Day 6.1 Cardio Flashcards
Causes of increased ESR
Infection (osteomyelitis) Inflammation (e.g. temporal arthritis, polymyalgia rheumatica) Cancer Pregnancy SLE
Causes of decreased ESR
Sickle cell (altered shape)
Polycythemia (too many)
CHF (unknown why)
Toxic side effects of TCA use
Convulsion
Coma
Cardiotoxicity (Tri C’s)
Repsi depression and hyperpyrexia
What anti-seizure drugs are used to treat bipolar disorder?
Lamotrigine
Carbamazepine
Valproate (Valproic acid)
Coronary arteries
RCA and LCA come off of aorta.
LCA gives LAD and CFX
RCA gives PDA (80%) and Acute marginal artery
What does the LAD supply?
Apex and anterior interventricular septum
What does CFX supply?
Posterior LV
What does PDA supply?
aka posterior interventricular artery
Posterior septum
Inferior part of LV
What does the AMA (acute marginal artery) supply?
RV
What supplies the SA and AV nodes?
RCA
Where does PDA arise from?
80% arise from RCA
20% arise from CFX (from LCA)
Most common site of coronary artery occlusion
LAD (anterior interventricular septum)
This is called an anterior wall MI
When do coronary arteries fill?
Diastole
Effects of LA enlargement
LA is most posterior part of heart.
Enlgmt causes dysphagia d/t compression of esophageal nerve
hoarseness d/t compression of recurrent laryngeal nerve (vagus)
CO eqn
CO = SV x HR
Fick principle eqn
CO = rate of O2 consumption / [arterial O2 content - venous O2 content]
MAP eqn
MAP = CO x TPR (P = Q x R)
MAP = 1/3 systolic + 2/3 diastolic
Pulse pressure
PP = systolic - diastolic
proportional to SV: if SV increases, PP increases.
SV eqn
SV = EDV- ESV
SV = CO / HR
What variables affect SV?
Contractility
Afterload
Preload
Increased contractility = increased SV
Increased afterload = decreased SV
Increased preload = increased SV
4 things that make contractility increase
and therefore SV increases too
- Catecholamines (B1 receptor)- increased activity of Ca2+ pump in SR
- Increased intracellular Ca2+
- Decreased extracellular sodium (so Na+/Ca2+ exchger works less, more Ca2+ stays inside cell)
- Digitalis (Increased intracellular Na+, so Na+/Ca2+ exchgr works less, more Ca2+ stays inside). aka digoxin.
5 things that make contractility decrease
and therefore SV decreases too
- B1 blockade
- Heart failure
- Acidosis
- Hypoxia/hypercapnia
- Non-dihydropyridine Ca2+ chnl blockers: Verapamil
What happens to CO during exercise?
Initially it goes up, bc of increased SV.
After prolonged exercise, CO increases as a result of increased HR.
What happens to CO if heart rate is too high?
Diastolic filling is incomplete (not enough time to fill) so CO decreases
eg in ventricular tachycardia
What is preload?
Preload = ventricular EDV
What is afterload?
Afterload = mean arterial prs (MAP)
proportional to TPR
Do venodilators affect preload or afterload?
They decrease preload (blood pools in veins, so less goes back to heart)
e.g. Nitroglycerin
Do vasodilators affect preload or afterload?
They decrease afterload bc they dilate arteries
Eg hydralazine
Afterload = Arterial!
In what conditions does SV increase?
Anx (bc catecholamine surge)
Exercise (bc increased preload, also increased catecholamines)
Pregnancy (higher blood vol, so higher preload)
What happens to SV in heart failure
decreases
What increases myocardial O2 demand?
Increased afterload (increased arterial prs)
Increased contractility
Increased HR
Increased heart size (increased wall tension)
Diff bt non-dyhydropyridine Ca2+ chnl blockers and dihydropyridine
Non-dyhydropyridine Ca2+ chnl blockers = verapamil. Works at heart.
Dyhydropyridine work at blood vessels.
Drugs that decrease O2 demand in heart attack
ACE inhibitors and ARBs decrease afterload
Beta-blockers (metoprolol) decrease HR and contractility
In what condition is there increased heart size?
