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Transcript of Cardiovascular support
Consultant Anaesthetics and Intensive Care
Queen Elizabeth Hospital Birmingham More or less boring definitions Cardiovascular physiology
- and what one can do about it More or less useful drugs A practical approach to the shocked patient Different patients on different ITU's Dakota tribal wisdom Inotropic agents Act on the heart by increasing the velocity and force of myocardial fibre shortening
Increase in contractility
Increase in cardiac output and blood pressure
cAMP dependent and non cAMP dependent
Examples: Dobutamine, Enoximone Vasopressors Exert a predominantly vasoconstrictive action on peripheral vasculature
Increase in vascular resistance
Increase in blood pressure
Examples: Phenylephrine, Metaraminol Vasodilators Veno- and/or arterial vasodilatation
Venodilatation leads to decreased preload
Arterial dilatation leads to decreased afterload
Examples: Nitroglycerine, Nitroprusside Don't forget:
Calcium channel blockers
ACE inhibitors and AT1 blockers
Inhaled nitric oxide
Intravenous prostaglandin E1 Vasoregulatory agents Modulate responsiveness of peripheral vessels to vasoactive drugs
Examples: Vasopressin, Corticosteroids Mean arterial pressure Cardiac output vs peripheral vasculature Cardiac output:
Preload and afterload
Heart rate and rhythm
Contractility Peripheral vasculature:
Impedance to ventricular ejection
SVR/ PVR Always remember that pressure does not mean flow and a certain mean arterial pressure does not mean adequate tissue oxygenation. Oxygen delivery total amount of oxygen delivered to the tissues per unit of time
depends on the volume of blood flowing through the microcirculation per unit of time = cardiac output CO
depends on the amount of oxygen contained in that blood = arterial oxygen content CaO2 What parameters can I influence?
DO2 = CO x CaO2
CO = SV x HR
CaO2 = Hb x SaO2 x 1.34
SV depends on preload, afterload and contractility Haemoglobin 1 g Hb binds 1.34 ml oxygen
maintenance of an adequate Hb is essential
blood flow also depends on viscosity
viscosity depends largely on the packed cell volume
keep the Hb above 8 g/dl (4.8 mmol/l) Arterial oxygen saturation sigmoid shape of oxyhaemoglobin dissociation curve clinically important
falls in PaO2 may be tolerated provided SaO2 remains above 90 %
increasing PaO2 above normal has only a minimal effect on oxygen content (Hb x SaO2 x 1.34)
keep SaO2 above 92 % Heart rate balance of sympathetic and parasympathetic nervous activity, related to metabolic rate
extreme bradycardias and tachycardias are bad
disturbances of rhythm - loss of atrial kick may cause CO to drop drastically
Maintenance of adequate heart rate and sinus rhythm important Stroke volume SV =
ventricular enddiastolic volume - ventricular endsystolic volume preload
afterload Preload tension of myocardial fibres at end- diastole
Starling's law: force of myocardial contraction is proportional to the initial fibre length
the greater the preload the greater the contractility ITU patients are far more commonly underfilled!
Fluid challenge = one of the simplest and most effective interventions Contractility Afterload refers to the ability of the heart to perform work independently of changes in pre- and afterload
mainly influenced by changes in pre- and afterload
is our target if we consider inotropic drugs One determinant of myocardial oxygen consumption!
