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Flashcards in Cardiology Deck (47):

What is the carbonic acid buffer system (CABBS)?

H + HCO3 = H2CO3 = H2O + CO2


What happens to CABBS during respiratory acidosis?

Increase in CO2/increase in H+
CO2 retention & decreased O2 binding affinity (due to low pH)

-Hypoventilation, respiratory failure/apnea/cyanosis
**Give ventilation’s via BVM & provide O2


What happens to CABBS during Respiratory alkalosis?

Decreased CO2 (eliminated due to increased RR)

S/S: hyperventilation, dizziness, paresthesia, decreased Ca2+, increased PaCO2
**Treat by decreasing respirations**


What happens to CABBS during metabolic acidosis?

(Increased H+ ions in system)
S/S: fever hypotensive, irregular RR, diaphoretic, tachycardia

Causes: DKA, sepsis, infection, renal failure, ASA, OD, lactic acidosis


What happens to CABBS during metabolic alkalosis?

- increase in PH/decrease in H+ ions/decrease in CO2

Vomiting may cause.

Increase in pH, dehydration, leads to greater affinity for binding of o2 (can’t offload into peripheral cells)

*give PT fluids!


What happens to sympathetic stimulation of bronchial SMC?

NT:ACh/R: nicotinic cholinergic —> NT: Norepi/R: B2 adrenergic —> binds to gPCR receptor —> cascade of RXNs = decreases Ca2+ —> SMC relaxation and bronchodilation. (Decreased Ca2+ = less interaction between actin and myosin)


What happens during ANS parasympathetic stimulation of bronchial SMC?

NT:ACh/R: nicotinic cholinergic —> NT: ACh/R: muscarinicic cholinergic —> binds to Muscarinic Acetylcholinergic receptor —> cascade of RXNs = increased Ca2+ —> SMC contraction and bronchodilation.


What are pacemaker cells? What do they do? Where are they located?

Found in the atrium/SA node.

Connected with gap junctions to allow passage of ions.

Stitched together with desomeres. Has cytoskeleton made of myofibrils (actin and myosin)


Conducting cells?

More cylindrical than pacemaker cells. Have the same organelles as pacemakers. Found in the AV-intermodal fibers.


Contracting cells?

Found mostly in ventricles. Have intercalated disks and striations allowing them to stretch.


What is the electrical pathway of the heart?

SA node —> intermodal bundle/Bachmann’s bundle —> AV node —> Bundle of His/Bundle Branches/Perkinge Fibers


Phases of Non-Pacemaker Action Potential?

Phase 4: resting potentional (-90mV)

Phase 0: depolarization to threshold (-65 mV leads to opening of Na+ FAST CHANNELS and rapid influx of Na+ to +30mV

Phase 1: opening of K+ channels —> rapid repolarization to about 0mV

Phase 2: (Plateau phase) —> @ 0mV Ca2+ channels open Ca2+ flows in as K+ continues to flow out. Maintains 0mV

Phase 3: main repolarization K+ flows out —> return to resting.


Phases of pacemaker action potential?

Phase 4: hyperpolarization. Activated Na+ channels open (slow Na+ entry)

-Threshold (-40mV)

Phase 0: Ca2+ channels open (fast Ca+ entry)


Phase 3: Ca2+ channels close/K+ open (slow K+ exit)



Where will you most commonly see Pacemaker action potential?

Occurs in SA nodal cells


Where will you most likely see Non-pacemaker action potential?

In the ventricles.


What is the first step of the cardiac cycle?

Atrial diastole/ Ventricle diastole: the atria and ventricles are at rest (valves open)
-70% blood in ventricles/ 30% blood in atria
-Depolarization of SA node
-depolarization of conducting and PM cells in atria


What is the second step of the cardiac cycle?

Atrial systole/ ventricle diastole: atrial contraction/ventricle relaxation
-depolarization of the AV node
-depolarization of ventricles


What is the third step of the cardiac cycle?

Atrial diastole/ ventricle systole: atrial relaxation/ ventricle contraction


How does the cardiac cycle relate to pT’s in A-fib or SVT?

MAP (mean arterial pressure) is still maintained because 70% of blood is still present and active in the ventricles allowing for perfusion throughout the system.


What is end diastolic volume?

Amount of blood in ventricles after atria contract.
-> Refers to END of ventricular diastole.


What is end systole volume?

Amount of blood in ventricles after ventricles contract and expel blood.
-> refers to the END of ventricular systole


What are the steps of muscle contraction?

1) Ca2+ binds to troponin, moves tropomyosin and reveals myosin binding site.

2) Cross bridge formation —> actin binds to myosin.

3) Powerstroke —> actin and myosin interact and shorten sarcomere.

4) ATP molecule arrives —> releases actin and myosin —> muscle relaxes.


What is vascular shunting?

Vascular shunting the process in which the precapillary sphincter closes and blood bypasses “true capillary bed”, returning blood to vital organs.


What are elastic arteries? Examples of?

Capable of stretching, have increased amount of baroreceptors, do NOT activate with vasoconstriction (NEVER constrict; they are the main suppliers).

