Cvs Notes 1st Part.docx

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1. CARDIAC CYCLE Definition: The cyclical changes that take place in the heart during each beat (one systole and one diastole) Duration for one cycle = 0.8 sec Phases:  Atrial systole - 0.1 sec  Atrial diastole- 0.7 sec  Ventricular systole – 0.3 sec  Ventricular diastole – 0.5 sec ATRIAL SYSTOLE

 Contraction of atria & expulsion of blood into ventricles  Contributes 25% of the ventricular filling  Last phase of ventricular diastole  Produces fourth heart sound ATRIAL DIASTOLE  Gradual filling of atria by blood brought by veins VENTRICULAR SYSTOLE

 Contraction of ventricles & expulsion of blood into respective blood vessels  Includes three phases Isovolumetric contraction-0.05sec Maximal ejection – 0.1 sec Reduced ejection – 0.15 sec Isovolumetric contraction  Period between closure of AV valves & opening of semilunar valves  Ventricles contract as closed chambers  No change in the volume of blood in the ventricles  Intraventricular pressure increases Maximal Ejection phase  Increase in intraventricular pressure  Semilunar valves are forced to open  Due to High Pressure gradient, blood is rapidly ejected out of ventricles  About 2/3rd of stroke volume is ejected Reduced ejection

 Due to decreased pressure gradient, the rate of ejection of blood is reduced  About 1/3rd of stroke volume is ejected VENTRICULAR DIASTOLE

 Filling of ventricles by the blood flowing from atria  Includes five phases Protodiastolic period – 0.04 Sec Isovolumetric relaxation – 0.08 Sec Rapid inflow – 0.11 Diastasis – 0.19 Atrial systole – 0.11

2 Protodiastolic phase  Ventricle relaxes  Intraventricular pressure in less than the pressure in the aorta/Pulmonary Arteries  Semilunar valves close to prevent the back flow of blood from arteries into ventricles  Closure of SLV produces second heart sound Isovolumetric relaxation  Period between closure of semilunar valves & opening of AV valves  SLV and AV valves are closed  Ventricle relaxes as closed chamber  No change in the volume of blood in the ventricles  Intraventricular pressure decreases Rapid inflow phase  Intraventricular pressure less than intra atrial pressure  Hence AV valves open  Blood flows from atria to ventricle at a faster rate  Turbulence due to rapid flow produces third heart sound Diastasis  Increase in intraventricular pressure  Blood flow from atria to ventricle at low rate or static Atrial systole  Last phase of ventricular diastole  Contributes additional 25% of ventricular filling HEART SOUNDS 4 recordable heart sounds (Phonocardiogram)  First heart sound-S1 – Caused by closure of AV valves. Occurs at the beginning of ventricular systole  Second heart sound S2- Caused by closure of Semi Lunar Valves. Occurs at the end of ventricular systole  Third heart sound- Due to rapid ventricular filling  Fourth heart sound- Caused by atrial systole HEMODYNAMIC CHANGES

Pressure and volume changes in the atria & ventricle during cardiac cycle  Intra atrial pressure curve  Intraventricular pressure curve  Aortic pressure curve  Ventricular volume curve Intra-atrial pressure curve 3 Positive waves – a, c & v (caused by increase in intraatrial pressure) 2 Negative waves - x & y (caused by decrease in intraatrial pressure)  ‘a’ wave - due to atrial systole  ‘c’ wave – due to bulging of AV valve into the ventricles during isovolumetric contraction  ‘v’ wave – due to filling of atria after the closure of AV valves

