Baroreceptors are activated when?
Systemic Bp is decreased it can sense the change in blood pressure.
Order these class II drugs from increasing to decreasing lipophilisity
Atenolol, Metoprolol, Propranolol, Esmolol
Propranolol>metoprolol>Esmolol=Atenolol
What is the normal rate of conductions for SA, AV, Purkinje Fibers, and myocytes?
SA-180-120
AV- 40-60
Purkinje- 30-40
Myocytes- cant do that
What is the counter regulator of the compensatory mechanisms during heart failure?
Natriuretic Peptides
What is the relavance of BNP levels to diagnose CHF
BNP levels are directly related to the severity of the CHF
What does long term compensatory mechanism cause?
Ventricular hypertrophy enlargement
The start of the Q wave to the end of the T wave, what occurs during this time?
Ventricular Depolarization followed by repolarization.
What do class II antiarrhythmics do?
Beta Receptor blocker
WHat is Adenosine mainly used for?
What can it cause?
how lond is it used?
Paraxyxmal Supraventricular tachycardia,
can cause arrhythmias
Used in the short term
How is heart rate regulated by the conduction sytem?
Im guessing right now. Im assuming first of all that the pacemaker the SA node is responsible for setting the tone for the initial depolarization and once the conductance is passed to the AV Node it passes through a slower conductance layer which provides the heart enough time to fully empty its atria/ventricles so there is no wasted effieciency? I need to find the actual answer though.
Normally this occurs in a cell
Sympathetic Stimulation–>NE release–>Activation of B1 receptors
causing
Increase in pacemaker current and Increase in Slope phase 4 depolarization
What do class II drugs do to change this pathway?
They block the stimulation of the Sympathetic system especially on the SA and AV node
This causes a Decrease in phase 4 slope and prolonged repolarization
Increase the duration of an action potential
Decrease automaticity, decrease rate, decrease re-entry currents
What are the BNP levels for a Class I CHF for men and women?
What about class 4?
146, 149
938, 858
Re-entry circuits are common in what?
tachyarrhythmias
What is the pathophysiology of Arrhythmias?
Ischemic tissue damage
Electrolyte abnormality
Excessive catecholamine exposure
Drug toxicity
There are two sounds that occur in the heart. At what phase do they occur and what is causing this sound?
The sounds are from the AV and SL valves closing the first sound S1 is from the AV valves closing the second sound is from the SL valves closing. The AV sounds occur during phase 2 or isovolumetric contraction during this time the ventricles are being depolarized and the AV valves close while still keeping the SL valve close- because it is close initally when start the phases. The second sound S2 which is the SL valves closing after previous phases opening (it during Phase 3 rapid ejection) occurs during Phase 5 or isovolumetric relaxation.
Na+ is the major depolarizing current in non-pacemaker cells, but what is the major current for pacemaker cells?
First of all pacemaker cells need no outside stimulus to produce their action potential. They have Na+ funny currents that initially depolarize the cell along with calcium L-type currents (non-pacemaker cells have these two) but there is no rapid uptake of sodium the key depolarizing current in pacemaker cells is Calcium, which sustains the action potential. I THINK!!!!
Class I C Drugs?
Flecainide, Encainide, Propfenone, Moricizine
Desribe the RAAS system
and the Activation of the Sympathetic NS
during compensatory mechanism
WHat is the ST segment?
End of S to start of T ventricular depol, plateau phase in AP
Propranolol is a Class ___ drug and it isnt widely use because why?
Propranolol is a Class II drug and it isnt selective for either B1 or B2. This is an issue because is can cause airway constriction and bronchospasms.
What effect does achetylcholine have on the Autonomic nervous systems and Calcium?
Acetylcholine reduces phosporylation of calcium channels and when this is effected during a membrane potential calcium entry is inhibited. It does this by coming from the parasympathetic NS and binds to muscarinic Ach receptor stimulating an inhibitory G protein and inhibiting adenylyl cyclase
What are the Defects in impulse conduction?
