Important terms:

1. Diastole: a period of relaxation during which heart fills with blood
2. Systole: a period of contraction during which the blood is ejected from the heart.
3. Isovolumetric: a phase when all valves are closed and ventricle behaves as a closed chamber and volume within ventricle remains constant

Time period of various events of cardiac cycle:

A)     Atrial Cycle: 0.8 sec

1. Systole: 0.1 sec

2. Diastole: 0.7 sec

B)      Ventricular Cycle: 0.8 sec

1. Systole: 0.3 sec

• Isovolumetric contraction: 0.05 sec
• Rapid ejection phase: 0.1 sec
• Reduced ejection phase: 0.15 sec

2. Diastole: 0.5 sec

• Isovolumetric relaxation: 0.1 sec
• Rapid filling phase: 0.1 sec
• Reduced filling phase (Diastasis): 0.2 sec
• Last Rapid filling phase (Atrial systole): 0.1 sec

Points to understand:

• Normally, atrial and ventricular systoles never coincide. Ventricular systole occurs during atrial diastole and atrial systole occurs during ventricular diastole.
• For a period of about 0.4 sec (Isovolumetric ventricular relaxation, Rapid ventricular filling phase and Reduced ventricular filling phase), both the ventricles and atria relax.

Events in Cardiac Cycle:

1. Atrial Systole:

• Preceded by ECG “P” wave  which begins due to spontaneous generation of action potential in SA node
• Contributes to last rapid phase of ventricular filling (20% filling) but is not essential for ventricular filling
• Filling of ventricle by atrial systole gives rise to 4^th Heart sound, which is not audible in normal adults
• “a” wave appears on atrial pressure curve due to increase in atrial pressure (4 to 6 mmHg in right atrium and 7 to 8 mmHg in left atrium)

2. Isovolumetric ventricular contraction:

• Ventricles are filled with blood: 80% filling occurred before atrial systole and 20% filling occurred during atrial systole
• Begins after onset of ECG “QRS” complex
• Immediately after ventricular contraction begins, pressure rises abruptly
• When Ventricular pressure > Atrial pressure, Atrioventricular (AV) valve closes giving rise to 2^nd heart sound (As mitral valve closes before tricuspid valve, 1^st heart sound may split)
• Since AV valves and semilunar valves (aortic and pulmonary valves) are both closed, isovolumetric contraction occurs and there is rapid rise in ventricular pressure.

3. Rapid Ventricular Ejection:

• When the left ventricular pressure rises above the aortic pressure (~80 mmHg), aortic valve opens and there is rapid ejection (70% ejection) of blood into the aorta.
• When the right ventricular pressure rises above the pulmonary pressure (~8 mmHg), pulmonary valve opens and there is rapid ejection (70% ejection) of blood into the pulmonary trunk.
• “c” wave appears on atrial pressure curve due to bulging AV valve on atria due to increasing ventricular pressure
• Pressure rise in the ventricles is slower because the blood flows into the arteries. The entry of blood into the arteries causes arteries to stretch and pressure increases. During this period, the pressure in the left ventricle and aorta reaches a maximum of 120 mmHg (systolic pressure) and that in right ventricle and pulmonary trunk reaches a maximum of 24 mmHg.
• Atrial filling begins
• Onset of ECG “T” wave marks end of both ventricular contraction and rapid ejection.

4. Reduced Ventricular Ejection:

• Ejection of blood (30% ejection) from the ventricles continues, but is slower
• Ventricular pressure begins to decrease
• Aortic and Pulmonary pressure also decreases because of runoff of blood from larger arteries into smaller arteries
• Atrial filling continues

5. Isovolumetric ventricular relaxation:

• Repolarization of Ventricles is now complete (marked by end of ECG “T” wave)
• Ventricular pressure begins to fall
• When the pressure in respective ventricles < pressure in aorta and pulmonary trunk, the semilunar valves close (closure of aortic valve followed by pulmonary valve) giving rise to 2^nd heart sound. Inspiration causes splitting of 2^nd heart sound.
• Dicrotic notch or incisura appears on aortic pressure curve as a “blip” after closure of aortic valve due to short period of backward flow of blood immediately before closure of the valve, followed by sudden cessation of the backflow.
• Since, AV valves and semilunar valves are both closed; isovolumetric relaxation
• Ventricular falls rapidly but the elastic walls of the arteries maintain a high pressure in the arteries, even during diastole although there is a fall in arterial pressure.
• “v” wave appears on atrial pressure curve due to accumulation of blood in atria against closed AV valves
• When ventricular pressure < atrial pressure, AV valves (Mitral and Tricuspid) open.

