Cardiac Pharmacology Flashcards
1
Q
What is th Bohr Effect
A
The presence of carbon dioxide aiding in the release and delivery of oxygen from hemoglobin.
2
Q
What is the amount of blood that is pumped out of the heart per unit of time?
A
Cardiac Output
3
Q
What is the lowest pressure reached right before ventricular ejection?
A
Diastolic blood pressure (DBP).
4
Q
What is the pressure that drives blood into the tissues, averaged over the entire cardiac cycle?
A
Mean Arterial Pressure (MAP).
5
Q
What are catecholamines?
A
Endogenous products that are secreted into the bloodstream and travel to nerve endings to stimulate an excitatory response.
One of a group of similar compounds having sympathomimetic action
6
Q
What is the link between atrial depolarization and ventricular depolarization?
A
AV Node
7
Q
What is the peak pressure reached during ventricular ejection?
A
Systolic blood pressure (SBP).
8
Q
What enzyme is responsible for the breakdown of cAMP?
A
Phosphodiesterase.
9
Q
What is A-fib?
A
A cardiac arrhythmia in which normal atrial contractions are replaced by rapid irregular twitchings of the muscular wall.
10
Q
What is vasopressor?
A
An agent that causes vasoconstriction (increase SVR)
Used to increase BP
Also results in an increase in coronary perfusion pressure
11
Q
What is an inotropic agent?
A
It is an agent affecting the strength of muscular contraction.
- Can be positive (increase contraction strength) or negative (decrease contraction strength)
12
Q
What is V-fib?
A
A cardiac arrhythmia in which normal ventricular contractions are replaced by rapid movements of the ventricular.
13
Q
What three factors does tissue perfusion depend on?
A
Cardiac function, vascular tone, and vascular volume.
14
Q
If a patient was in cardiogenic shock and had a decreased CO, would a pulse oximeter attached to the index finger be an accurate way to measure oxygenation status?
A
No, if perfusion was limited due to decreased CO the patient’s pulse rate in the finger may not be adequate enough for the proper functioning of a pulse oximeter.
15
Q
What is a Chronotrope
A
- An agent that affects heart rate
- Can be positive (increase HR) or negative (decrease HR)
16
Q
What is a Dromotrope
A
- An agent that affects the rate of conduction
- Can be positive (increase conduction velocity) or negative (decrease conduction velocity)
17
Q
What is a vasoactive drug
A
An agent that affects blood vessel tone (dilation/contraction)
18
Q
Where are alpha Adrenergic Recpetors located
A
- Primary located in the peripheral vasculature where they will regulate smooth vascular tone
- Alpha 1 receptors are located in the peripheral blood vessels
- Alpha 2 receptors are located in the presynaptic sympathetic neurons and CNS
19
Q
Alpha Recpetor Stimulation
A
- Agonist stimulation results in vasoconstriction and therefore
- Increased arterial blood pressure
- Increased coronary and cerebral perfusion pressure
- Will regulate cardiac, vascular, bronchiolar, and GI smooth muscle tone
- Will have a minimal inotropic effect due to the fact that there is few alpha receptors in the myocardium
20
Q
Stimulation of Alpha 2 Receptors
A
- Alpha 2 receptors are located in the presynaptic sympathetic neurons and CNS
- Stimulation here inhibits the release of norepinephrine resulting in vasodilation
21
Q
Examples of Alpha Agonists
A
- Norepinephrine +++
- Epinephrine++
- Dopamine (high dose) +++
22
Q
Where are Beta 1 Receptors Located
A
Located within the heart (mostly in the sinus node and ventricles)
23
Q
Agonist Stimulation of Beta 1 Receptors
A
- Increased heart rate (positive chronotrope)
- Increased myocardial contraction (positive inotrope)
- Increased rate of conduction (positive dromotrope)
24
Q
Negative Effects of Stimulation of Beta 1 Receptors
A
- Increased myocardial irritability
- Increased myocardial oxygen demand
25
Beta 2 Receptors
* Located in the heart, vascular bed and bronchial smooth muscle
* Agonist stimulation will result in bronchodilation (primary effect) and peripheral vasodilation (minimal effect, opposes alpha one stimulation)
26
Dopaminergic Receptors
* Located in the smooth muscle in the cerebral, coronary, renal, and splanchnic vascular beds
* Agonist stimulation will results in vasodilation and therefore increased blood flow to these areas
27
After administration of epinephrine, stimulation of what receptor type is likely to produce a net effect of tachycardia?