Re-entry currents- important for arrhythmias
Conduction block
Accessory Tracts
Describe preload and afterload
Preload the volume of blood when returning to the heart increases the pressure, if the preload is increased like in the compensatory mechanism by vasopressin angiotensin II, and aldosterone the blood that is being ejected has a greater force and the amount of blood flow increases.
Afterload- The peripheral resistance to blood flow during systole resistance to blood ejection.
Class IA drugs are for what type of arrhythmias and what do they do?
SV and ventricular
Prolong action potential duration (APD up) (ERP up)
Class IB drugs are only for ______ arrhythmias? and do what?
For ventricular arrhythmias, reduce the duration of an action potential ERP down as well
What does Angiotensin II do?
Decreases renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys this increases the preload, which increases the blood flow
What are the compensatory mechanisms used during heart failure? All of these things are trying to do what?
Epinephrine, Angiotensin II, Vasopressin,aldosterone
All are trying to increase the flow of blood
What is the pathway of blood through the heart?
What does vasopressin do?
Increases water retention thus increasing preload
What does Aldosterone do?
Increases sodium rentention which increases water rentention which increase the preload which increases the flow of blood
Class III?
Potassium Blocker
WHat is adenosines MOA
Opens a G-protein coupled K channels and decreases Ca2+ depedent action potential
this is used in the short term in electroversion
All arrhythmias result from what?
Disturbance in impulse formation
Disturbance in impulse conduction
or both
Cardiac output equals=?
HRxstroke volume
Esmolol and Atenolol are very similar but the key difference is?
Esmolol can only be administer though an IV, but Atenolol can be administer orally.
WHat is the sequence of excitation in the heart muscles?
SA Node—-> AV Node —-> Bundle of his —> Purkinje Fibers —> Ventricular myocytes
What are Class IV drugs mainly used for?
Atrial fibrilation and flutter
Name the class II drugs
Propranolol, Metoprolol, Atenolol, Esmolol
Out of the Class IV drus which ones are nondihydropyridine or Dihydropyridine?
NON-Verapamil, and Dilitiazen
DI-Nifedipine
If you increase the preload what happens?
You increase the blood supply
Class II drugs can cause fatigue why?
They can have negative inotrophy
Inotrophy is decreased contractility so if the body is getting nutrients like it normally would thats going to make you tired.
What effects does Epinephrine have on the Autonomic nervous system and Calcium?
Epinephrine increases the opening productivity of voltage gated calcium channels in a cardiac action,it does this by binding to beta adrenergic receptors and increasing cAMP
Nutrients is supplied to myocytes by what type of artery? Name the major arteries that perform this talk.
HINT: Their are six
I was in my car. I looked right then I looked left. Then I kept driving but i noticed that the anterior look kind of marginal on my right seat. So I decided to post up and take the circumfrance of my tire.
Coronary arteries supply nutrient to the myocytes.
- Right and Left Coronary Artery
- Posterior and Anterior Intraventricular coronary artery
- Circumplex Coronary artery
- RIght marginal coronary artery
What does epinephrine do during compensatory mechanism? Where does it come from?
Increases contractility in the heart and increase the rate and pressure.
Comes from the sympathetic NS
Class IV?
Calcium channel blocker
What is the mechanism of action of Class II drugs?
B1 receptor antagonists in SA and AV node, they reduce cAMP, and Calcium currents, they decrease automaticity, decrease mortalily after MI, and are relatively safe. THEY are the most widely used drugs.
What are the defects in impulse formation?
Altered automaticity- altered sympathetic and vegal input to SA node
Triggered Automaticity
Early afterdepolarization- Occurs at phase 2 and 3 could lead to torsades de pointes, this is when a normal action potential triggers an extra AP
With a prolonged phase 2 some of the Na channels can recover and cause another depolarization changing the membrane potential EAD
Also
Delayed afterdepolarization
Happens shortly after repolarization may or may not trigger an AP
What is the difference in ECG between Ventricular Tachycardia and Torsades De Pointes?
