BIO 202: Lecture - Heart

What system/circuit does each side of the heart contain

Right heart: pulmonary circuit
Left heart: systemic circuit

Where is the heart located

Right behind mediastinum

What do heart valves do

Ensure unidirectional flow of blood through the heart (prevent back flow of blood)

Which valve is on the left and right side of the heart

Left: bicuspid/mitral/left atrioventricular valve and aortic semilunar valve
Right: tricuspid/right atrioventricular valve and pulmonary semilunar valve

What are chordae tendineae and papillary muscle

Chordae tendineae: heart strings that are attached to tricuspid valve flap
Papillary muscle: stabilize AV valve cusps during ventricular contraction

How does the atrioventricular (AV) valves function

1. Blood returning to heart fills the atria, pressing against the AV valve. The increased pressure forces the AV valves to open

2. As ventricles fill, AV valve flaps hang limply into ventricles

3. Atria contract, forcing additional blood into ventricles

(atrial valves open; atrial pressure greater than ventricular pressure)

How does the semilunar (SL) valves function

Semilunar valves open: as ventricles contract and interventricular pressure rises, blood is pushed up against semilunar valves, forcing them open
Semilunar valves closed: as ventricles relax and interventricular pressure falls, blood flows back from arteries, filling the cusps of semilunar valves and forcing them to close

What direction do arteries and veins carry blood

Arteries send blood away from heart
Veins bring blood towards heart

Because the heart is a double pump, describe the pathway of the heart regarding oxygen-poor blood

Oxygen-poor blood return from body to heart by superior vena cava/inferior vena cava/Coronary sinus → right atrium → tricuspid valve → right ventricle → pulmonary semilunar valve → pulmonary trunk → lungs

Because the heart is a double pump, describe the pathway of the heart regarding oxygen-rich blood

Oxygen-rich blood returns to heart by 4 pulmonary veins → left atrium → mitral valve → left ventricle → aortic semilunar valve → aorta → oxygen-rich blood is delivered to body tissues (systemic circuit)

How much volume of blood is pumped to pulmonary and systemic circuits with the pathway of blood through heart

Isovolumetric ejection of blood (iso: the same, volume, ejection: of blood): equal volumes of blood are pumped to pulmonary and systemic circuits (with every contractions, it has to be equal)

Describe the circulation in pulmonary circuit and systemic circuit and how does the anatomy of the ventricles reflect these differences

Pulmonary circuit is short, low-pressure circulation
Systemic circuit is long, high-friction circulation
This is shown by the left ventricle walls are 3x thicker than right as it pumps with greater pressure

What in the heart that is part of coronary circulation is sometimes covered in fat

Coronary sinus

Describe the histology of the heart and what it is made up of. What is the heart described as

The heart has cardiac muscle cell, nucleus, and intercalated discs. The intercalated discs have gap junctions that electrically connect myocytes and desmosome that keep myocytes from pulling apart.
The heart will be described as syncytium (meaning cells acting as a single unit)

What is the difference between cardiac and skeletal muscle

Cardiac muscle cells are self-excitable → the heart does not need input from nervous system to contract and it will contract by itself

What are the 2 kinds of cardiac myocytes and describe them

Contractile cells: responsible for contraction
Pacemaker cells: noncontractile cells that spontaneously depolarize (specialized muscle cells)
*Pacemaker cells trigger contractile cells to contract & contractile cells are the ones doing the beating and is most numerous

How does the heart contract compared to skeletal and what does it ensure

Heart contracts as a unit → all cardiomyocytes contract as a unit (functional syncytium) or none contract. This ensures effective pumping action
Skeletal muscles contract independently

What does an influx of Ca2+ from extracellular fluid trigger

- It triggers Ca2+ release from SR:
- Depolarization opens slow Ca2+ channels in sarcolemma, allowing Ca2+ to enter cell
- Extracellular Ca2+ then causes SR to release its intracellular Ca2+
- Skeletal muscles do not use extracellular Ca2+

Can tetanic contractions (a type of cramp) occur in cardiac muscles

No, tetanic contractions cannot occur in cardiac muscles as cardiac muscle fibers have longer absolute refractory period than skeletal muscle fibers → this allows heart to relax and fill as needed to be an efficient pump
(heart muscle cells (cardiac fibers) take longer before they can respond to another stimulus compared to skeletal muscle cells)

What respiration does the heart rely on and why

- The heart relies almost exclusively on aerobic respiration and heart muscles do not fatigue.
- Cardiac muscle has more mitochondria than skeletal muscle so it has a greater dependance on oxygen (it cannot function without oxygen) whereas skeletal muscle can use fermentation when oxygen isn’t present
- Cardiac is more adaptable to other fuels, like lactic acid, but it must have oxygen

