Vol.3-Ch.2 "Cardiology" (Part 1 - Mostly Overview Review) Flashcards
Quick heart anatomy review
TISSUE LAYERS:
- Endocardium (inner most/bathed in blood)
- Myocardium (middle, has conduction cells)
- Pericardium (outermost, visceral & parietal; visceral aka epicardium contacts muscle, parietal is tough fibrous outer coating; has pericardial fluid in pericardial cavity that separates the two)
VALVES:
- Atrioventricular (tricuspid - atria/vena cava ; bicuspid or mitral - pulm vein/L atria)
- Semilunar (pulmonary/aorta)
3 BRANCHES OFF AORTA:
- Ascending aorta
- Thoracic aorta
- Abdominal aorta
CORONARY ARTERIES:
- originate in the aorta just above the leaflets of the aortic valve, receive blood during diastole, drain back to sup vena cava by the anterior great cardiac vein and marginal veins that dump into the coronary sinus
- Left Coronary Artery has two branches Anterior Descending artery and Circumflex artery
- Right Coronary Artery has two branches Posterior Descending Artery and Marginal Artery
COLLATERAL CIRCULATION:
- it is a protective mechanism that provides alternative path for blood flow in case of a blockage. ANASTOMOSES are communications between two or more vessels
LAYER OF VESSELS:
- Tunica Intima (inner most, single cell layer thick)
- Tunica Media (middle, elastic fibers and muscle)
- Tunica Adventitia (outer most, fibrous tissue covering)
What is ejection fraction?
What are the 3 factors that affect stroke volume?
It is the % or fraction of blood ejected out of the ventricles during systole. This is typically 2/3 and between 60-100mL (stroke volume)
Stroke Volume depends on:
- preload
- cardiac contractility
- afterload
What is Starling’s Law of the Heart?
It states that the more the myocardial muscle stretches during preload the harder it will contract.
Therefore, the more preload that can be obtained, the greater the stroke volume and therefore the higher the cardiac output
Nervous System of the Heart Review
The heart is controlled by Sympathetic and Parasympathetic components of the Autonomic Nervous System
SYMPATHETIC NERVOUS SYSTEM:
- Innervates the heart through the Cardiac Plexus, a network of nerves at the base of the heart that originates from the thoracic and lumber spine.
- Its main neurotransmitter is Norepinephrine, its release causes increased heart rate and cardiac contractibility
- It acts on the two main type of receptors Alpha and Beta.
- Alpha receptors located in the peripheral blood vessels are responsible for vasoconstriction
- Beta 1 receptors located in the heart, increase heart rate and contractility.
- Beta 2 receptors located in the lungs and peripheral blood vessels cause bronchodilation and peripheral vasodilation
PARASYMPATHETIC NERVOUS SYSTEM:
- Innervates the heart via the Vagus nerve that originates in the brain (10th cranial nerve)
- Its main neurotransmitter is Acetylcholine, its release slows the heart rate and atrioventricular conduction
Chronotropy VS Inotropy VS Dromotropy
Chronotropy refers to heart rate ; a positive chronotropy agent increases the heart
Inotropy refers to the strength of cardiac muscle contraction ; a positive inotropic agent strengthens contractility
Dromotropy refers to the rate of nervous impulse conduction; a positive Dromotropy agent speeds impulse conduction
The heart can also function as an endocrine organ, it can secrete _____ causing _____ in response to hemodynamic stress.
What are the 3 types secreted?
The heart can also function as an endocrine organ, it can secrete NATRIURETIC PEPTIDES causing DIURESIS (loss of water), NATRIURESIS (loss of sodium), and VASODILATION in response to hemodynamic stress.
ATRIAL NATRIURETIC PEPTIDE (ANP):
It is made, stored, and secreted in the atrial muscle. It responds to atrial distention and sympathetic stimulation. It counters the renin-angiotensin-aldosterone system and causes a reduction in blood volume resulting in decreased central venous pressure, cardiac output, and blood pressure.