B1 receptors because they are densely populated in the myocardium.
28
Why do patients receiving a phenylephrine infusion has developed reflex bradycardia?
Patients on phenylephrine infusions develop a reflex bradycardia due to the unopposed alpha 1 stimulation in the vasculature causing increased SVR.
29
Why would you use drug that will alter CO and SVR
* Stabilize hemodynamic status and avert cardiovascular collapse
* Restore perfusion pressure
* Improve CO and organ perfusion
30
Cautions of CO and SVR Drugs
* The increase BP and increase HR increases myocardial oxygen demand and may cause myocardial ischemia
* β1 properties markedly increases myocardial oxygen consumption which may exacerbate myocardial infarct/ischemia
31
32
Epinephrine Mechanism of Action
* Both an alpha and beta adrenergic agent
* Both vasopressor and inotropic, chronotropic, and dromotropic properties
* Will increase both cerebral and coronary prefusion pressure
33
Epinephrine Effect on Heart Rate
* Increase rate firing of the SA node
* Increased rate of conduction through the AV node
* Decreased refractory time
* This can make the heart prone to arrhythmias
34
Epinephrine Beta 2 Stimulation
The beta two stimulation will result in bronchodilation, the peripheral vasodilation will not win out against the strong alpha effects (though there will be some vasodilation occurring via the B2 stimulation)
35
Indications for Epinephrine
* Cardiac arrest
* Given as a bolus
* Used in pulseless arrhythmias, VF, VT, PEA, asystole
* Epinephrine makes VF more responsive to defibrillation
* Hypotension
* Given as an infusion
* Anaphylaxis and severe allergic reactions
* Given via SQ/ IM
36
Epinephrine Routes of Administration
* Can be given via the ETT
* 2-2.5 mg in 10 cc normal saline
* i.e. 2-2.5 x normal bolus of 1 mg
* Other Routes
* Inhaled in 5 mg for adults and therefore 5 mL of 1:1000
37
What is the major determinant of blood pressure and ventricular contractility?
CO and the volume of blood filling in the ventricles (preload).
38
What are two determinants of MAP?
Systemic vascular resistance and CO.
39
What is stroke volume?
The amount of blood ejected from the heart during systole.
40
What would be the 1st line therapy to improve the hypotension if a patient has just suffered severe blood loss due to the arterial lines becoming dislodged?
Fluids are the mainstay for improving hypotensive episodes.
41
What measurement would likely be alerted if a patient’s hemodynamic parameters are currently being measured and patient’s fluid overloads?
CVP would be increased.
42
What is the clinical indication for the use of Levophed?
The need to increase MAP
* Hypotension due to a low SVR
* Ex. Distributive shock (septic, anaphylactic, neurogenic)
* Should be used with extreme caution in cardiogenic shock
* The higher BP achieved may severely limit the blood flow to flow organs
* In non septic patient can produce severe renal and splanchnic vasoconstriction
* Is an important endogenous neurotransmitter
43
Why is the use of isoproterenol which can be used to relax the smooth muscle of the bronchi, limited and what is the brand name?
Limited because of its pronounced stimulatory effect on the HR. Isuprel.
44
Why is Norepinephrine more appropriate treatment than dopamine in treating a patient with septic shock?
There is an increased risk of tachyarrhythmias as compared to the risk with other vasopressors.
45
What is the indication of epinephrine in advanced life support?
Potent vasoconstrictor.
46
What medications would be indicated to increase blood flow to the myocardium and the CNS during CPR?
Epinephrine.
