Complications of Heart Disease Flashcards
Anatomy of Heart
1) why is the ventricle on the left larger than that on the right
2) How many cardiac valves are there, what are their names, between what features of the heart and what are they made of
1) Ventricle on the left is larger than the ventricle on the right because it has to pump blood to the rest of the body
2) All lie in same plane of fibrous ring of fibrous tissue (not cardiac muscle .˙. unexcitable/can’t have AP, insulates A + V)
♣ Tricuspid valve (3 cusps)
* Between RA + RV
♣ Pulmonary valve (semilunar) (outlet)
* Between RV + pulmonary trunk (to lungs)
♣ Mitral/bicuspid valve (2 cusps)
* Between LA + LV
♣ Aortic valve (semilunar) (outlet)
* Between LV + aorta (to the body)
Flow of oxygenated and deoxygenated blood in the heart:
- All deoxygenated blood from the body is sent to the heart through the vena cava from the right-hand side of the heart
o Pulmonary artery brings deoxygenated blood to the lungs
o Pulmonary vein brings oxygenated blood from the lungs back to the heart
♣ To be pumped out by the aorta
Anatomy of Heart - Nodes and Bundle of His
1) What are the nodes and their purposes
2) What does the bundle of His do
1) SA Node:
♣ Pace maker activity
♣ Small collection of cells that initiate atrial systole
NA Node:
♣ Provides delay in impulse transmission
♣ Protects ventricles from atrial fibrillation
2) Bundle of His
♣ Divides R and L bundles
♣ Provides orderly depolarization of ventricles
* Spread around heart muscle, even depolarization in both ventricles
* Everything behind the wave of depolarization is hyperpolarized and cannot be stimulated by another AP so the depolarization only spreads forward
Cardiac Cycle: Systole
1) Describe Isovolumetric Contraction
2) Describe Ventricular Ejection
1)
a. Ventricles are contracting but all valves are closed so no blood is ejected
b. Blood volume remains constant but the ventricular walls are squeezing to generate pressure (all valves are closed)
2)
a. The blood from the ventricles is forced out as the ventricular muscles shorten
i. Once this pressure generated exceeds that of the aorta + pulmonary trunk, pulmonary + aortic valves open (bi + tri are closed)
b. Volume of blood ejected in this scenario is the stroke volume (SV) (70mL)
Cardiac Cycle: Diastole
1) Describe Isovolumetric Ventricular Relaxation
2) Describe Ventricular Filling
1) Isovolumetric ventricular relaxation
a. Pressure in ventricles is less than that of the pulmonary trunk + aorta therefore all the valves are closed
2) Ventricular filling
b. Tricuspid and bicuspid valves are open because of pressure difference and blood flows into the atria
c. Pressure in atria is higher than ventricles so blood flows to ventricles
i. SA node fires
What is the order of the whole cardiac cycle
1) Ventricle filling
2) Isovolumetric ventricular contraction
3) Ventricular ejection
4) Isovolumetric ventricular relaxation
EKG:
1) Why are there different shaped waves on the EKG
2) What are the different waves
3) Describe what happens in each wave/what each wave shows
1) Different shapes of waves due to different types of voltage gated ion channels in cardiac tissue
2)
- P-wave
- Q-wave
- R + S wave
- T-wave
3)
- P-wave:
- Shape Very small due to small structures being activated
o Atrial excitation:
♣ SA node activates
♣ RA activated
o AV node activated
♣ LA activated
♣ Bundle of HIS
♣ Bundle branches
♣ Perkinje fibers
- Q-wave:
o Ventricular excitation begins
o LA + RA relax
o Activation of septum
♣ From LR
♣ From TB
- R + S wave: o Ventricular excitation is complete o Activation of RV + LV free walls ♣ Simultaneous - T-Wave: o Ventricular relaxation ♣ Repolarization of ventricles
Cardiac Arrythmias
1) Definition
2) Causes (2)
3) Risk factors (8)
4) Treatment (3)
1) Irregular beating of heart
2)
- Abnormal pacemaker activity
- Disturbance of cardiac conduction
3)
- Ischemia
- Hypoxia
- Drug toxicity (antiarythmic drugs)
- Electrolyte abnormalities
- Diseased heart tissue/scarring
4)
- Electrical devices
- Electrical ablation of normal pathways (in surgery)
- Drugs treatment
Molecular Components of AP:
1) Beginning of AP what happens
2) What happens once it passes threshold
3) After depolarization, what comes and how
1) Small number of Na+ channels open where Na+ influxes for a short period of time (milliseconds) causing a rapid rising phase/depolarization of the cell until it reaches threshold
* Then the Na+ channels inactivate and close quickly
2) The depolarization and passing of threshold causes the Ca2+ channels to open
* (they don’t inactivate as quickly as Na+)
* Ca2+ enters the cell and causes contraction
3) Hyperpolarization occurs and this is whereK+ channels open where K+ effluxes from the cell
Ion Channels Adopting Different Conformational States (Na+)
1) What is the structure when the channel is resting
2) What is the structure when the channel is activated
3) What is the structure when the channel is inactivated
4) whats similar and different between ion channels of different ions
1) Resting:
* m-shape closes the channel while h remains intracellular
2) Activated
* m-shape removes itself from channel exposing the channel
* Drug can bind the inside of the channel
* Na+ ions can influx into the cell through the channel
3) Inactivated:
* h-shape blocks the Na+ channel/pops into the pore inactivating the channel
4) Similar functional behaviours is also found with K+ and Ca2+ channels
♣ The difference is the voltage range of activation + inactivation
Impulse Formation and Pacemaker Activity:
1) Why are pacemakers inserted into patients
2) What are the 3 different ways of slowing pacemaker activity and restore normal pacemaker activity
1) In attempt to normalize the pacemaker cells activity, a pacemaker is inserted into the patent
♣ However, they can be problematic when they act unpredictably
2)
a) More negative diastolic potential
b) Reduction of diastolic depolarization (rate)
c) More positive threshold potential
Impulse Formation and Pacemaker Activity:
1) Describe the 3 different ways of slowing pacemaker activity
1) More negative diastolic potential
* By opening K+ channels = more hyperpolarized cell
* Changing resting potential so its takes longer to reach the threshold for an AP by Na+ channel opening
2) Reduction of diastolic depolarization (rate)
* By blocking Na+ or Ca2+ channels
* Blocking will slow the rate of rise of depolarization of cardiac tissue delay in AP
* AP peak will be smaller seen as though its delayed
3) More positive threshold potential
* Shift in voltage sensitivity
* More depolarized potential = delay in opening of the channel
o Requires more depolarization to reach threshold of AP
Pathophysiology of Arrhythmia:
1) Define afterdepolarization
2) What are the 2 types of afterdepolarization that cause arrhythmias
1) After depolarization is a wave of depolarization during or after depolarization phase
2) ♣ Early afterdepolarization
* Often occurs at slower heart rate
* Arises from plateau of AP
* Mainly driven by voltage oscillations in the repolarizing phase of the AP
♣ Delayed afterdepolarization
* Occur at fast heart rates
* Arises from resting potential
* Driven by spontaneous Ca2+ release during diastole
Cardiac Conduction:
1) What is normal tissue conduction
2) What is a common disturbance of conduction and why is it caused
3) Describe this disturbance of conduction
1) Tissue behind wave of depolarization is hyperpolarized and cannot be reactivated
- When 2 waves of different AP meet, they distinguish each other and the cells in this region remain hyperpolarized
2) Region of re-entry and it is usually due to a depressed region of heart muscle
o I.E scar tissue due to heart attack, etc.
3) When the AP meet, they do not distinguish each other and instead start going in circles forming a re-entry loop
* Muscle starts to contract
o Can cause ventricular fibrillation if it spreads to other muscle areas of the heart
Pharmacological Intervention of Arrhythmias:
1) What are the 5 groups of antiarrhythmic drugs and an example of each
1)
I. Na+ Channel Blockers
- EX: Quinidine
II. Beta blockers
- EX: Propranolol
III. K+ channel blockers
- EX: Sotalol
IV. L-type Ca2+ channel blockers
- EX: Verapamil
V. Miscellaneous
- EX: Adenosine, K+, Mg2+ ions
