Cardiothoracic ICU

Beta-phenylethylamine

1) vasoconstriction in vascular smooth muscle, pupillary dolatation (mydriasis), sphincter contraction

2) inhibits norepinephrine release which causes vasodilatation

1) HEART --> chronotropy, dromotyromy (increased conduction), reduced refractoriness within the AV node, inotropy
B1 cells also found on juxtaglomerular cells --> increases renin release

2) HEART/Vasculature: vasodilitation, enhanced diastolic relaxation (lusitropy). AND bronchodilation/uterine & bladder relxation/ decreased GI motility

Metabolism of non-catelcholamine sympathomimetics (i.e.ephedrine, phenylephrine) is mostly vis MAO--> could have prolonged/exaggerate hemodynamic responses to these meds.

Beta effects: + inotrope and + chronotrope

alpha receptor mediated vasoconstriction predominates --> increases CO while maintaining coronary perfusion pressure.

- sinus tachycardia
- atrial/vent arrhythmias
- metabolic distrubance: hyperglycemia, hypokalemia, lactod acidosis

alpah and Beta 1

- blood pressure is reliably increased, but effects on cardiac output variable.

apha, beta, type 1 and 2 dopamine (DA) receptors

DA 1: renal, mescenteric, cerebral ciculations

DA2: found presynaptically and inhibit norepinephrine release

potent Beta receptor:
increased contractility, HR, vasodilitation.

--> CO is reliably increased, and BP typically falls
note: PT with CAD, it may precipitate myocardial ischemia

Symptomatic bradycardia or heart block

arrhythmias, hypotension, metabolic distrubances

.01-.05 ug/kg/min

synthetic catelocholamine with specificity for Beta 1 receptors.

non-catelcholamine direct acting Alpa agonist ) no Beta receptor activity).

It increases coronary perfusion pressure without increasing HR.

Decreased Cardiac output secondary to increased afterload and baroreceptor -mediated reflex bradycardia.

Inodilators --> increase contractility and cause pulmonary and systemic vasodilation.

They are potent vasodilators of coronary grafts and cause LESS tachycardia and Afib than dobutmaine

(also can combine with B1 agonist)

low dose norepinephrine

phenylnephrine

Milrinone, Enoximone, Amrinone

2.5 hours

- decreases afterload
- improves peripheral tissue perfusion and redistributes heat to the periphery

0.1 ug/kg/min to max
8 ug/kg/min

- reduced ventricular compliance exacerbated by myocardial edema from ischemia/reperfusion injury
- lack of atrioventricular synchrony (with impaired ventricular filling)
- impaired RV functioning
- excessive use of inotropes

- administer fluid --> raise PCWP 20-25 mmHg (increase LV end diastolic volume)
- Lusitropic drugs that relax LV --> inamrinone or milrinone
- low dose CCB/BB to improve diastolic relaxatin
- Aggressive diuresis to reduce interstitial edema AND provide colloid to maintain intravascular volume

Surgical vs. medical
causes-->
1) surgical bleeding sites
2) heaprin effect, residual or rebound
3) Platelet dysfunction
4) clotting factor deficiency
6) fibrinolysis

30-50%
...the duration of CPB and the degree of hypothermia after bypass.

- hepatic dysfunction
- residual coumadin effect
- vitamin K-dependent clotting factor def.
- von Willebrands disease
- thrombolytic therapy

50X, Factor V is decreased by 80%.
- cell saving devices

coumadin - 4 days

Low-molecular weight heaprin - 12 hrs ( it is only 80% reversible with protamine)

ASA - 3 days

Can give DDAVP or Amicar to help stop bleeding.

Plavix - 5-7 days (antiplatelet activity lasts for life of plt)
Inhibition of platelet 2hrs post administration. Achievement of steady state with 50% inhibition of platelet aggregation occurs 6hrs after 300 mg loading dose.

Ticlid - 7 days, abnormal bleeding time may be normalized within 2hrs --> Methylprednisolone 20 mg iv

80% Platelets function recovers within 4-6 hrs

stop 4 hrs prior to surgery

half life 12 hours. Give platelet transfusion b/c this drug has very little circulating unbound drug.

Antifibrinolytic AND preserves platelet function: inhibits conversion of plasminogen to plasmin

5g post induction
5g on pump
1g/hr during procedure

It gives a qualitative measurement of clot strenght. It evaluates the interaction of Plt and the coagulation cascade.

