Flashcards in Day 6.2 Cardio Deck (135):
EKG P wave
EKG PR interval
conduction delay through AV node
usu < 200msec
EKG QRS complex
usu <120 msec
EKG QT interval
mechanical contraction of ventricles
EKG T wave
T-wave inversion indicates recent MI
Why isn't atrial repolarization on an EKG?
it's masked by QRS complex
EKG ST segment
isoelectric, ventricles are depolarized
EKG U wave
can be caused by hypokalemia or bradycardia
On EKG: what waves are up, what are down?
P is up
Q is down
R is up high
S is down
T is up
What is the PR interval?
From the beginning of the P wave to the start of the QRS complex (so until the Q wave)
Prolonged in AV block. Prolonged means >200 msec
Torsades de pointes
Ventricular tachycardia, see shifting sinusoidal waveforms on EKG.
Can progress to v-fib
Anything that prolongs the QT interval can predispose to TdeP
What drugs prolong the QT interval (and therefore predispose to TdeP)?
Antimalarials (chloroquine, mefloquine)
Protease inhibitors (HIV)
Anti-arrhythmics (Class 1A, Class III)
Congenital long QT interval
usu due to defects in cardiac Na+ chnls or K+ chnls.
Can px w severe congenital sensorineural deafness (Jervell and Lange-Nielsen syndrome)
Wolf Parkinson White
Ventricular pre-excitation syndrome.
Accessory pathway (bundle of Kent) from atria to ventricle, which bypasses AV node
So, ventricles partially depolarize earlier-->
classic delta wave on EKG.
Can result in reentry current, leading to SVT
Rx procainamide or amiodarone
Where is a delta wave?
After P wave, right at start of QRS should be.
It's leading up to the R, you don't really see a Q
Where is the ST segment?
After QRS until the beginning of T wave
So from end of S wave to T.
EKG Segment vs Interval
Segment = flat part bt 2 waves
Interval = includes one segment (flat part) and at least one wave.
How many leads are on an EKG? What are they?
aVR, aVL, aVF
I, II, III (bipolar)
points from heart to right arm
points from heart to left arm
points from heart to foot
limb lead I
points from right arm to left arm
limb lead II
points from right arm to foot
limb lead III
points from left arm to foot
Normal net electrical signal
Down and to the left
aVR net signal
negative deflection of QRS
aVL net signal
positive deflection of QRS
Limb lead I net signal
positive deflection of QRS
(means that signal is going to left)
Limb lead II net signal
positive deflection of QRS
(means that signal is going down and left)
T/F you can combine limb leads I and II and their overlap is the direction that the signal is going
Positive QRS deflection in aVL and in aVR
Left axis deviation
Causes of left axis deviation
Interior wall MI
Left anterior fasicular block
Positive QRS in limb lead III
Right axis deviation (probably)
Causes of right axis deviation
Acute R heart strain (ex massive pulm embolism)
Left posterior fascicular block
Dextrocardia (heart pointed toward right/on right side of body)
Quickest way to know if heart has normal axis
Look at limb leads I and II
If they both have positive QRS then it's normal.
Positive deflection in aVR
almost always abnormal- completely the opposite way of where the heart should be pointing.
EKG: amt of time in 1mm (little) box
EKG: amt of time in 5mm (big) box
0.2 sec (200 msec)
Length of normal PR interval
Beginning of P wave to start of QRS complex should be less than 200 msec (1 big box)
Length of normal QRS
the ventricular depolarization should happen to both ventricles at the same time, so it should be quick- less than 120 msec (3 tiny boxes).
If both ventricles are depolarizing at the same time, it will take longer. This could be a ventricular rhythm- one that is originating from the ventricles rather than the AV node.
What ion do T waves give info about?
Peaked T waves = hyperkalemia
Flat T waves = hypokalemia
Speed of conduction- which places have fast conduction? Slow conduction?
Fastest to slowest:
Purkinje (v fast)
AV node (v slow)
What is the pacemaker? What serves as the pacemaker if it stops working?
If no SA, then AV node
If no AV, then bundle of His & purkinje fibers
^These will all cause normal narrow QRS. If ALL fail, then ventricles will take over- and will have wide QRS
No distinct P waves
No pattern to how often there is a QRS, can't see P waves bt QRS.
No distinct SA nodes. (A-fib is common if there is atrial enlargement.)
