cardiac meds
DESCRIPTION
Cardiac Meds. Cardiac Output. =. X. Stroke Volume. Heart Rate. Afterload. Preload. Contractility. Sympathetic Stimulation. Meds. PVR. Venous Return. Viscosity. Ventricular Compliance. Aortic Impedance. Preload. - PowerPoint PPT PresentationTRANSCRIPT
Cardiac Meds
Cardiac Output
Stroke Volume Heart Rate
Meds Sympathetic Stimulation
Afterload Preload Contractility
X
=
PVR
Viscosity
Aortic Impedance
Venous Return
VentricularCompliance
Preload
• Function of the volume of blood to the LV and the compliance (ability of the ventricle to stretch) of the ventricles at the end of diastole (LVEDP)
• Factors affecting are: venous return, total blood volume and atrial kick
• Hypovolemic patient has too little preload• Heart failure patient has too much preload
Afterload
• Ventricular wall tension or stress during systolic ejection
• Increase in afterload relates to an increase in the work of the heart
• Increased afterload R/T:– Aortic stenosis– Vasoconstriction and SVR– Blood volume and viscosity
• To decrease, use vasodilators, decrease myocardial oxygen demand
Contractility
• Inotrophy or enhancing strength, can be positive or negative
• Sympathetic medications increase contractility• Ca++ is a medication that will increase
contractility by increasing actin and myosin contractions
• Digoxin also works to increase Ca++ channels by slowing the Na/Ca pump
Control of Heart Rate• SNS- sympathetic nervous system
– Fight or flight– Increase HR, BP, respirations, dilate pupils
• PNS- parasympathetic system– Decreases contractility, rate– Vagus nerves to the SA and AV nodes
• Baroreceptors- pressure sensors in carotids and aortic arches• Chemoreceptors- pH levels in aortic arch• ANF- atrial natriuretic factor- hormone secreted by the atria in
response to atrial pressure– Causes Na and water to be excreted and also vasodilates
Control of Stroke Volume
• Preload– Increase use:
• Fluid resusitation– Decrease use:
• Diuretics and vasodilators
• Afterload– Increase use:
• Vasopressors• Volume expanders
• Afterload– Decrease use:
• Vasodilators• Diuretics• Decrease sympathetic
stimulation
• Contractility– Increase use:
• Sympathetic stimulants– Decrease use:
• CCB’s• Decrease sympathetics
Vasopressors
• Sympathomimetic-inotrophic• Medications that mimic the sympathetic
system, work on alpha, beta and dopamineric receptors
• Require continuous monitoring of BP and heart rate
• Alpha: vasoconstricts peripheral arterioles• Beta 1: Increased HR, contractility• Beta 2: Bronchodilation
Vasopressor• Dopamine
– Stimulates alpha and beta receptors
– In small doses (2-5 mcg/kg/min) produces renal vasodilation
– Larger doses (max 20 mcg/kg/min) alpha and beta stimulation
– Increases HR and BP
• Precautions:– Give IV only, can
sloughing of tissue with extravasation, if it does infiltrate, give phentolamine IV to the site
– Tachyarrhythmias, palpations, hypotension if not hydrated, headache, dyspnea
Vasopressor• Epinephrine
– Alpha-Adrenergic, beta 1 and beta 2 stimulant
– Produces bronchodilation and vasoconstriction
– Increases HR, BP and bronchodilates
– Given IV, SQ and inhalation
– Max is 20 mcg/min
• Precautions:– Tachyarrhythmias– Angina– Nervousness, tremors– Hypertension– Works almost
immediately IV– Watch for chest pain and
HR >120, can cause cardiac arrest with too last a rate
Vasopressor
• Norepinephrine– Stimulates alpha, beta
receptors– Need to hydrate patient– Lacks beta 2 effects– Marked alpha
vasoconstriction– Used in shock states– Max is 16 mcg/min
• Precautions:– Closely monitor HR and
BP, can elevate quickly– Monitor for peripheral
vasoconstriction, in high doses, can constrict all extremities
– Can decrease the C.O. if rate is too high
Vasopressor• Dobutamine
– Synthetic cathecholamine with mainly beta effects
– Mild stimulation of beta 2
– Increases myocardial contractility
– Useful with heart failure patients
– Max is 20 mcg/kg/min
• Precautions:– Monitor for increased
HR and BP– PVC’s and angina– Watch for shortness of
breath– May be given over a long
infusion for heart failure patients
Vasopressors- Phosphodiesterase Inhibitors
• Cause increased levels of AMP and Ca++
• Medications:– Amrinone (Inocor)– Milrinone (Primacor)
• Cause an increase in cardiac output and some decreased afterload
• Effective in heart failure patients to increase C.O.
