Exam 2 - Wendt (Arrhythmia/CHF) Flashcards
_______ cells have automaticity
Pacemaker
pacemaker cells have (what ion) dependent spikes
Ca2+
Ventricular myocytes have (what ion) dependent spikes
Na+
Pacemaker Cells or Ventricular Cells?
have a very fast/immediate/vertical depolarization
Ventricular cells
Pacemaker Cells or Ventricular Cells?
have Ca2+ dependent spikes
Pacemaker
Pacemaker Cells or Ventricular Cells?
have Na+ dependent spikes
Ventricular
Pacemaker Cells or Ventricular Cells?
Have high automaticity
pacemakers
Pacemaker Cells or Ventricular Cells?
have low automaticity
ventricular
Pacemaker Cells or Ventricular Cells?
are specialized non-contractile cells
Pacemaker
Pacemaker Cells or Ventricular Cells?
are contractile cells
ventricular
what are the phases of a Pacemaker cells action potential?
In order: Phase 4,0,3,4
what is phase 4 in pacemaker cell action potential
“funny” current makes diastolic pacemaker current
annnnd
K+ channels/current is activated by vagus
what is phase 0 in pacemaker cell action potential
calcium channel carries AP upstroke
what is phase 3 in pacemaker cell action potential
repolarizing K+ current
Myocyte action potential phases? (in order)
IN ORDER: Phases 4,0,1,2,3,4
what is phase 0 in myocyte cells action potential
Na+ channel carries AP upstroke
what is phase 1 in myocyte cells action potential
repolarizing K+ current (“transient upward”???)
what is phase 2 in myocyte cells action potential
plateau Ca2+ current critical for muscle contraction
what is phase 3 in myocyte cells action potential
repolarizing K+ current
what is phase 4 in myocyte cells action potential
pacemaker current (very minimal?)
Acetylcholine decrease _____ and ____ currents
HCN; Ca2+
ACH activates ______ which causes hyperpolarization
GIRK
_____ activates GIRK which causes hyperpolarizaiton
ACH
ACH stimulates the G_____ channel
G (alpha I)
ACH is a a part of the (sympathetic or parasympathetic) system
PARAsympathetic
what does the GIRK channel do when activated?
it causes hyperpolarization by kicking K+ out of the cell
how many classes of antiarrhythmic drugs are there (according to Vaughn-Williams-Singh Scale)
4
what are the 4 classes of antiarryhthmic drugs
according to Vaughn-Williams-Singh Scale
1 - Na+ channel blockers
2- Beta adrenergic antagonists
3- K+ channel blockers aka drugs that prolong refractory period
4 - Ca2+ Channel blockers
If another signal happens when an area is still under its refractory period what happens?
nothin’ — if still in refractory period a new beat won’t occur
what are the common arrhythymias
atrial sinus arrhythmia re-entry arrhythmia a.fib wolf-parkinson white monomorphic ventricular tachycardia AV nodal re-entrant tachycardia Premature ventricular complexes
what beta blockers dose wendt mention
Esmolol, Acebutolol, Propranolol
Beta Blockers:
slow ______ and _____ currents in SA/AV Node
Pacemaker/Ca2+
Beta Blockers:
(increase or decrease) refractoriness of SA/AV node
INCREASE
Beta Blockers:
(increase or decrease) P-R interval
increase
Beta Blockers:
are good when the arrhythmia involves ______
catecholamines…
Ca2+ Channel Blocker Options for arrhytmias?