How much does the SA node beat and what happens if you cut all the nodes from the heart like the SA node/AV node

SA node: intrinsic rhythm ~100bpm
If you cut all these nodes from the heart, it will still beat at 100 bpm

What is the ion sequence of cardiocytes

1. Pacemaker potential: starts with sodium (Na+) influx:
   pacemaker cells = slow Na+ & contractile cells = fast Na+

2. Depolarization: Ca2+ influx
   pacemaker cells = fast Ca2+ & contractile cells = slow Ca2+

3. Repolarization: K+ efflux (outflow)

Both have the same sequences: sodium → calcium → potassium
Pacemaker cell: slow sodium → fast calcium → potassium efflux (outflow)
Contractile cell: fast sodium → slow calcium → potassium efflux (outflow)

What is the pattern of conduction during 1 heartbeat

1. Sinoatrial (SA) node (pacemaker) generates impulses
   internode pathway

2. Impulses pause (0.1 s) at the atrioventricular (AV) node

3. Atrioventricular (AV) bundle connects atria to the ventricles

4. Bundle branches conduct impulses through interventricular septum

5. Subendocardial conducting network (aka purkinje fibers) depolarizes contractile cells of both ventricles

What does ANS autonomic fibers change

Heart rate and force of contraction

Describe the sympathetics and parasympathetics in regards to heart rate and conduction force

Sympathetic: increases heart rate and increases conduction force
Parasympathetic: decrease heart rate and lowers conduction force
At rest, heart rate is 75 bpm

What do cardiac muscle fibers make up and responsible for

Make up bulk of heart and are responsible for pumping action → different from skeletal muscle contraction because cardiac muscle action potentials have plateau (prolongs depolarization/contraction period)

What are the steps involved in an action potential for contractile cells

1. Depolarization (from pacemaker cells) opens fast voltage-gated Na+ channels; Na enters cell (from -90mV to +30mV)

2. Depolarization by Na+ also opens slow Ca2+ channels (at 30+mV, Na channels close but slow Ca channels remain open → prolonging depolarization called plateau phase)

3. After ~200ms, slow Ca2+ channels are closed, and voltage-gated K+ channels are open (rapid efflux of K+ repolarizes cell to resting membrane potential & Ca2+ is pumped both back into SR and out of cell into extracellular space)

What are 3 major features on an ECG/EKG → electrocardiogram

P wave: atrial depolarization (depolarization → contraction)
QRS complex: ventricular depolarization (depolarization → contraction)
T wave: ventricular repolarization (repolarization → relaxation)

What is a normal sinus rhythm

Can see P, QRS Complex, and T wave
Rhythmic, evenly spaced out in time

What is junctional rhythm (abnormal)

Sa node is nonfunctional, which results in P waves being absent and AV node paces the heart at 40-60 beats per minute
(This is a good rhythm for a pacemaker as heart is still working, just not well)

What is second-degree heart block

AV node fails to conduct some SA node impulses, as a result there are more P waves than QRS complex.
(this means there is some sort of disruption in conduction system of heart - arrhythmia)

What is ventricular fibrillation

Electrical activity is disorganized. Action potentials occur randomly throughout ventricles.
Results in chaotic, grossly abnormal ECG deflections
See in acute heart attach and after an electric shock
(Nothing is recognizable, if not corrected the person will die, some people are just prone to this)

What is systole and diastole and what number goes at the top/bottom

Systole: period of heart contraction
Diastole: period of heart relaxation
In BP: systolic BP/diastolic BP (normal rate is 120/80)

What is the cardiac cycle (what is atrial systole/diastole followed by and what does the cycle represent)

Blood flow through heart during one complete heartbeat.
Atrial systole and diastole are followed by ventricular systole and diastole
Cycle represent series of pressure and blood volume changes
Mechanical events follow electrical events seen on ECG

What sound does AV valves and semilunar valves closing cause

AV valves closing cause a softer sound
Semilunar valves closing cause a sharper sound

What are the 3 phases of the cardiac cycle

EDV: end diastolic volume
SV: stoke volume
ESV: end systolic volume

What is EDV, ESV, and SV and what do they do

End diastolic volume: max ventricular volume because they are relaxed
End systolic volume: min ventricular volume when contracted
Stroke volume: how much blood gets ejected from ventricles
*This is opposite of blood pressure (in BP, diastolic is min and systolic is max)

How do you calculate stroke volume

SV = EDV (end diastolic volume/max) - ESV (end systolic volume/min)
Normal SV = 120 ml - 50 ml = 70 ml/beat
EDV is affected by length of ventricular diastole and venous pressure (~120)
ESV is affected by arterial BP and force of ventricular contraction (~50)
*Stoke volume should always be positive