Heart rate and afterload > preload and SV! refers to myocardial wall tension developed during systolic ejection
resistance imposed by the aortic valve and the peripheral vasculature
Laplace's law: T = Ptm x /2H
Ptm = transmural pressure
R = ventricular radius
H = ventricular wall thickness Dopamine Precursor of noradrenaline
Dopaminergic DA1/DA2, beta1>beta2
SVR should go down, CI should increase, dilatation of splanchnic and renal vessels
increase NA release and may cause splanchnic ischaemia
betareceptor effects: tachycardia, arrhythmias
2- 20 цg/kg/min Dobutamine Strong βbeta 1 inotropic effect
Mild βbeta 2 vasodilatation
lowers SVR↓, increases CI↑
Most useful in low CO with high SVR
Tachycardia may restrict use
5- 20 цg/kg/min Dopexamine Analogue of dopamine
βbeta2 > betaβ1, DA1>DA2
Very weak positive inotrope
Powerful splanchnic vasodilator, improving blood flow to vital organs
Higher doses lead to a marked drop in SVR↓↓
1- 4 цg/kg/min Adrenaline Very potent inotrope, may prove successful when other agents have failed
Might stimulate myocardial alphaα-receptors
Low dose: HR goes up, CI goes up↑, SVR drops ↓(betaβ1, betaβ2)
High dose: SVR↑ increases (alpha-actionα)
With increasing doses danger of metabolic acidosis, reduction in renal blood flow, ARF
0.01- 0.5 цg/kg/min Noradrenaline αalpha>betaβ, but has significant inotropic effect
Most suitable when low SVR
Higher doses may promote impaired organ perfusion
0.01- 0.5 (- 1.5) цg/kg/min Isoprenaline beta1 and 2 receptor agonist
increases HR and CI,
SVR drops and blood flow might be diverted away from vital organs
used after cardiac transplant to maintain HR of 100- 110 /min
0.01- 0.1 цg/kg/min Phosphodiesterase inhibitors Phosphodiesterase inhibitors Non-receptor mediated inhibition of phosphodiesterase isoenzymes resulting in increased levels of cAMP
cAMP also effects diastolic heart function through regulation of phospholamban, the regulatory subunit of the calcium pump of the SR, which leads to calcium re-sequestration and diastolic relaxation
PDI cause potent vasodilatation and reduction in PVR, combined use with catecholamines may be necessary Excretion is predominantly renal
PDI have place in patients with beta- receptor downregulation (chronic heart failure)
Effects additive to catecholamines
inotropic effect > vasodilation
0.5 – 1 mg/kg bolus 10 min
5 – 20 µg/kg/min infusion Glucagon Stimulation of adenyl cyclase via specific receptor leads to increase in cAMP
Reports of its use in severe betablocker, calcium antagonist and tricyclic poisening
Large doses are required which are associated with metabolic side effects Digoxin inhibition of Na/K membrane pump
increase in intracellular sodium slows down the Na/Ca exchange pump, leading to an increase in intracellular calcium
Narrow therapeutic index
Highly protein bound
Excreted unchanged in urine
Half-life varies between 35h to 5 days according to renal function
Role in acute cardiac failure is questionable, inotropic effect is negligible in presence of high levels of sympathethic activity
Potential for toxicity is increased by low potassium, low magnesium and high calcium
Short acting inotropes and amiodarone have superseded its use Calcium Numerous studies in isolated heart muscles have shown that increasing the concentration of extracellular calcium leads to an increase in myocardial contractility
Inotropic effect if hypocalcaemia (<0.8 mmol/l)
Increase in SVR independent of calcium level
Small doses of calcium may be useful to increase the vascular resistance or to treat hypocalcaemia or an overdose in calcium channel blockers
Useful in hyperkalaemia thyroid hormone Required for synthesis of contractile proteins and normal myocardial contraction
Positive inotropic effect due to increased aerobic metabolism and synthesis of high-energy phosphates
Increase of myocyte contractile performance independent of and additive to beta stimulation
Regulates synthesis of adrenergic receptors
Treatment of patients with low levels of thyroid hormone
0.2- 0.8 цg/kg bolus, 0.12 цg/kg/h Levosimendan Calcium sensitiser increase myofilament sensitivity for calcium by binding to troponin C
Vasodilatation through opening of K channels and PDE III inhibitory action producing venous, arterial and coronary vasodilatation
Resultant increase in tension development, myocardial contractility.
Does not affect total intracellular calcium concentration.
Therefore, enhanced myocardial performance achieved without increasing myocardial oxygen consumption and without provoking fatal arrhythmias Decompensated low-output heart failure (cardiac index <2.5/l/min/m2 or PCWP >16mmHg or LVEF <0.4)
Bolus injection followed by infusion 0.05-0.2 ug/kg/min for 24 hours
Outcome benefits included regression of dyspnoea, improved hemodynamic index, increased urine output, shortened hospital and ICU stay, and lower 180-day mortality
Effects last for 3-4 days due to long acting metabolite (half-life 80 hours)
Repetitive administration at intervals of 4-8 weeks maintained clinical improvement in 6 out of 9 patients in a small study
Left ventricular failure in acute coronary artery disease
Reduced 180-day mortality
Reduce infarct size in animal studies
Prevent myocardial stunning after coronary reperfusion in a case series of 18 patients
No formal controlled studies
In several clinical observations, improved hemodynamics if combined with noradrenaline to maintain adequate perfusion pressure
Infusion 0.05-0.2ug/kg/min for 24 hours without bolus
Perioperative treatment in patients undergoing cardiac surgery
No formal controlled studies
In several clinical observations, improved hemodynamics, improved/prevented postoperative ischemic cardiac depression
Given as bolus 12ug/kg or as infusion 0.2ug/kg/min for 6 hours or both over 24 hrs Vasopressors Vascular contraction is slow but sustained.
Cytosolic free Ca is the primary factor governing contraction. Phenylephrine and Metaraminol:
direct acting alpha1 agonists leading to venous and arterial vasoconstriction
Patients may become refractory after several hours of infusion
May cause reflex bradycardia
May be useful in correcting hypotension from pure vasodilatory states
Phenylephrine: 0.05- 1.5 цg/kg/min
direct and indirect acting alpha and beta agonist leading to modest positive chronotropy and inotropy Vasodilators Nitroglycerin:
0.1 – 10 µg/kg/min
Primarily venodilatation = reduction in preload and filling pressures
Arterial dilatation in higher doses
Dilates coronary conductance vessels
Produces metHb: cyanosis, acidosis,
progressive weakness if > 15- 20%
(treatment methylene blue 1 mg/kg iv) Nitroprusside:
0.1 – 8 µg/kg/min
Predominantly relaxes arterial smooth muscle with decreased afterload
Lesser effect on venous vessels
Cave! Dangerous drug!!!
Thiocyanate toxicity! Vasoregulatory drugs Vasopressin:
Local mediators like vasopressin, corticosteroids, nitric oxide, endothelin
naturally occurring peptide secreted by the posterior pituitary gland
V1a - vasoconstriction, gluconeogenesis in the liver, platelet aggregation and release of factor VIII and von Willebrand factor.
V1b - corticotropin secretion from the pituitary gland.
V2 - control of free water reabsorption in the collecting ducts of the kidneys
Effects seem to be independent of any direct vasopressor action
„catecholamine sparing“ effect?? Dose in sepsis: 0.04 U/min
Dose in CPR: 40 U bolus (not longer recommended)
Dose in cardiac surgery: studies with up to 0.1 U/min
Dose for control of variceal bleeding: start with 0.2 U/min and gradual increase to 1 U/min (max 2U/min) Corticosteroids (Hydrocortisone)
Replacement of „stress response“ doses (200 mg/d) may improve vasoresponsiveness to catecholamine infusions
Consider intravenous hydrocortisone for adult septic shock when hypotension remains poorly responsive to adequate fluid resuscitation and vasopressors.(2C)
ACTH stimulation test is not recommended to identify the subset of adults with septic shock who should receive hydrocortisone.(2B) Assess the patient rapidly and thoroughly,
time is essential!!! Try to address the underlying cause! Patients who have lost intravascular volume – the heart has little to pump
Patients with extrinsic causes of pump failure – cardiac tamponade, tension pneu
Patients with intrinsic causes of pump failure – MI, valvular reasons
Patients with peripheral circulatory failure – sepsis Ensure adequate volume status! Clinical assessment
Adequate cFT – oesophageal doppler
Adequate left sided filling as assessed by transthoracic echo
Adequate left sided filling as assessed by TOE
Various metabolic parameters and indices of organ perfusion – pHi, lactate
Evidence of adequate vital organ perfusion Aggressively sustain the blood pressure at the set target, do not wait for your fluids to fail. Start inotropes soon and at a reasonable dose. Traditional MAP > 60 mmHg was considered to be adequate.