• Precautions:– Given as a continuous IV
infusion– Can cause PVC’s and V tach
because of increased contraction
– Monitor for drops in BP R/T decreased afterload
– Watch for thrombocytopenia and abnormal liver function
Other Vasopressors
• Phenylephrine (neo-synephrine)– Stimulates alpha
receptors only– Used by anesthesia– Can increase myocardial
demand– Works very quickly
• Vasopressin (antidiuretic hormone)– Nonadrenergic
peripheral vasoconstrictor
– Used in VF and pulseless VT, 40Units
– Used as an IV infusion in sepsis with peripheral vasodilation
Vasodilators- Direct Smooth Muscle Relaxants
• Decrease PVR• Arterial and venous dilation• Improves cardiac output• Medications:
– Nitroprusside (Nipride)– Nitroglyceride– Hydralazine (Apresoline)
• Precautions:– Closely monitor BP, can drop
dramatically, especially nipride
– Long term nitroprusside therapy can lead to thiocyanate toxicity
– NTG is used with unstable angina (given 5-300 mcg/min
– Apresoline is not a continuous infusion, major side effect is tachycardia
Vasodilators- Ca++ Channel Blockers
• Arterial vasodilation• Reduce the influx of
calcium and decrease resistance
• Used mostly for hypertension
• Also to slow rapid rhythms, such as SVT, and Atrial fib
• Medications:– Nicardipine (Cardene)– Nifedipine (Procardia)– Diltiazem (Cardizem)– Verapamil (Calan)
• Side effects:– Hypotension,
bradycardia, nausea, heart failure and peripheral edema
Vasodilators-ACE inhibitors• Vasodilate by blocking
the conversion of angiotensin I to angiotensin II, decreases PVR
• May drop BP dramatically if volume depleted
• Stops Na and water retention
• Medications:– Captopril (Capoten)– Enalapril (Vasotec)
• Precautions:– Hypotension, chronic
cough, neutropenia and elevated liver enzymes
Vasodilators- Alpha adrenergic blockers
• Block peripheral alpha receptors in arteries and veins
• Orthostatic changes may result
• May lead to fluid retention
• Medications:– Labetalol (normadyne)
• Alpha & beta blocker• Decreased BP without
increased HR• Used in aortic dissections
– Phentolamine (Regitine)• Peripheral alpha blocker,
decreases afterload• Used with
pheochromocytomas
Vasodilators- DA-1 receptor agonists & Synthetic BNP
• Dopamine DA-1 receptor agonists, vasodilates peripheral and renal arteries
• Medication:– Fenoldopam (Corlapam)
• Hypertensive emergencies
• Watch for hypotension and tachycardia
• Natrecor:– Brain naturietic peptide– Used for decompensated
HR with dyspnea– Vasodilates pulmonary
bed, reduces SVR and PVR
– Lowers BNP levels– Infusion runs for 6-48
hours
Vaughn Williams Classification- Used for Antiarrhythmics
• Class I agents interfere with the sodium (Na+) channel.
• Class II agents are anti-sympathetic nervous system agents. Most agents in this class are beta blockers.
• Class III agents affect potassium (K+) efflux. • Class IV agents affect calcium channels and the
AV node. • Class V agents work by other or unknown
mechanisms.
