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CVRN Cardiovascular Pharmacology
Terms in this set (116)
Frank Starling's curve
↑ preload = ↑ SV = ↑ CO in normal circumstances with a compliant ventricle
In a non-compliant ventricle, a large increase in preload actually decreases CO
- The ability of the ventricles to distend when preload enters the ventricles during diastole
- In normal ventricles, increased preload (volume) results in increased distention and increased CO
- If myocardial oxygenation is low (MI), fibrosis or hypertrophy has occurred, the ventricles are less compliant and CO decreases with increased preload
- Resistance or pressure in the systemic system that the left ventricle needs to overcome by increasing force and contraction to the point which opens the aortic valve and blood is propelled into the circulation
- Clinically measured by Systemic Vascular Resistance (SVR)
What factors affect afterload?
- Arterial resistance (hypertension)
- Aortic valve problems
- Blood viscosity
- Use of vasoconstrictor or vasodilator drugs
- Heart's intrinsic contractile strength that is independent of the other determinants of CO
- There is no non-invasive way to measure contractility
- Ejection fraction is a surrogate for contractility
- Physiological determinants of contractility are oxygenation, pH, electrolyte balance, and temperature
Pathological factors effect reduced contractility
Acute MI, open heart surgery, ventricular dysfunction seen in cardiomyopathy and heart failure
Pathological factors effect increased contractility
Early ventricular hypertrophy
Positive inotropic drugs
increase contractility of the heart
Negative inotropic drugs
decrease contractility of the heart
increase heart rate
decrease heart rate
How do "βeta 1 receptors" effect cardiac function?
- Simulation of βeta 1 receptors (β1) with β1 adrenergic medications causes a positive chronotropic effect, positive inotropic effect
- If blocked, all of the above decrease
How do "βeta 2 receptors" effect cardiac function?
Simulation of βeta 2 receptors (β2) with β2 adrenergic medications causes a vasodilation of the coronary arteries as well as relaxation of bronchial smooth muscle and dilation of major blood vessels
How do "alpha receptors" (α) effect cardiac function?
Simulation of α receptors causes vasoconstriction of vascular beds throughout the body
Act at alpha, βeta 1 & 2, and dopaminergic receptor sites
- Low cardiac output states due to MI, cardiac
- Acute decompensated heart failure
- Shock states, including cardiogenic shock and
Sympathomimetic drugs action
- Mimic the action of norepinephrine or epinephrine stimulating α and β receptors either directly or indirectly by causing the release of natural neurohormones at storage sites
- Result in peripheral vasoconstriction, increased cardiac contraction, increase HR, and bronchodilation
- Results in increased contraction, CO and SV as well as increased renal blood flow and sodium excretion
Other shock states with low BP
Inotropin (Dopamine®) doses
Low dose: 0.5-2 mcg/kg/min
- Activation of dopaminergic receptors causing vasodilation of renal, mesenteric, coronary and intracerebral vasculature
Intermediate dose: 2-10 mcg/kg/min
- Stimulation of Beta-1 receptors causing increased contractility, HR, and cardiac output
High dose: 10-20 mcg/kg/min
- Stimulation primarily of alpha receptors leading to vasoconstriction
- Stimulates β1 receptors resulting in increased contractility, CO, and SV with minor effects on HR
- Stimulation of B2 receptors causes vasodilation which decreases preload and afterload (which indirectly increases cardiac output)
Also has alpha-1 effects
Treatment of decreased cardiac contractility resulting from myocardial disease, injury, or cardiac surgery
Acute heart failure
- Marked stimulation of alpha, β1 and β2 receptors, resulting in increased contractility, heart rate, stroke volume, cardiac output, and coronary blood flow and bronchodilation (positive inotropic and positive chronotropic effects)
- Produces profound vasoconstriction of the periphery, especially of renal and splanchnic beds
Hypotension resistant to conventional measures
Symptomatic bradycardia unresponsive to atropine
- Predominantly an α agonist but also stimulates β1 receptors at low doses
- Produces vasoconstriction in all vascular beds
Hypotension caused by sepsis, MI, or other hypotensive crisis refractory to fluids
- Pure α agonist producing pronounced
vasoconstriction, increasing both systolic and
diastolic BP, and a reflex decrease in HR
- First line vasopressor if tachyarrythmias preclude
use of norepinephrine
• Vascular failure in shock states
- Pronounced stimulation of β1 and β2, and minimal alpha effect
- Positive inotropic and chronotropic effects
Serious heart blocks
- Acts on the kidneys to increase water reabsorption, to prevent water loss
- Constricts blood vessels to raise blood pressure
Asystole (Use for asystole not approved by the FDA)
Ventricular tachycardia or ventricular fibrillation
Sympathomimetic drugs list
Bipyridine Inotrope / Vasodilator: Milrinone (Primacor®)
- Direct acting inotropic agent as well as direct arterial vasodilating agent
- Improves diastolic relaxation
- Produces increase in CO, decrease in afterload and preload without increase in HR or myocardial oxygen consumption
Short term treatment of decompensated CHF
Post op cardiac surgery;
Pulmonary hypertension and right-sided heart failure
- Use cautiously in patients with renal failure (renally excreted)
In the post-MI patient, what is the drug of choice to manage decreased cardiac output?
