Radial pulse and other peripheral pulses.pptx

normal characteristics of radial pulse

1. ARTERIAL PULSE

2. Pulse:  The pulse is defined as rhythmic expansion of the arterial wall due to transmission of pressure waves along the walls of the arteries that are produced during each systole  Carotid: 30ms  Radial: 80ms  Femoral: 75ms  Brachial: 60ms

3. I M P O R T A N C E :  Also called the mirror of heart  Information about arterial wall condition  Rough estimation of SBP n DBP  State of heart n circulation  Detect and diagnosis of arrythmia  Diagnosis in case of AR and acute LVF

4.  The arterial pulse should be examined in all 4 limbs and both sides of the neck Radials Brachials Carotids Femorals Popliteals Temporal Facial Peripheral arteries of the legs :Dorsalis pedis Posterior tibial

5. How to feel the Pulse  The Radial pulse:  The 3 middle fingers are used  The palmar surface of the fingers overlies the radial A. and encircles the wrist  At first the artery is completely occluded, then gradually release the pressure until maximum feeling of the pulse wave is perceived.

6. The Carotids  The patient lies down with the head of the bed elevated 30 degrees  Carotid pulsations may be visible just medial to sternomastoid  Place the left thumb on the right carotid A. in the lower third of the neck at the level of the cricoid cartilage, just inside the medial border of the sternomastoid and press posteriorly  Never press both carotids at same time

7. Comment on the Pulse Rate Rhythm Volume ( amplitude) Comparison of the two sides Special character Condition of the arterial wall

8. Rate Rate of the pulse at radial artery Normal at rest : 60- 10 0 beat s / min if irregular count at apex weak beats may not be felt (pulsus deficit) Apex pulse deficit: > 10 suggestive of AF

9. Tachycardia Causes Physiological Pathological Exercise After meals Anger Emotion & excitement Infants & children Pregnancy High environmental temperature Fever Hyperthyroidism Anemia Beriberi A-V fistula Heart failure PSVT AT, VT

10. Bradycardia Causes Physiological Pathological Athletes Fear Grief Old age Meditation Myxedema/ Hypothyroidism Increased Intra cranial pressure Obstructive Jaundie Heart blocks Drugs: digitalis, propranolol

11. Rhythm Is the rhythm regular or irregular? 1. Normally regularly regular 2. Sinus arrhythmia: phasic irregularity with respiration, 3. Irregular: 1. Regularly irregular: 1. PAT with Fixed AV Block Atrial flutter 2. 3. Ventricular bigeminy or trigeminy 2. Irregularly irregular: 1. APCs, AF VPCs 2. 3. PAT with varying degree of block

12. Volume (Amplitude) Degree of expansion between systole and diastole Measurement of pulse pressure  Hyperdynamic : ( high PP , SV)  Anxiety  Exercise  AR  Fever  Anemia  Thyrotoxicosis  AVF  Beriberi  Hypovolemic: (low PP, SV)  Shock  CHF  Hypovolemia  Stenotic Valvular disease  My o carditis  Cardiomyopathies

13. Force and tension:  Force Indicates SBP High in : I solated S ystolic H TN , AR PDA, Hyperdynamic states: Low in: Shock, Cardiac failure, Stenotic Valvular lesion, Cardiac Temponade  Tension: Indicates DBP

14. Comparison of both sides Causes of unequal pulse 1. Genetic absence or change in the cours e of radial artery (anomalous radial artery) 2. Compression of the vessel Atheromatous plaque Embolus 3. 4.

15. Percussion wave (P): ejection phase of ventricles Tidal wave (T): falling blood column in slow ejection phase Dicrotic notch (N): closure of aortic valve..marks end of ventricular systole Dicrotic wave (D): rebound of blood column from closed aortic valve

16.  Anacrotic Pulse (Pulsus Tardus ):  Slow rise, slow fall  Duration of pulse is prolonged  Amplitude is small  Lazy in character (Tardus)  In aortic stenosis  Dicrotic Pulse:  One peak in systole, one in diastole  Myocardial disease with reduced CO and TPR  LVF  Cardiac Tamponade  Dehydration

17. Collapsing and Water hammer pulse , C orriagan , bounding pulse  Rapid upstroke  Rapid down stroke  High amplitude  Short duration  Causes:  Aortic incompetence  PDA  Hyperdynamic states: Fever, Anaemia, Thyrotoxicosis, pregnancy and AV fistula

