Wiggers Diagram =)

A Wiggers diagram is a standard diagram used in cardiac physiology.

The X axis is used to plot time, while the Y axis contains all of the following on a single grid:

• Blood pressure
  • Aortic pressure (RED)
    
  • Ventricular pressure (BLUE)
    
  • Atrial pressure (YELLOW)
    
• Ventricular volume
• Electrocardiogram
• Arterial flow
  
• Heart sounds
  

By illustrating the coordinated variation of these values, it becomes easier to illustrate the relationship between these values in the cardiac cycle.

Note that during isovolumetric/isovolumic contraction and relaxation, all the heart valves are closed. At no time are all the heart valves open.

• S3 and S4 heart sounds are associated with pathologies and are not routinely heard.

Electrocardiogram

The electrocardiogram (ECG) is a recording of the electrical activity of the heart. It is the vector sum of the depolarization and repolarization potentials of all myocardial cells . At the body surface these generate potential differences of about 1 mV, and the fluctuations of these potentials create the familiar P-QRS-T pattern. At rest the intracellular voltage of the myocardium is polarized at -90 mV compared with that of the extracellular space. This diastolic voltage difference occurs because of the high intracellular potassium concentration, which is maintained by the sodium-potassium pump despite the free membrane permeability to potassium. Depolarization of cardiac cells occurs when there is a sudden increase in the permeability of the membrane to sodium. Sodium rushes into the cell and the negative resting voltage is lost (phase 0). The depolarization of a myocardial cell causes the depolarization of adjacent cells and, in the healthy heart, the entire myocardium is depolarized in a coordinated fashion. During repolarization, cellular electrolyte balance is slowly restored (phases 1, 2 and 3). Slow diastolic depolarization (phase 4) follows until the threshold potential is reached. Another action potential then follows.

I· ECG Waveform

i. The first deflection is caused by atrial depolarization, and it is a low-amplitude slow deflection called a P wave.

ii. The QRS complex reflects ventricular activation or depolarization and is sharper and larger in amplitude than the P wave. An initial downward deflection is called the Q wave. An initial upward deflection is called an R wave. The S wave is the last part of ventricular activation.

iii. The T wave is another slow and low-amplitude deflection that results from ventricular repolarization

iv. The PR interval is the length of time from the start of the P wave to the start of the QRS complex. It is the time taken for activation to pass from the sinus node, through the atrium, AV node and the His-Purkinje system to the ventricle

v. The PR interval is the length of time from the start of the P wave to the start of the QRS complex. It is the time taken for activation to pass from the sinus node, through the atrium, AV node and the His-Purkinje system to the ventricle

vi. The QT interval extends from the start of the QRS complex to the end of the T wave. This interval represents the time taken to depolarize and repolarize the ventricular myocardium. QT interval varies greatly with heart rate and is often represented as a corrected QT interval (or QTc) for a given heart rate

vii. The QT interval extends from the start of the QRS complex to the end of the T wave. This interval represents the time taken to depolarize and repolarize the ventricular myocardium. QT interval varies greatly with heart rate and is often represented as a corrected QT interval (or QTc) for a given heart rate

2.

3.

Examination of the Cardiovascular System

Again, some information regarding the examination of CVS which I took from Kumar and Clark's relating mainly to the examination mentioned in Part A of this PCL.

Arterial Pulse

· Pulse rate

o Pulse rate – between 60-80 bpm when adult patient is lying quietly in bed

o Young children maybe have higher pulse rates where else athletes and elderly adults may have slower rates.

o When pulse is irregular not all ventricular systolic beats maybe be detected by palpation of the radial pulse.

o Apex-radial pulse deficits maybe appreciated by counting the radial pulse simultaneously while listening to the heartbeat with a stethoscope. Commonly associated with atrial fibrillation and ventricular ectopy.

Blood Pressure

Jugular venous pressure

o There are no valves between the internal jugular vein and the right atrium.

o Observation of the column of blood in the internal jugular system is therefore a good measure of right atrial pressure.

o The external jugular cannot be relied upon because of its valves and because it may be obstructed by the fascial and muscular layers through which it passes; it can only be used if typical venous pulsation is seen, indicating no obstruction to flow.

o Measurement:

§ Hepatojugular reflex – When abdomen compressed causing temporary increase in central and hence jugular venous pressure. Confirms venous nature of a pulsation in the neck

§ Cannot be measure if low jugular venous pressure due to haemorrhage or other forms or hypovolemia

Intepretation Of The Jugular Venous Pressure Wave

This consists of three peaks and two troughs .The peaks are described as a, c and v waves and the troughs are known as x and y descents:

· The a wave is produced by atrial systole. Distinguished from the v wave by observing venous pulse while palpating the carotid artery. a wave occurs immediately after carotid pulsation while v wave occurs simultaneously.

· The x descent occurs when the atrial contraction finishes.