Dopamine or norepinephrine (SOAP II trial) are the
drugs of choice due to their vasopressor abilities
Severe hypotension caused by cardiogenic shock which has been nonresponsive to dopamine and dobutamine, what is another drug choice?
Dopamine at 15 mcg/kg/min has what hemodynamic effect?
At 15 mcg/kg/min the effect is mostly α with resulting vasoconstriction of the periphery and renal blood flow is impaired
When infusing epinephrine, what should you monitor closely besides the patients hemodynamics?
- Blood glucose levels should be monitored very closely as epinephrine stimulates glucose release from the liver
- IV insulin infusions maybe necessary
- Also monitor for acidosis
In a combined drug therapy of dopamine at 2mcg/kg/min and dobutamine at 7mcg/kg/ min, what are the expected hemodynamic changes?
- Increased CO from increased contractility resulting in increased SV; possible decreased preload
- Decreased SVR
- Improved renal blood flow, with improved renal output and decreased preload
In an acute MI with symptomatic bradycardia unresponsive to atropine, what would be a drug of choice?
- Dopamine or epinephrine infusions, per ACLS guidelines
- Cardiac pacing
Is preferable after a MI
What is the drug of choice to treat right sided heart failure?
Dobutamine is the drug of choice in treating right sided heart failure to increase contractility, SV, and CO
If right heart failure is due to pulmonary HTN, then Milrinone would be a better choice
What is a major concern in use of vasopressor drugs when the patient has hypovolemia?
Vasoconstriction can worsen already inadequate organ perfusion
Always volume resuscitate a hypovolemic patient before instituting therapy with a vasopressor agent unless life-threatening hypotension is present while volume is infusing
When titrating down vasopressors or
inotropes, what factors influence how quickly
- Drug half-life
- Hemodynamic stability
- How many the patient is on; titrate one at a time taking into consideration the drug actions
Which sympathomimetic would not be a drug of choice to treat hypotension resulting from an acute MI?
- As a pure α drug, the resulting vasoconstriction and increase in SVR would increase myocardial oxygen demand
When infusing vasopressors, what parameters need to be monitored?
- Infusion site: Monitor for signs of extravasation which can cause tissue necrosis; use central line if possible
- Hemodynamic profile if patient has a PA catheter
- Volume status
- Vital signs including I/O, temperature, limb circulation, pulse strength through out the body
- Electrolyte balance
What vasodilator would be the drug of choice to treat pulmonary hypertension?
Milrinone due to its primary effects on increasing contractility, SV and CO and pulmonary vasodilation
What is the most common drug combination seen in acute heart failure to treat hypotension?
- Dopamine or norepinephrine
- Dobutamine at doses to support cardiac output
What factor needs to be taken into account when using vasopressors or inotropes in severe coronary atherosclerosis?
Severe atherosclerosis results in low coronary blood flow; the addition of a sympathomimetic increases the myocardial oxygen demand; the coronary arteries may not be able to deliver the needed blood flow; ischemia, angina, or MI may result
What is the antagonist used when catecholamines (epinephrine, norepinephrine) are infiltrated into the tissues?