18. Pulsus Bisferiens Pulse has 2 peaks:  two peaks in systole  d/t ejection of rapid jet of blood  AS + AR  Severe AR  HOCM A double pulse is felt and seen in the carotid

19. Pulsus Par v us :  Small volume pulse  Low CO  A/w Tachycardia, thready pulse  Physiological: cold, anxiety  Vessel occlusion  CoA of Aorta  Severe Hypotension (Shock)  Severe AS PS  MI  Severe PAH Pulsus magnus

20.  Jerky pulse:  Small volume & collapsing  HOCM  Severe MR  AR with LVF  Pulsus alterans:  Alternate large and small volume pulse  LV Failure  Cardia Arrythmias

21. Pulsus paradoxus:  Exaggerated decrease in strength of arterial pulse during inspiration, Inspiratory fall of SBP >10mmHg  Cardiac temponade  Constrictive pericarditis  Acute asthma  SVC obstruction  Reverse pulsus paradoxus:  HOCM  AV dissociaton

22. JVP Jugular venous pulse

23. JUGULAR VENOUS PULSE Pressure change in atrium is directly reflected in internal jugular veins. Waves of JVP Jugular venous pulse (JVP) has five waves: three positive waves and two negative waves (descents). The positive waves are a , c , and v waves, and two descents are x and y descents. a wave: This is due to atrial contraction . c wave: This wave coincides with the onset of ventricular systole and results from the bulging of tricuspid valve ring into the right atrium as the right ventricular pressure rises. v wave: indicates the passive rise in pressure in the right atrium as venous return continues while the tricuspid valve remains closed.

24. JUGULAR VENOUS PULSE Waves of JVP Jugular venous pulse (JVP) has five waves: three positive waves and two negative waves (descents). The positive waves are a , c , and v waves, and two descents are x and y descents. x descent: caused by a fall of right atrial pressure due to relaxation of the right atrium. y descent: due to fall in right atrial pressure when blood enters into the right ventricle as tricuspid valve opens.

25. Measurement of JVP

26. Abnormal JVP Waves Conditions of raised JVP 1. Right-side heart failure 2. Obstruction of superior vena cava 3. Increase in circulating blood volume Pregnancy Acute nephritis Over-enthusiastic treatment with IV fluids 4. Congestive heart failure 5. Constrictive pericarditis 6. Tricuspid incompetence

27. Prominent ‘a’ Wave 1. Pulmonary stenosis 2. Pulmonary hypertension 3. Tricuspid stenosis (if atrial fibrillation is associated with it, a wave may not be seen). 4.  Myxoma of right atrium 5. Distended right atrium in atrial septal defect 6.  Cardiomyopathy PHYSIOLOGICAL BASIS: Prominent ‘a’ wave occurs due to increased force of right atrial contraction associated with right atrial hypertrophy or hypertrophy of right ventricle. When right atrium contracts against increased resistance , prominent a wave occurs.

28. Cannon Wave When amplitude of ‘a‘ wave is abnormally big, it is called giant ‘a’ wave or cannon wave. It occurs when right atrium contracts against a closed tricuspid valve . Canon wave is seen in: 1. Complete heart block when atrial and ventricular systoles coincide. 2. Nodal rhythm when the atrium and ventricle are activated simultaneously.

29. Absence of ‘a’ Wave: in atrial fibrillation . Prominent ‘v’ Wave: seen in tricuspid regurgitation because when ventricle contracts during systole blood enters into right atrium through the incompetent tricuspid valve.

30. PATHOPHYSIOLOGY OF HEART FAILURE

31. Definition This is a pathophysiologic state in which an abnormality of cardiac function results in inability of the heart to pump blood at a rate adequate for the requirements of the tissues of the body. Occurs due to either decreased myocardial contractility or increased pressure or volume overload. The usual physiological alterations - decreased stroke volume (in forward failure) and damming of blood in the venous compartment (in backward failure ).

32. Types of Heart Failure Acute vs. Chronic Failure Acute heart failure occurs following acute myocardial infarction or rupture of a heart valve. Sudden decrease in cardiac output causes severe hypotension (therefore, edema is not a feature ). Chronic failure occurs due to a slowly progressive disease in which blood pressure may be maintained ( edema in the dependent parts is a feature ).