The ECG is polymorphic meaning it can originate in a single or in multiple sites in the ventricle. VTs are monomorphic.
The PR interval is?
the conduction through the AV node
What are the Class I B Drugs?
Lidocaine, Mexiletine, Phenytoin
What do class I antiarrhythimic agents do? And what are the classes?
Class I antiarrhythmics Block Sodium channels
A,B,C
Class IC drugs do what?
Decrease the rate of Phase 0 they have a proarrythmic potential so they are a last resort
Especially with nonselective beta blockers (propranolol) they should not be used in patients with what?
Asthma
The entire compensatory mechnism causes what?
Ventricular remodeling
What are the functions of T-tubules, sacromeres, sarcoplasmic reticulum, ryanodine receptors calcium release channel, myosin, troponin, tropomyosin, and sarcoplasmic reticulum calcium adenosine triphosphatase pump (SERCA).
- T-tubule responsible for uptake of calcium into myocardial cell
- Sacromere is the function unit of contractile myocardial cells
- Myosin- Thick myofilament, is able to hydrolyze ATP using ATPase
- Troponin- Is a complex of 3 proteins
- TnC- Binding site for calcium in thin filament
- TnI- Binds to actin inhibiting contraction
- TnT- Bind to Tropomyosin
- Tropomyosin- BInds to actin
- SERCA- ATPase- When there is leftover calcium in the cytoplasm after calcium spark this pumps Calcium back into the sarcoplamic reticulum for storage.
- Sarcoplasmic Reticulum- Inner membrane system stores calcium and releases it for contraction
- Ryanodine Receptor Calcium Release channel- Channel in the sarcoplasmic reticulum once calcium enters the cell through DHPR (L-type channel) this channel is activated and releases calcium into the cytoplasm to bind to the TnC site on the thin filament
What are the serious adverse effects of Verapamil and DIltiazem?
CHF and SInus node depression
What do cytokines cause?
Cause optosis of cardiac myocytes
WHat is an EKG and what are the waves present?
Waves and intervals in the conduction of an action potential in the heart
p wave is atrial depolarization
QRS is Ventricular Depol and Atrial repol
T wave- ventricular repol
Define Systolic heart failure
diastolic heart failure
right heart failure
Systolic heart failure- Left ventricle contractile dysfunction most common from ischemic heart disease (decreased blood flow and oxygen) Their are 4 classes of the failure ranging from little limitations to complete inability to lead a normal life without getting tired with most minut amount of activity.
Left ventricular failure can lead to pulmonary adema from dyspnea.
Blood starts to move backward into the left atrium and causes an increase in pressure,
Fluid often fills the alveoli taking up space and preventing the alveoli from transfering O2 correctly.
diastolic heart failure- Contractile functions are preserved, impaired relaxation though, chronic HTN and LVH are often the reason for this
right heart failure- often results in left heart
Name the Class I Drugs subtype A
Quinidine, Procainamide, Disopyramide
What is the mechanism of action of Class IV drugs?
Preferentially act on SA and AV nodes and block calcium channels, this slows the phase 0 and slows conduction through the AV node.
When would you not want to use a Class IV drug?
Someone with WPW sydrome, Calcium channel blockers have proven to be harmful
What are propranolol, metoprolol, atenolol, esmolol used to treat?
Treat Ventricular tachycardia, and Supraventricular tachycardia
WHat is special about amiodarone?
Has clas I, II, and III effects very effects in SV and Ventricular
but has dose dependent side effects interacts with lipid membrane
not useful in PVC
What are the Class III drugs and what is their MOA
Ibutilide, Sotalol, Bretylium, Amiodarone
Block K+ channels resulting in longer action potential plateau and prolonged repol
ERP is up early after depol risk