Term
| class 1a antiarrhythmic drugs MOA and ex's |
|
Definition
slows conduction velocity (less than class IC) and prolongs action potential duration
Disopyramide
Procainamide*
Quinidine |
|
|
Term
| class 1b antiarrhythmic drugs MOA and ex's |
|
Definition
has no effect on conduction velocity and may shorten APD
Lidocaine*
Mexiletine
Phenytoin |
|
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Term
| class 1c antiarrhythmic drugs MOA and esx's |
|
Definition
slows conduction and may prolong APD (mild)
Flecainide
Propafenone |
|
|
Term
| class II antiarrhythmic drugs MOA and ex's |
|
Definition
blocks beta adrenergic receptors
Beta blockers |
|
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Term
| class III antiarrhythmic drugs MOA and ex's |
|
Definition
prolongs APD and has no effect on conduction
Amiodarone
Dofetilide
Ibutilide*
Sotalol¶
Dronedarone |
|
|
Term
|
Definition
| ¶ l-sotalol has beta blocking and class III activities; d-sotalol is a pure class III agent. Commercially available sotalol is a racemic (equal part) mixture. |
|
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Term
| class IV antiarrhythmic drugs MOA and ex's |
|
Definition
calcium channel blockers
Non-dihydropyridine calcium channel blockers (verapamil and dilitiazem) |
|
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Term
|
Definition
|
|
Term
| toxic ecg findings, 2 types of proarrythmias |
|
Definition
|
|
Term
| when to use rate vs rhythm control situations |
|
Definition
|
|
Term
| af rate control recommendations |
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Definition
|
|
Term
| af rate control drugs classes and agents |
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Definition
|
|
Term
| af rhythm control agents, interactions, advantages, adverse effects |
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Definition
|
|
Term
|
Definition
|
|
Term
| vt/vf pharmacology best treatment and goals |
|
Definition
• No RCT evidence in VT/VF of ↑ survival for 1° or 2° prevention
• Except beta blockers (metoprolol succinate, carvedilol)
Goal
• Control arrhythmias • Improve symptoms |
|
|
Term
| VF treatments table agents, receptors, physiologic effects, ADE |
|
Definition
|
|
Term
has ADE
Cardiac: Hypotension,
bradycardia, AVB, TdP, slows VT below programmed ICD detection rate, increases defibrillation threshold
Other: Corneal microdeposits, thyroid abnormalities, ataxia, nausea, emesis, constipation, photosensitivity, skin discoloration, ataxia, dizziness, peripheral neuropathy, tremor, hepatitis, cirrhosis, pulmonary fibrosis or pneumonitis |
|
Definition
|
|
Term
Has ADE
Cardiac : Bradycardia, hemodynamic collapse, AVB, sinus arrest Other: Delirium, psychosis, seizure, nausea, tinnitus, dyspnea, bronchospasm |
|
Definition
|
|
Term
Has ADE
Cardiac: HF, AVB
Other: Lightheaded, tremor, ataxia, paresthesias, nausea, blood dyscrasias |
|
Definition
|
|
Term
has ADE
Cardiac: Syncope, TdP,
AVB
Other: Dizziness,
diarrhea, nausea, esophagitis, emesis,
tinnitus, blurred vision,
rash, weakness, tremor; blood dyscrasias |
|
Definition
|
|
Term
has ADE
Cardiac: Bradycardia, hypotension, HF, syncope, TdP
Other: Fatigue, dizziness, weakness, dyspnea, bronchitis, depression, nausea, diarrhea |
|
Definition
|
|
Term
|
Definition
| Amidarone, Lidocaine, Mexiletine, Quinidine, Solatol |
|
|
Term
uses: VT, VF, PVC,
targets: INa, ICa, IKr, IK1, IKs, Ito,Beta receptor, Alpha receptor nuclear T3 receptor
effects: Sinus rate slowed
QRS prolonged
