6070 exam 2- cardiology

BP = Q* (cardiac output) x TPR (total peripheral resistance)

the equation for blood pressure

what does the Na/K pump do?

3 Na+ out with 2 K+ in

what is the charge of the inside of the cardiac cell?

negative

which node has the closest to 0 threshold?

what is this node able to set

SA node

responsible for the heartbeat

what are the pacemaker cells modulated by?

autonomic nervous system

what are the 3 phases of SA node pacemaker cells in order?

1. phase 4- diastolic depolarization due to gradual Na+ influx with Ca2+ influx and gradual decrease in K+ efflux

2. phase 0- depolarization (Ca 2+ channels open

3. phase 3- repolarization (K+ channels open (delayed))

what is the MDP?

maximum diastolic potential (most neg charge)

instead of resting membrane potential

what does the parasympathetic system do to the membrane potential of the SA node while we sit at rest?

causes blockage of SA node action by ACH

slower increase in phase 4, 

lower frequency of SA node signals

what does the sympathetic system do to the SA node depolarization

quickens this up with norepinephrine

what is the resting potential of the cardiac myocyte?

-90 mV

what is the depolarization of the cardiac myocyte ? x 5 things

• phase 0 - rapid upstroke attributable to Na+ influx

• Phase 1- slight repolarization bc of closure of Na+ channels and beginning of K+ leaving

• phase 2- plateau due to equalized influx calcium and exiting K+

• phase 3- Ca channels close and K+ efflux increases, rapid repolarization

• phase 4- membrane potential reached and all channels closed

why are atrial action potentials shorter than ventricular APs?

shorter due to reduced phase 2

what does sympathetic innervation do to the heart? x 3 things

how is this done?

1. increases HR (chronotropic effect)

2. speed of conduction (dromotropic effect)

3. force of contraction (inotropic effect)

binding of norepinephrine to B receptors

what does the parasympathetic nerve do to the heart?

uses the vagus nerve to send ACh to the muscarinic receptors. This causes 

1. reduced HR

2. reduced speed of action potential conduction

   1. reduced inotropy

what nerve supplies the SA node?

what supplies the AV node?

right vagus nerve

left vagus nerve

what is inotropy

what is positive inotropy?

magnitude of contraction

more squeezing of the heart

what is chronotropy?

the rate of the heart

what is dromotropy?

the way the signal moves through the heart

what is a beta blocker

what is a Ca channel blocker?

negative inotrope

negative inotrope

ca is what?

epi is what?

positive inotropes

what does P wave correspond to ?

QRS complex?

atrial depolarization

ventricular depolarization

what does T wave represent

What does u wave mean?

ventricular repolarization

slow heart rate and low potassium

what are the gap junction proteins called between cardio myocyte cells?

what do they form?

connexins

low resistance pathway, electrical coupling between cells

having an mi causes what system to kick in?

what action comes after this?

sympathetic

causes more ca2+ to enter the cells

the area of the MI after the sympathetic increase does what to the MP in the area?

what does this have possible influence into?

brings it more positive, now has MP that is closer to 0

tachyarrythmias

why are neighboring regions predisposed to ectopic dysrhythmias after MIs/ischemia?

due to the closer to 0 MP

the neighboring cells are ‘jumpy’

hyperkalemia is what?

what is this caused by?

increased extra-cellular K+

diffusion gradient from inside to outside is reduced

IN the case of hyperkalemia, at RMP, what happens to k+ efflux?

what happens inside the cell?

there is less of it

inside is more positive, partial depolarization

in the setting of hyperkalemia, some na+ channels open, but 

not enought to generate an AP

what is a peaked T wave indicative of?

if you lose the p wave, what is this due to ?

hyperkalemia

locked K+ in the cell, sodium locked in cell, arresting cell activity

what are the 2 ways that impulse generation is done incorrectly for dysrhythmias?

1. abnormal rate of impulse generation from normal pacemaker

   1. impulse generation from abnormal (ectopic) site

what are the 3 mechs for abnormal circular depolarizaiton?

1. abnormal automaticity

2. triggered activity from depolarization

3. reentrant circuits

what is the mechanism of reentry circuit in the dysrhythmia?

1. wave of depolarization that travels slowly or by an abnormal pathway may encounter myocardium that has had time to recover and can restimulate it

2. could result in an extra beat and depolarization could chase it’s tail in a circuit

   1. resulting fibrillation

It is not possible for a cardiomyocyte to be acitvate during what phase?

when is this premature reactivation possible?

1-2 aka absolute refractory period

in #3 or relative refractory period

what is triggered activity?

occurs when an impulse is generated during or just after repolarization

when does early afterdepolarization in ventricular cell occur?

what is this due to ?

in phase threew

some voltage-gated ca channels open

when does late/delayed afterdepolarization occur in what phase?

why does this happen?

phase 4

Ca ions spontaneously released from SR after repolarization

what is an R on T wave?

r wave occuring on top of T wave means that the cells were prematurely depolarized again

R on T syndrome predisposes some patients to what ?

long QT syndrome

in long QT syndrome, what channel function is reduced?

what does this lead to?