47
Norepinephrine (Levophed)
Mechanism of Action
* Powerful alpha and beta 1 receptor agonist
* The beta 1 effect is primarily an increase in myocardial contraction
* The effect on Hr is less prounced
48
Dopamine (Intropin)
MEchanism of Action
* A precursor to norepinephrine
* Will agonise the effect of norepeine
* Stimulates alpha, beta 1, and dopaminergic receptor
49
Dopamine
Low Dose
* **Low Dose (1-5 ug/kg/min)**
* Renal dose
* Causes vasodilation of renal and splanchnic arteries increasing urine output
* No longer used to treat oliguria
50
Dopamine
Moderate Dose
* Cardiac dose
* Beta one effects dominate
* The effects on the renal system are enhanced due to an increase cardiac output
* Used to treat bradycardias
51
Dopamine High Dose
* **High Dose (10-20 ug/kg/min)**
* Vasopressor dose
* Alpha effects are seen increasing SVR and splanchnic vasoconstriction
52
Phenylephrine (Neo-Synephrine)
Mechanism of Action
* Alpha agonist with minimal beta stimulation and almost no inotropic or chronotropic properties
53
Phenylephrine (Neo-Synephrine) Indications
* Hypotension due to distributive shock
* Vasoconstriction that lasts 20 min after IV
54
Phenylephrine (Neo-Synephrine) Cautions
* Don’t use to treat low heart rates
* Reflex bradycardia response can be blocked by atropine
55
Vasopressin
Mechanism of Action
* A non-adrenergic peripheral vasopressor
* A naturally occurring hormone (aka ADH)
* An advantage is that it does not have β stimulation (which can lead to increased myocardial irritability)!
* Vasopressin in resuscitation: once ROSC then less likely to have a tachyarrhythmia then compared with Epi
* Long half life, that’s why only used once.
ETT dose not known
56
Vasopressin
Indications
* May be used as an alternative pressor to epinephrine (1st or 2nd dose) in pulseless arrhythmias: VF, pulseless VT arrest, PEA, asystole (as a bolus)
* Hypotension due to distributive shocks (as a infusion)
* Treat diabetes insipidus (it’s original use)
57
Dobutamine (Dobutrex)
Mechanism of Action
* A synthetic catecholamine that produces predominantly β1 effects (\ primarily an inotrope)
* Net change on BP can be increased/ decreased /Ø
* Has minimal effect on α receptors, and actually can cause a slight in SVR because it may have a minimal effect on b2
58
Dobutamine (Dobutrex)
Indications
* Pt’s with pump problems who have adequate systolic blood pressure (\> 70-100 mmHg) (ie. Cardiogenic Shock)
* Need adequate BP in case the net BP change causes a decrease!
* The increased myocardial demand is compensated by the increased coronary blood flow
59
Dobutamine Cautions
* Contraindicated in severe hypotension and distributive shocks
* May cause tachyarrhythmias
60
Isoproterenol (Isuprel)
Mechanism of Action
* Nearly a pure β agonist (β1 and β2)
* Therefore a potent inotrope and chronotrope (b/c of β1) but BP and SVR due to β2
61
Isoproterenol (Isuprel)
Indication
* Never an “agent of choice” due to better drugs
* May be used in refractory bradycardia or to treat β-blocker OD
62
Inamrinone and Milrinone
Mechanism of Action
* Phosphodiesterase III inhibitors that have inotropic and vasodilatory properties (aka “inodilators”)
* In the heart causes inotropic effects
* In the periphery results in vasodilation
63
Inamrinone and Milrinone
Indication
Severe CHF or cardiogenic shock
Cause inotropic effects
In the periphery results in vasodilation
More for short-term management of CHF!
* Does not react with digitalis and patients should be on this prior as inamrinone may increase ventricular response as it increases conduction through the AV node
* Contains sulphites and may cause allergic reactions (in asthmatics \> non-asthmatics)
64
Atropine
Mechanism of Action
* A parasympatholytic that enhances both automaticity of the SA node (to increase rate) and AV conduction
* increase conduction thru AV node---helpful in some heart blocks
65
Atropine
Indications
* Symptomatic bradyarrhythmias
* **BUT,** it may not work in higher level blocks (2° type II or 3° blocks)
* **New ACLS doesn’t have atropine in the PEA/asystole anymore.**
66
Anti-Arrhythmics
Classification
* _Class I_: Sodium channel blockers (Lidocaine)
* _Class II_: β-Blockers (Metoprolol, Propanolol, Lobetalol…)
* _Class III_: Potassium channel blockers (Amiodarone)
* _Class IV_: Calcium channel blockers (Diltiazem, Verapamil)
67
Sodium-Channel Blockers (Lidocain)
Mechanism of Action
* Suppresses ventricular arrhythmias and decreases myocardial conduction
* Increases VF threshold
* If block the sodium channels then it takes more stimulus to result in depolarization
* Can be given IV/IO or via the ETT!
68
Sodium-Channel Blockers (Lidocain)
Indications
* Shock refractory VF/pulseless VT
* Manage PVCs/ventricular irritability
* Think _ventricular_ arrhythmias!