Hypertrophic cardiomyopathy.
Higher risk for heart attack and sudden cardiac death since this increases O2 demand on the heart.
What does the starling curve show?
That the force of contraction is proportional to the initial length of cardiac muscle fiber (preload).
Plots CO or SV against Ventricular EDV or preload
EF eqn
EF = SV / EDV
EF = [EDV -ESV] / EDV
What is EF normally?
> = 55%
It’s an index of ventricular contractility
Eqn for resistance, prs, flow
P = Q x R (MAP = CO x TPR)
Eqn for resistance
R = 8nl / [pi x r^4]
8.viscosity.length / pi.radius to the 4th
directly prop to visc, inversely prop to radius^4
What determines velocity, physiologically?
Mostly the hematocrit. As you increase velocity, you increase resistance. Viscosity is increased in: polycythemia (too many RBCs) hyperproteinemic states (mult myeloma) hereditary spherocytosis
Which vessels account for most of the TPR?
Arterioles
they regulate capillary flow
Resistance of vessels in a series
Rseries = R1 + R2 + R3…
Resistance of vessels in parallel
Rparallel = 1/R1 + 1/R2 + 1/R3…
Cardiac cycle Phase 1
Isovolumetric contraction
- period bt mitral valve closing and aortic valve opening
- highest O2 consumption
- this is systole
Cardiac cycle Phase 2
Systolic ejection
- period bt aortic valve opening and closing
- lose SV
Cardiac cycle Phase 3
Isovolumetric relaxaing
-period bt aortic valve closing and mitral valve opening
Cardiac cycle Phase 4 & 5
4: Rapid filling (just after mitral opens)
5: Reduced filling (just before mitral valve closing)
- gain the SV
S1
Mitral and tricuspid closure
Loudest at mitral area
point bt phase 5 and phase 1
S2
Aortic and pulmonary valve closure
loudest at left sternal border
point bt phase 2 and 3
S3
In early diastole during rapid ventricular filling phase (phase 4)
assoc w increased filling prs
more common in dilated ventricles
normal in kids and prego
S4
“atrial kick” in late diastole (phase 5)
high atrial prs
assoc w ventricular hypertrophy
LA has to push against a stiff LV wall
Waves of the jugular venous pulse
JVP: a, c, x, v, y (at carter’s x-ing, vehicles yield
a wave: atrial contraction
c wave: RV contraction (tricuspid valve bulges into atrium)
x descent: ventricles empty
v wave: increased atrial prs d/t filling against closed tricuspid valve.
y descent: diastole. atria empty into ventricles.
S2 splitting (normal)
aortic valve closes slightly before pulmonic.
inspiration increases this difference.
inspiration means a drop in intrathoracic prs, which increases the capacity of pulmonary circulation.
pulmonic valve closes later to accommodate more blood entering the lungs
aortic valve closes earlier bc of decreased return to left heart.
normal in athletes and young ppl
Wide S2 split
a/w pulmonic stenosis or RBBB
(slightly) more with inspiration
seen in conditions that delay RV emptying. delay in emptying causes delayed pulmonic sound (on both insp and expiration). an exaggeration of normal splitting.
Fixed splitting in S2
a/w ASD
doesn’t chg w inspiration
ASD leads to L–>R shunt and therefore flow thru pulmonic valve is increased- so regardless of breath, pulmonic closure is very delayed.
Paradoxial splitting S2
A/w aortic stenosis or LBBB
pulmonary shuts before aortic!
thus it’s decreased(!) on inspiration
seen in conditions that delay LV emptying.
normal order of valve closure is reversed.
on inspiration, the later P and the earlier aortic sounds move closer to each other, “paradoxically” eliminating the split.
Starling curve: what happens to the curve with exercise?
Shifts up (kinda left)
for a given preload, you are pushing out more blood during exercise
d/t the increased contractility w exercise.
anything that causes increased contractility will do this (catecholamines, digitalis, sympathetic stimulation)
Starling curve: what happens to the curve with CHF or digitalis?