K channel sluggishnes

prolongation of AP of ventricular myocytes and prolongation of QT interval

curve is shifted to the R

delayed repolarization

what genes might be messed up if the person is experiencing long QT syndrome?

what function of these genes is changed?

KCNQ1 (K+ channel LOF)

KCNH2 (K+ channel LOF)

what is given that can prevent ca reentry and stop tachyarrythmias?

magnesium

what is the main problem with long QT syndrome?

sluggish k channel

slow depolarization

what are contractive units called?

what type of muscle is this?

sarcomeres

slow twitch

what is the process of cardiac myocyte contraction/excititation? x 6 things

1. calcium enters cell (phase 2)

2. ca enters the SR

3. SR releases stored Ca into cytoplasm of the cell (ryanidine receptor)

4. CA binds to troponin

5. troponin bound to tropomyosin moves tropomyosin

6. actin and myosin interact, pull the sarcomeres to squeeze

what is the diastolic phase of cardiac myocytes? x 5

1. as repolarization happens, the ca inside the cell is resequestered to SR through sarcopump (which requires ATP)

2. ca could be pumped out of cell w atp

3. sodium calcium exchanger

4. sodium potassium pump

5. ca into the mitochondria

how is the ca resequestered to the SR during diastole?

resequestration into sr through sarcopump that needs ATP to survive

in ischemic heart disease, the heart is low on energy. 

what does this do the the calcium in the cardiomyocytes and the resulting tension of the heart?

ca stuck in cytoplasm during diastole

stiff heart

what is muscle relaxation?

lusitropy

is significant energy needed for lusitropy?

yes

more ca equals what inotropy level

more ca = more inotropy

what is the equation for stroke volume

EDVlv - ESVlv = sv

what is EDV?

vol of blood in the ventricle prior to ejection

what is ESV?

vol of blood that remains in the ventricle after ejection

what is a normal ejection fraction?

60-80%

what is normal resting cardiac output

what is the equation of Co?

5-6 L/min

CO =  sv x hr

what are tje 3 determinants of stroke vol?

1. preload

2. afterload

3. contractility

what does increased afterload do to stroke volume?

decrease stroke vol

what does preload and contractility do to the SV?

increase it

B adrenergeic activation

1. epi/norepi bind to b receptors

2. pka is activated, phosphorylates ca channel

3. ca can enter the cell easier, Ca out of SR easily

4. increases inotropy

B adrenergic activation during diastole

1. epi/norepi bind

2. pka phosphylates plb

3. enhances uptake of ca into SR

parasympathetic binding of Ach to m2, what is the pathway for systole and diastole 

1. ach binds to m2 receptors

2. G protein inhibits ac

3. less pka to be phosphorylating

4. less ca entrance, less release from S

b blocker does what?

controls inotropy, limits it

what can angiotensin II increase entry of into the heart cell?

what does this do to the heart?

Ca entry

this induces heart growth that leads to HF

angiotensin is a what?

constrictor

what do stable plaques of artherosclerosis have?

more collagen and fibrin

stable cap

plaque formation =

1. endothelial dysfunction, monocyte adhesion and emigration

2. smooth muscle emigration from media to intima. macrophage activation

3. engulfed lipids, foam cells

   1. collagen deposition, smooth muscle proliferation

what is a stemi?

chest pain and proof on ECG of ST segment elevation, + biomarkers

what is an nstemi?

what might these be treated with ?

sx of unstable angina but no ST elevation, + biomarker

antiplatelet drugs

what is unstable angina?

chest pain, no st elevation, neg biomarkers

what are serum marker changes in nstemi and stemi? x 4

1. myoglobin

2. troponin

3. lactate dehydrogenase

4. creatinine kinase

after an MI, which autonomic system is activated? x 2

sympathetic nervous system and angiotensin/aldosterone systems

HFREF is what type of HF?

what is the basic vibe of this?

what is the result of this?

systolic

❤ can’t sustain CO to meet needs of body

results in pooled blood flow in systemic or pulm veins

what is the neuro hormonal change in HFREF? x 3

sympathetic system activation

renin-angiotensin system activation

vasopressin release

what are some sx of hfref

ascites, dyspnea, cardio megaly

what is the diff between hfref and hfpef

impaired contractility

disordered relaxation

what does the RAAS system do?

results in increased sodium and water retention

what remodels happen after hf? x 3

sns activation

increased preload

myocardial hypertrophy

what is released from the heart when it is chronically stretched?

what does this tell the kidneys to do?

ANP/BNP

stimulate kidney to pee off more sodium and water

WHAT IS THE ACC/AHA STAGE OF HF?

STAGE A: high risk, w/o structure change or sx

stage b: w structure change, w/o s/sx of hf

stage c: w structure heart disease, w prior or current sx of heart disease

stage d: sx at rest need intervention

ny hf stages

1 no limitation

2 slight limitation

3 incapacity w slight exertion

4 incapacity w rest