No coordinated atrial contraction (that's why there are no distinct P waves)
Can result in atrial stasis and lead to stroke (pooling of blood leads to clots --> pulm embolism, or if patent FO, then anywhere in body --> stroke)
Predisposes to SVT
Rx for A-fib
If new A-fib ( drugs- K+ chnl blockers (sotalol or amiodarone)
Prophylax against thromboembolism w warfarin/coumadin
Rapid identical back-to-back atrial depolarization waves- do have distinct P waves, just a lot of them!
220-300bpm (once it's >300 it's A-fib)
Rx for atrial flutter
Try to convert to sinus rhythm
Use Class 1a, 1c, or III anti-arrhythmics
1st degree AV block
Prolonged PR interval
PR should be <200 msec, so this is more than that- aka greater than one big box.
Asymptomatic, benign- but more likely to go into 2nd degree block.
What organism can cause 1st degree AV block?
2nd degree heart block: what are the types?
Mobius Type 1 = Wenckebach
Mobius Type 2
Mobius Type 1 (2nd degree heart block)
Progressive lengthening of the PR interval until a beat is dropped- there is a P wave which is NOT followed by a QRS.
Usu asymptomatic, benign
Mobius Type 2 (2nd degree heart block)
Dropped beats that are NOT preceded by a change in length of PR interval (so no warning, just have a missed QRS all of the sudden)
The abrupt non-conducted P waves result in a pathologic condition.
Often found as 2:1 block, where there are 2 P waves for every 1 QRS response.
Can progress to 3rd degree AV block, so treat w pacemaker to prevent this.
3rd Degree heart block
Atria and ventricle beat completely independently of each other- so have both P waves and QRS, but no connection between the two.
SA node is not communicating w AV node
Atrial rate (P waves) is faster than the ventricular rate (QRS).
Usu treated w pacemaker
What disease can cause 3rd degree heart block?
Completely erratic rhythm w no identifiable waves.
Fatal arrythmia w/o immed CPR and defibrillation.
Count the boxes- 5 big boxes is 60
(300, 150, 100. 75, 60, 50)- count from e.g. peak of QRS to peak of next QRS.
Narrow QRS w fast rhythm
Wide QRS w fast rhythm
Ventricular premature beats
See QRS w/o a P wave. (on top of normal P QRS T, P QRS T rhythm)
How does an MI change w time on EKG?
Acute: ST elevation
Hours: ST elevation + R wave is decreased + Q wave appears
Day 1-2: Deeper Q wave + T wave inversion (plus ST elev, decrsd R wave from before)
Days later: ST normal, R back up high, T wave still inverted, still have Q wave
Weeks later: ST normal T wave normal, still have Q wave (every thing looks normal except for Q)
Where is angiotensinogen released from?
Where is renin released from?
JG cells of kidney
What causes renin rls?
Decreased BP (sensed by JG cells)
Increased Na+ delivery (sensed by MD cells)
Increased sympathetic tone
What is the role of renin?
Converts angiotensinogen from liver to AT I
What converts AT I to AT II?
ACE from the lungs and kidneys
(ACE also breaks down bradykinin)
What does AT II do (6 things)?
Acts on ATII receptors on smth musc
Constricts eff arteriole of glomerulus
Causes aldosterone secretion (from adrenal gland)
Causes ADH secretion (from post pit)
Increases proximal tube Na+/H+ activity
When AT II acts on receptors of vascular smooth musc, what is the effect?
AT tenses angios!
It causes vasoconstriction, which elevates BP
When AT II constricts the efferent arteriole of the glomerulus, what is the effect?
It increases the filtration fraction to preserve renal fn (GFR) in low-volume states
eg when RBF is decreased
When AT II causes aldo rls from adrenal glands, what is the effect?
Aldo causes increased Na+ chnl and increased Na+/K+ insertion into principle cells.
It enhances K+ and H+ excretion by upregulating principle cell K+ chnls and intercalated cell H+ chnls
Together, these create a favorable Na+ gradient for Na+ and H2O reabsorption.
When more Na+ and H2O stay in the body, blood prs is increased!
When AT II causes ADH rls from the post pit, what is the effect?
ADH causes insertion of H2O chnls in principle cells, which leads to increased H2O reabsorption
When AT II causes increased proximal tubule Na+/H+ activity, what is the effect?
can permit contraction alkalosis
When AT II stimulates the hypothalamus, what is the effect?
AT II affects barocepter function- what is the result of this?
It limits reflex bradycardia.
Normally, when there is increased BP, the HR will go down. This dampens that effect.
Released from atria in response to increased blood volume in atria
Can act as a check on renin-AT-aldo system
Relaxes vascular smooth musc via cGMP, causing increased GFR and decreased renin.