69
Beta Blockers Mechanism of Action
* Blocks the β-adrenergic receptors reducing the effects of circulating catecholamines
* This results in:
* Decrease HR
* Decrease BP
* Decrease myocardial contractility
* Decrease myocardial oxygen consumption
* (mild vasoconstriction due to blocking of the β2 receptors on the peripheral vasculature)
* _Overall BP is decreased_ as the drop in HR is greater than the minimal increase in SVR
70
**Common** **_β-Blockers:_**
Metoprolol, Propanolol, Labetalol, Atenolol, Esmolol
71
Beta Blockers Indications
* Acute coronary syndromes
* Hypertension
* Acute Tachyarrhythmias (SVTs)
72
Cautions of Beta Blockers
May result in hypotension and/or bradycardias
Avoid in bronchospastic diseases!
73
Potassium-Channel Blockers
Amiodarone (Cordarone)
Indications
* Shock-refractory VF/pulseless VT
* Treat tachyarrhythmias
* Commonly used to treat aFib (but this is off-label)
74
Amiodarone Cautions
* May produce vasodilation and decrease BP
* May have negative inotropic effects
* Can have toxic effects---"Amiodarone lung”, “Smurf Syndrome”
75
Calcium Channel Blockers Subgroups
## Footnote
###
* One used to treat arrhythmias
* One to treat hypertension
76
Calcium Channel Blockers
Mechanism of Action
* Decrease SA node automaticity
* Slows AV node conduction
* Increase AV node refractory period
77
Calcium Channel Blockers
Indications
* Narrow complex tachycardia (SVTs)
* First drug of choice for afib/flutter over digoxin
* Second line agents after adenosine (along with β-blockers)
78
Calcium Channel Blockers
Common Drugs
* Diltiazem
* Verapamil
79
Calcium Channel Blockers
Cautions
* Do not give to tachycardias with a wide-complex or WPW
* Expect BP to drop due to peripheral vasodilation
* Do not give to patients who are receiving β-blockers (can cause profound hypotension)
80
Adenosine Mechanism of Action
##
Depresses both SA and AV nodes
81
Adenosine Indications
* To treat SVTs
* Can also be used “diagnostically”--slow down the rhythm to identify if there is p waves in a wide complex tachy (ie. Classify the specific arrhythmia---help with treatment options
* First drug of choice for narrow complex tachycardias (SVTs), including WPW
* BUT, will not convert AFib/AFlutter or VT
* Vagal maneuvers should be tried first
82
Adenosine Cautions
* Warn patient of the possible symptoms they may feel during administration (heat, flushing, chest pain/tightness)
* Expect a few seconds of asystole/bradycardia
* Contraindicated in asthma due to risk of bronchospasm
* VERY short lived drug ~ 5 sec half-life
83
Adenosine Administration
* Adenosine and Saline flush both into port, clamp IV tubing_, fast_ bolus adenosine followed by the flush, unclamp tubing.
84
Digoxin
* Is a positive inotrope and a negative chronotrope
* Slows conduction thru the AV node
85
Digoxin Indications
* To decrease the ventricular response in AFib or Aflutter, especially chronic cases
86
Digoxin Cautions
* A very narrow therapeutic range!!! (Especially if potassium depletion is present)
* Digitoxicity may cause serious arrhythmias and precipitate cardiac arrest!
87
Nitrates MEchanism of Action
* Will breakdown nitric oxide that binds to vascular receptors and produce venodilation and arterial dilation
* Reduce preload and increase capacitance of veins
* Increase CO by reducing SVR and in turn afterload
* Will dilate large coronary arteries and collaterals improving blood supply to myocardium
88
Nitrates Indications
* Angina, AMI, CHF, hypertensive crisis
89
Nitrates Cautions
Hypotension
90
ACE Inhibitors Mechanism of Action
* Prevents the synthesis of Angiotensin II (a vasoconstrictor); thus, the end result is systemic vasodilation and decrease BP
91
ACE Inhibitors Common Medications
Captopril, Enalapril and Ramipril
92
Anticoagulants
**Heparin**-Inhibits clot formation by inhibiting specific factors of the clotting pathway
**Coumadin**-Often used post-heparin therapy
93
Antiplatelets
**Aspirin (ASA)**
**Reopro (Abciximab)**
**Plavix (Clopidogrel)**
94
Common Thrombolytics
Alteplase (tPA)
Reteplase (Retavase)
Streptokinase (Streptase)
Tenecteplase (TNK)
95
What condition is vasopressin used for?
Septic shock.