It moves down (to the right)
For a given preload, you are pumping out less blood.
D/t less contractility
anything that decreases contractility will decrease CO or SV. (drugs, loss of myocardium in MI)
In very bad CHF, curve will be a lot lower and more toward the right.
What causes the aortic valve to open?
Prs in ventricle exceeds prs in aorta
What causes mitral valve to open?
Prs in LA exceeds prs in LV
In what dz’s do you lose elasticity of the aorta?
Marfan’s
Syphilis (tree-barking)
What can cause rapid ventricular filling (S3)?
CHF
Mitral regurg
L–>R shunt (ASD, VSD, PDA)
Dilated cardiomyopathy
What does QRS represent?
Ventricular contraction
Heart sound are not actually d/t valves closing. What causes them?
The turbulent flow right AFTER the valves close.
So on graph will see mitral closing, then S1; Aortic closing, then S2
What can cause atrial kick S4?
Hypertrophic cardiomyopathy
Aortic stenosis
Chronic HTN w LVH
After an MI
Windkessel effect
Dicrotic notch in aortic prs curve.
After systole, the aortic prs drops, but goes up again slightly right after the ejection. Prs increases d/t elasticity of the aorta (like rubber band).
This is when the coronary arteries fill!
What happens to the cardiac cycle graph when preload is increased?
It gets wider (to the right) bc increased preload increases SV
The width of the graph is the SV.
What happens to the cardiac cycle graph when you increase afterload?
It gets taller and skinnier in width.
Increased afterload means increased aortic prs (so taller) and decreased SV (so skinnier)
Increasing the afterload also increases ESV.
What happens to the cardiac cycle graph when contractility is increased?
It gets wider (on both sides) and taller.
Increasing contractility increases SV (so wider) and increases EF and decreases ESV.
These mean that the pressure is increased (so taller).
What is TPR a measurement of?
Afterload
Cardiac and vascular fn curve: what 2 things are plotted?
CO and Venous return (wrt RA pressure or EDV)
If the cardiac and vasc fn curve of CO shifts right, what happened?
Either decreased contractility (inotropy)
Or increased afterload (increased TPR)
If the cardiac and vasc fn curve of CO shifts left, what happened?
Either increased contractility
Or decreased afterload
What happens to pressure and blood flow on inspiration?
Inspire - diaphragm goes down.
ITP increases
More space for blood to fill heart- so RV vol increases. This is why you get splitting on inspiration.
Ventricular AP: Phase 0
Rapid upstroke
Volt-gated Na+ chnls open (Na+ comes in)
Ventricular AP: Phase 1
Initial repolarization
Volt-gated Na+ chnls are inactived
Volt-gated K+ chnls start to open (K+ goes out)
Ventricular AP: Phase 2
Plateau
Ca2+ influx thru volt-gated Ca2+ chnls balances K+ efflux.
Ca2+ coming in triggers rls of even more Ca2+ from SR- this causes myocyte contraction.
Ventricular AP: Phase 3
Rapid repolarization
Massive K+ efflux d/t opening of volt-gated slow K+ chnls and closure of Ca2+ chnls
Ventricular AP: Phase 4
Resting potential
High K+ permeability through K+ chnls (“leak” current is K+ efflux)
What are the leak currents?
K+ going out
Na+ coming in
Ca2+ coming in
What are the pumps/exchgrs?
Na+/K+ pump (Na+ out / K+ in)
note: the leak channels go in the opp direction
Na+ in, Ca2+ out
note: Ca2+ leak chnl is back in
Na+ leak chnl is in tho, bc of the Na+/K+ pump
Where does the ventricle AP also occur?
bundle of His and purkinje fibers
How is cardiac musc contraction different than skeletal musc?
Cardiac musc AP has a plateau (d/t Ca2+ influx)
Cardiac nodal cells spontaneously depolarize, resulting in automaticity d/t I(f) channels
Cardiac myocytes are electrically coupled to each other by gap jns
If the mbr were freely permeable to each of these (individually) what would the voltage be?