QTc prolonged
AV nodal refractoriness increased; increased DFT |
|
Definition
|
|
Term
uses: VT, VF
target: INa
effect: No marked effect on most intervals: QTc can slightly shorten |
|
Definition
|
|
Term
uses: VT, VF, PVC,
has a role in patients with LQT3
target: INa
effects: No marked effect
on most intervals;
QTc can slightly shorten |
|
Definition
|
|
Term
uses: T, VF, (including short QT syndrome, Brugada)
targets: INa, Ito, IKr, M, Alpha receptor
effects: QRS prolonged QTc prolonged; increased DFT |
|
Definition
|
|
Term
uses: VT, VF, PVC
targets: IKr, Beta 1 and 2 receptor
effects: Sinus rate slowed
QTc prolonged
AV nodal refractoriness increased;
decreased DFT |
|
Definition
|
|
Term
| sustained VT treatment algorithm and agents for each class |
|
Definition
|
|
Term
|
Definition
| Procainamide, Beta blockers, CCB |
|
|
Term
use: VT
targets: INa, IKr
electrophysical effects: QRS prolonged QTc prolonged; increased DFT
ADE: Cardiac: TdP; AVB, hypotension and exacerbation of HFrEF Other: Lupus symptoms, diarrhea, nausea, blood dyscrasias |
|
Definition
|
|
Term
| beta blocker electrophysical effects |
|
Definition
Sinus rate slowed
AV nodal refractoriness increased |
|
|
Term
| beta blockers for VT that target beta1 only |
|
Definition
| acebutolol, atenolol, bisprolol, esmolol, metoprolol |
|
|
Term
| beta blockers for VT taht target beta 1 and 2 |
|
Definition
|
|
Term
| beta blockers for VT that target beta1,2 and alpha |
|
Definition
|
|
Term
| ADE: bradycardia, hypotension, HF, fatigue, dizziness |
|
Definition
|
|
Term
| ADE: hypotension, edema, HF, AVB, bradycardia, headache, rash |
|
Definition
| Calcium channel blockers (Dilitazem, Verapamil) |
|
|
Term
uses: VT (specifically RVOT, verapamil sensitive idiopathic LVT)
target: ICa-L
effects: Sinus rate slowed
PR prolonged
AV nodal conduction slowed |
|
Definition
|
|
Term
uses: VT specifically RVOT,
idiopathic LVT
target: ICa-L
effects: Sinus rate slowed
PR prolonged
AV nodal conduction slowed |
|
Definition
|
|
Term
| causes for QT prolongation and remedy |
|
Definition
digoxin: digoxin ab's
medication induced torsades de pointes: iv magnesium sulfate, inc HR w atrial/ventricular pacing or isopreterenol, potassium repletion
sodium-channel blocker toxicity: discontinue medicine or reprogram device
-avoid QT prolongation medications in pts w congenital or acquired long QT syndrome |
|
|
Term
| Integrative Cardiovascular Control of Blood Flow, ways to regulate |
|
Definition
• Autoregulation
• Active hypermia
• Reactive hyperemia
• Fluid regulation (RAA), baroreceptors (ADH)
• Autonomic nervous system
• Vasoactive compounds
• Baroreceptors
• Chemoreceptors |
|
|
Term
|
Definition
Autoregulation: In some tissues (kidneys, brain, heart, skeletal muscle), the arterioles can constrict or dilate in response to increased or decreased pressure in order to maintain constant blood flow.
-->
Myogenic hypothesis to explain autoregulation: Increased stretching of the arteriolar smooth muscle increases intracellular Ca2+ and hence contractility.
--> example
Afferent arteriole of the nephron constricts in response to raised pressure—this maintains constant flow rate in the nephron. |
|
|
Term
| active hyperemia and reactive hyperemia |
|
Definition
Active hyperemia: Increased metabolic demand will stimulate vasodilation to increase blood flow (e.g., skeletal muscle during exercise).
Reactive hyperemia: Blood flow increases following occlusion to restore O2 levels—seen in coronary circulation.