3 Intraventricular pressure curve: (Left ventricular pressure)  During isovolumetric contraction phase – Pressure rises steeply due to a rise in tension  Maximum ejection phase – Maximum pressure (120 mmHg) develops as the ventricle is contracting with a maximum force  Reduced ejection phase – Pressure is less during this phase Aortic pressure Curve:  During diastole of heart, the aortic pressure is maintained at 80 mmHg  During systole of the heart, it rises to 120 mmHg Ventricular volume curve:  End diastolic volume – During diastole, ventricular volume increases. The maximum volume of blood in the ventricle at the end of diastole is called End Diastolic volume. It is normally 130 ml.  Stroke Volume: Volume of blood ejected out from ventricle during systole. It is 80 ml  End Systolic Volume: The minimal volume of blood remaining in the heart at the end of systole ECG: “P” wave = is due to atrial depolarization which occurs before atrial systole “QRS” complex = is due to ventricular depolarization which occurs before ventricular Systole “T” wave is due to ventricular repolarization which occurs before ventricular diastole Wiggers Chart

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2. CARDIAC OUTPUT A) Definition: Cardiac output (CO) – Volume of blood ejected by each ventricle / minute Stroke volume (SV) – Volume of blood ejected by each ventricle / beat Cardiac Index (CI) – Cardiac output / square meter of the body surface Area End Diastolic Volume (EDV) – Volume of the blood in the ventricle at the end of diastole Ejection Fraction (EF) – Fraction of the end diastolic volume that is ejected Peripheral Resistance (PR) – The resistance offered to the blood flow in the peripheral blood vessels B) Normal values: Cardiac output – 5 lts / min Stroke volume – 70 ml/ beat Cardiac index – 3 lts/ min/square metre of body surface area End diastolic volume – 120 ml Ejection Fraction -- 65% METHODS TO DETERMINE CARDIAC OUTPUT Direct method Indirect method  Fick principle  Dilution principle (Dye. Isotope & Thermo dilution)  Ballistocardiography  Pulse pressure contour  X – ray cardiometry FICK PRINCIPLE The cardiac output is calculated by the following formula X Q = ---------A – V difference Q – Blood flow X – Amount of substance taken up by an organ A -- V difference = Arterio venous difference in the concentration of a substance As pulmonary blood flow is equal to cardiac output, pulmonary blood flow determined by Fick principle is taken as cardiac output. Pulmonary blood flow = amount of O2 taken by the lungs/minute -------------------------------------------------Arterio venous difference of O2 For example Amount of oxygen taken by lungs / minute = 250 ml (Determined by spirometer) Arterial oxygen content = 20 ml / 100 ml of blood (Estimated from any peripheral artery) Venous oxygen content = 15 ml / 100 ml of blood (Estimated from right atrium) Pulmonary blood flow = 250 --------- X 100 = 5000 ml 0r 5 lts 20 - 15

5 As pulmonary blood flow = cardiac output, CO = 5 lts DYE DILUTION PRINCIPLE

A known amount of dye is injected into the peripheral vein and blood samples are collected from the peripheral artery and the concentration of the dye in each sample is estimated. Cardiac output can be calculated by using the following formula: Amount of the dye injected ----------------------------------------Mean concentration of the dye over a period of 1 minute The commonly used dye is EVAN”S BLUE (T—1824) C) Regulation of Cardiac output: Cardiac output = Stroke volume x Heart rate ------------------------------------Peripheral resistance Stroke volume = Myocardial contractility X End Diastolic Volume (EDV)

Heart rate (chronotropic)

End Diastolic Volume (Pre load)

Cardiac Output

Myocardial Contractility (Ionotropic)

Peripheral resistance (After load)

Cardiac Output Regulation

Heterometric regulation (Factors which cause an increase in the initial length of cardiac muscle before contraction)

Homometric regulation (Factors which do not cause any change in the initial length of cardiac muscle before contraction)

Heterometric regulation of cardiac output I.

Intrinsic factors regulating myocardial contractility Frank – Starling Phenomenon: The force of contraction is directly proportional to the initial length of the cardiac muscle. The initial length of the muscle depends on the end diastolic volume. Any increase in the EDV stretches the ventricular myocardium, increasing the length of the muscle fiber Importance: – helps to match the stroke volume of the ventricles – helps to maintain the minute output – prevents venous engorgement

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II.

