Cardiovascular System and Heart Anatomy

Cardiovascular System

• The cardiovascular system's main components are the heart and blood vessels
• The circulatory system delivers blood to organs and tissues.

Functional Anatomy Of The Heart

• The heart is a hollow muscular organ enclosed in the pericardium
• The pericardium protects the heart and facilitates contraction with minimal friction
• The heart's wall consists of cardiac muscle, divided into right and left halves
• Each half is comprised of one atrium and one ventricle

Heart Valves

• The right atrium is separated from the right ventricle by the tricuspid valve
• The left atrium is separated from the left ventricle by the bicuspid, or mitral, valve
• The atrioventricular valves, also known as A-V valves, include both the tricuspid and bicuspid valves
• Papillary muscles in the ventricles connect to the A-V valves via chordae tendineae
• These muscles and tendons prevent the valves from everting into the atria during ventricular contraction
• The aorta originates from the left ventricle, and its opening is guarded by the aortic valve
• The pulmonary artery originates from the right ventricle, and its opening is guarded by the pulmonary valve
• The heart valves help to ensure that blood flows in only one direction

Functional Histology of Cardiac Muscle

• The heart is a functional syncytium
• Gap junctions provide paths of low resistance between cells
• Intercalated discs offer a degree of mechanical cohesion between cells

Cardiac Muscle Properties

• Cardiac muscle is automatic, rhythmic (autorhythmic), excitable, conductive, and contractile

Autorhythmicity

• Autorhythmicity refers to the heart's capacity to independently produce electrical impulses and beat regularly
• The SA node serves as the heart’s electrical generator and emits impulses at a rate of 60-90 per minute
• The AV node acts as backup pacemaker
• If the AV node fails, Purkinje fibers become the tertiary pacemaker
• Autorhythmic cells are characterized by a low resting membrane potential (RMP)
• Autorhythmic cells have less permeability to K⁺ and more permeability to Na⁺ and Ca⁺⁺

Fast vs Slow Response Fibers

• Fast response fibers are more negative at resting membrane potential (phase 4)
• The upstrokes (phase 0) are steeper in fast response fibers
• Overshoots and action potential amplitudes are greater in fast response fibers
• Fast response fibers use Fast Na channels
• Slow response fibers use Slow Ca channels
• RRP ends at phase 4 in fast response fibers
• RRP extends into phase 4 in slow response fibers
• Fast response fibers show fast conduction velocity
• Slow response fibers show slow conduction velocity

Factors Affecting Autorhythmicity

• Positive chronotropic factors include sympathetic stimulation, fever, mild alkalosis, and mild hypoxia
• Negative chronotropic factors include parasympathetic stimulation, hypothermia, mild acidosis, and severe hypoxia

Excitability

• Excitability is the capacity of a cardiac impulse to trigger an action potential given adequate stimulation
• Cardiac muscle excitability is nil during the absolute refractory period
• During the relative refractory period, cardiac muscle excitability increases but remains below-normal
• Cardiac muscle cannot be tetanized because it has a longer refractory period

Conductivity

• Conductivity is cardiac muscle's capacity to transmit an action potential from one cell to the next

Contractility

• Contractility refers to the ability of cardiac muscle to transform chemical energy into mechanical energy, resulting in tension, work, and pressure
• Contraction starts with an increase in intracellular Ca⁺⁺ from extracellular fluid (ECF) and the sarcoplasmic reticulum (SR)
• Positive inotropic factors include sympathetic stimulation, catecholamines, and elevated Ca⁺⁺ in ECF
• Negative inotropic factors include parasympathetic stimulation, ether anesthetic, bacterial toxins/ischemia and elevated K⁺ in ECF

Determinants of the Force of Contraction

• Preload: Increased preload causes more shortening of cardiac muscle
• Contractility
• Afterload: Increased afterload results in less shortening of cardiac muscle

Cardiac Cycle

• The cardiac cycle is a sequence of mechanical events inside the heart during one heartbeat
• It lasts 0.8 seconds and consists of systole and diastole
• The number of cardiac cycles per minute is the heart rate