Increases the level of procoagulant (VIII:c) and raises the level of von Willebrand factor (VIII:vWF) by about 50% -->

by releasing it from tissue stores

--> in essense helping platelet adhesion to subendothelium

CALCIUM
give calcium chloride b/c it provides three x more ionized calcium

(instead of calcium gluconate)

1) untapering mediastinal bleeding

- More than 400 ml/hr for 1 hour
- More that 300 ml/hr for 2-3 hours
- More than 200 mL/h for 4 hours

2) suspected tamponade

1) exsanguinating hemorrhage
2) tamponade w/ incipient cardiac arrest

hemodynamic compromise with elevated filling pressures
- sudden cessation of sig med bleeding
- low CO + Hypotension w/ resp variation and narrowing of pulse pressure
- equilibration of intracardiac pressures
- CxR = widened mediastinum
- decreased electrocardiographic voltage

CO = HR x SV

Preload refers to the LV end-diastolic fiber length

i.e. end-diastolic volume

Afterload is determined by both: Preload and SVR

Contractility is intrinsic strength of myocardial contraction at constant preload and afterload

- Hg level
- coronary blood flow (could be influence by stenosis, thrombus, spasm)
- the duration of diastole
- coronary perfusion pressure
- arterial oxygen saturation

- poor peripheral perfusion --> pale, cool extremities + diaphoresis
- pulmonary congestion + poor oxygenation
- impaired renal perfusion _ oliguria
- metabolic acidosis

Abnormal
- PRELOAD
- AFTERLOAD
- CONTRACTILITY
- HEART RATE

or in patients with normal systolic function, but marked LVH + diastolic dysfunction

1) hypovolemia
2) cardiac tamponade
3)positive pressure ventilation & PEEP
4) RV dysfunction (RV infarction, pulmonary HTN)
5) Tension Pneumothorax

1) Low EF
2) Myocardial Stunning seconcary to transient ischmeic/reperfusion injur, myocardial ischemia, or infarction

1) Vasoconstriction
2) Fluid overload and ventricular distention
3) LV outflow tract obstruction following mitral valve repair/replacement

- Thin VENTRICULAR SIZE and COMPLIANCE

BP = CO x SVR
a satisfactory blood pressure/ or elevated is not necessary a sign of good cardiac performance.

1) optimize preload with CVP 18-20
2) Ensure AV conduction
3) Maintain adequate systemic perfusion pressure with vasoactive meds or IABP
4) Lower RV afterload (PVR) and improve RV contractility

- Nesiritide
- Inhaled NO
- nhaled prostacyclin
- IV prostaglandin E
- Adenosine
- Endothelin agonists

Synthetic B- type natiuretic peptide

--> powerful vasodilator that lowers preload and afterload, indirectly improving CO, renal perfusion and diuretic effect (synergistic when given with loop).

2 ug/kg IV bolus
.01-.03 ug/kg/min infusion

selective pulmonary vasodilator with minimal effect on SVR.
- it may reverse hypoxic vasoconstriction
- improve Pa02/Fio2 ratio

10-40 ppm

Dipyridamole (persantine) 0.2 mg/kg IV

methemoglobin

Decrease the dose by no more than20% every 30 minutes. Inhalation can be stopped at 6 ppm

1) Impaired systolic relaxation

2) decreased diastolic compliance

1) ACE inhibitors--> can iimprove diastolic compliance
2) Lusitropic drugs (CCB, nesiritide, milrinone) --> can improve relaxation
3) Bradycardic drugs (BB/CCB) --> can help innapropriate tachycardia
4) Aggreesive diuresis --> can decreased myocardial edema contributing to reduced compliance

--> potent B1 inotropic agent
--> B2 bronchodilation

At doses < .03 ug/kg/min --> B2 effects w/ mild peripheral vasodilation but maintained CO

At doses > .03ug/kg/min alpa - increased SVR and BP

positive inotropic agent with strong Beta 1 effect: increases HR in dose dependent manner AND contractility

- mild vasoconstrictive alpha1 effect
- mild vasodilatory Beta 2 effect

(increase myocardial oxygen demand but aguements myocardial blood flow.

They provide comparable hemodynamic support, but Dobutmaine is associated w/ more:

- HTN
- Tachycardia
-increased chance of triggering AF

Note (when used together, synergistic effect to improve CO)

"inodilator" --> improve CO by reducing SVR/PVR

and

"lusitropic" --> relaxant properties

- modest increase in HR
- lowering filling pressurs and SVR
- vasodilate arterioles (beneficial in suspected coronary spasm pt who requires inotropic support)

2.3 hours

50 ug/kg IV bolus over 10 min followed by

.375-.75 ug/kg/min

powerful catelcholamine with alpha and beta adregnergic properties.

- Increases SVR, BP, contractility, HR

(increases myocardial O2 demand)

pure alpha- agent:
- increases SVR that may cause reflex DECREASE In HR.