If extravasation occurs, infiltrate area with
phentolamine (Regitine®) to counter act the
Beta Blockers actions
- Binds with beta adrenergic receptors to block the response to sympathetic impulses, circulating catecholamines, or adrenergic drugs
- β1 blocking specific drugs result in decreased HR, slower AV conduction, decreased contractility and CO leading to lower BP
- β2 blocking specific drugs increase airway resistance and inhibits peripheral vasodilating effects of catecholamines
- There are combined or specificβ1 and β2 blocking agents
Beta Blockers uses
- MI & CHF
Calcium Channel Blockers actions
- Inhibit the influx of calcium through the cell membrane, resulting in depressed automaticity and conduction velocity in smooth and cardiac muscle leading to depressed contraction
- In coronary vessels, dilation occurs in both normal and ischemic tissues and inhibits coronary spasms
- Decreases SVR, thus lowering cardiac oxygen demand
- Slows AV conduction and atria conduction
Calcium Channel Blockers uses
Prinzmetal's (Variant)angina, chronic stable angina, paroxysmal supraventricular tachycardia, hypertension, atrial fibrillation/flutter
ACE Inhibitors actions
- Suppresses the renin-angiotensin-aldosterone system by inhibiting the conversion of angiotensin I to angiotensin II resulting in a decrease in peripheral resistance and lower aldosterone secretion (leading to less fluid and sodium reabsorption)
- End result is lower BP, and possible increase in CO due to the lower SVR
ACE Inhibitors uses
- Heart failure(except in acute decompensated heart failure with hypotension)
- CHF post MI
- Left ventricular dysfunction
ACE Inhibitors side effects
- Hyperkalemia (especially with underlying kidney disease)
- Bronchospasm in patients with underlying reactive airway disease
ACE Inhibitors cautions
- Patients with bilateral renal artery stenosis, hyperkalemia, increased creatinine
- Use for all MI patients within 24 hrs unless there is hypotension or other contraindications
Angiotensin II Receptor Blockers actions
- Block angiotensin II receptors in vascular smooth muscle and the adrenal gland
- This blocks the vasoconstriction and aldosterone secreting effects of angiotensin II
- BP is lowered with minimal orthostatic hypotension
- Does not effect the enzyme that converts angiotensin I to angiotensin II (ACE)
Angiotensin II Receptor Blockers uses
- Heart failure
- investigational: CHF in combination with ACE or ARB (not both) reduces morbidity and mortality
Alpha-1-Adrenergic Blocking Agents
- Blocks alpha-1 adrenergic receptors resulting in dilation of arterioles and veins which decreases BP
Nitrate Vasodilators actions
- Relax vascular smooth muscle which dilates peripheral veins and arteries
- Decrease venous return to the heart results from increased venous capacitance
- Preload, afterload and BP are reduced as is myocardial oxygen consumption and workload
- Reflex tachycardia may result
- Venous response higher at lower doses, with arterial response greater at higher does
Nitrate Vasodilators uses
- First line for unstable angina and prophylaxis in chronic stable angina
- Hypertension and CHF
- MI and pulmonary edema
Nitroprusside (Nipride) actions
- Direct acting on smooth muscles leading to peripheral vasodilation of both arteries and veins
- Interrupts the influx and activation of intracellular calcium
- Is somewhat more active on veins than arteries
- Decreases preload, afterload and may improve CO
- Has short half-life (2 min)
Nitroprusside (Nipride) uses
- Hypertensive crisis; controlled hypotension during procedures/surgery; acute CHF
- Can cause severe hypotension quickly, especially in hypovolemic patients
- Cyanide toxicity occurs in renal patients very quickly
Nitroprusside (Nipride) caution
in patients with renal or hepatic disease
Loop Diuretics actions
- Decreases the rate sodium and chloride are reabsorbed by the distal renal tubules of the kidney
- Increased excretion of sodium and chloride increases water excretion
- They also have direct vasodilation effect to the arterioles
Loop Diuretics uses
- Nephrotic syndrome
- Renal impairment
- Hypertension and pulmonary hypertension
Antihyperlipidemia Agents actions
- Inhibit HMG-CoA reductase which results in the interruption of the early steps in the synthesis of cholesterol
- Increase HDL cholesterol and decrease LDL cholesterol , total cholesterol, VLDL cholesterol, and plasma triglycerides
- Maximum effect seem in 4-6 weeks
- Avoid grapefruit juice to avoid potential increase in drug serum concentrations
Antihyperlipidemia Agents uses
- Primary hypercholesterolemia; mixed dyslipidemia; hypertriglyceridemia
- Prevention of coronary artery disease and MI
- Significantly reduces CV events
- Common drug group name: "statins"
In the post acute MI patient, what is the role of a beta blocker?
- Blocks sympathetic stimulation in the heart
- Decreases contractility, slows heart rate, decreases systolic BP, decreases myocardial oxygen demand
- Slower heart rate means a longer diastole and filling time as well as coronary perfusion time resulting in increase myocardial oxygenation
- Reduces infarct size and early mortality when started early after an MI and increases survival long term
When are beta blockers contraindicated?
- Severe CHF
- Cardiogenic shock
- Obstructive pulmonary diseases and acute bronchospasm
- AV block and symptomatic bradycardias
Which are the most common cardio-selective beta blockers that can be used in patients with obstructive pulmonary diseases?