Where are each of the valves heart

Aortic valve: sound heard in 2nd intercostal space at right sternal margin
Pulmonary valve: sound heart in 2nd intercostal space at left sternal margin
Mitral valve: sound heart over heart apex in 5th intercostal space in line with middle clavicle
Tricuspid valve: sound typically heart in right sternal margin of 5 intercostal space

What is cardiac output and how do you calculate it

Volume of blood pumped by each ventricle in 1 minute.
CO = heart rate (HR) x stroke volume (SV)
HR=number of beats per minute, SV=volume of blood pumped out by 1 ventricle with each beat
Normal CO = 5.25 L/min (at rest) → CO = 75bpm (HR) x 70mL/beat (SV)

What is cardiac reserve and how does CO changes

Difference between resting and maximum cardiac output
(basically what can the body do above+beyond what it normally does it you really push it)
CO changes (increase/decrease) if either or both SV and HR is changed

CO is affected by factors leading to?

Regulation of stroke volume & regulation of heart rates

What are 3 main factors that affect SV

Preload: amount of blood in ventricles before contracting/proportional to EDV
Contractility: force of heart contraction
Afterload: proportional to ESV

What is preload

- Most important factor in preload stretching of cardiac muscle is venous return (the amount of blood returning to heart)
- Increased venous return distends (stretches) ventricles and increases contraction force!!
- Heart respond to increased venous return by ejecting more blood
- Slow heart beat and exercise increase venous return
- If venous return increases → EDV increases → SV increases → CO increases
(preload basically the amount of tension in ventricular cardiac muscle cells prior to contracting)

What is frank-starling law of heart in preload

The harder we make the heart work, the more efficiency it is
(the greater the tension on the cells, the more forcefully they contract)

What is contractility

Contractile strength at given muscle length that is independent of muscle stretch and EDV
Increased contractility lowers ESV: caused by sympathetic epinephrine release stimulates increased Ca2+ influx, leading to more cross bridge formations & positive inotropic agents (medicine that increase force of cardiac contraction, improving heart’s ability to pump blood) increase contractility
Decreased by negative inotropic agents (weakens heart contraction)

What is afterload

Back pressure exerted by arterial blood (how much blood is left over). It is proportional to ESV.
Afterload is pressure that ventricles must overcome to eject blood: back pressure from arterial blood pushing on SL valves is major pressure (aortic pressure is 80mmHg and pulmonary pressure is 10mmHg)
*We want to decrease afterload because when it increases, it is called congestive heart failure.)

What increases afterload and what does that effect

Hypertension increases afterload, resulting in increased ESV and reduced SV, which is the start of congestive heart failure

What chemicals regulate heart rate and what happens to sympathetic/parasympathetic system

Chemical regulation of heart rate: hormones and ions
Heart rate increase cause sympathetics to increase and parasympathetic to decrease

How does hormones chemically regulate heart rate

Epinephrine from adrenal medulla increases heart rate and contractility
Thyroxine increases heart rate; enhances effects of norepinephrine and epinephrine

How does ions chemically regulate heart rate

Intra- and extracellular ion concentrations (like Ca and K) must be maintained for normal heart function. Imbalances are very dangerous to heart, especially potassium

What are other factors that influence heart rate

Age (fetus has fastest HR), gender (which both fall into body size) (females have faster HR than males), exercise (trained athletes have slow HR), body temperature (HR increase with body temp)

What is congestive heart failure (CHF)

Heart is inefficient. Progressive condition; CO is so low that blood circulation is inadequate to meet tissue needs
Reflects weakened myocardium caused by: coronary atherosclerosis → clogged arteries cause by fat buildup; impairs oxygen delivery to cardiac cells
Heart becomes hypoxic, contracts inefficiently

What are factors that contribute to congestive heart failure (CHF)

Persistent high blood pressure (aoritc pressure > 90)
Multiple myocardial infarcts (heart weaken as contractile cell become scar tiss)
Dilated cardiomyopathy (DCM) (ventricles stretch and become flabby, myocardium deteriorates)

How does congestive heart failure affect each side of the heart
(NEED TO KNOW FOR EXAM)

Left-side failure results in pulmonary congestion: blood backs up in lungs
Right-side failure results in peripheral congestion: blood pools in body organs, causing edema (swelling caused by fluid)
*Failure of either side weakens the other side: it leads to decompensated, seriously weakened heart.
Treatment: removal of fluid, drugs to reduce afterload (pressure heart must exert to pump blood out of ventricles) and increase contractility