6. Rapid Ventricular Filling:

• Rapid flow of blood, long accumulated in the atria to the ventricles gives rise to the 3^rd heart sound, which is normal in children but pathologic in adults.

7. Reduced ventricular filling (Diastasis):

• Longest phase of cardiac cycle
• Only a small amount of blood flows into the ventricles at a slower rate from the great veins via atria.
• During this period, the blood in both atrium and ventricle becomes continuous as if a single cavity.
• Time required for diastasis and ventricular filling depends on the heart rate. Increase in heart rate decreases the time available for ventricular filling.

8. Last rapid filling phase:

• Coincides with the atrial systole

Summary:

Phases in Left Ventricle:

• Isovolumetric contraction: period between mitral valve closure and aortic valve opening; period of highest O2 consumption
• Systolic ejection: period between aortic valve opening and closing
• Isovolumetric relaxation: period between aortic valve closing and mitral valve opening
• Rapid filling: period just after mitral valve opening
• Reduced filling: period just before mitral valve closure

Heart Sounds:

• S1: mitral and tricuspid valve closure; loudest at mitral area.
• S2: aortic and pulmonary valve closure; loudest at left sternal border.
• S3: in early diastole during rapid ventricular filling phase.
• Associated with ↑ filling pressures and more common in dilated ventricles (but normal in children and pregnant women).
• S4: in late ventricular diastole or atrial systole.
• Associated with ventricular hypertrophy. Left atrium must push against stiff LV wall.

Jugular venous pulse (JVP):

• a wave: atrial contraction
• c wave: RV contraction (tricuspid valve bulging into atrium).
• v wave: ↑ atrial pressure due to filling against closed tricuspid valve.

Flowchart:

1) Juxtaglomerular cells (modified smooth muscle cells) of afferent arteriole including renin containing (synthesizes and stores renin) and sympathetically innervated granulated cells which function as mechanoreceptors to sense blood pressure.

2) Macula densa cells (Na+ sensors) of Distal Convoluted Tubule (DCT) which function as chemoreceptors to sense changes in the solute concentration and flow rate of filtrate.

3) Juxtaglomerular/Extraglomerular mesangial cells (Lacis cells) forming connections via actin and microtubules which allow for selective vasoconstriction/vasodilation of the renal afferent and efferent arterioles with mesangial cell contraction.

Functions of Juxtaglomerlar Apparatus (JGA):

1. Local transmission of Tubuloglomerular Feedback (TGF) at its own nephron via angiotensin II (AT II)
2. Systemic production of Angiotensin II (AT II) as part of Renin-Angiotensin-Aldosterone System (RAAS)

Tubuloglomerular Feedback (TGF) Mechanism

The tubuloglomerular feedback mechanism has 2 components that act together to control GFR:

1. Afferent arteriolar feedback mechanism
2. Efferent arteriolar feedback mechanism

Increased renal arterial pressure leads to an increased delivery of fluid (increased osmolality or increased flow rate) to the macula densa. The macula densa senses the load and causes constriction of nearby afferent arteriole, increasing the resistance. This will return osmolality and filtrate flow rate to normal.

Decreased renal arterial pressure leads to a decreased delivery of fluid (decreased osmolality or decreased flow rate) to the macula densa. The macula densa senses this and causes:

1. Vasodilation of afferent arteriole
2. Constriction of efferent arteriole as a result of renin release by stimulated JG cells

Renin Angiotensin Aldosterone System (RAAS)

When systemic blood pressure decreases, there is decreased stretch of JG cells, which leads to their release of renin. Renin release causes the activation of renin-angiotensin mechanism, which ultimately leads to an increased blood pressure.

Korotkoff sounds:

When the cuff pressure is great enough to close the artery during part of the arterial pressure cycle, a sound then is heard with each pulsation. These sounds are called Korotkoff sounds believed to be caused mainly by blood jetting through the partly occluded vessel. The jet causes turbulence in the vessel beyond the cuff, and this sets up the vibrations heard through the stethoscope.

