Cardiac Physiology: Heart Anatomy and Function

• Cardiac physiology focuses on the heart

Objectives

• To explain the basic anatomy of the heart and how it influences cardiac function
• To explain the pathway a wave of depolarization follows as it moves from the SA node through the heart to bring about a synchronized cardiac contraction
• To explain the role of the AV node in the propagation of the electrical signal
• To discuss the functional significance of the refractory period of the heart
• To describe the events of the cardiac cycle in terms of volume and pressure changes and electrical signaling
• To define cardiac output (Q) and identify the 3 determinants of Q
• To explain how each of these determinants help to determine cardiac output
• To distinguish EF from SV

Cardiopulmonary System

• It's important to understand the fundamental function of the cardiopulmonary and vascular system, their interactions and the signs and symptoms of disfunction

Gross Structure of the Heart

• The heart has four chambers
• The right and left sides of the heart are separated by a continuous septum (atrial and ventricular septa)
• Chambers on the right (N=2) and left sides (N=2) are connected via one-way valves (atrioventricular valves)
• There are 2 parallel but separate pumps
  • These pumps work in parallel
• There are 2 parallel but separate paths of blood flow
  • These paths go different places

Heart Valves

• Heart valves ensure one way flow of blood and prevent backward or retrograde flow of blood
• Tricuspid valve is the right atrioventricular valve
• Mitral valve is the left atrioventricular valve
• Pulmonic semilunar valve-RV into pulmonary artery
• Aortic Valve – LV into the aorta

Layers of the Heart

• Epicardium is the same as the visceral pericardium
• Myocardium is the middle layer, and the thickest region of the heart
  • It contains the myocytes
• Endocardium is a thin layer of connective tissue that covers the valves and is continuous with the endothelium layer of the vessels

Cardiac Muscle Cells

• Cardiac muscle cells are arranged in layers
• Cardiac muscle cells lack different fiber types and fibers are all slow-oxidative
• It is innervated like smooth muscle
  • This involves the sympathetic and parasympathetic
• It has an absolute refractory period
• It is highly aerobic that requires a continuous O₂ supply
• Myocytes on both sides contract simultaneously but do so in a graded fashion
  • Strength of muscle contraction is driven by intracellular Ca2+ concentrations
  • Calcium regulation of contra, Ca2+ induced Ca2+ release

Gap Junctions

• Gap Junctions/intercalated disks
  • Mediate the cell-to-cell movement of ions and small metabolites
  • Play an important role in impulse conduction
  • Action potential can spread and structures contract as a whole (atria, ventricles, etc.)
• Intrinsic heart rate(SA Node) (Pacemaker, fires 60-100 bpm)
• Purkinje fibers are modified cardiac muscle cells
  • Their function is to facilitate the conduction of an AP through the myocardium myocyte

Cardiac Function

• Cardiac Cycle notes
• Blood moves when a pressure gradient exists
  • Blood will move from an area of high pressure to an area of lower pressure
• Pressure gradients lead to the movement of blood from one chamber to the next, changing the volume and pressure in both chambers.
• Cardiac valves control blood flow in the context of these pressure gradients
• Chamber contraction(muscle cell contraction) increases pressure in that chamber and expels a bolus of blood
  • This is when Work is being done in this process when energy is being expended
• Chamber relaxation leads to a decrease in chamber pressure, ventricular relaxation and a refilling of the ventricles
• The heart undergoes a repeating pattern of contractions (systole) and relaxations (diastole) of the chambers
• The heart is constantly challenged to match blood delivery(O₂ delivery) with a tissue's need for oxygen/blood(cardiac regulation and coordination)

Atrial Diastole

• Atria are relaxed
• Atrial pressure < vena cava pressure
• Blood is moving into the atria and on into the ventricles
• Venous Return
  • The flow of blood back to the heart
  • Under steady-state conditions, venous return must equal cardiac output (CO) when averaged over time
• If not blood would accumulate in either the systemic or pulmonary circulations