---> (both lead to)
Metabolic hypothesis: Metabolites such as CO2, H+, lactate, and adenosine produced during high levels of cellular activity, or as a response to temporarily reduced blood flow, can induce vasodilation to promote blood flow.
---> (examples)
-Skeletal muscle and other tissues during high activity
-Coronary circulation after brief occlusion |
|
|
Term
| Vasoactive compounds integrative cardiovascular control |
|
Definition
• Vasoactive compounds released locally
• Histamine and bradykinin dilate arterioles/constrict
venules to promote filtration and produce edema
• Serotonin constricts blood vessels at injury sites
• Prostaglandins can be vasodilators or vasoconstrictors
• ADH |
|
|
Term
| fluid regulation integrative cardiovacular control |
|
Definition
| • Reduced blood volume is detected by juxtaglomerular cells (RAA) and baroreceptors (ANS), while increased volume is sensed by cardiac atrial cells (ANP/BNP) |
|
|
Term
| ADH release, receptors, effects |
|
Definition
• ADH release simulated by osmoreceptors
• ADH has three receptors: one in the kidney collecting ducts (V2) stimulates aquaporin insertion into membranes and water reabsorption
• ADH(a.k.a.vasopressin)released in response to low-pressure baroreceptors in the atria
• Receptor V1 is found in vascular smooth muscle and stimulates vasoconstriction
• V3 is in the pituitary gland and has less well understood functions in hormonal regulation |
|
|
Term
| ANS and cardiovascular control of blood flow |
|
Definition
• Parasympathetic and sympathetic branches respond to information from a variety of sources to neuronally regulate dilation or constriction of arterioles in different tissues
• Sympathetic nervous system stimulates alpha and beta receptors and stimulates release of adrenaline from the adrenal gland
• Parasympathetic nervous system stimulates acetylcholine receptors—similar to but not the same as the neuromuscular junction |
|
|
Term
|
Definition
| • Neurons in the atria, aorta, and carotid arteries that sense changes in blood volume by changes in pressure and relay to autonomic nervous system via the brainstem |
|
|
Term
| peripheral chemoreceptors |
|
Definition
| • Neurons in the aorta and carotid arteries that sense O2 levels; when O2 is decreased, these neurons stimulate vasoconstriction, decrease heart rate, and then increase oxygen intake |
|
|
Term
|
Definition
| • Neurons in the brainstem sense changes in ventilation via changes in CO2 and H+; they stimulate sympathetic nervous system to increase total peripheral resistance, which can be very dangerous. |
|
|
Term
|
Definition
local responses: inc vasodilator metabolites -> dilation of skeletal muscle arterioles, dec TPR -> inc blood flow to skeletal muscle
Central command: inc sympathetic outflow, dec parasympathetic outflow (HR only) -> inc HR inc contractility inc CO, constriction of aretrioles (splanchnic and renal), constriction of veins and dec unstressed volume inc venous return -> inc blood flow to skeletal muscle |
|
|
Term
|
Definition
| the brain,including higher cognitive and executive areas of the cerebral cortex, coordinates autonomic nervous system responses that stimulate vasoconstriction to visceral organs (excluding heart) and vasodilation in skeletal muscle; cardiac output increased, total peripheral resistance decreased—best of all possible worlds |
|
|
Term
|
Definition
| as muscle metabolic rate increases during exercise, metabolites, including CO2, H+, lactate, and adenosine, are increased and these promote further vasodilation of skeletal muscle |
|
|
Term
| hemorrhage (dec Pa) leads to? |
|
Definition
Baroreceptor reflex: inc sympathetic outflow -> inc HR inc Contractility inc CO, constriction of arterioles and inc TPR/ total peripheral resistantce, constriction of veins and dec unstressed volume(volume in veins) inc venous return -> inc Pa toward normal
Renin-Angiotensin II-Aldosterone: inc angiotensin II -> inc TPR, inc aldosterone->inc Na reabsorption->inc blood volume--> inc Pa toward normal
Capillaries: dec Pc (capillary hydrostatic pressure)-> inc fluid absorption->inc blood volume-> inc Pa toward normal |
|
|
Term
|
Definition
pooling of blood in veins -> dec xPa -> Baroreceptor -> inc Sympathetic outflow which causes:
inc HR, inc Contractility, inc CO
constriction of arterioles, inc TPR
Constriction of veins, dec unstressed volume, dec venous return
-->
inc Pa toward normal |
|
|
Term
| orthostatic hypotension explanation |
|
Definition
• The baroreceptor reflex operates anytime one moves from a supine to a standing position or when one stands still for extended periods. We usually don’t notice it.