Diltiazem and Verapamil
Ca2+ Channel Blocker:
have a __________ block
frequency dependent
Ca2+ Channel Blocker:
(increase or decrease) refractoriness of AV node
INCREASE!
not SA node like beta blockers
Ca2+ Channel Blocker:
(increase or decrease) the P-R interval
increase
what are the 3 different classes of Na+ Channel blockers (aka Class 1 Na+ Channel blockers)
1A; 1B; 1C
what antiarrhythmic drug class is class 1
Na+ channel blockers
what antiarrhythmic drug class is class 2
beta adrenergic antagonists
what antiarrhythmic drug class is class 3
K+ channel blockers (agents that prolong refractory period)
what antiarrhythmic drug class is class 4
Ca2+ channel blockers
what antiarrhythmic drugs are a part of Class 1A
quinidine
procainamide
disopyramide
what antiarrhythmic drugs are a part of Class 1B
lidocaine
tocainide
Mexilitine
Phenytoin
what antiarrhythmic drugs are a part of Class 1C
Propafenone
Flecainide
Moricizine
what antiarrhythmic drugs are a part of Class 3
(the K+ channel blockers) Amiodarone Dronedarone Sotalol Ibutilide
what antiarrhythmic drugs are a part of Class 5
These are all the misc. Drugs Digoxin Magnesium Chloride Potassium Chloride Adenosine
When beta adrenergic receptors are stimulated cAMP increases which directly increases activity of _____ channels –> increased ______ currents
HCN channels; DEPOLARIZING currents
When beta adrenergic receptors are stimulated cAMP increases which increases phosphorylation of _______ channels which increases amount of current these channels can pass and allows them to open at more _____ membrane potentials
L-type voltage gated Ca2+ channels; negative
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
does pure sodium channel block
1B and 1C
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
both widens QRS complex AND prolongs Q-T interval
1A
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
can reduce QT interval (but not clinically significant)
1B
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
Widens QRS complex
1A & 1C
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
will block both the open and inactivated state
1B
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
preferentially blocks open state
1A & 1C
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
ONLY blocks open state
1C
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
has VERY slow dissociation (> 10 secs)
1C
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
has rapid dissociation (millisecond)
1B
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
has moderate to slow dissociation (seconds)
1A
QT interval is known as the time from the beginning of _________ to the end of _________
beg. of ventricular depolarization; to end of ventricular repolarization
what are the 3 mechanisms that can cause arrhythmia
enhanced automaticity
triggered activity
re-entry
the ____ Node cells exhibit the highest rate of automaticity
SA
Arrhythmias can be caused by trigger activity — what does trigger activity mean?
depolarizations that arise abnormally from a normally generated sinus action potential
what does EAD and DAD stand for
EAD - early afterdepolarizaiton
DAD - delayed after depolarization
what are the different types of trigger activity that cause arrythmias
EAD or DAD
Triggered Activity - EAD
is caused by ________
Arises from a _________ Vm
Caused by (rapid or slow) HR, or _____kalemia, or ______ syndrome
caused by PROLONGED AP
from a DEPOLARIZED
SLOWED HR, HYPOkalemia, or LONG QT syndrome
Triggered Activity - DAD caused by \_\_\_\_\_\_\_\_ (increase or decrease) NCX current arises from a \_\_\_\_\_\_ Vm often seen with: (rapid or slow) HR, MI, \_\_\_\_\_\_\_ stress, or \_\_\_\_\_\_\_ intoxication
caused by Ca2+ overload
INCREASE in NCX current
arise from NORMAL Vm
RAPID HR; adrenergic stress, digoxin intoxication
what two things make up cardiac output
Stroke Volume and HEART RATE
what are the consequences of decreased cardiac output
Cardiovascular:
Tachycardia, Cardiomelgia, Arrhythmias, Fatigue/exercise intolerance
Respiratory: SOB Pulmonary Edema Cyanosis Orthopnea
definition of stroke volume
amount of blood ejected from da ventricles during contraction
______ increase stroke volume
what hemodynamic concept..
contractility
what are the axis on a FrankSterling Relationship
Y-axis: Stroke Volume
X-axis: PreLoad (aka left ventricular diastolic volume)
Preload is also known as ……
LV (left ventricular) End diastolic volume
Afterload and ____ are inversely related
SV (stroke volume)
Frank-Starling Relationship
a failing heart can’t compensate and increase _____ when _____ increases
can’t increase SV when preload increases
what are the axis in a force tension graph
Y-axis: Stroke Volume
X-axis: Afterload
what are the two types of CHF
Systolic Failure
or Diastolic Failure
Types of CHF:
Systolic Failure has….