Atrial Systole

• Atria contract
• Atria are filled passively
• Atrial contraction moves blood through AV valves and into ventricles;
  • This action “tops off the tank” in the ventricles
• P Wave- initiates atrial contraction
• Atria are not depleted of blood

Ventricular Diastole

• The period during which the two ventricles are relaxing from the contortions/wringing of contraction, then dilating and filling
• Atria are also relaxing and filling with blood
• Blood is flowing from the atria into the ventricles
  • The AV valves are open
• Ventricular volume is increasing

Ventricular Systole(Ventricular Contraction)

• QRS complex/ Ventricles begin to contract
  • The pressure in the ventricles rise, and AV valves close
• Isovolumetric contraction:
  • Pressure is developing in each of the ventricles but no blood is flowing
• Blood begins to flow out of the ventricles (ejection) when chamber pressure > vessel (aorta or pulmonary artery) pressure.
• As ejection occurs with ventricular volume and pressure decrease
• Ejection continues until ventricular pressure vessel pressure
• Ventricular pressure continues to fall/declines after the aortic valve closes and the myocardium relaxes
• Coordination of chamber contraction in the context of parallel pumps
• Volume of blood ejected by LV = volume of blood ejected by RV
• Assessing volume of blood ejected by LV/RV which is the stroke volume
  • Stroke Volume is the Volume of blood ejected from a ventricle during ventricular contraction

Important Factors Affecting Stroke Volume

• Preload: Venous return (more volume thing)
• Afterload: Systemic blood pressure (more pressure thing)
• Contractility
• Other ventricular volumes to note
• EDV= End diastolic volume
• ESV = End systolic volume (after contraction/ejection)
• SV = EDV – ESV

Pulmonary Circulation Pressure

• Pressure changes in the right ventricle and pulmonary arteries are qualitatively similar to those described for the LV
• But it's quantitatively smaller
• Pulmonary arterial systolic and diastolic pressures are 25 (vs. 120) and 10 ( vs. 80) mmHg respectively
• The pulmonary circulation is a low-pressure system

Electrical Activity - Electrocardiogram

• PR Interval
  • Delay of AV node to allow filling of ventricles
• QRS Complex
  • Depolarization of ventricles, triggers main pumping contractions.
• ST Segment is the beginning of ventricle repolarization
  • This should be flat
• T Wave is the Ventricular repolarization
• P-Wave
  • Depolarization of atria in response to SA node triggering.

Refractory periods

• The absolute refractory period is a period where it is completely impossible for another action potential to occur:
  • regardless of the size of the trigger stimulus, this is because the sodium channels are inactivated until hyperpolarization is completed

Sinoatrial Node (SA Node)

• The SA Node is responsible for the initiation of the heartbeat
  • Including automaticity
• Heart cells beats on its own
• SA node cells spontaneously depolarize [PacemakerPotential]
• Fires 60-100 times per minute
• This wave of depolarization courses over the atria and can only move into the ventricles only at the AV (atrioventricular) node
• SA function can be regulated by the autonomic NS
  • Stimulation of the parasympathetic vagus N. decreases the discharge rate of the SA node
  • Stimulation of the sympathetic nerves to the SA node increases the discharge rate of the SA node

Regulation of Heart Rate

• Actual HR is created by the summed effects of the antagonistic/opposing influences of the sympathetic and parasympathetic influences
• Positive chronotropic effect increases HR (Sympathetic NS)
• Negative chronotropic effect decreases HR (Parasympathetic)

Sympathetic Innervation

• Increases HR Also increases the strength of contraction
• The net effect is an increase in cardiac output (CO)
• Inhibition of sympathetic nerves or reduced sympathetic outflow → ↓ HR and contractility
• Parasympathetic Innervation
  • Also referred to as vagal stimulation
• Vagal fibers are distributed mainly to SA and AV nodes Actions:
  • Slows heart rate, decreases the strength of contraction and decreases CO
  • Vagal stimulation regulates HR more than contractility