Atenolol, esmolol, metoprolol are all β1 selective and less likely to cause bronchospasms (β1 selectivity is not absolute)
What effect do beta blockers have on diabetics?
They may mask signs (tachycardia, tremors) of hypoglycemia in diabetic patients on insulin or oral hypoglycemic agents
Why are ACE inhibitors used in post MI patients?
- Studies have shown that they prevent and retard LV dysfunction and remodeling that occurs post MI
- Use also decreases risk of CHF post MI as well as recurrent infarction
- Long term use shows improvement in endothelium in abnormal coronary arteries
How quickly after an MI should an ACE inhibitor be started on a hemodynamically stable patient?
Within 24 hours has the best result in decreasing mortality rates
Which organ is adversely effected by the use
Caution should be used in renal insufficiency or renal stenosis
- Monitor creatinine levels closely
- Can use in end stage renal failure as the kidneys are already gone
Which drug is used to treat Prinzmetal's (Variant) angina?
Calcium channel blockers are used due to their relaxing effects on the smooth muscle cells, decreasing the vasospasms associated with Prinzmetal's angina
When are calcium channel blockers used in the post MI?
- They are not recommended post MI
- Used successfully in angina with patients who cannot take beta blockers and in patients post MI with preserved EF
When beginning new angiotensin II receptor blocker therapy, what is the most common side effect?
How do angiotensin II receptor blockers work differently than ACE inhibitors?
- Block angiotensin II receptors in vascular smooth muscle and the adrenal gland
- This blocks the vasoconstriction and aldosterone secreting effects of angiotensin II
- Does not effect the angiotensin converting enzyme, as do ACE inhibitors
What are the physical results of α-1 adrenergic blocking agents?
- Dilation of both arterioles and veins
- Decreased BP, especially diastolic BP
What precautions should be taken when initiating α-1 adrenergic blocking agents?
- Postural hypotension may be a problem in patients
- Recommend changing position from lying to sitting
to standing slowly
What is the most common combination of drugs given post MI?
- Beta blocker
- ACE inhibitor
- Platelet inhibitor
What are the major effects of nitroglycerin in CHF patients?
Decrease preload by increased venous blood pooling which relieves over worked heart muscle and decreases oxygen consumption
Nitroglycerin post MI helps in what hemodynamic changes?
- Decreased preload, afterload, and BP
- Increased myocardial oxygen delivery from coronary dilation
- Decreased myocardial oxygen consumption
Which vasodilator is associated with cyanide toxicity?
- Use with caution in the renal impaired patient
What are the major hemodynamic effects of nitroprusside?
- Decrease SVR
- Decreased afterload and preload
What is the major electrolyte imbalance associated with loop diuretics?
What are the major side effects to using diuretics?
- Electrolyte imbalances
If a patient is sensitive to sulfonamides, which diuretic class should they use with caution?
What are the most common side effects patients complain about while on statins?
Body aches, joint pain, fatigue
Anticoagulant drugs classes and types
Additional classifications of anticoagulants
- P2Y12 platelet inhibitors
- Indirect Factor Xa inhibitors
- GP Iib/IIIa Platelet inhibitors
- Unfractionated heparin (is the old standard)
- Low molecular weight heparins (are newer)
- Oral anticoagulants
- Direct thrombin inhibitor anticoagulants
Anticoagulant drugs uses
Pulmonary emboli; prophylaxis/treatment of DVT; atrial fibrillation with embolization; DIC; adjunct to treat coronary occlusion in acute MI; embolic stroke; cardiac surgery/procedures
Anticoagulant drugs actions
Inhibit the development and enlargement of clots by actions in the coagulation phase blocking the action of clotting factors or platelets. They do not lyse clots nor affect the fibrinolytic pathways.