96
What is a clinical situation in which midodrine would be indicated?
Management of orthostatic hypotension in refractory pts with orthostatic hypotension.
97
What is the clinical indication for dobutamine?
For the short-term treatment of decompensated heart failure secondary to depressed contractility.
98
Why would milrinone be chosen over inamrinone to manage patient’s hemodynamic status?
Milrione has a shorter half-life than inamrinone and is less likely to cause thrombocytopenia.
99
What chronic condition is Digoxin, the only drug in the cardiac glycoside class, issued in management?
Heart Failure
100
When is a catheter ablation indicated and what is involved in the procedure?
A-fib. Inserting a catheter into a blood vessel. The tip causes an arrhythmia and electrical current burns a small hole.
101
In general, amiodarone is used to treat?
Supraventricular and ventricular arrhythmias.
102
## Footnote
**What are Class IV drugs referred to as?**
Calcium channel blockers.
103
What is the indication of magnesium sulfate in advanced life support?
Prolonged conduction time
104
What drugs can be administered through an endotracheal tube if IV access is not available?
Naloxone, atropine, vasopressin, epinephrine, and lidocaine. Remember NAVEL.
105
What pressure best evaluates a patient-specific response to fluid therapy and vasoactive therapy?
CVP.
106
What therapies are used in the management of shock?
Fluids, inotropes, vasopressors, and cardiac glycosides.
107
What types of drugs are norepinephrine and epinephrine?
Catecholamines
108
What medication is best indicated for the management of septic shock?
Norepinephrine (Levophed).
109
What is the only glycoside that used in the management of chronic heart failure?
Digoxin
110
What drug is used for the treatment of life-threating ventricular arrhythmias?
Procainamide.
111
When administering medications down an endotracheal tube, how much normal saline should be used to dilute the medication?
10 mL
112
What is distributive/shock syndrome?
Abnormal distribution of blood flow in the smallest blood vessels results in adequate supply of blood to the body’s tissues and organs. It is usually caused by sepsis (a life-threatening complication of an infection).
113
What is cardiogenic shock?
Heart suddenly cannot pump enough blood to meet your body’s needs. It is most often caused by a severe heart attack.
114
What is dopamine (Inotropin)?
Catecholamine, directly stimulates B receptors, chronotropic and inotropic effects lead to increase CO, increases SVR and do not give to patients in septic shock.
115
What is Phenylephrine?
Catecholamine, purely an agonist, induces vasoconstriction, elevates SBP and DBP, and due to unopposed a1 stimulation, reflex bradycardia when infusing.
116
What is Vasopressin (Pitressin)?
It is an antidiuretic hormone that increases BP by increasing circulation of blood volume, catecholamine, used in the setting of septic shock, naturally occurring hormone (ADH), should not be used as a sole agent for hypotension in the setting of septic shock and should be given when other vasopressors are not enough.
117
What are the initial signs and symptoms of vasopressor-induced extravasations?
Pain, swelling, erythema, blistering, mottling and to decrease risk administer vasopressor via central line.
118
What is Dobutamine (Dobutrex)?
Inotropic agent; for short-term treatment of heart failure second to depressed contractility; r isomer: causes positive inotropic and chronotropic effects; and, adverse effects: tachyphylaxis, tachycardia, and hypotension.
119
What is Digoxin (Lanoxin)?
It is an inotropic agent used for the management of chronic heart failure, it inhibits the vagus nerve, it has no hypotensive effects, and it has a narrow therapeutic margin (0.5-2ng/ml).
120
Atrial Fibrillation is caused by what?
By irritation, that causes a twitch in that region and can be due to acid, hypoxemia, or imbalances in electrolytes.
121
What defines a hypertensive crisis?
Any SBP greater than 180 and any DBP greater than 120 encompasses an urgency/emergency.
122
What are ACE inhibitors?
Block conversion of angiotensin I to angiotensin II by competing with physiologic substrate angiotensin I for the active site of ACE.
123
What is the biggest concern for respiratory therapists when it comes to beta blockers?
May cause bronchospasm.
124
What is Adenosine?
It is used via rapid IV push to terminate SVT.
125
What is Atropine?
Used for bradycardia
126
What are the categories of thrombolytic?
Anticoagulants, antiplatelet, and thrombolytic.
127
What does Protamine sulfate do?
It reverses heparin.
128
What is the treatment for Torsades de Pointes?
Magnesium sulfate.