· As the pressure falls there is a small transient increase that produces a positive deflection called the c wave. This is caused by transmission of the rapidly increasing right ventricular pressure before the tricuspid valve closes.

· The v wave develops as the venous return fills the right atrium during continued ventricular systole.

· The y descent follows the v wave when the tricuspid valve opens.

Main abnormalities:

· Large a waves –

o Causes

§ resistance to ventricular filling, as seen with right ventricular hypertrophy due to pulmonary hypertension or pulmonary stenosis

§ tricuspid stenosis, but unusual because patients with tricuspid stenosis are usually in atrial fibrillation and therefore do not have a waves.

o A very large a wave occurs when the atrium contracts against a closed tricuspid valve; this is known as a 'cannon wave'. Cannon waves occur irregularly in complete heart block and in ventricular tachycardia.

· Large v waves –

o Caused by tricuspid regurgitation because the right ventricular pressure is transmitted directly to the right atrium and the great veins.

· Steep y descent –

o Diastolic collapse of elevated venous pressure can occur in right ventricular failure but is more dramatic in constrictive pericarditis and tricuspid regurgitation.

o At the end of ventricular systole the elevated atrial pressure suddenly falls when the tricuspid valve opens.

o However, the ventricles are stiff and cannot be distended and therefore, the venous pressure rapidly rises again. This rapid fall and rise of the jugular venous pulse is known as Friedreich's sign.

General Signs and Symptoms of CVS

Hey people, these are some of the things I prepared before the previous PCL. Below is the informations I summarised and gathered from Kumar and Clark's Clinical Medicine (: Unfortunately, there isn't much corellation with the pathogenesis but I hope it still helps (:

SYMPTOMS OF HEART DISEASE:

· Chest pain:

o Causes: Angina pectoris and myocardial infarction due to myocardial hypoxia.

o Pain usually described as crushing, gripping, heavy pain behind sternum in the middle of the chest and may radiate. Parasthesia, pain or heaviness or upper limb/s may also be associated with.

o Angina pectoris – Usually provoked on strenuous activity. Relieved by short acting nitrates.

o Pain radiating to the back – Enlarging thoracic aortic aneurysm

· Dyspnoea:

o Abnormal awareness or breathlessness

o Causes:

§ Pain in chest or abdomen may lead to dyspnoea

§ Main causes – cardiac and pulmonary pathologies – notably left ventricular failure (LVF)

o Pathophysiology

§ Oedema of the pulmonary interstitium and alveoli à Lungs being stiff and less compliant à more respiratory effort required to ventilate the lungs

· Palpitations:

o Increased awareness of the normal heartbeat or sensation of slow rapid or irregular heart rhythms.

o Normal heartbeat may be sensed due to anxiety, excitement or recumbency of the left side. Therefore, careful history must be taken to rule out.

o Most common arrhythmias felt as palpitations are:

§ Premature ectopic beats:

· Pause followed by forceful beat

· Pause present because heart resets itself before the next normal beat. Forceful beat present due to longer diastolic period and therefore heart is filled with more blood.

§ Paroxysmal tachycardia:

· Start abruputly and felt as racing heartbeat. May terminate suddenly but also tend to slow down first leading to sensation og palpitations fading away.

· Paroxysmal atrial fibrillation- irregular rhythm but other supraventricular or ventricular tachycardia - regular

· Symptoms: Syncope, presyncope, dyspnoea or chest pain. Polyuria after palpitations owing the release of atrial natiuretic peptide (ANP) which leads to sodium and water lost from kidneys.

o Different arrhythmias have different characteristics. One way to determine is to ask patient to tap out the rate and rhythm or their palpitations.

o Postural Orthostatic Tachycardia Syndrome: tachycardia on standing – mild drop in BP with dizziness and near syncope

o Maybe also caused by bradycardia but usually not common.

· Syncope

o Transient loss of consciousness due to inadequate cerebral blood flow

o Cardiovascular causes

§ Vascular – usually due to bradycardia and vasodilation

· Neurocardiogenic (Vasovagal attack)

· Postural hypotension – Pooling of blood

· Postbrandial hypotension – After a meal, BP drops

· Micturition syncope – Parasympathetic overactivity after bladder evacuated

· Carotid sinus syncope

§ Obstructive

· Aortic stenosis

· Pulmonary stenosis... etc

§ Arrhythmias

· Rapid tacchycardias

· Profound Bradycardia ( Stokes-Adams)

· Significant pauses in rhythm

· Artificial pacemaker failure

· Fatigue:

o Inadequate systemic perfusion in heart failure

o Other factors can be

§ poor sleep due to paroxysmal nocturnal dyspnoea, orthopnoea, decubitus angina, nocturia (due to diuretic therapy) or nightmares (due to amiodarone therapy)

§ direct side-effect of medication, particularly beta-blockers

§ electrolyte imbalance due to diuretic therapy

§ as a systemic manifestation of infection such as endocarditis.

· Peripheral oedema: