1. 2 - Cardiovascular Physiology

Pericarditis

Inflammation of the pericardium, fluid accumulation in pericardial cavity, restricts heart movement, heart is unable to pump

Chordae Tendinae

Anchors AV valves to papillary muscle, prevents back-flow

Papillary muscle

Control tension on chordae tendinae

Stenosis

Narrowing of heart valve, faulty opening

Valve regurgitation (insufficiency)

Faulty closure, backflow

Rheumatic heart disease

Autoimmune disorder caused by strep infection

When is stenosis heard?

Heard during open valve, whistling

When are insufficiencies heard?

Head when valve should be closed, whirring

Ventricular torsion

Allows for more efficient ejection

Produces diastolic suction (more efficient filling)

Intercalated disks

desmosomes and gap junctions

Desmosomes

Withstand stress

Gap junctions

Movement if ions, electrical impulses

Autorhythmic cells

Generates and spreads action potentials, pacemaker cells, conducting cells

Contractile cells

99% of cardiac muscle cells, mechanical work of contraction

Typical action potential events

Na influx, Ca influx, K efflux

Pacemaker potential

The slow rise in depolarization prior to an AP in the SA node, no refraction period

Events in Pacemaker potential

T-type Ca channels open (volt-sensitive), calcium moves in but does not stay open long, pacemaker potential continues to rise to threshold

Threshold reached in Pacemaker potential

L-type Ca channels open, calcium moves in, rapid depolarization and action potential

Repolarization of Pacemaker potential

L-type Ca channels close, K channels open, K moves out of SA node cells

SA node

pacemaker of the heart, auto-rhythmic, self-generated, events repeat 70/min

Other Pacemaker regions

Av node, Purkinje fibres

AP of Myocardial contractile cells

Depolarization (Na moves in), Plateau (Ca moves in , stays depolarized), Repolarization (K moves out)

Modulation of HR by sympathetic nervous system

Pacemaker cells are more depolarized, closer to threshold, will reach threshold faster, increased HR

Modulation of HR by parasympathetic nervous system

Further from threshold, longer to reach threshold, slower HR (normal resting condition)

Specialized conduction system of heart

Sa node, internodal pathway, AV node, bundle of his (AV bundle), Purkinje fibres

Electrocardiogram

External recording of electrical events, waves of the ECG can be correlated to specific electrical events

P-wave

atrial depolarization (contraction), initiated in SA node, spreads via gap junctions and internodal pathway

AV delay

Delay of signal, allows for ventricular contraction after atrial contraction and ventricular filling

QRS complex

Ventricular depolarization and atrial repolarization, impulse moves to Bundle of HIS, to bundle of branches then to purkinje fibres

T-wave

Ventricular Repolarization, initiates ventricular relaxation, reversed repolarization wave from apex

Sinus Rhythm

Normal heart rhythm, 60-120 BPM

Tachycardia

Rapid heart rate of more than 100 BPM, ex. Heart disease, anxiety, fear, Sinus (normal) or Ventricular (Irregular)

Bradycardia

Slow heart rate of less than 60 BPM, can be normal in athletes or abnormal (ez. Thyroid issue), risk of fainting

Arrythmias

Abnormal heart rhythms, can cause sudden death, fainting, heart failure, dizziness, palpitations or no symptoms at all

Causes of Arrythmias

Hypoxia, caffeine, smoking, alcohol, purkinje excitation

Premature Ventricular Contraction

Extra systoles, often caused by ectopic foci, atrial or ventricular, trigger extra beats

Risk factors of PVC's

Stress, lack of sleep, caffeine, medications

Atrial flutter

Extra P waves

Heart Block

Interruption in conduction system, impulses from atria cant always reach ventricles, normal p waves but fewer QRS waves, symptoms include fatigue painting and chest pain

Supra Ventricular Tachycardia

Abnormally fast heart rhythm, originating in the atria, ex. Wolff-parkinson-white syndrome, symptoms include palpatiins, fainting, sweating, shortness of breath, or chest pain

Atrial fibrillation

No organized electrical pattern in the atria, no p-waves, risk factors include caffeine stress and genetics, symptoms include palpitations, discomfort or fainting

Treatment of Atrial fibrillation

Electric conversion, ablation, anti-coagulants

Causes of heart block

Aging, heart-disease, stress, caffeine, alcohol

Ventricular Fibrillation

No organized pattern of depolarization, no organized contraction, no ejection, leads to death

Cardiac Cycle

Electrical events correspond to mechanical events in the heart

Atrial pressure

3-10 mmHg

RV pressure

3-35 mmHg

LV pressure

3-125 mmHg

4 phases of cardiac cycle

Diastolic filling, isovolumic contraction, ejection, isovolumic relaxation

Properties of the cardiac cycle

Electrical events precede mechanical events, left and right sides contract simultaneously, pressure changes due to changes in volume or changes in contractile state

Diastolic Filling

LAP>LVP, Mitral Valve open, LVP

Isovolumic Contraction

QRS - LV contracts ,LVP increases, Once LVP>LAP, Mitral valve closes, Both valves closed, Pressure still increasing

Ejection

Once LVP>AP, aortic valve opens, blood ejected into aorta

Isovolumic Relaxation

T-wave, LVP decreases, once LVP

Stroke Volume

Amount of blood pumped in one beat, SV=EDV-ESV

Factors that Regulate Stroke Volume

preload, contractility, afterload

Preload

The amount of myocardial stretching, greater=greater SV

Contractility

The amount of force produced during a contraction at a given preload

Greater=Greater SV, affected by sympathetic tone, length of muscle fibre

Afterload

The tension required for the LV to open the aortic semilunar valve, Greater=Lower SV

Venous Return

Amount of blood entering heart, affected by skeletal muscle pump, respiratory pump and sympathetic innervation

Frank-Starling Law

SV increases as EDV increases

Inotropic Effect

The effect of increased sympathetic tone contractility of the heart

Role of (Nor)epinephrine on Heart

Increases contractility and HR, harder and faster contractions

Cardiac Output

Amount of blood pumped in a minute, CO= SV x HR

Factors Effecting Heart Rate

Autonomic Nervous System, Age, Gender, Physical Fitness, Body Temperature

ANS on HR

Sympathetic NS raises HR, Parasympathetic lowers HR,

Hormones- E/NE increases HR, Ach lowers

Age on HR

Older people have greater HR

Gender on HR

females have faster HR than males

Physical fitness on HR

Low fitness raises HR

Body temperature on HR

Increased Temp increases HR

Thyroid Hormone on HR

Increased number of adrenergic receptors on SA node cells

Caffeine on HR

Inhibits breakdown of cAMP

Nicotine on HR

Increases Norepinephrine release

Cocaine on HR

Inhibits reuptake of norepinephrine, longer response

In Exercise effect on CO

Higher demand for oxygen and blood flow, increases epinephrine, these both increase CO

Heart Muscle Metabolism

•Heart muscle is highly oxidative

- abundant mitochondria and myoglobin

- Gets oxygen from coronary circulation

Coronary Circulation during exercise

HR increases, diastole time decreases, heart still gets adequate blood due to dilation of coronary arteries

Long-term benefits of exercise

Bigger heart increases SV, resting HR decreases, increase coronary artery diameter which increases coronary blood flow, increases collateral blood vessels which lower ischemia

Cardiac Remodelling

Pathological or Physiological

Pathological Cardiac Remodelling

Consequence of heart disease, high BP, heart failure, infarct

Physiological Heart Remodelling

Consequence of training of pregnancy

Myocardial Ischemia

Heart attack, Inadequate delivery of oxygenated blood to heart tissue

Fibrosis in Heart

Necrosis in Heart

Death of the heart muscle cells

Acute Myocardial Infarction

Blood vessel supplying area of heart is blocked or ruptured

Characteristics of Ischemia

Transient, no permanent muscle damage, symptoms occur when cardiac demand increases beyond what the heart can match, symptoms ease when demand lowers

Characteristics of Infarcts

Permanent Blockage, muscle cells permanently damaged, symptoms remain and worsen, Heart attack, chest pain sweating nausea are symptoms

Treatment of Ischemia and Infarct

-Coronary artery bypass (CABG)

-Vasodilators (widens blood vessels)

-Angioplasty (unblocking of coronary artery)

-Reduce risk factors (ie: diet, exercise, less smoking)

Arterial Hypertension Causes

- smoking

- stress

- diet

- age/genetics