decreased  broken pump
Decreased  primary
problem
Increased  compensatory
mechanism
Increase  backed up fluids
Decrease  primary problem
Increased  compensatory
mechanism
Decreased  primary
problem
Neutral
Decreased  primary
problem
Pump is broken
Increased  compensatory
mechanism
Increased  compensatory
mechanism
Treatment
Fluids
O2
Stop the loss
Increased- compensatory
mechanism
Diuresis  decrease preload
O2
ACE inhibitors (block
angiotensin 2) Decrease
afterload
IABP intra-aortic balloon
pump
Distributive (massive
vasodilation; body fluids are
displaced)
Anaphylactic, neurogenic,
septic
Increased  compensatory
mechanism
Increased  compensatory
mechanism
NEUROGENIC SHOCK 
bradycardia is the hallmark
rhythm
Fluid resuscitation
Vasopressors
O2
Treat the cause
Septic shock draw blood
cultures, draw labs and
lactates, give broad-spectrum
abx
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