• When fluid volume is low—for example, following illness where water was lost—the effect is noticeable as light-headedness (decreased cerebral blood flow) and racing heart (sympathetic response exacerbated by inadequate fluid volume) |
|
|
Term
| list of special circulatory situations |
|
Definition
• Coronary blood flow
• Pulmonary blood flow
• Renal blood flow
• Hepatic portal blood flow
• Cerebral blood flow
• Placental and fetal blood flow |
|
|
Term
| coronary blood flow mechanism |
|
Definition
• Coronary arteries feed the cardiac muscle
• Arise adjacent to the aortic valve • High pressure
• Small diameter
• Compressed during systole—increased resistance creates “O2 debt”
• Muscular compression: normal mechanism
• Vasoconstriction: autoregulation of blood flow—high hydrostatic pressure induces arteriolar vasoconstriction—can cause angina |
|
|
Term
| pulmonary blood flow mechanism |
|
Definition
• The lungs receive huge cardiac output via the right heart, and gas exchange, which takes place at the pulmonary alveoli, is managed via this circulation.
• The conducting airway, bronchi, bronchioles, and trachea have a separate blood supply via the bronchial artery. |
|
|
Term
| renal blood flow mechanism |
|
Definition
~25% of cardiac output
• Glomerular filtration rate (GFR) is dependent on afferent arteriolar pressure but can be influenced by efferent arteriolar pressure. The diameter of the efferent arteriole can be managed independently of the afferent arteriole in order to adjust GFR.
• Low pressure in the afferent arteriole stimulates what? |
|
|
Term
| hepatic portal blood flow |
|
Definition
• The liver receives oxygenated blood from the hepatic artery.
• The liver receives all venous return from the abdominal organs before it goes back to the heart.
• Hepatic portal circulation • Why? To detoxify.
• What impact?
• Liver obstruction?
• Ascites, heart failure
• Signs include varices, hemorrhoids, ascites, and abdominal distension with bulging veins (caput medusae) |
|
|
Term
| cirrhosis of liver can cause? |
|
Definition
portal hypertension
-destruction of sinusoidal architecture due to cirrhosis of liver leads to inc resistence in veins and portal hypertension
-scarred and nodular cirrhotic liver leads to scar tissue in liver
-portal systemic collaterals can bleed
-splenomegaly
-back pressure in portal vein leads to hyertension |
|
|
Term
|
Definition
• Blood flow to the brain is so important that the circulatory system of the brain is specialized to do two things.
• Circle of Willis: series of anastomoses that ensure blood will always flow to the brain
• Blood brain barrier: special, very tight capillaries that prevent a lot of compounds from entering the interstitial tissue (a.k.a. the parenchyma) of the brain
• Drugs for neurological and psychological conditions have to be assessed for their ability to cross the blood brain barrier.
• Drugs with toxic neurological side effects can sometimes be used if they don’t cross the blood brain barrier. |
|
|
Term
| placental and fetal blood flow |
|
Definition
• Maternal effects of preeclampsia: High blood pressure, strokes, convulsions, death
• Fetal effects of preeclampsia: Hypoxia, poor nourishment, abruption, early delivery, death
-ductus arteriosus shunts blood from pulmonary artery to aorta
-foramen ovale shunts blood from right to lef atrium
-ductus venosus bypasses maternal blood from liver straight to heart
-umbilical vein from placenta
-umbilical arteries to placents |
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