Cardiac Tropism describes the effects of cardiac drugs on various heart muscle properties with a brief focus on anesthetics

1. CARDIAC TROPISM
BY MEHDI HADAVI
ANESTHESIOLOGIST

2. PROPERTIES OF THE CARDIAC CELLS=>
• Automaticity: capability of contract even in the absence of neural
control
• Rhythmicity: heart beats are extremely regular
• Contractibility: cardiac muscle contracts in response to a stimulus
• Excitability: ability of the cardiac muscle to respond to different
stimuli
• Conductivity: impulses produced in the SA node is conducted by
the specialized conducting pathway

3. CARDIOTROPY BASED ON CARDIAC MUSCLE
PROPERTIES
• Chronotropic (Heart rate)
• Inotropic (Contractility)
• Dromotropic (Conduction velocity)
• Bathmotropic (Excitability)
• Lusitropic (Relaxation)

4. CHRONOTROPY
• From chrono-, meaning time.
• Chronotrope Affects heart rate.

5. CHRONOTROPY
 Negative Chronotropes:
-Beta-blockers such as Metoprolol
-Acetylcholine
-Digoxin
-The non-dihydropyridine calcium
channel blockers diltiazem and
verapamil
 Positive Chronotropes:
-Atropine
-Dopamine
-Dobutamine
-Epinephrine
-Isoproterenol

6. INOTROPY
• From Greek in-, meaning fibre or sinew.
• An inotrope is an agent that alters the force or energy of
muscular contractions
• positive inotropy: increase contractile force of heart -->
ventricles empty more completely --> cardiac output improved
• negative inotropy: weaken/decrease the force of myocardial
contraction

7. INOTROPY
• Positive Inotropes:
-Dgoxine
-Bipyridine derivatives
-Calcium and Ca sensitizing
agents
-Cathecolamines
-Eicosanoids
-Phosphodiesterase inhibitors
-Glucagon
• Negative Inotropes:
-Beta blockers
-Calcium channel blockers
-Class 1A antiarrhythmic drugs
-Class 1C antiarrhythmic drugs

8. INOTROPY

9. DROMOTROPY
• from the Greek word "Dromos", meaning running, a course, a
race
• Dromotrope Affects Atrioventricular node (AV node) conduction
• Agents that are dromotropic are often (but not always)
inotropic and chronotropic

10. • Positive dromotropic:
-Isoproterenol
-Phenytoin
• Negative dromotropic:
-Verapamil
-Adenosine
DROMOTROPY

11. BATHMOTROPY
• From the Greek word "Bathmos," meaning step or threshold
• Bathmotrope Refers to modification of the degree of
excitability, (threshold of excitation), of musculature in general,
and of heart musculature specifically
• Positive Bathmotropic effects increase the response of muscle
to stimulation
• Negative Bathmotropic effects decrease the response of muscle
to stimulation

12. BATHMOTROPY
• Positive Bathmotropes:
-Norepinephrine and sympathetic stimulation in
general
-Digitalis - Converts the normal Purkinje action
potential of heart muscle to the automaticity typ
e, which increases myocardial irritability.
-Adrenaline
-Hypocalcemia
-Mild to Moderate Hyperkalemia
-Mild hypoxia
-Ischaemia
-Propanolol
-Quinidine and other Class A Antiarrhythmic
Agents
-Calcium Channel Blockers
-Parasympathetic stimulation (only of atrial
muscle cells)
-Hyponatremia - decreases external sodium
concentration
-Marked Hyperkalemia
-Hypokalemia
-Hypercalcemia
-Hyponatremia
-Acetylcholine
-Marked Hypoxia

13. LUSITROPY
• from Gr. lusis, variant of lysis
• Lusiotrope Describes myocardial relaxation.
• The increase in calcium uptake by cardiomyocytes leads to increased myocar
dial contractility (positive inotropic effect), but the myocardial relaxation, or
lusitropy, decreases
• Increased catecholamine levels promote positive lusitropy, enabling the hear
t to relax more rapidly

14. LUSITROPY
• Positive Lusitropy:
-Beta adrenergic agonists phosphorylate phospholamban via cAMP, reducing
calcium available for binding with troponin. Phospholamban is antagonist of
SERCA in the non phosphorylated state
• Negative Lusitropy:
-High calcium
-Reduced rate of calcium removal from myocyte through pumps
-Impaired sarcoplasmic reticulum calcium ATPase (SERCA)
-Increase affinity of troponin C
-Alkalosis that increases calcium sensitivity