Cardiac cycle phases

• Atrial Systole: Atria contract, ventricles relax, A-V valves are open, and semilunar valves are closed
• Isovolumetric Contraction: Atria relax, ventricles contract, and both A-V and semilunar valves are closed
• Rapid Ejection Phase: Atria relax, ventricles contract, A-V valves close, and semilunar valves open
• Slow Ejection Phase: Atria relax, ventricles contract, A-V valves close, and semilunar valves open
• Isovolumetric Relaxation: Atria relax, ventricles relax, and both A-V and semilunar valves are closed
• Early Ventricular Diastole: Atria and ventricles are relaxed, A-V valves are open, and semilunar valves are closed
• Mid Ventricular Diastole: Atria and ventricles are relaxed, A-V valves are open, and semilunar valves are closed
• Atrial Systole: Atria contract, ventricles relax, A-V valves are open, and semilunar valves are closed

Cardiac Output

• Cardiac output is the volume of blood pumped by either the right or left ventricle per minute
• A normal rate is an average of 5.5 L/minute under basal or resting conditions
• The heart is considered functionally normal as long as the measured cardiac output satisfies the body's requirements
• Cardiac index (CI) is cardiac output divided by body surface area, typically averaging 3.2 L/min./m²
• Body surface area serves as an important determinant of metabolic rate

Determinants of Cardiac Output

• Cardiac output (CO) is determined by stroke volume (SV) x heart rate (HR)
• Alterations in cardiac output are brought about by alterations in either the stroke volume or the Heart rate
• Stroke Volume (SV) averages 80 ml and is affected by preload, contractility, and afterload

Stroke Volume

• Stroke volume (SV) averages 80 ml and is affected by:
• Preload: Increased preload results in an increased Stroke Volume
• Contractility: Increased contractility results in an increased Stroke Volume
• Afterload: Increased afterload results in a decreased Stroke Volume

Factors That affect Cardiac Output

• Nervous factors: Sympathetic stimulation increases CO
• Parasympathetic stimulation reduces CO
• Hormonal factors: Catecholamines and glucagon increase CO
• Drugs: Beta-agonists (caffeine & theophylline, glucagon, digitalis) increase CO
• Beta-blockers and barbiturates decrease CO
• Ions: Increased calcium levels in blood prolong and increase cardiac contractility, predisposing the heart to stop in systole
• Increased potassium levels decrease cardiac contractility, predisposing the heart to stop in diastole
• Body temperature: Moderate increases in body temperature increase cardiac contractility and cardiac output (e.g., during muscular exercise)
• Marked increases in body temperature decrease cardiac contractility and cardiac output (e.g., fevers)
• Blood gases: Hypoxia, hypercapnea, and acidosis depress cardiac contractility

Blood Vessels

• Elastic arteries (Windkessel vessels) and the aorta are examples of elastic arteries
• Muscular arteries such as big arteries (Conduit vessels)
• Arterioles, also known as Resistance vessels
• Capillaries, also known as Exchange vessels
• Veins, also known as Capacitance vessels

Arterial Blood Pressure

• Arterial blood pressure should be defined, and its functions mentioned
• Determinants of arterial blood pressure should be recognized
• Regulation of arterial blood pressure should be discussed

Arterial Blood Pressure Functions

• Arterial blood pressure is the force that pushes blood, and therefore ensures proper tissue perfusion
• Arterial blood pressure allows for capillary filtration
• Mean arterial blood pressure = Diastolic pressure + 1/3 pulse pressure (90-95 mmHg)
• Pulse pressure = Systolic pressure - diastolic pressure (30-50 mmHg)
• Physiological variations in arterial blood pressure include age, sex, diurnal variations, sleep, emotions, exercise, and gravity
• Arterial blood pressure (ABP) is the product of cardiac output (CO) and peripheral resistance (PR)

Hypertension

• Hypertension manifests with blood pressure greater than 140/90 in young adults, greater than 150/100 up to age 50, and over 160/100 in adults older than 50
• Primary hypertension: In 90% of cases, there is no explicit cause
• Primary hypertension is characterized by narrow arterioles due to hyperactivity of the vascular system to constrictor stimuli
• Secondary hypertension constitutes 10% of cases, and is due to an underlying cause
• Causes of secondary hypertension include renal failure, atherosclerosis, and endocrine disorders
• Predisposing factors to hypertension include smoking, obesity, and excess salt intake

Venous Return

• Venous return describes veins as a passage for blood to reach the heart and is essential for proper circulation
• Venous return needs to be defined
• Vein functions include:
  • Draining capillary blood to the heart
  • Blood returned to the heart by veins determines cardiac output (CO)
• Veins facilitate cardiac output by draining capillary blood back