K+, Na+, Ca2+
K+ -75mV
Na+ +55mV
Ca2+ +20mV
How do anti-arrhythmics slow down the heart rate?
By increasing ERP- effective refractory period.
During ERP, another AP can’t occur. (another contraction can’t occur)
What drugs prolong phase 3 (ventricular AP)?
K+ chnls blockers
Which phase do Na+ chnl blockers prolong?
Phase 0 (ventricular AP)
Pacemaker AP- where does this take place?
In the pacemakers- SA and AV nodes.
In contrast to the ventricular AP, which occurs in the ventricles
Pacemaker AP- what are the phases?
Phase 0, 3, 4
Pacemaker AP: phase 0
Upstroke = opening of volt-gated Ca2+ chnls
Ca2+ comes in
Unlike ventricular myocytes, the pacemaker cells don’t have fast volt-gated Na+ chnls.
Thus, there is a slow conduction velocity- this allows the AV node to prolong the transmission from atria to ventricles (to allow for filling)
Pacemaker AP: phase 3
Inactivation of Ca2+ chnls
Increased activation of K+ chnls, so increased K+ efflux
Pacemaker AP: phase 4
Slow diastolic depolarization- the mbr potential spontaneously depolarizes as Na+ conductance increases. Accounts for automaticity of SA and AV node.
What part of the pacemaker AP determines the HR?
the slope of phase 4 (slow depolarization)
ACh decreases the rate of diastolic depolarization and so decreases HR
Catecholamines increase depolarization and therefore increase HR.
Sympathetic stimulation increases the chance that the I(f) Na+ chnls are open (so makes depol faster)
Which drugs inhibit phase 0 of the pacemaker AP?
Ca2+ chnl blockers
How do beta blockers affect the pacemaker AP?
They decrease the slope of phase 4 (and thus reduce HR)
Mne for anti-arrhythmics
No Bad Boy Keeps Clean I- Na+ blockers II- B-blockers III- K+ blockers IV- Ca2+ blockers
How do Na+ chnls blockers work on the myocyte AP?
They decrease the slope of phase 0, thereby prolonging the ERP.
What are the Na+ chnl blockers
PDQ TLM FPE
Police Dept Questioned The Little (pudgy) Man For Pushing Ecstacy
Class I-A:
Procainamide
Disopyramide
Quinidine (not quinine!)
Class I-B: Tocainide Lidocain (Phenytoin) Mexiletine
Class I-C:
Flecainide
Propafenone
Encainide
Procainamide
Class IA anti-arrythmic (Na+ chnl blocker)
Used for WPW
Can cause drug-induced SLP (shipP, anti-histone Ab)
What is WPW?
abnormal electrical pathway bt atria and ventricles- bundle of Kent. can stimulate ventricles to contract too early, causing atrioventricular reciprocating tachycarding- a type of SVT. EKG: short PR interval and delta waves Rx: Procainamide (class 1a) or amiodarone (class III)
Effect of Class Ia anti-arrhythmics
Increase AP duration, so increase ERP
EKG: increased QT interval
affect both atrial and ventricular arrhythmias, esp re-entrant and ectopic supraventricular or ventricular tachycardia.
Side effects of quinidine
Cinchonism: headache and tinnitus
Thrombocytopenia
Torsades de pointes d/t increased QT interval
Effect of class I-B ant-arrhythmics
I-B = tocainide, lidocaine, (pheytoin), mexiletine
Decrease the AP duration. (yes, decrease)
Preferentially affect ischemic or depolarized purkinje and ventricular tsu
useful in acute ventricular tachy-arrythmias (esp post-MI) and in arrythmias caused by digitalis
Toxicity of class 1-B
Local anesthetic (lidocaine!)
CNS stim/deprsn
CV deprsn
Effect of class 1-C
Flecainide, Propafenone, Encainide
Have no effect on AP duration (really)
Useful in V-tach that progresses to VF, and in intractible SVT.
Usu last resort.
For pts w/o structural abn.
Toxicity of Class 1c
pro-arrythmic, esp post-MI (contraindicated)
Signif prolongs the refactory period in the AV node.