Class Ia
• Medications:– Quinidine– Procainamide– Disopyramide
• Type:– Na+ channel block
intermediate
• Use:• Ventricular arrhythmias• Prevents recurrent atrial
fib, triggered by overactive vagal stimulation (Wolff-Parkinson-White syndrome)
Class Ib
• Medication:– Lidocaine– Phenytoin– Mexiletine
• Type:– Na+ channel block fast
• Use:– Ventricular tachycardia– Atrial fib– Prevention during and
immediately after an MI, but it is now discouraged R/T increased risk of asystole
Class Ic
• Medications:– Flecainide– Propafenone– Moricizine
• Type:– Na+ channel block slow
• Use:– Prevents paroxysmal
atrial fib– Treats recurrent
tachyarrhythmias of abnormal conduction system
Class II• Medications:
– Propranolol– Esmolol– Timolol– Metoprolol– Atenolol
• Type:– Beta Blocker
• Use:– Decrease myocardial
infarction mortality, used post MI
– Prevent recurrence of tachyarrhythmias
– Decrease Beta 1 and 2 stimulation, decrease HR and BP
– Side effects of bradycardia, fatigue, wt. gain, impotence, depression
Class III
• Medications:– Amiodarone– Sotalol (also a Beta)– Ibutilide– Dofetilide
• Type:– K+ channel blocker
• Use:– Ventricular tachyarrhythmias– Atrial flutter and atrial fib– Wolff-Parkinson-White
syndrome• Side effects:
– SOB, bronchospasm, renal or hepatic insufficiency
– Photosensitive, use sunscreen and sunglasses, may cause bluing of periphery
Class IV
• Medications:– Verapamil– Diltiazem
• Type:– Ca++ channel blocker
• Use:– Prevent recurrence of
paroxysmal SVT– Reduce ventricular rate in
patients with atrial fib– Decrease the contraction of
muscle tissue, prevents slide of actin and myosin
– Avoid grapefruit juice it can increase serum levels, as do high fat meals
– Monitor thyroid function
Class VMedications:
AdenosineDigoxin
Type:Work by other methods,
direct nodal inhibitionNa/Ca pump
Use: Supraventricular arrhythmias Contraindicated in ventricular
arrhythmiasSide effects:
Digoxin- bradycardia, anorexia, nausea & vomiting, yellow/green halos, heart blocks, arrhythmias, causes hypocalcemia and hypokalemia
Aspirin
• Acts to reduce inflammation by inhibiting the production of prostaglandins
• Decreases platelet aggregation, decreases the incidence of TIA’s and MI
• Dosage of 81 mg maintenance, not enteric coated in MI
• Monitor for GI bleeding, exfoliative dermatitis, Stevens-Johnson syndrome, tinnitus
Other Emergency Medications
• Atropine:– Parasympathicolytic, enhances
the SA node and AV node conduction
– Used for bradycardia and asystole
– Side effects:• Tachycardia, urinary
retention, blurred vision, bowel obstruction, not for Complete heart block
• Calcium Cl:– Enhances myocardial
contractility for pts with elevated K, Mg and low Ca and CCB toxicity
– Side effects:• Coronary and cerebral
vasospasm, ventricular irritability, cautious if on Digoxin
Other Emergency Medications
• Magnesium– Reduces post infarction
arrhythmias and pump failure– Hypomagnesemia can cause
refractory V fib and sudden cardiac death
– Side effects:• Flushing, sweating,
hypotension, sensation of heat, flaccid paralysis, circulatory collapse
• Diprivan (Propofol)– Short acting sedative,
used for sedation with patients who have airway and ventilatory support
– Side effects:• Hypotension, rebound
tachycardia and increased ICP when wean off, hepatotoxicity
Other Emergency Medications
• Lorazepam (Ativan)– Benzodiazepine sedative– Effects last 6-8 hours– If given intraarterial can cause
gangrene and limb loss– CNS depression is prominent if
over 50– Contraindicated if glaucoma– Watch for airway depression
• Midazolam (Versed)– Benzodiazepine sedative– Effects last 1.5-2 hours– Depresses respiratory rate,
apnea, can cause hypotension– Hiccups, headache, nausea,
amnesia, confusion– Can be reserved with romazicon
(flumazenil)
Other Emergency Medications
• Succinylcholine– Neuromuscular blocking agent– Rapid acting agent for intubation– Side effects:
• Hypotention, tachycardia, hyperkalemia, severe in neurologic patients myoglobinuria, malignant hyperthemia
• Rocuronium or vecuronium– Neuromuscular blocking agent– Lasts 20-60 minutes– Can cause tachycardia,
hypotension and bronchospasm in some patients, prolonged weakness if renal involvement