We need to know the individual autoregulatory threshold!
If we know a person‘s pre-morbid blood pressure we can predict that reduction in mean pressure of over 30 % will result in a substantial decrease in perfusion of vital organs.
If we have absolutely no idea of what the patient‘s „normal blood pressure“ runs at, we should be generous in our estimates. Dopamine – dose dependent
Dobutamine - increases HR and contractility↑, lowers SVR ↑
Adrenaline – dose dependent, βbeta>alphaα
Noradrenaline – dose dependant, αalpha>betaβ
Enoximone – non-betaβ-receptor action, drop in SVR↓
Isoprenaline – βbeta2 and β1 action, lowers SVR↓, increases HR↑
Phenylephrine, Metaraminol - increase in SVR↑, bradycardia↓
Vasopressin - increase in SVR↑, noradrenaline sparing!? Ensure organ function !!! ☞adequate perfusion pressure? Elevated venous pressure? Abdominal compartment syndrome?
☞good brain function? Do not needlessly sedate or even paralyse the patient.
☞good heart function? Chest pain? Pulmonary crackles? Echo? ECG?
☞good kidney function? Urine output? Serial changes in creatinine and urea?
☞good splanchnic function? pHi? The best test is that it works!
☞good overall metabolic function? Serial changes in lactate! Mixed venous saturation ! Trauma Burns Cardiac Liver Neuro Sepsis haemorrhage: chest, abdomen, pelvis, long bones etc – intracranial bleed???
other causes of shock in trauma patient?
tension pneumothorax? Cardiac tamponade?
endpoints for resuscitation?
thoracic and abdominal trauma vs head trauma external and internal fluid losses
maximum oedema formation first 6 to 8 hrs and continues for 24 hrs
Baxter or Parkland formula:
4 ml/kgBW/%BBSA with ½ first 8hrs
myocardial depressant factor
significant airway burn post- bypass?
vasodilatation and myocardial stunning
shock usually after >40% myocardium is dead
high filling pressures, HR high, SVR high vasodilation and high cardiac output
maldistribution of microcirculatory flow
increase of capillary permeability
bleeding, high ICP often management of high ICP and CPP
other problems you can think about?
spinal shock (high thor and cerv injuries)
autonomic dysreflexia (above T6)
diabetes insipidus (common)
SIADH and cerebral salt wasting peripheral vascular failure with hypovolaemia
high cardiac output but myocardial depressant factor
disturbed cellular metabolism with myochondrial dysfunction
tissue dysoxia and supply dependency Sepsis Resuscitation Bundle < 4 hrs Serum lactate measured
Blood cultures obtained prior to antibiotic administration
From the time of presentation, broad-spectrum antibiotics administered within 1 hour
In the event of hypotension and/or lactate > 4 mmol/L:
Deliver an initial minimum of 20 ml/kg of crystalloid
Apply vasopressors for hypotension not responding to initial fluid resuscitation to maintain mean arterial pressure (MAP) > 65 mm Hg
In the event of persistent hypotension despite fluid resuscitation (septic shock) and/or lactate > 4 mmol/L:
Achieve central venous pressure (CVP) of > 8 mmHg
Achieve central venous oxygen saturation (ScvO2) of > 70% What did we miss??? Ventilation
Right ventricular failure and pulmonary hypertension
Intraaortic Balloon Counterpulsation
Circulatory assist devices: LVAD, RVAD, BiVAD
Extracorporeal membrane oxygen