As long as the pressure in the cuff is higher than the systolic blood pressure of the patient, blood doesn’t jet through the completely occluded artery, hence no sound is heard. If the pressure is dropped to a level equal to that of the patient’s systolic blood pressure, the first Korotkoff sound will be heard. As the pressure is further gradually lowered down, following korotkoff sounds are heard:

Phase 1 (K1): Clear tapping sounds representing systolic pressure
Phase 2 (K2): Softer tones
Phase 3 (K3): Louder once again
Phase 4 (K4): Muffled Tones sounds representing diastolic pressure
Phase 5 (K5): Tones cease

Auscultatory Gap:

An auscultatory gap also called as silent gap is the interval of pressure where korotkoff sounds indicating true systolic pressure fade away and reappear at a lower pressure point during the manual measurement of blood pressure by auscultatory method. The auscultory gap happens when the first Korotkoff sound fades out for about 20-50 mmHg only to return. It can result in following erroneous blood pressure reading:

1. Underestimation of systolic blood pressure
2. Overestimation of diastolic blood pressure

Example:

The patient’s actual systolic pressure is 200 with a gap from 170 to 140 and a diastolic of 110. You inflate the cuff to 170 and hear nothing until the manometer reaches 140, which you presume is the systolic pressure. Also if you, inflate the cuff to 200, you may read 170 as the diastolic pressure which is the beginning of auscultatory gap.

When recording a blood pressure with an auscultatory gap, always list your complete findings. eg. BP 200/110 with the auscultatory gap from 170 to 140.

Auscultatory gap has been found to occur due to venous pooling of blood. The auscultatory gap is most likely to appear in the obese arm, especially if the physician pumps up the cuff slowly and traps a great deal of blood in the arm’s venous compartment. Another way to trap blood is to pump the cuff 2nd time immediately after 1st determination, without allowing 1-2 minutes for the trapped blood to escape.

Auscultatory gap in Hypertension

An auscultatory gap is common in elderly hypertensive patients. It occurs in some hypertensive patients only. Auscultatory gaps are related to carotid atherosclerosis and to increased arterial stiffness in hypertensive patients, independent of age.

Types:

3 types of auscultatory gaps, have been identified by using wideband external pulse recording.

1. G1: occurs with cuff pressure just below systolic and is characterized by the presence of K1 and K2 with intermittent disappearance of K2. G1 gaps are related to a phasic decrease of arterial (systolic) pressure.
2. G2: are related to a phasic increase of arterial (diastolic) pressure, occur when cuff pressure is just above diastolic, and are characterized by the presence of K1, K2, and K3 with intermittent disappearance of K2.
3. G3: occurs with cuff pressure between systolic and diastolic and are characterized by an underdeveloped or blunted K2 signal.

Mechanism:

• The mechanism of origin of auscultatory gap has not been understood clearly.
• Cavallani recently showed that the early loss of audible sound during cuff deflation is associated with blunted high frequency K2 signals associated with korotkoff sound (detected by wideband external pulse recording) likely related to the altered physical properties of a stiffer arterial wall.

Precautions:

1. Determining systolic blood pressure by palpatory method before recording the blood pressure with auscultatory method.
2. Inflating the blood pressure cuff to 20-40 mmHg higher than the pressure required to occlude the brachial pulse.

Tidal Volume (TV)- Volume of gas inspired or expired in each breath during normal quiet respiration. It is 400-500 ml ie 10ml/kg

Inspiratory Reserve Volume ( IRV)- It is the maximum volume of gas which a person can inhale from end inspiratory position. It is 2400 to 2600 ml.

Inspiratory Capacity ( IC)- It is the maximum volume which can be inhaled from end expiratory position ie, IRV + TV. It is 2500 + 500= 3000 ml or 3 L

Expiratory Reserve Volume- Maximum volume of gas that can be expired after normal expiration. It is 1200 to 1500 ml.

Vital Capacity- Maximum volume of gas that can be exhaled after maximum inhalation ie, it is IRV+TV+ ERV. Its value is 4200 to 4500 ml ( 75-80 ml/kg).

Functional Expiratory Volume ( FEV)- It is vital capacity per time. FEV1 is VC in 1^st sec.

Residual Volume- It is the volume of gas still present in lungs after maximal expiration. It is 1200-1500 ml.

Maximum breathing capacity- Maximum volume of air that can be breathed/minute. It is 120-170 litre/min ( normally it can be measured for 15 sec and expressed as litre/min)

Minute Volume- It is tidal volume X Respiratory rate. It is 500 X 12= 6000 ml/min

Total Lung volume- IRV+TV+ERV+RV = 5500 to 6000ml

Functional Residual Capacity( FRC)- It is the volume of gas in lungs after end expiration. It is ERV + RV. It is 2400-2600 ml. During anaesthesia FRC decreases by 15-20%.

DEAD SPACE: It is the volume of the respiratory tract that does not participate in gas exchange. It is approximately 300 ml in normal lungs.

a.ANATOMIC DEAD SPACE: Volume of the conducting airways, approximately 150 ml

b.PHYSIOLOGIC DEAD SPACE: The volume of the lung that does not participate in gas exchange.In normal lungs, is equal to the anatomic dead space (150 ml). May increase in several lung diseases.

Reference- Short Text book of Anesthesia- A. Yadav, Web.