Introducing
Your new presentation assistant.
Refine, enhance, and tailor your content, source relevant images, and edit visuals quicker than ever before.
Trending searches
Stoelting, R., Hines, R., & Marschall, K. (2013). Handbook for Stoelting's anesthesia and co-existing disease. Philadelphia, PA: Elsevier/Saunders. Chapter 4
Positive Pressure ventilation:cardiac effects
Increases intrathoracic pressure which reduces venous return and preload, causing decrease in CO.
Changes in the partial pressure of carbon dioxide (PaCO2) resulting from changes in ventilation will also have cardiovascular effects.
A low PaCO2, which commonly occurs during controlled ventilation, causes peripheral vasoconstriction by a direct effect.
This increases systemic vascular resistance, increases afterload and can result in a fall in cardiac output
Most volatile anesthetic agents are coronary vasodilators
Volatile agents appear to exert beneficial effects in the setting of myocardial ischemia and infarction
**They reduce myocardial oxygen requirements
Surgery
Co-existing Diseases
Critically ill patients coming to the OR..
Anesthesia:
Cardiac Failure
Massive MI
Severe CHF
Failing Heart...waiting for transplant
Trauma
Shock states
Neurological
What meds are we used to using:
Epinephrine
Levophed
Dopamine/Dobutamine
Can be an acute or chronic condition!
Predisposing conditions:
Most significant clinical consequence is stroke!!
Nitrous Oxide
In Vitro: theoretically depresses myocardial contractility
However, CO, BP and HR remain unchanged.
Very good adjunct anesthetic….
For the right procedure and patient
Airway obstruction
Absence of air
Near drowning
Suffocation
Pulmonary embolus
Pneumothorax
Hypovolemic
Cardiogenic shock
Coronary insufficiency
Infarction
Reduced serum potassium (hypokalemia)
And to a lesser degree, epinephrine-like substances
(Beta 1 adrenergic stimulants)
Anesthetic management:
Cardiac dysrhythmias:
Conduction disturbances:
degree of blockade
Clinical significance depends on effects to vital signs and potential for deterioration into a life threatening rhythm
Healthy patients = compensate
Unhealthy cardiac patients= compensatory mechanisms are disrupted by anesthesia, end result can be catastrophic
Atropine
Glycopyrrolate
Sympathomimetic drugs
Caffeine
Nicotine
Cocaine
Amphetamines
Myocardial ischemia/infarction
CHF
PE
Hyperthyroidism
Pericarditis
Pericardial Tamponade
MH
ETOH withdrawal
Three Mechanisms:
1. Increased automaticity in the normal conduction tissue OR an ectopic focus
2. Reentry via abnormal pathways
3. Triggering of abnormal cardiac potentials due to "afterdepolarizations"
Depresses sinoatrial node automaticity
Dilates coronary arteries
(but is not as potent as Nitroglycerin or Adenosine)
How is cardiac output maintained?
Increased HR
Conflicting studies about whether coronary steal causes regional myocardial ischemia during episodes of tachycardia or drops in BP
Coronary Steal:
When a drug is given to a person with partial obstruction in a coronary artery, all the coronary vessels dilate. Hence blood will flow preferentially to the non-obstructed vessels, reducing the flow in the region of the obstructed vessel. Hence the drug given to improve the circulation will predispose to stealing of the blood into other regions.
Can be hard to determine...
if unstable - cardioversion!
Judgement:
Is it acceptable?
Does the patient continue to be hemodynamically stable with arrhythmia?
Similar cardiac effects to those of Isoflurane
Dose related Increase in BP but Decrease in SVR
Minimal CO effects with 1-2 MAC
Does not cause increased coronary blood flow (such as Isoflurane)
Rapid Increased MAC –Inc. BP, HR, and catecholamine levels
Tx: Narcotics and Esmolol
Mildly depresses cardiac contractility
Less decrease in SVR and BP than Iso or Des
Little increase in HR
No evidence of coronary steal
May prolong Q-T interval
Cardiac effects of Local:
Can depress the contractility and conduction
High concentrations depresses conduction by binding to fast sodium channels.
Many uses during surgery: local injection by surgeon, IV to block intubation response, regional blockade or neuraxial anesthesia
High spinal with cardiac arrest: high incidence, even in healthy patients - Tx is supportive measures
Local with Epinephrine (and or cocaine) during ENT/oral surgery
Be careful with patients with stenotic valvular lesions
and epinephrine ~ causes tachycardia!
Fentanyl/Morphine type opioids
In general do not affect cardiac function
Vagal mediated bradycardia
***Meperidine may increase HR, structurally similar to Atropine
Benzodiazepines: variable HR seen with
induction suggests may alter vagal tone
Ketamine: Increases arterial BP, HR and CO
Increases Cardiac Workload, avoid in CHF and patients with uncontrolled hypertension.
-Anxiety
-Patient is non-compliant with medications
-Patient stops cardiac medications prior to surgery thinking that they may interfere with anesthesia
History?
Hypertension, CAD, MI, Cardiomyopathy, Chronic Chest Pain?
Medications?
Lasix, Digoxin, Metoprolol, Nitroglycerin, Lisinopril, Cardizem, etc....?
Type of surgery?
Preparing for surgery?
NPO - how long?
Bowel preparations?
Any medications held?
The more risk factors the increased chance of poor outcome
Vagal stimulation:
Surgical Stimulation:
Caused by volatile anesthetic/or repeat doses of Succinylcholine
What type of drug is this?
Depolarizing Skeletal Muscle Relaxant
Cardiac Effects:
Slight increased HR
Be careful of repeated doses=bradycardia
Thought to be due to its metabolite succinylmonocholine which stimulates cholinergic receptors in the SA node
What is the main cause of succinylcholine induced arrhythmias?
A normal intubating dose causes the K+ levels to increase by 0.5 to 1 mEq/L
Not a problem with normokalemic patients but conditions which predispose patients to an increase in potassium
this increase could be fatal!
Labetalol:
5-20 mg IV over 2 minutes - reassess
Total dose not to exceed 300mg
* very unusual to give this large dose in anesthetized pt.
Metoprolol:
Acute Tachyarrhythmia - 5 mg IV over 1-2 min; total dose not to exceed 15mg
Afib/Flutter or SVT:
2.5 mg - 5mg IV Q2-5min; not to exceed 15 mg over 10-15 min
(Medscape App)
HR of 100-160
Normal P waves before every QRS
Normal PR interval
Treatment aimed at correcting underlying cause if increased sympathetic stimulation!
If not related to hypovolemia or compensation for maintaining CO ..... may be appropriate to give a Beta-Blocker
Untreated ST contributes to myocardial ischemia and CHF in susceptible patients
Labetalol:
7:1 with IV administration
Metoprolol: Selective inhibitor of alpha-1 adrenergic receptors; competitively binds with beta-1 receptors; little or no effect on beta-2
Better for treating HR than BP