The Heart

First heart sound “lubb”

Cause by blood punching atrioventricular valves closed when ventricles contract

Second heart sound “dupp”

Cause by arterial blood pushing semilunar valves closed when ventricles relax

Heart murmur

Abnormal heart sound, can indicate a valve problem

Stress EKG or stress test

Measures hearts response to exercise

Holster monitor

Records a continuous ECG for 24 hours

A sinus rhythm =

Normal rhythm

Arrhythmia

An abnormal heart rhythm due to a problem in the conduction system. Rhythm may be too fast too slow or irregular

Causes of arrhythmias

• Caffeine

• Nicotine

• Alcohol

• Other drugs

• Stress

• Hyperthyroidism

• Hypokalemia (low K+)

• Heart disorders (like MI or valve problems)

Bradycardia

Heart rate < 60 bpm

Tachycardia

Heart rate > 100 bpm

Heart block

Spread if action potential is slowed/blocked usually AV node

Atrial flutter

Rapid atrial contractions with AV block

Atrial fibrillation

Unsynchronized/uncoordinated contraction of atrial fibers

• results in atria being unable to pump blood

• May cause clots to form which can travel & cause a stroke

Ventricular tachycardia

Ventricles beat too fast

• usually caused by heart disease/MI

• Can develop into v fib

Ventricular fibrillation

Unsynchronized/uncoordinated contraction of ventricular fibers (quiver rather than contract)

• results in cardiac arrest(ventricles stop pumping blood)

• Leads to death in minutes

Asystole

Heart has stopped “flat line”

Treatment of arrhythmias

• some aren’t treated

• Medication

• Defibrillation/cardioversion

• Cardiac ablation

Defibrillation/cardioversion

Electrical shock applied to chest

Cardiac ablation

Procedure which destroys abnormal electrical conduction pathways in heart

Cardiac cycle

All the events of one heartbeat

Systole

Contraction

Diastole

Relaxation

Blood flows/moves from an area of

High pressure to low pressure

Atrial systole

Atria contract which forces remaining blood into ventricles

End diastolic volume (EDV)

Volume of blood into ventricles at end of rest

Ventricular systole

Ventricles contract which forces blood into arteries

Isovolumetric contraction

Ventricles start to contract which closes AV valves

Ventricular ejection

Ventricle contraction opens SL valves and ejects blood

Stroke volume (SV)

Amount of blood pumped in one ventricular systole (about 70 ml)

End systolic volume (ESV)

Volume of blood into ventricles ventricles at end of contraction

Ejection fraction

Stroke volume (SV) / End diastolic volume (EDV)

Isovolumetric relaxation

SL valves close and atria start filling with blood

Ventricular filling

AV valves open & ventricles start filling with blood

Cardiac output

The amount of blood pumped by a ventricle in one minute

Heart rate

Number of beats per minute

Cardiac output calculation

Stroke volume x Heart rate

Average CO (resting adult)

5.25 L/min

Factors that increase stroke volume or heart rate will also increase…

Cardiac output

Cardiac reserve

An increase in cardiac output above its level at rest

Positive chronotropic agents

Increase heart rate

Negative chronotropic agents

Decrease heart rate

Preload

How much myocardium is stretched before it contracts

• The more it’s stretched the stronger it will contract

• Overstretched in heart failure = weak contraction

Myocardial contractility

Strength/force of contraction

• Sympathetic NS, hormones & various chemicals alter contractility

• Inotropic agents

Inotropic agents

Alter force of contraction

Valvular (mitral or aortic) insufficiency/ incompetence

Valve doesn’t completely close, results in backflow of blood (into previous chamber)

Valvular (mitral or aortic) stenosis

Narrowed valve due to scarring

Rheumatic heart disease

Strep bacteria trigger an immune response wheee antibodies inflame and damage various connective tissues, including joints and heart valves

Mitral valve prolapse

Valves balloons up into left atrium

Significant valve dysfunction may lead to

Heart failure

Conduction system

Group of specialized cells in the heart that are autorhythmic (self excitable). They generate & pass along action potentials which stimulate heart contraction

Pacemaker potential

Ability to reach threshold without stimulation

Sinoatrial (SA) node (AKA pacemaker)

• Located in right atrium

• Creates action potential which causes atrial contraction

Atrioventricular (AV) node

Located in interatrial septum; signal is slowed down through AV node which gives atria time to finish contracting

right and left bundle branches

Located in interventricular septum

Purkinje fibers

Spread the action potential throughout walls of ventricles which causes ventricular contraction

If SA node fails…

AV node takes over

If AV node fails need to implant an…

Artificial pacemaker

Parasympathetic nervous system —— heart rate

Decreases

Sympathetic nervous system —— heart rate and force of contraction

Increases

Electrocardiogram (ECG or EKG)

A recording of the electrical changes in the heart

P wave

Represents atrial depolarization

ORS complex

Represents ventricular depolarization

T wave

Represents ventricular repolarization

ECG or EKG is used to detect:

• Abnormal heart rhythms

• Hypertrophy (enlarged heart)

• Ischemia

• Regions of heart damage

After load

Arterial pressure that must be overcome by heart

• Hypertension & atherosclerosis incr. afterload which decreases stroke volume

Increased preload = ?

Increased stroke volume

Increased force of contraction =?

Increased stroke volume

Increased afterload =?

Decreased stroke volume

Coarctation of the aorta

part of the aorta is narrowed

Patent ductus arteriosus

Ductus arteriosus fails to close

Atrial septal defect

Foramen ovale fails to close

Ventricular septal defect

Hole in interventricular septum

Tetralogy of Fallot (consists of 4 defects)

1. Ventricular septal defect

2. Pulmonary stenosis - narrow pulmonary trunk & valve

3. Aorta emerging from both ventricles

4. Enlarged right ventricle