Force Frequency relation: Any increase in the frequency of heart beat increases myocardial contractility within physiological limits. The increase in contractility is due to accumulation of intracellular calcium ions End Diastolic volume: End Diastolic Volume (EDV) is the volume of blood in the ventricles at the end of diastole. Any increase in the EDV increases the cardiac output by increasing the stroke volume. Mechanism: Increase in EDV  stretching of ventricular muscle fibres  Increase in the length of fibres  stronger muscle contraction Increase in cardiac output (Frank Starling’s law) Factors influencing EDV: i) Venous return ii) Ventricular compliance iii) Diastolic pause iv) Atrial systole Venous return: The volume of blood that returns to the atria through the veins in one minute. This increases EDV & there by increases cardiac output. Factors influencing venous return: 1. Cardiac pump: The pumping action of ventricles increases venous return by 2 forces:  Vis – a – tergo (propelling force from behind): - Left ventricular contraction during systole and elastic recoiling of arteries during diastole push the blood from aorta towards the right atrium  Vis – a –fronte (suction force from front) – Right atrial pressure: - Less pressure in right atrium during diastole helps in suction of blood from the great veins into the right atrium 2. Capacity of venous reservoir: This factor is inversely proportional to venous return . Venoconstriction  decrease in venous capacity  increase in venous return 3. Blood Volume: Directly proportional to venous return. e.g., hemorrhage  decrease in blood volume  decrease in venous return 4. Respiratory pump: Venous return increases during inspiration Inspiration  negative intrathoracic pressure  suction of blood into thoracic big veins  increased venous return 5. Muscle pump: Intermittent contractions of skeletal muscle particularly leg muscle  squeeze the veins  increases the flow of venous blood towards the heart  increase in venous return

7 6. Abdominal pump: Contractions of abdominal muscles  compresses the great veins, pushing venous blood towards the heart Right atrial pressure Blood volume Cardiac pump

Abdominal pump

Respiratory pump Vascular capacity

Venous return

Muscle pump

Ventricular compliance: - refers to the stretchability of ventricular myocardium - any increase in the compliance reduces EDV and thereby stroke volume e.g constrictive pericarditis & pericardial effusion Diastolic pause: - refers to the duration of diastole of ventricles - this influences the ventricular filling - this factor is directly related to EDV within physiological limits Atrial systole: - contributes 20% of ventricular filling at rest - influences EDV directly e.g - increase in atrial systole during exercise  increase in EDV - in atrial flutter & fibrillation, the contribution of atrial systole in ventricular filling is reduced

Homometric Regulation of Cardiac Output I . Extrinsic Factors Regulating Myocardial Contractility a) Neural factors: Sympathetic stimulation: Releases nor-epinephrine  binds to β1 receptors  increases cAMP  increase in intracellular calcium  increase in myocardial contractility Parasympathetic stimulation: Releases acetylcholine  binds to muscarinic receptors (M2)  hyperpolarization of SA nodal and myocardial cells  decrease in myocardial contractility b) Hormones: Epinephrine & Nor-epinephrine: Bind to β1 receptors increase in cAMP  increase in intracellular calcium  increase in myocardial contractility Glucagon: Increases myocardial contractility by increasing intracellular calcium without binding to β1 receptors Thyroxine: Increases the myocardial contractility by increasing the metabolic rate. c) Ions: Sodium & Potassium – decreases the myocardial contractility Calcium – increases the myocardial contractility

8 d) Drugs: β – blockers: e.g Propanaolol – block the β – receptors and decreases the myocardial contractility Calcium-channel blocker: e.g Verapramill – block the calcium channel  decrease in intracellular calcium  decrease in myocardial contractility Digitalis: Blocks Na+ - K+ ATPase  decrease in Na+ gradient across the membrane  calcium accumulation inside the cell  increase in myocardial contractility e) Coronary blood flow: Decrease in coronary blood flow ↓ Hypoxia, hypercapnia & acidosis ↓ Decrease in myocardial contractility