15. VASCULAR EFFECTS OF SOME INOTROPE DRUG

16. INOTROPE EFFECTS ON BP AND CO

17. HEMODYNAMIC EFFECTS OF INOTROPES

18. INOTROPE EFFECTS, MECHANISMS AND DOSAGE IN SOCK
SITUATIONS

19. DOSE-DEPENDENT ACTIONS OF INOTROPES AND
CHRONOTROPES
Miller:

20. CARDIOTRPIC EFFECT OF VOLATILE
• Volatile anesthetics exert profound effects on the cardiovascular system by altering the
inotropic, chronotropic, dromotropic, and lusitropic state of the heart
• Volatile anesthetics produce dose-related prolongation of LV isovolumic relaxation in vivo.
This delay of isovolumic relaxation is associated with declines in early LV filling but is not of
sufficient magnitude to affect LV chamber stiffness.
• Coronary blood flow is elevated during isovolumic relaxation, and delays in relaxation
produced by volatile anesthetics contribute to impairment of coronary flow during early
diastole.
• Prolongation of LV relaxation probably occurs as a result of simultaneous depression of
myocardial contractility and not because of a direct negative lusitropic effect.
• In fact, volatile anesthetics modestly enhanced the rate of relaxation of isolated myocardium in
vitro. Volatile anesthetics also cause concentration-related decreases in the rate and extent of
early LV filling concomitant with negative inotropic effects.
• Further, volatile anesthetics reduced LV filling during atrial systole.

21. CARDIOTRPIC EFFECT OF VOLATILE
• inhalation anesthetics have direct inhibitory effects on sinoatrial node activity, which would
decrease heart rate in the absence of other compensatory mechanisms
• Rapid increases in the inhaled concentrations of desflurane, and to a lesser extent those of
isoflurane, may cause marked increases in heart rate due to sympathetic nervous system
activation. Sevoflurane, in contrast, has minimal effects on heart rate
• Isoflurane, desflurane, and sevoflurane did not alter invasively derived indices of regional
myocardial or chamber stiffness, indicating that LV distensibility was unaffected by these
volatile anesthetics.
• favorable reduction in myocardial O2 demand (reductions in ischemic burden) concomitant
with preservation of energy-dependent vital cellular processes because volatile anesthetics
cause direct negative inotropic, lusitropic, and chronotropic effects and are vasodilators.
• N2O has been demonstrated to depress various measures of LV contractile function, although
to a lesser extent than potent inhaled agents do
• N2O increases heart rate through stimulation of the sympathetic nervous system

22. CARDIOTROPIC EFFECT OF HYPNOTICS, SEDATIVE AND
OPIOIDS
• High concentrations of propofol abolish the inotropic effect of α- but
not β-adrenoreceptor stimulation, and enhance the lusitropic
(relaxation) effect of β-adrenoreceptor stimulation
• Systolic shortening can be impaired by propofol, especially at high
doses but sedative concentrations of propofol (0.65 to 2.6 g/mL)
produce significant vasodilation and hemodynamic disturbances but
not direct negative inotropic effects.
• Increases in plasma histamine after morphine administration cause
dilatation of terminal arterioles and direct positive cardiac
chronotropic and inotropic actions
• Combinations of vecuronium and high doses of opioids may produce
negative chronotropic and inotropic effects

23. CARDIOTROPIC EFFECT OF HYPNOTICS, SEDATIVE AND
OPIOIDS
• Diazepam and midazolam exert a direct myocardial depressant effect
. Negative inotropic effects of benzodiazepines have also been
reported in isolated organ preparations, although debate exists . In
vivo human studies of benzodiazepine effects, which also reflect
central and local reflex compensatory changes after drug
administration, do not indicate that these negative inotropic actions
are problematic or very significant.
• The dose-dependent negative inotropic actions of barbiturates are
greater than those produced by benzodiazepines, etomidate, or
ketamine but probably not as great as the depression that can be
produced by potent inhaled anesthetics.
• The inotropic effects of etomidate are slight; the drug itself has mild
positive inotropic actions in vitro, but propylene glycol, the solvent
that is used for the preparation of etomidate, may produce a slight

24. CARDIOTROPIC EFFECT OF HYPNOTICS, SEDATIVE AND
OPIOIDS
• Ketamine cardiovascular stimulation probably results from
central nervous system-mediated effects and sympathoneural
and systemic release of norepinephrine. Ketamine also
produces direct positive inotropic actions secondary to
increased myocardial calcium influx

25. CARDIOTROPIC EFFECT OF NEUROMUSCULAR BLOCKING
DRUGS
• Important cardiovascular effects mediated by muscarinic stimulation
are primarily related to parasympathetic cardiac actions
• Succinylcholine:low doses=>negative inotropic and chronotropic
Large doses=> effects may become positive
• Pancuronium, d-tubocurarine, and, to a lesser extent, rapacuronium,
rocuronium, and metocurine produce increases in heart rate due to
muscarinic blockade
• a positive chronotropic effect that places emphasis on the vagolytic
mechanism of pancuronium has not been found in humans
• tachycardia seen with benzylisoquinolinium compounds is the result
of histamine release

26. CHRONOTROPIC/INOTROPIC ACTIONS OF
HORMONES
Miller: