Cardiovascular Support

8/13/2019 Cardiovascular Support

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Cardiovascular support

Tom Woodcock

Southampton University Hospitalshttp://www.scolopax.co.uk/


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Systemic Inflammatory Response Syndrome

The clinical manifestation ofhypermetabolism that may occur after a life-threatening insult

Defined (SCCM) as two or more of thefollowing;

Pyrexia (>38C) or hypothermia (90bpm)

Tachypnoea (>20 bpm or PaCO2 12x10-9/L or 10%band forms


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Sepsis & MODS definitions (SCCM)

SepsisSystemic inflammatory response toinfection. Criteria as for SIRS.

Severe sepsisSepsis associated w ith organ dysfunction,perfusion abnormality, or hypotension.

Septic shock

Sepsis w ith hypotension (unresponsive toadequate fluid resuscitation) and perfusionabnormality (e.g. lactic acidosis, oliguria,acute alteration in mental status).

HypotensionSystolic blood pressure


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SIRS/MODS initiators

Trauma accidental

surgical

multiple bloodtransfusions

fat embolism syndrome

Burns

Non-septicinflammatory disease pancreatitis

amniotic fluid embolism

diabetic ketoacidosis

Sepsis Primary infections

Nosocomial infections

Shock (ischaemic &reperfusion injury) hypovolaemic,

cardiogenic, distributive.

Ventilator induced lunginjury (VILI)

Double hit theory priming the immune

system?


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SIRS/MODS pathophysiology

direct tissue cell injury by angry whitecell attack

systemic inflammatory response

compensating anti-inflammatory response indirect tissue cell injury by dysoxia

VO2/DO2 mitochondrial utilisation block

the gut as the motor of sepsis translocation of organisms and toxins


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SIRS/MODS risk factors

inadequate or delayedresuscitation

persisting septic or

inflammatory process chronic organ

dysfunction or failure

age

alcohol abuse, hepaticdysfunction or cirrhosis

bowel infarction,surgical misadventures

diabetes mellitus

immune impairment;malignancy, malnutrition,morphine, steroids, AIDS.


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Improving the outcome fromSIRS/Sepsis

Resuscitation Early, rapid

Anti-microbial therapy

Fluid balance; ARDS is usually

preceded by positivefluid balance (weightgain) and hypo-proteinaemia

Ventilator prescription; supported ventilation

preferred to controlled

use normal tidalvolumes during PPV.

Posture; supine position is bad

for you

Feeding; enteral is best.

Insulin resistance i.v. insulin to keep

blood glucose in normalrange.

Anti-inflammatorytherapy

rhAPC (whenavailable).

Hydrocortisone?

Thromboprophylaxis


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Pre-emptive therapy I-trying to reduce morbidity and mortality in

surgical patients

surgical patients achieving supranormal

(150%) DO2 have lower risk ofmortality.

sympathomimetic therapy to achievesupranormal DO

2can reduce

postoperative mortality for very highrisk groups (>20% mortality in controlgroup)


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Pre-emptive therapy II-trying to reduce morbidity and mortality in

surgical patients volume challenge (gelofusin) against stroke

volume (Doppler aortography) can reducepost-operative morbidity

Sympatholytic therapy (beta blockade withatenolol or bisoprolol) can reduce cardiacmorbidity and mortality after major surgeryin patients with or at risk of ischaemic heart

disease Speculation; are other sympatholytics such as alpha-2

agonists or thoracic epidural analgesia as efficacious?


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Shock and resuscitation.

Shock is an acute syndrome ofcirculatory insufficiency leading toinadequate tissue perfusion andcellular dysfunction.

Hypotension (systolic


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Get a diagnosis for specific treatments.

High venous pressure Tension pneumothorax

Pulmonary embolism

Pericardial tamponade Acute coronary

syndromes

Ventricular dysfunction

Mechanical (valvular

dysfunction, VSD etc)

Low venous pressure Haemorrhage

Severe extra cellular fluiddepletion

Vasoparesis

Anaphylaxis

Fulminant hepaticfailure

Endocrine emergency Septicaemia

Tissue hypoxia

Other causes of MODS


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Shock reversal goals;cardiac output vs oxygenation

core-peripheraltemperaturegradient

indicator dilutiontechniques

Doppler flow

velocity ascending aorta

descending aorta

perfusionabnormalities

gastric tonometry

intramucosal pH,regional-arterialPCO2difference

mixed venous bloodanalysis

oxygen saturation,acid base status


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Sequential resuscitation.

I Oxygen therapy. Initially high FIO2

II Cardiac output/ oxygen delivery by A intravascular volume therapy

B inotropes? Early window of opportunity?

III Perfusion pressure to autoregulatoryrange by pressors.

IV Augment microvascular perfusion?


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Fluids or inotropes to increase thecardiac output?

fluids inotropes

Improved

DO2 with preserved

autoregulation

possible steal

Increased Qt

with increased

stroke volume

increased

heart rate

Excess leads

to oedema cardiacischaemia

Receptor

down-

regulation a problem.


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Which fluids?

increased mortality for resuscitation with colloids

increased mortality for resuscitation with albumin

increased mortality for liberal red cell

transfusion in intensive care Crystalloids are mainstay of fluid therapy but

avoid drowning Special caution in acute lung injury and hepatic

failure Restrictive / selective approach to use of

colloids/ albumin/ blood products. E.g. hepatorenal syndrome.

E.g. acute coronary syndromes.


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Functional assessments of adequacyof ventricular preload

filling pressures are a poor index of ventricularpreload so

continue fluid resuscitation until the strokevolume no longer responds to changes inpreload

stroke volume assessed by Doppler aortic flow, indicatordilution

square wave arterial pressure response during strainphase of Valsalva manoeuvre

Systolic pressure variation, pulse pressure variation.


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Systolic pressure variation as an indicator of hypovolemia

Rooke G. A. Current Opinion in Anaesthesiology1995,

8:511-515.

Delta Down is the difference in

systolic pressure at end-

expiration and the nadir during

the respiratory cycle.

during mechanical ventilation

the nadir occurs in the earlyphase of expiration.

Delta Down < 5 mmHg

significant hypovolemia is

unlikely,

Delta Down > 10 mmHg appears to be associated

with a blood volume deficit

of at least 0.5

Compare pulsus

paradoxus in lungdiseases.


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Filling pressures

ventricular preload not alwaysproportionate to CVP or PAOP

pulmonary capillary pressure notreliably measured by PAOP

SVC pressure important in ALI as it

determines thoracic duct pressure. intrathoracic blood volume a useful

concept?


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PAOP and LV preload

end diastolic muscle fibre length

end diastolic volume

end diastolic transmural pressure compliance

pericardial/ pleural pressure

left atrial pressure mitral valve dysfunction

pulmonary artery occlusion pressure West zone

tachycardia


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Transmural vascular pressure

Transmural = vascular - pleural pressure

Transpulmonary = alveolar - pleural


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Perfusion pressure.

normal autoregulatory range is MAP70-140mmHg.

may be higher in chronic hypertensive

patients. consider perfusion pressure if ICP (for

brain) or intraabdominal pressure ( for

kidney) elevated.judicious use of pressors in patients

with hyperdynamic circulation canrestore function of these vital organs.


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Regulating vascular tone

sympathetic vasopressin Renin/angiotensin

Mediators ofconstriction

Norepi, epi AVP Angiotensin(plasma reninactivity)

Pharm.

antagonists

Alpha and betaantagonists

ACEI


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Commonly used adrenergics

Norepinephrine(0.02-0.2mcg/kg/min) pressor

Epinephrine (0.02-0.2 mcg/kg/min) inopressor

may cause lactic acidosis

Dopamine (5-20 mcg/kg/min) inopressor

inhibits anterior pituitary hormones

Dobutamine (2.5-25 mcg/kg/min) inotrope

Dopexamine (0.5-2 mcg/kg/min) Inodilator

Flexible combinations, e.g Norepi + Dob


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Phosphodiesterase inhibitors

... competitively inhibit cyclicnucleotidase phosphodiesterase FIII in

cardiac and vascular smooth muscle. bipyridine amrinone, milrinone

imidazole

enoximone, piroximone specific for cGMP sensitive enzyme

benzimidazole sulmazole, pimobendan


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Adrenocortical insufficiency?

absolute; cortisol < 280nmol/L Give hydrocortisone +/- fludrocortisone

relative? response to Synacthen; rise


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Resistance to alpha 1 agonists

alternative pressors vasopressin infusion, terlipressin

angiotensin II infusion

iNOS / Guanylate cyclase overactivity steroids

false NOS substrate eg N-methyl aspartate

methylene blue

NO scavengers diaspirin or polyoxyethylene cross-linked haemoglobin


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Augment microvascular perfusion? renal dose dopamine agonists

splanchnic vasodilation, GI mucosa protection

GTN, vasodilator prostanoids (epoprostenol,alprostadil)

general vasodilation n-acetyl cysteine

corrects glutathione depletion

free radical scavenger

increases VO2and DO2

pentoxifylline

red cell deformability,

TNF levels reduced


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Mechanical circulatory assist

Ventricular assistdevices as a bridgeto transplant and

for post- cardiacsurgical shock

(ECMO for

meningococcalshock)

Intra-aortic ballooncounterpulsationstabilises mortally ill

patients with acutecoronary syndromes

(MAST, external

lower bodycounterpulsation)


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Recommended drugs;

for high-risk surgery

seeEagle & Fleisher NEJM2001;345:1677-82

Identify risk factors

Higher risk surgery

Heart disease (ischaemic, ventricular failure etc) Diabetes mellitus

Renal insufficiency

Poor functional status

Beta-block

Atenolol or metoprolol; hr


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Recommended drugs;

Shock complicating acutecoronary syndromes

Lancet 2000 vol 356:749

estimated LVEDP high,

systolic BP >100

Diuretic + inodilator

systolic BP


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Recommended drugs;

Vasodilatory shock

see Landry & Oliver NEJM2001;345:588-95

Volume loading

Norepinephrine

Consider hydrocortisone, vasopressin (orterlipressin).


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Recommended drugs;

Anaphylaxis

Epinephrine

Volume loading

Hydrocortisone, antihistamines

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