Intrinsic Factors Frank-Starling phenomenon

Force – Frequency relation

M Y O C A R D I A L C O N T R A C T I L I T Y

Extrinsic Factors Sympathetic Neural Parasympathetic Catecholamines Hormonal Glucagon Thyroxine Ions (Na+, K+ & Ca2+) β-blockers Drugs Calcium channel blockers Digitalis Coronary blood flow

Influence of heart rate on cardiac output - Direct relationship between heart rate and cardiac output Increase in HR ↓ Increase in intracellular calcium ↓ Increase in force of contraction

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This happens by two ways: 1. As a multiplying factor 2. Staircase phenomenon (This relation is linear upto 180 BPM. Beyond this level, venous return falls  decrease in cardiac output) Influence of peripheral resistance on cardiac output: - Initially, the variation in peripheral resistance tends to influence cardiac output - But the indirect effects maintain the cardiac output ---------------------------------------------------------------------------------------------------------------------

3. BLOOD PRESSURE Definition: Blood Pressure

: The lateral pressure exerted by the moving column of blood on the walls of the arteries Systolic BP : The maximum BP in the arteries during systole of the heart. Diastolic BP : The minimum BP in the arteries during diastole of the heart. Pulse pressure : The difference between systolic and diastolic pressure Mean Arterial BP : The average BP in the arteries. This is calculated as Diastolic BP + 1/3 of pulse pressure Normal Values: Blood Pressure : 120/80 mm Hg Systolic BP : 90 – 140 mm Hg Diastolic BP : 60 – 90 mm Hg Pulse pressure : 40 mm Hg Mean Arterial BP : 95 mm Hg Regulation Of Arterial Blood Presssure: Short – Term or Rapid Acting Mechanisms 1. Baroreceptor reflex 2. Chemoreceptor reflex 3. Cushing reflex 4. Stress relaxation & inverse stress relaxation 5. Capillary fluid shift 6. Hormones Baroreceptor reflex: - Also called as “Marey’s reflex” or “Sino-Aortic reflex” - Initiated by increase in blood pressure - Receptors are mechanoreceptors which respond to stretch in blood vessel wall - Receptors are called “Baroreceptors”. They are present in the carotid sinus and aortic arch - This mechanism can correct 2/3rd of fall in BP - The working range of BP is 60-200 mm Hg

10 Increase in BP ↓ Stimulation of baroreceptors (Carotid sinus and aortic arch) ↓ Stimulation of NTS (Nucleus of Tractus Solitarius) in medulla ↓ Inhibition of VMC (Vasomotor center)

Stimulation of CVC (Cardiovascular centerNucleus Ambiguus)

Inhibition of SNS (Sympathetic Nervous System)

Stimulation of vagus

Decreased sympathetic tone

Blood vessel

Vasodilatation Venodilatation

Increased vagal tone

Adrenal medulla

Decreased catecholamine secretion

Heart

Bradycardia

Net effect: Decreased Peripheral resistance & Decrease in cardiac output

 Decrease in BP

Decrease in BP ↓ Inhibition of baroreceptors (Carotid sinus and aortic arch) ↓ NTS is not stimulated ↓ stimulation of VMC (Vasomotor center)

Inhibition of CVC (Cardiovascular centerNucleus Ambiguus)

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Stimulation of SNS (Sympathetic Nervous System)

Inhibition of vagus

Increased sympathetic tone

Decreased vagal tone

Blood vessel

Adrenal medulla

Heart

Vasoconstriction Venoconstriction

Increased catecholamine secretion

Tachycardia

Net effect: Increased Peripheral resistance & Increase in cardiac output

 Increase in BP

CNS ischemic response: - This mechanism occurs due to ischaemia of brain - This may result due to severe fall in BP below 40 mmHg - If this response is specifically due to increase in intracranial pressure, it is called as “Cushing reflex” - The response is called “last ditch effort” as it tries to prevent the death of a person - The working range for this mechanism is 15-50 mm Hg - It can correct 90% of the fall in BP Decrease in BP (below 40 mm hg) ↓ Decreased blood flow to the brain ↓ Ischemia of brain ↓ Stimulation of VMC (Vasomotor center)

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Stimulation of SNS (Sympathetic Nervous System)

Increased sympathetic tone

Blood vessel

Vasoconstriction

Increase in BP Chemoreceptor Reflex: - Receptors respond to chemicals. So called as chemoreceptors - Two types of receptors – peripheral & central chemoreceptors - Peripheral chemoreceptors - Carotid bodies & Aortic bodies - Stimuli for receptors : Hypoxia, Hypercapnia & Acidosis Decrease in BP (<40 mm Hg) Cerebral hypoxia, hypercapnia & acidosis

Stimulation of VMC (Vasomotor center)

Stimulation of SNS (Sympathetic Nervous System) Increased sympathetic tone

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Blood vessel

Vasoconstriction Stress relaxation and reverse stress relaxation mechanism: Increase in BP  Stretching of blood vessels  Stress relaxation  Loss of vasomotor tone  increased capacity of vascular bed  Pooling of blood  Decrease in circulating blood volume  Decrease in BP Decrease in BP Blood vessels are not stretchedIncrease in vasomotor tone  decreased capacity of vascular bed Increase in circulating blood volume Increase in BP Capillary Fluid Shift Mechanism:

Increase in BP

Decrease in BP

Increase in capillary Hydrostatic pressure Fluid

Decrease in capillary Hydrostatic pressure Decrease in BP

Interstitial space

Fluid

Increase in BP

Interstitial space

Hormones: 1. Catecholamines: Fall in BP  release of catecholamines (epinephrine & norepinephrine) from adrenal medulla  Vasoconstriction & increase in cardiac output  increase in BP 2. ADH: In large amounts ADH causes vasoconstriction  increase in BP 3. Glucocorticoids: Cortisol and corticosterone sensitize the vascular smooth muscle to the action of catecholamines (permissive role) 4. Nitric oxide (Endothelium Derived Relaxing factor) :released by endothelium and acts locally causing vasodilatation

Long Term Regulation of Blood Pressure 1. Renal body fluid mechanism 2. Renin-Angiotensin mechanism 3. Hormones – Aldosterone & ADH

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Renal body fluid mechanism: Increase in BP

Decrease in BP

Increase in renal blood flow

Decrease in renal blood flow

Increase in GFR

Decrease in GFR

Increase in urine formation

Decrease in ECF volume

Decrease in urine formation

Increase in ECF volume

Decrease in BP (Restoration of BP)

Increase in BP (Restoration of BP)

Renin – Angiotensin Mechanism: Decrease in BP

Decrease in renal blood flow

Decrease in GFR

Renal ischemia or decreased Na+ & Cl- at macula densa

Release of renin from juxtaglomerular cells of kidney

15 Angiotensinogen

Angiotensin I

Angiotensin II & Angiotensin III Angiotensin II & Angiotensin III

Vasoconstriction

reabsorption of Na+ & Cl(direct effect on kidney)

Aldosterone secretion

ADH secretion

reabsorption of Na+ & Cl-

reabsorption of water

Increase in ECF volume

Increase in blood volume Increase in blood pressure

Hormones Regulating Blood Pressure: Aldosterone: Secreted from adrenal cortex in response to decrease in ECF volume. Increases the reabsorption of Na+ & Cl- in kidney tubules. This causes increase in ECF volume and blood pressure ADH: Secreted from posterior pituitary. Increases water reabsorption from kidney  increase in ECF volume and blood pressure ANP: Secreted from atrial myocardium in response to increase in ECF volume facilitates Na+, Cl-& H2O excretion into urine  decrease in ECF volume & blood pressure