Venous Return Volume

• The volume of blood that enters the right ventricle per minute
• Venous return is equivalent to cardiac output

Arteries vs veins

• Arteries have small diameters
• Veins have large diameters
• Arteries have thin walls
• Veins have thick walls
• Arteries have thick smooth muscle layers
• Veins have thin smooth muscle layers
• Arteries have many elastic fibers
• Veins have few elastic fibers
• Arteries have circular shapes
• Veins have variable shapes
• Arteries have conduit functions
• Veins have reservoir functions

Venous Pressure

• Understanding vein function requires knowledge of the pressures in veins and affecting them
• All systemic veins empty into the right atrium; the central venous pressure (CVP) in the right atrium measures about 0 mmHg
• Peripheral venous pressure (PVP) indicates the pressure in veins nearest the tissues and varies depending on body part, but it is greater than zero
• Venous flow is always towards the heart
• Valves support the unidirectional flow of blood
• The force for venous flow is a pressure gradient between peripheral venous pressure (PVP) and central venous pressure (CVP).

Factors Affecting Venous Return

• Thoracic pump: Inspiration lowers intrathoracic pressure which reduces pressure in the big veins, decreasing CVP (central venous pressure), and increasing venous return
• Deep inspiration increases venous return
• Venous return diminishes during expiration
• Cardiac suction: Occurs during rapid ejection and rapid filling phases
• Rapid ejection phase: Atrioventricular ring moves down, lowering atrial pressure and CVP
• Rapid filling phase: Blood moves from atria to ventricles, causing atrial pressure to decrease and increasing venous return (VR)
• Muscle pump: Skeletal muscle contraction raises pressure in surrounding veins
• increased PVP (peripheral venous pressure) and VR (venous return) due to nearby tense skeletal muscles
• Arterial pulsations: Arterial pulsation pressure on the nearby veins increases PVP and venous return (VR)
• Venomotor tone: Sympathetic stimulation causes peripheral veins to vasoconstrict causing an increase in PVP and VR
• Blood volume: Increased volume raises venous pressure, in turn augmenting venous return (VR)

Capillary Circulation

• Recognize Starling forces
• Describe interstitial fluid formation
• Discuss causes of edema

Capillary Function

• Serves as a crucial point for the interchange of nutrients and waste between blood and tissue cells

Diffusion

• It is the most important mechanism for exchange of water and dissolved substances
• There is net movement of O2&glucose out of capillaries and net movement of Co2 into the capillaries
• Molecules can diffuse across the capillary wall either through the water filled pores or directly through the endothelial cells.

Bulk Flow

• The exchange of water and solutes through the capillary pores occurs by bulk flow depending on the pressure gradient between the inside and outside of the capillaries
• Water and solutes go through pores due to pressure differences between the inside and outside of the capillary
• Gradient pressure is always from inside to outside the capillary
• Fluid exchange is limited
• This mechanism is vital for maintaining blood volume in circulation

Starling Forces

• Oncotic pressure in the plasma proteins
• Capillary hydrostatic pressure

Causes of Edema

• Decreased plasma proteins due to malnutrition, liver disease, or kidney disease
• Increased capillary hydrostatic pressure due to venous obstruction, heart failure
• Increased capillary permeability and lymphatic obstruction

Circulatory Shock

• Circulatory shock needs to be defined
• The types of circulatory shock need to be listed
• The outcome of a shocked person needs to be predicted
• Compensatory measures to shock need to be recognized.

Hemorrhage

• Hemorrhage pertains to blood loss in the cardiovascular system, whether external or internal, and it is dangerous because internal bleeding is hard to identify
• Shock refers to reducing tissue perfusion, inhibiting the delivery of nutrients and oxygen to cells
• The body can compensate for blood loss of less than 20% of the total blood volume
• Compensatory functions are often deficient when over 20% blood is lost
• When compensatory systems fail, death can occur without a blood transfusion

Circulatory shock pathophysiology

• Decreased blood volume leads to decreased venous return, resulting in decreased cardiac output, and eventually culminating in decreased tissue perfusion or shock

Compensatory Mechanisms During Circulatory Shock

• Immediate compensatory functions include the constriction of veins and arterioles and cardiac acceleration

• Stimulation of the adrenal medulla to secrete catecholamine

• Secretion of aldosterone and ADH helps to increase plasma

• Delayed compensatory mechanisms include restoration of plasma volume, proteins, and red blood cells