Cardiac Output

• Cardiac output (CO or Q) is the volume of blood pumped per minute by each ventricle
• Cardiac output = stroke volume X heart rate (ml/minute) = (ml/beat) (beats/min)
• Stroke volume (SV) is the blood ejected by a ventricle with each heartbeat

Factors Determining Stroke Volume (SV)

• Extrinsic control of SV is regulated by three variables

  • Preload is known as the end diastolic volume (EDV)
  • Afterload is also known as Total Peripheral Resistance
  • Contractility (strength of ventricular contraction)

• The Frank-Starling Law describes the intrinsic ability of the heart to adapt to changes in the volume of inflowing blood (venous return or preload)

  • It must automatically accommodate to the blood that comes into it

• Increased venous return → increased amount of blood returned to the right atrium → increases amount of blood moved from the RA to the RV → ↑RVEDV → increases the strength of cardiac contraction → ↑ SV (blood headed to the lungs)

• Increased EDV stretches the myocardium, which increases the stretch on the heart muscle (length-tension) and increases the sensitivity of cardiac myocytes to Ca2+

• The net effect is an increase in the strength of contraction and ejection of blood, where is an optimal EDV

• Both ventricles are similarly stretched, so the SV is similar for both ventricles

• Frank-Starling mechanism allows for a rapid adjustment for a rise in peripheral resistance i.e. afterload!

  • Increased peripheral resistance will temporally decrease stroke volume causing a backup of blood in the ventricles as a result

• Increase venous return and control it

• Includes R atrium EDV, total blood volume, Venous blood pressure (driving force for blood return) and Muscle pump

• Other important factors are respiration, gravity/posture and Right atrial pressure/increased thoracic pressure Valsalva maneuver

Afterload

• Increased afterload i.e. arterial pressure tends to reduce stroke volume also
  • Arterial pressure constitutes a “load” that contracting ventricular muscle must work against when it is ejecting blood
• Total peripheral resistance is the resistance offered by the systemic circulation
• Examples that contribute to afterload are hypertension and high blood pressure

Contractility

• This is the extrinsic control regulated by three variables

  • Preload (EDV), Afterload (Total Peripheral Resistance) , and Contractility

• Contractility is a measure of cardiac pump function and the degree to which muscle fibers can shorten and generate force It's the intrinsic ability of the heart to contractCardiac performance independent of preload and afterload

• It reflects the force or strength of cardiac contraction and ejection fraction

  • Under resting conditions EF normally averages between 50% and 75%.
  • Increased contractility increases EF and Decreased contractility decreases EF
  • EF reflects basic muscle mechanics- the rate and amount of cross bridge cycling
  • Increased sympathetic stimulation results in a reduced ESV (more blood ejected)
  • Decreased such as Parasympathetic stimulation, Hypoxia or Hyperkalemia result in an increased ESV (less blood ejected)

Key points

• 4 Chambers forming 2 parallel and separate pumps
• Heart valves help to ensure unidirectional blood flow and prevents retrograde blood flow
• Understanding the Characteristics of cardiac muscle cells and coronary arteries
• Cardiac Cycle/Wiggers Diagram
• Difference between SV and EF, the Characteristics of pulmonary circulation
• Electrical characteristics of the heart
• ANS regulation of cardiac function (HR & Contractility)
• Cardiac output and its regulation (Frank Starling Law,Venous Return/preload, Afterload and Contractility) Signs and Symptoms of Cardiovascular diseases
  • Shortness of breath with activity or when lying down
  • Chest pain, chest tightness, chest pressure and chest discomfort (angina)
  • Fatigue and weakness
  • Swelling in the legs, ankles and feet
    • Exercise intolerance
  • Dizziness or fainitng