deficit in _______
and a ______ heart
deficit in CONTRACTION
THIN/DILATED heart
Types of CHF:
Diastolic Failure has….
deficit in _______
_______ walls that cannot relax
deficit in FILLING
STIFF/THICK that cannot relax
what are the 3 types of cardiac remodeling (due to CHF is why we talked about them)
Cardiac Dilation
Pathological Hypertrophy
Physiological Hypertrophy
CHF - Cardiac Remodeling:
which one does NOT have fibrosis
Physiological hypertrophy
CHF - Cardiac Remodeling:
which one has thinning walls
cardiac dilation
CHF - Cardiac Remodeling:
what can cause pathological hypertrophy
Chronic HTN
Aortic valve stenosis
CHF - Cardiac Remodeling:
what can cause physiological hypertrophy
Chronic Exercise
Pregnancy
CHF - Cardiac Remodeling:
what can cause cardiac dilation
MI or other insults (like HF)
Renin/Angiotensin System:
______ makes angiotensinogen
Liver
Renin/Angiotensin System:
_____ makes Renin
kidney
Renin/Angiotensin System:
______ makes ACE
Lungs
Renin/Angiotensin System:
Angiotensin II causes _____ and _____ secretion
Aldosterone/ADH
Renin/Angiotensin System:
overall leads to
increased ________ and increase _______ and increased __________
water retention; blood volume; sympathetic activity
2 Main CHF Tx Strategies
Manipulate Hemodynamics
Inhibit compensation
CHF Tx Strategies
Manipulate Hemodynamics and Inhibit Compensation -
which one improves mortality
inhibiting compensation
CHF Drugs
what drugs are used to manipulate hemodynamics
vasodilators (organic nitrates, hydralazine)
diuretics
angiotensin inhibitors
inotropic agents (digoxin, PDE3 inhibitors, Bera-adrenergic agonists)
what are the 3 classes of inotropic agents used in CHF and are they used for chronic or for acute therapy only?
Cardiac glycosides - chronic
PDE (phosphodiesterase) inhibitors - acute only
Beta adrenergic agonists - acute only
what drugs are known as PDE inhibitors and used in CHF as inotropic agents
milrinone and inamrinone
what drugs are known as Beta adrenergic agonists and used in CHF as inotropic agents
dopamine; dobutamine
how does Na+/K+ ATPase blockade cause higher contractility
when the ATPase is inhibited it creates more Na+ inside - the NCX channel then compensates and kicks out Na+ and brings in Ca2+ which causes more contraction/greater contraction
what drug is a cardiac glycoside
digoxin
what are some common digoxin toxicities
psychiatric - delirium/fatigue/malaise/confusion
G.I - anorexia, N/V, abdominal pain
Respiratory - increased response to hypoxia
C.V - pro-arrhythmic (atrial tachy, AV block)
what drugs are Vasopressin receptor antagonists
tolvaptan
conivaptan
Tolvaptan or Conivaptan:
which one is V2 selective
Conivaptan
Tolvaptan or Conivaptan:
which one is V1A/V2 receptors
Tolvaptan
Vasopressin Receptor Antagonists are used for treating ________ in HF and ______
hyponatremia; SIADH
ADEs of Vasopressin Receptor Antagonists
hypotension
osmotic demyelination
why is neprilysin inhibition helpful in CHF
under normal circumstances, neprilysin breaks down natriuretic peptides. but natriuretic peptides cause VSMC relaxation
what drug is a neprilysin inhibitor
Sacubitril
Class 1 Antiarhythmics:
Class 1A, 1B, or 1C?
has mixed block for Na+ and K+
1A