Primarily regulates osmolarity (inserts water channels), but also reacts to low blood volume, which is more imp than osmolarity.
Primarily regulates blood volume.
In low-vol states, both ADH and aldo help out.
Vasodilator, lowers BP
Bradykinin is broken down by ACE.
ACE-inhibitors are used for HTN bc they stop ACE and therefore stop the breakdown of bradykinin- meaning it can vasodilate like it normally does.
ACE and Bradykinin
ACE breaks down bradykinin
What is the "long term" way to fix a decreased MAP?
JGA senses decreased MAP
Renin-AT system is activated
AT II causes vasoconstriction, which increases TPR, plus Aldo increases blood vol, which increases CO.
MAP is increased d/t increased TPR and CO
What is the "short term" way to fix a decreased MAP
Baroreceptor fires less often, this is sensed by the medullary vasomotor center
Causes increased sympathetic activity in heart and vasculature
B1: increased HR and contractility lead to increased CO
alpha1: venoconstriction means greater venous return, which increases CO
alpha1: arteriorlar vasoconstriction increases TPR
MAP is incrsd d/t increased TPR and CO
When is ANP released? What does it do?
Diuretic, rlsd from atria in response to increased bld vol and increased atrial prs.
Causes general vascular relaxation.
Constricts efferent renal arterioles, but dilates afferent arterioles.
Involved in "escape from aldosterone" mechanism.
Where are the baroreceptors?
Aortic arch and carotid sinus
How does the baroreceptor on the aortic arch transmit info?
Transmits via vagus nerve, to medulla
ONLY responds to INCREASED BP, not decreased.
How does the baroreceptor on the carotid sinus transmit info?
Transmits via glossopharyngeal nerve, to the solitary nucleus of the medulla.
Responds to both increases and decreases in BP.
When there is hypotension, how do baroreceptors sense it, and what do they do?
Carotid sinus (only) senses decreased arterial prs bc there is decreased stretch, and therefore decreased afferent baroreceptor firing (to glossopharyngeal)
This causes increased efferent sympathetic and decreased efferent parasympathetic.
The increased symp means alpha1 vasoconstriction, B1 increased HR and contractility, so increased BP
Overall this is a short term mechanism, but it's imp in response to severe hemorrhage.
How does carotid massage change the heart rate?
Increased prs on carotid artery means increased stretch- this means increased afferent baroreceptor firing (glossopharyngeal nerve), and so decreased HR.
How does glossopharyngeal nerve firing relate to HR?
decreased nerve firing means HR will increase (as in hypotensive response)
increased firing means HR will decrease (as in carotid massage)
When is carotid massage performed?
But, not in elderly/in ppl w plaques, bc could dislodge plaque.
If massage doesn't work, use adenosine for SVT.
Where are the peripheral chemoreceptors?
on carotids and aortic arch.
What do the peripheral chemreceptors have a response to?
Carotid bodies and Aortic bodies respond to decreased PO2 (<60mmHg)- that is, the amt of O2 dissolved in blood (nothing to do w Hb).
They also respond to increased PCO2 and to acidosis (decreased pH of blood).
What do central chemoreceptors respond to?
Centrals respond to chgs in pH and PCO2 not of blood in arteries, but in the brain interstitial fluid. (The pH and PCO2 in the brain are influenced by arterial CO2 tho.
They do NOT respond directly to PCO2.
Responsible for Cushing triad.
What is the Cushing triad?
HTN, bradycardia, and respi depression
Increased ICP constricts arterioles, leading to cerebral ischemia, which leads to HTN (sympathetic response), leading to reflex bradycardia.
pushes fluid out of capillary (it's the fluid inside tho, that's pushing out)
higher at beginning of capillary (w force of heart/aorta behind it)
interstitial fluid prs
pushes fluid into capillary (it's the fluid outside that's pushing in)
higher at end of capillary
(that was supposed to be pi)
plasma colloid oncotic prs
pulls fluid into capillaries
(proteins in blood)
(that was supposed to be pi)
interstitial fluid colloid osmotic prs
pulls fluid out of capillaries
(proteins in interstitial fluid)
What is the net filtration prs eqn?
Pnet = (Pc - Pi) - (TTc - TTi)
So, (prs d/t fluid inside - fluid outside), minus (pressure d/t proteins inside - proteins outside)
What is edema?
