Download Hemodynamic Monitoring

Hemodynamic Monitoring
Goal: maintain an adequate preload while keeping afterload to a minimum
Heart rate
Blood pressure
Cardiac output
Stroke volume
Description
If HR ↑ too much, SV may be compromised due to
inadequate time for ventricle filling; myocardial O2
demand may be enhanced
BP/MAP = CO x SVR = HR x SV x SVR
CO = HR x SV
Echo – gives EF
Lactate ↑ in anaerobic
Central venous catheter should show ScvO2 of 70-80%
4 factors that affect SV:
1. Diastolic filling pressure (preload)
2. Distensibility of ventricle
3. Mycoardial contractility
4. Aortic pressure (afterload)
Pulse pressure parallels stroke volume
Total systemic
vascular resistance
Pulmonary
vascular resistance
Mixed venous O2
saturation (SvO2)
Mean arterial
pressure (MAP)
Central venous
pressure (CVP)
Pulmonary artery
systolic pressure
Normal Values
60-100 bpm
90-140/60-90
4-8 L/min
CI: 2.5-4 L/min/m2
60-70 mL/beat
900-1200 absolute units
150-250 absolute units
High (80-95%) – high O2 delivery; low O2 demand/
inability of tissues to extract O2 due to hypothermia,
sepsis
Low (< 60%) – low O2 delivery due to anemia, hypoV,
hypoxemia, low CO; high O2 demand due to
hyperthermia, shivering, sz, pain, anxiety
(SBP + 2DBP)/3
Measured with arterial line that sits in radial, femoral or
pedial artery
Pressure in the right atrium
At the end of diastole, when tricuspid valve is open (RA
& RV are 1 chamber), CVP = pressure in RV  good
indicator of RV function
↓ - hypovolemia from fluid imbalance, hemorrhage,
extreme vasodilation
↑ - hypervolemia
Problems in right heart have most direct influence on
CVP
Pressure ↑ in pulmonary circulation (dz, embolism) will
affect CVP less directly
**doesn’t provide direct clues to left heart function
**changes show up later than in PADP and PCWP
Reflects pressure in the right ventricle
Pressure in PA when RV is contracting  reflects RV
60-80%
> 65 mm Hg
0-5 mm Hg
Positive ventilator: 8-12
20-30 mm Hg
(PASP)
Pulmonary artery
diastolic pressure
(PADP)
Pulmonary
capillary wedge
pressure (PCWP)
Right ventricular
pressure
Left atrial pressure
Left ventricular
pressure
Urine output
function
Reflects pressure in the left ventricle at end of diastole
**isn’t always most accurate indicator of left-heart
function b/c pulmonary pressures & LV pressures
influence it; only accurately mirrors if no significant
pulmonary dz
**can be used alone to monitor left heart function
except if obstructive pulmonary dz, PE (↑ PADP >
PCWP)
Direct indicator of left ventricle pressure
Most accurate indication of left-heart function
7-12 mm Hg
8-12 mm Hg
20-30 mm Hg (systolic)
0-5 mm Hg (diastolic)
2-7 mm Hg
90-140 mm Hg (syst)
2-7 mm Hg (diast)
0.5 mL/kg/hr
During systole – pulmonic and aortic valves are open; tricuspid and mitral valves closed
During diastole – tricuspid and mitral valves open; pulmonic and aortic valves closed
Receptors
α1 – smooth muscle vasoconstriction; increased cardiac contractility
α2 – post-synaptic; vasodilation by NO production
β1 – positive chronotrope (increases HR via increased SA nodal conduction) and inotrope
(increases contractility via increased automaticity and conduction of ventricular cardiac muscle
and increased AV nodal conduction)
β2 – vasodilation; mild chronotropic and inotropic improvements
D4 – increases CO by improving myocardial contractility and at certain doses increases HR
D1/2 – kidneys; stimulate diuresis
D1/2/4/5 – pulmonary; vasorelaxive effects
Vasopressin – peptide hormone; antidiuretic hormone; regulates body’s retention of water;
released when body is dehydrated, causing kidneys to conserve water (not salt), concentrating
the urine and reducing urine volume; increases BP by inducing moderate vasoconstriction
through V1 stimulation in peripheral arterioles
Alpha agonists cause vascular
constriction
Beta agonists increase CO by increasing HR
in SA node, increasing atrial cardiac muscle
contractility, increasing contractility and
automaticity of ventricular cardiac muscles
and AV node
VASST Trial
 Vasopression vs. NE in septic shock
 Only patients with previous administration of low-dosage NE demonstrated improved
survival with vasopressin
 In general, no survival benefit with vasopressin over NE
Drug
Dobutamine
Dopamine
Epinephrine
Norepinephrine
Effects
β1 agonist properties mainly = ↑ CO by ↑
inotrope
β2 = vasodilation;  systemic/pulm. vascular
resistance
DOC for cardiogenic shock w/ low CO and ↑
afterload
Dose 1: ↑ CO by ↑ inotrope (minimal); renal
and visceral vasodilation
Dose 2: ↑ SVR/CO by ↑ inotrope/HR
Dose 3: ↑ SVR
Used as vasoconstrictor in vasodilatory shock
Used as inotrope in low CO
**Indicated in vasodilatory shock with
bradycardia
↑ SVR at high doses (alpha > beta)
↑ CO by ↑ inotrope/HR at low doses
Low dose: primarily β
1st line catecholamine in cardiopulmonary
resuscitation & anaphylactic shock
2nd line vasopressor and inotrope
↑↑ SVR (arterial and vasoconstriction) from
alpha
Inotropic effects offset by increases in
afterload
ADRs
CVS: ↑ HR, BP
LYTE: hypoK
Tachyarrhythmias, AF
Ischemic gut; ischemic peripherals
Monitor pulmonary fxn, HR, BP, site of
infusion for blanching/extravasation
CNS: Tremor, weakness
HEENT: ocular irritation
RESP: pulmonary edema/HTN
CVS: tachyarrhythmia, MI
GI: lactic acidosis
ENDO: hyperglycemia (due to
hypermetabolism, suppression of insulin
release and glycolysis)
CVS: peripheral ischemia; MI
DERM: skin necrosis
Increases MAP, effective circulating blood volume, venous
return/preload, with minimal increase of HR or SV
Phenylephrine
Vasopressin
Milrinone
More potent than dopamine; associated with
some survival benefit in septic shock vs.
dopamine and epi
1st line for distributive shock
↑↑ in SVR
Used temporarily to restore MAP, SVR and
CVP in hypoT w/ vasodilation and adequate
CO
↑↑ SVR
 CO and redistribute CO to
hepatosplanchnic microcirculation
↑ CO by PDE5 inhibition  mobilize
intracellular Ca
2nd line in cardiogenic shock
CNS: tremor, weakness
CVS: ischemia; reflex bradycardia
DERM: extravasation
CVS: MI, venous thrombosis
GI: mesenteric ischemia
DERM: ischemic skin lesions,
circumoral pallor; diaphoresis
CVS: ventricular arrhythmia