Ex: Aorta, pulmonary trunk, pulmonary arteries, common carotid, common iliac.


What are muscular arteries? Examples of?

Carry blood to specific organs/ can be effected by vasoconstriction/ moderate diameter/ have SMC to help with blood volume.

Ex. External carotid, brachial, femoral, mesenteric.


What are arterioles?

Arteries small in diameter, most have only endothelium and SMC.
Can change in diameter for local, neural, and hormonal stimuli.


Let’s talk about veins....

Have less pressure, thinner walls, contain valves. These valves are made of folds in the tunica intima.

Venules are small veins (0.01mm-0.1mm in diameter)


What is local regulation?

Process that provides adequate nutrients to active muscle/tissue with ‘vascular shunt’

Precapillary sphincters —> relaxed —> allow blood to enter the ‘true capillary bed’ —> allows exchange/adequate perfusion.


What is neural regulation?

Neural regulation of arteries is triggered by a decrease in MAP, when baroreceptors sense a decrease in pressure, or with sympathetic activation.

B1R —> metabotropic —> increase Ca2+ in cardiac PM cells = increase in HR
increases Ca2+ in ventricular cells.


What is hormonal regulation?

Chemical messengers are released/ interact with distant tissues.


What happens to hormonal regulation when there is a decrease in MAP or BP?

Release of angiotensin II

1) vasoconstriction
2) vasoconstriction of efferent arteriole
3) ADH regulates H2O excretion from kidneys
4) Aldosterone regulates Na+ reabsorption.


What happens with hormonal regulation if there is an increase in BP?

Release ANP

1) vasodilation
2) vasodilation of efferent arteriole
3) inhibit reverse of ADH and Aldosterone


Let’s talk about alveolar/capillary gas exchange....

-Pressure gradient of CO2/O2 is what the gas molecules move along
-Air water boundary in alveoli is where the gases dissolve into the blood stream. (Henry’s law)
-o2 collected by RBC’s and bound to hemoglobin.


What is Dalton’s law?

Total pressure = sum of all partial pressures (Ptot = PCO2 + O2)


What is Boyle’s Law?

Pressure and volume have an inverse relationship at constant temperature. In a larger container gas molecules spread out, and there is lower pressure. The opposite is true in smaller containers.

P1V1 = P2V2


What are the steps of calcium induced calcium release in muscle contraction?

1) Ca2+ VG channel opens on sarcolemma —> Ca2+ enters cytosol.

2) Ca2+ in cytosol opens Ca2+ channel on SR (sarcoplasmic reticulum) —> releases Ca2+.

3) Ca2+ moves down filaments and binds to troponin.


What is MOA of adenosine?

A1 R agonist — slows AV conduction by activation of G-protein 2nd messengers.
-decreases cAMP
-inhibits Ca2+ entry into cardiac pacemaker cells


What is the MOA of Nitro?

NO activates GTP —> cGMP + 2 Pi in VSMC

CGMP activates cascade of RXNs, causes reduction in intracellular Ca2+, VSMC relax in arterioles.

Decreases cardia preload and afterload.


MOA of metoprolol?

B1 R - antagonist —> inhibits extracellular ca2+ entry and Ca2+ release from sarcoplasmic reticulum.

Positive chronotropic, inotropic, and dromotropic effect.


MOA of Magnesium Sulfate?

In cardiac cells it is a Ca2+ channel blocker. Positive chronotropic, inotropic, and dromotropic effects.


What is the MOA of Levalbuterol?

B2 agonist —> promotes sympathetic stimulation of bronchial SMC reducing interaction between actin and myosin causing smooth muscle relaxation.


MOA of Ipratropium Bromide?

Muscarinic ACh-R antagonist —> inhibits parasympathetic stimulation in bronchial SMC, submucosal glands, and goblet cells.

Allows bronchodilation.


MOA of Epi?

A1 agonist —> 2nd messenger release of Ca2+ in VSMC —> peripheral vasoconstriction —> increase in SVR and BP

B1 agonist —> increased intracellular Ca2+ in cardiac cells (positive inotropic, chronotropic, and dromotropic effect)

B2 agonist —> bronchial smooth muscle relaxation/bronchodilation.


MOA of Diltiazem?

SMC Ca2+ channel blocker —> inhibits Ca2+ entry and interaction Bren actin and myosin in SMC

Smooth muscle relaxation and dilation of blood vessels.


MOA of dexamethasone?

**immunosuppressant** diffuses across cell membranes of various cells present and binds to DNA inhibits/regulates inflammatory agents


MOA of atropine?

Muscarinic ACh-R antagonist —> inhibits parasympathetic stimulation in SA/AV nodal cells.

-prevents K eflux and hyperpolarization

- ‘+’ chronotropic, inotropic effect.


MOA of amiodarone?

K+ channel blocker : prolongs phase 3 repolarization and refractory period of non-pacemaker action potential

Na+ channel blocker: decreases amplitude of phase 0 depolarization of non-pacemaker cells

Non-competitive Beta blocker: negative chronotropic, inotropic, dromotropic effects

Weak Ca2+ channel blocker: negative chronotropic, inotropic, dromotropic effects