Unfractionated Heparin actions
- Activates antithrombin III which is needed to inactivate thrombin and factor Xa activity
- This Inhibits thrombin which is needed for the conversion of fibrinogen to fibrin
- Inhibits the activation of fibrin stabilizing factor preventing the formation of a stable clot
Unfractionated Heparin uses
- NSTEMI & STEMI
- DVT prophylaxis & DIC
- Pulmonary embolism
- Venous thrombosis & peripheral arterial occlusive disease
Low Molecular Weight Heparins
- Inhibit Factor Xa and thrombin
- DVT prophylaxis in high risk patients
- Dalteparin (Fragmin®
- Enoxaparin (Lovenox®)
Direct factor Xa inhibitors
- Prophylaxis and treatment DVT
- Prophylaxis and treatment of atrial fibrillation
- Prophylaxis and treatment of pulmonary emboli
Old standby which interferes with the making of vtamin K-dependent clotting factors resulting in epletion of clotting factors
Direct factor Xa inhibitors
- Factor Xa inhibitors prevent the formation of thrombin in the clotting cascade
- Example: Apixaban (Eliquis®), edoxaban
Direct thrombin inhibitor actions
- Direct thrombin inhibitor reversibly binds to the thrombin active sites
- Does not require antithrombin III for antithrombotic action
- Inhibits both free and clot contained thrombin
Direct Thrombin Inhibitor uses
- Heparin induced thrombocytopenia
- Those at risk for heparin induced thrombocytopenia ndergoing percutaneous coronary intervention
Direct Thrombin Inhibitor medications
- Bivalirudin, Argatroban
New oral medication
- Dabigatran (Pradaxa®)
Antiplatelet drugs actions
- Clopidogrel, Ticagrelor and Prasugrel inhibit the P2Y12 adenosine diphosphate (ADP) platelet receptors which prevents platelet activation and aggregation
- Aspirin: Inhibits thromboxane A2 mediated platelet
Antiplatelet drugs uses
- Post percutaneous coronary procedure to prevent lot formation on stents and in newly opened vessels
- STEMI +/- PCI (except those who received lytics in the rior 24 hours)
- NSTEMI patients getting PCI or being medically anaged
- Prophylaxis of arterial thrombosis
- Management post MI and stroke
Platelet Glycoprotein GPIIb/IIIa Antagonists
- Interrupt the action between fibrinogen and Von illebrand's factor with the platelet complex GPIIb/IIIa esulting in the interruption of platelet aggregation
- UA/NSTEMI/STEMI patients undergoing PCI
- They are plasminogen activators that cause ibrinogenolysis in the clot
- Newer drugs are more "clot specific" than older drugs nd therefore massive systemic lysis can be avoided
- Severe pulmonary emboli
- Arterial thrombus
- Acute ischemic stroke
- Acute MI
Thrombolytics side effects
- Bleeding at procedure sites as well as any other area
- Major hemorrhage with the side effects of major leeding at any site
Thrombolytics special considerations
Reocclusion may occur quickly after lysis of clot. Therefore concurrent treatment is recommended with heparin, aspirin, and/or other antiplatelet drugs to reduce the risk of major reocclusion with life threatening consequences
In what bleeding disorder would you see heparin ordered as the treatment of choice?
DIC: disseminated intravascular coagulation
What is the major action of anticoagulants?
Inhibit the development and enlargement of clots by actions in the coagulation cascade by blocking the actions of clotting factors or platelets
What is the most major and common side effect of anticoagulants?
- Can lead to hypovolemic shock
If a patient has heparin induced thrombocytopenia with thrombosis , what is the anticoagulant class of choice?
Direct thrombin inhibitor anticoagulants like argatroban or bivalirudin
Which patient population is at greater risk for bleeding complications from antiplatelet therapy?
Female geriatric patients with low body weight and renal insufficiency have a much higher incidence of bleeding with antiplatelet therapy
What diagnosis are low molecular weight
heparins most commonly used in?
Prevention or treatment of DVT
What drug classification would you not see
combined with heparin in the cardiac
- Direct thrombin inhibitors
- Direct thrombin inhibitors are used in patients who
cannot take heparin (if they have heparin induced
What laboratory level is monitored closely when a patient is on warfarin?
- INR is monitored daily during loading of the drug until it is in therapeutic range
- INR is monitored frequently in patients on an outpatient basis
What is the antidote for an overdose of heparin?
- Protamine sulfate
- May also give fresh frozen plasma to aid in clotting
Post percutaneous coronary intervention (PCI) with stent placement, what class of drug would you ordered for the patient?
What are the major contraindications for thrombolytic therapy?
- Intracranial hemorrhage
- Active bleeding
- Recent CPR (relative contraindication if > 10 minutes)
- Malignant intracranial neoplasm
- Ischemic stroke within last 3 months
- Suspected aortic dissection
- Closed Head or facial trauma within last 3 months
- Recent major surgery
What is the usual concurrent therapy seen with thrombolytic therapy?
- Aspirin and/or other antiplatelet drug
- The goal is to prevent reocclusion or reclotting after the thrombolytic has caused lysis of the clot
When is thrombolytic therapy the first choice in treatment of an acute MI?
When a skilled practitioner who can perform a PCI is not available or the facility does not have a cardiac catheterization lab to perform a PCI
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