Excessive fluid outflow into interstitium. Can be pitting (excess fluid w/o colloid) or non-pitting (lots of colloid in interstitium, so fluid comes to balance it)
4 common causes of edema
1. increased capillary prs (Pc)- typically at end of capillary (it's already big at beginning). see in heart failure
2. decreased plasma proteins (TTc) d/t nephrotic syndrome (peeing them out) or liver failure (not making enough)
3. Increased capillary permeability (Kf) caused by toxins, infection, burn, septic shock. histamines and bradykinin cause capillaries to be leaky.
4. increased interstitial fluid colloid osmotic prs (TTi) d/t lymphatic blockage
Net fluid flow eqn
Pnet x Kf
What is Kf?
filtration constant (aka capillary permeability)
What is PCWP (wedge prs) a good estimate of?
(also LV end diastolic prs)
Measure w a Swan-Ganz catheter, which goes thru R heart and into pulm artery.
In mitral stenosis, PCWP > LV diastolic prs.
What factors determine autoregulation of perfusion prs in the heart?
Local metabolites- O2, adenosine, NO
if O2 decreases, coronary arteries dilate
adenosine is a potent vasodilator
NO dilates the coronary arteries
What factors determine autoregulation of perfusion prs in the brain
local metabolites: CO2 (regulates pH)
What factors determine autoregulation of perfusion prs in the kidneys?
myogenic and tubuloglomerular feedback
What factors determine autoregulation of perfusion prs in the lungs?
Hypoxia causes vasoconstriction
This is the opp of the rest of the body, but for good reason: don't want to perfuse areas that are poorly oxygenated, bc it means the blood that goes to that area won't take up much O2- and then you will be delivering O2-poor blood to the body.
What factors determine autoregulation of perfusion prs in the skeletal musc
local metabolites- lactate, adenosine, K+
What factors determine autoregulation of perfusion prs in the skin?
Sympathetic stimulation is the most imp mech- esp for temp control.
Normal prs in heart (RV, LV, etc)
RA = < 10 (the 10 is PCWP)
LA = <130 / 90
Dx: HTN + paroxysms of increased SNS tone: anx, palpitations, diaphoresis
Dx: HTN, onset bt 20-50yo
Dx: HTN + elevated serum creatinine and abn urinalysis
Dx: HTN + abd bruits
Renal artery stenosis
Dx: HTN + BP in arms > legs
Coarctation of aorta
Dx: HTN + fam hx of HTN
Dx: HTN + tachycardia, heat intolerance, diarrhea
Dx: HTN + hyperkalemia
Dx: HTN + Episodic sweating and tachycardia
Dx: HTN w/ abrupt onset in pt 50, and depressed serum K+ levels (hypoK+)
(high aldo in blood)
Dx: HTN + central obesity, moon-face, hirsutism
Dx: HTN + normal urinalysis, normal serum K+
Dx: HTN + young pt w acute onset tachycardia
stimulant abuse (cocaine, meth)
Dx: HTN + hypokalemia
Or, renal artery stenosis
Dx: HTN + proteinuria
HTN features and risk factors
BP > 140/90
PreHTN BP >130/85
90% is primary/essential and related to increased CO or increased TPR
other 10% is secondary to renal dz.
Malignant HTN is severe and rapidly progressing.
Risk: increased age, obesity, diabetes, smoking, genetics, black>white>asian
What does HTN predispose to?
early form of end-organ dz caused by HTN
causes stiffened LV -- so hear S4 heart sound
as musc size increases, it chgs the inside (not outside) of heart- affects the luminal diameter, so LV can't fill as well.
Precursor to L-sided heart failure, precursor to MI
Rx for essential HTN
Ca2+ chnl blockers
T/F Beta blockers are contraindicated in decompensated CHF.
You can only use B-blockers for STABLE heart failure.
What 4 BP drugs can be used in pregnancy?
Nifedipine (Ca2+ chnl blocker)
Used to treat severe HTN, CHF. First-line for HTN in prego (w methyldopa).
Increases cGMP, causing smooth musc relaxation.
Vasodilates arterioles more than venuloes (unique!) so causes reduction in afterload.
Why is hydralazine often given along w a beta-blocker?
To prevent reflex tachycardia.
Any time you vasodilate, you can get reflex tachycardia
Toxicity of Hydralazine
Compensatory tachycardia (contraindicated in angina/CAD. give beta-blocker).
Used for severe HTN.
K+ chnl opener- hyperpolarizes and relaxes vasc smth musc.
Tox: Hypertrichosis (it's Rogaine!), pericardial effusion, reflex tachycardia (use a B-blocker), angina, salt retention.