Which of the Na+ blocking classes is best post-MI? worst?
Best = 1B Contraindicated = 1C
What electrolyte imbalance increases toxicity for all class 1 drugs?
Hyperkalemia
Class II anti-arrythmics
Beta-blockers
Propranolol, esmolol (short acting), metoprolol, atenolol, timolol
Mech: decrs cAMP (bc B receptors are Gs- so if you block them, will decrs it) and decrs Ca2+ currents
They suppress abn pacemakers by decreasing the slope of phase 4
EKG: increased PR interval (AV node is esp sensitive)
Use for v-tach, SVT, slowing ventricular rate during a-fib and a-flutter
Toxicity of Class 2 anti-arrythmics
Impotence Exacerbation of asthma CV: bradycardia, AV block, CHF CNS: sedation, sleep alteration Can mask signs of hypoglycemia, so be careful in diabetic pts Metoprolol can cause dyslipidemia Treat OD w glucagon.
Class III anti-arrhythmics
K+ channel blockers Sotalol, amiodarone, ibutilide, bretylium, dofetilide Increase AP duration, so increase ERP. Used when other anti-arrhythmics fail. EKG: increased QT interval
What is sotalol used for?
Toxicity?
rhythm control for a-fib
tox: torsades de pointes (incrsd QT), excessive Beta-block
Toxicity of ibutilide (class 3)
torsades de pointes (increased QT)
Toxicity of bretylium
new arrythmias, hypotension
note: guanethidine and bretylium are the drugs that inhibit NE rls from adrenergic (sympathetic) neurons
Toxicity of amiodarone
Pulmonary fibrosis,
hepatotoxicity,
hypo- or hyperthyroidism (amiodarone is 40% iodine by weight. only organ in body that uses iodine is thyroid!)
Check PFTs, LFTs, TFTs when using amiodarone
Also, corneal deposits, skin deposits (blue/gray) resulting in photodermatitis, neurologic effects, constipation, CV effects (bradycardia, heart block, CHF)
What is unique about the effects of amiodarone on the ventricular AP?
It has class I, II, III, and IV effects bc it alters the lipid mbr Mostly class III, but used to be listed as class Ia
What phase of the ventricular AP do the K+ chnl blockers affect?
Class 3 = Phase 3 effects
What drugs cause photosensitivity?
SAT for a photo:
Sulfonamides
Amiodarone (class III anti-arrythmic)
Tetracycline
What are the 2 kinds of Ca2+ chnl blockers?
dihydropyridine- these work at the vessels
non-dihydropyridine- these work at the heart (these are the anti-arrhythmics)
Class IV anti-arrhythmics
Ca2+ channel blockers (non-dihydropyridine)
Verapamil, diltiazem
Primarily affect AV nodal cells
Decrease conduction velocity (decrease slope of phase 0 in pacemaker AP), increase ERP
EKG: increased PR interval
Used to prevent nodal arrhythmias (eg SVT)
Toxicity of Class IV
constipation, flushing, edema, CV effects (CHF, heart block, sinus node deprsn)
Get heart block if you combine them w other anti-arrythmics, esp B-blockers
Which anti-arrhythmics increase the QT interval?
Class Ia (Na+ blockers) Class III (K+ blockers) Increasing QT means at risk for torsades de pointes
Which anti-arrhythmics increase the PR interval?
Class II (beta-blockers) Class IV (Ca2+ blockers)
Other than the 4 classes, what are the other anti-arrythmics?
Adenosine, K+, Mg2+
Adenosine
Antiarrhythmic
Increases K+ efflux out of cells, leading to hyperpolarization of the cell and decreased inward Ca2+.
Drug of choice for dx’ing or abolishing SVT
V short acting (~15 sec!)
Toxicity: flushing, hypotension, chest pain- these effects are blocked by theophylline (methylxanthine bronchodilator)
K+ as an anti-arrhythmic
Depresses ectopic pacemakers in hypokalemia (e.g. digoxin toxicity)
Mg2+ as an anti-arrhythmic
Effective in torsades de pointes (long QT) and digoxin toxicity