BRAIN NATRIURETIC PEPTIDE (BNP):
Initially discovered in the brain, it actually secretes in the ventricles in response to excessive stretching of the myocytes. It also counters the renin-angiotensin-aldosterone system and causes a reduction in blood volume resulting in decreased central venous pressure, cardiac output, and blood pressure. However, its HALF LIFE IS 2X AS LONG AS ANP
C-TYPE NATRIURETIC PEPTIDE:
Secreted from endothelium of blood vessels and appears to have vasodilatory effect
**(BNP levels elevate in CHF and mark the presence of CHF and can also be administered as a treatment for it)
Overview of electrolytes and their function in the heart
Major Electrolytes include Sodium (Na+), Potassium (K+), Calcium (Ca+), Chloride (Cl-), and Magnesium (Mg++)
Sodium plays major role in depolarization
Potassium plays major role in repolarization
- Hyperkalemia decreases automacity and conduction
- Hypokalemia increases irritability
Calcium plays major role in depolarization and contraction
- Hypercalcemia results in increased contractility
- Hypocalcemia decreases contractility and increased electrical irritability
Electrophysiology Review
The heart has 3 types of cardiac muscle:
- Atrial
- Ventricle
- Specialized excitatory and conductive fibers
The atria and ventricle muscles are similar to skeletal muscle except they have intercalated disks that speed up cell to cell impulses up to 400x faster
Syncytium - is the ability of the heart muscles to spread an impulse rapidly across an entire group of cells to allow for a type of “flow” contraction
- The atrial syncytium depolarizes superior to inferior
- The ventricle syncytium depolarizes inferior to superior
At Resting Potential (-70mV) in a myocardial cell there are 3 sodium ions outside and 2 potassium ions inside the cell, leaving the cell interior negatively charged. When the impulse hits the cells and the cell wall changes to allow sodium in, the entered sodium changes the polarity to +30mV inside the cell, this event is called the Action Potential. Calcium channels also open at that point, and as Calcium goes through it raises the mV even higher.
The 4 special properties of cardiac conduction cells are:
- Excitability: Cells can respond to an electrical stimulus, like all other myocardial cells
- Conductivity: The cells can propagate the electrical impulse from one cell to another
- Automacity: The ability of the individual cells to depolarize without an outside electrical stimulus, aka Self-Excitation.
- Contractility: The ability to cause contraction
On a cardiac action potential graph the parts are:
0 = Depolarization (where it goes straight up)
1 = Repolarization
2 = Plateau
3 = Repolarization
4 = Resting Potential
How is an ECG tracing affected by;
- Ischemia?
- Injury?
- Necrosis?
- Ischemia causes ST segment depression or an inverted T wave
- Injury causes ST segment elevation, often in early MIs
- Necrosis/severe damage causes pathological Q waves which are those that are 0.4seconds or more long OR are at least 1/3 of the height of the QRS complex
MAKE SURE YOU CAN STILL DRAW OUT LEADS AND WHAT VIEW THEY ARE W/ WHAT ARTERY SUPPLIES
MAKE SURE YOU CAN STILL DRAW OUT LEADS AND WHAT VIEW THEY ARE W/ WHAT ARTERY SUPPLIES
Sinus Arrest vs Sinus Pause
They both involve a completely normal ecg findings other than the fact there there are one or more missed complexes.
Sinus Arrest is when there are MORE than 1 beat missing
Sinus Pause is when there is ONLY one beat missing
*unless symptomatic, there is no treatment required. If there are signs and symptoms of poor perfusion then prepare Atropine dosages (book says 0.5mg per 3-5min but new 2020 AHA says 1mg per 3-5min) and after the max 3mg has been given, prepare for TCP if refractory
What is Sick Sinus Syndrome?
Sick Sinus Syndrome is when the Sinus node is diseased or ischemic and will cause a wild swing in heart rate on an ECG from a severe bradycardia to a severe tachycardia and back.
What is Paroxysmal Supraventricular Tachycardia?
Paroxysmal means that it “starts and stops”
It is referencing when an irritable atrial foci takes over pacemaking for minutes to hours then dissipates
Fixed rate pace makers VS demand pace makers VS Dual Chambered pacemaker/AV sequential pace makes.
What are some problems with pacemakers?
When might you use a magnet on a PM and why?
Fixed rate PMs continuously fire at a preset rate
Demand PMs have a sensor that detects when the heart rate drops below a set rate and then starts firing
Most pace makers are placed in the right atria alone but there are Dual Chambered PMs aka AV Sequential PMs that go in the right atria and ventricle that fire the atria first and then the ventricles
Pace maker batteries can fail, or as they get low it can “run away” where it starts discharging faster, for demand PMs they can sometimes not shut off when the natural heart rate goes back above preset rate and then it competes with natural rate for pacemaking function, sometime landing on a relative refractory period and precipitating VFib
When you have a runaway PM you can use a magnet to “reset” its functions, usually to a preset 70bpm, b/c the magnet interferes with sensors and forces it to rest
What are the 3 general categories of conduction disorders that cause an arrhythmia?
- AV blocks
- Disturbances in Vent conduction (bundle branch blocks)
- Preexcitation syndromes
A Preexcitation syndrome is when the ventricles are prematurely stimulated b/c the impulse was able to bypass the AV node. Typically it is done by accesses the BUNDLE OF KENT, an extra conduction pathway b/w the atria and ventricles that bypasses the AV node. This is what occurs in WOLF-PARKINSON-WHITE syndrome. It is characterized by a SHORT PRI, b/c it is not delayed by the AV node, a WIDE QRS, and a DELTA WAVE which is a slur often seen on the upstroke of the R wave.