33. Types of Heart Failure Left-sided vs. Right-sided Failure Left ventricular failure - C ongestion occurs in the pulmonary circulation ; therefore presents with dyspnea and orthopnea. Right-sided failure - Congestion occurs in the systemic circulation , therefore, increased JVP, hepatomegaly, and edema in the dependent parts are usual features.

34. High Output vs. Low Output Failure H igh output failure - Heart pumps abnormally large quantities of blood to deliver adequate oxygen to the tissues. This occurs in conditions like severe anemia, Hyperthyroidism, Beriberi, Arterio -venous fistula and Paget’s disease Low output failure occurs due to failure of the heart to pump blood (due to decreased myocardial contractility ).

35. Forward vs. Backward Failure B ackward heart failure - P ressure and volume in the atrium and venous compartment behind the failed ventricle are more, therefore, edema occurs. F orward heart failure - Inability of the ventricle to pump blood causes tissue hypoxia that increases renin secretion. This activates rennin-angiotensin-aldosterone axis, therefore, edema (due to water retention) may be seen.

36. Systolic vs. Diastolic Failure The systolic heart failure occurs due to the systolic ventricular dysfunction . It is commonly seen in ischemic heart disease or due to dilated cardiomyopathy. The diastolic failure occurs due to the failure of relaxation of the ventricle . This is usually seen in restrictive cardiomyopathy as seen in amyloidosis in which the heart muscle is infiltrated by amyloid proteins. Due to inability of the ventricles to relax, the end-diastolic volume and therefore, cardiac output decreases.

37. Cardiac Changes in Heart Failure Pressure Overload In pressure overload, increased blood pressure increases the afterload . Heart pumps blood against increased resistance . Early Stage: Increased afterload results in concentric hypertrophy of the ventricles The functional capacity of ventricle in such a situation depends on the stress exerted on the ventricle . According to Laplace law, stress in the ventricular wall is the product of pressure and radius of ventricular cavity divided by ventricular wall thickness. Ventricular wall stress increases.

38. Cardiac Changes in Heart Failure Pressure Overload 2. Stage of Compensation (Concentric Hypertrophy): W all stress normalizes due to increase in wall thickness and decrease in cavity radius of ventricle. Therefore , ventricular function is maintained. 3. Stage of Hypertrophy & Dilatation : V entricular stress increases due to proportionate increase in radius caused by chamber dilation, which leads to failure of the myocardium to pump blood, causing systolic failure

39. Volume Overload In volume overload, due to increased venous return , diastolic pressure increases . This causes chamber enlargement that mainly results in eccentric hypertrophy . Early Stage (Stage of Dilation) : W all stress increases due to increased radius of the ventricular chamber. Stage of Eccentric Hypertrophy : Subsequently , wall stress is normalized due to increased wall thickness and decreased radius of the chamber. Thus, ventricular function is maintained in this stage. Later, in the stage of further dilation , wall stress becomes more due to increased radius of ventricular chamber that finally causes heart failure.

40. Clinical Features Dyspnea This occurs due to failure of the left ventricle to pump blood effectively that produces tissue hypoxia. Heart failure (early stage) - D yspnea occurs during due to failure of left ventricular output to meet oxygen demand during exercise. Heart failure(advanced stage) - D yspnea occurs even at rest due to increased pulmonary venous pressure or due to inadequacy of ventricular pumping.

41. Clinical Features Orthopnea - D yspnea in recumbent position . It is usually relieved by sitting upright . The difficulty in breathing in supine posture occurs due to: i )  Redistribution of blood from abdomen and lower extremities into the chest during recumbency causes an increase in pulmonary hydrostatic pressure. Pooling of blood in the pulmonary vascular bed adds to the already congested lungs. ii) Reduction in vital capacity occurs as diaphragm is pushed towards lungs in supine position. This is aggravated by hepatomegaly or ascites .

42. Paroxysmal Nocturnal Dyspnea - Episodes of dyspnea and cough of sudden onset in nights that usually awaken the patient from sleep. O ccurs partly due to the depression of respiratory centers during sleep and partly to the accumulation of excess fluid in the lungs in recumbent posture in sleep. During sleep, pulmonary venous pressure and pulmonary capillary pressure increase. This results in transudation of fluid into the air spaces. Gets immediate relief as the pulmonary vascular congestion decreases in upright posture . However , many such episodes occur in paroxysms . Therefore, it is called paroxysmal dyspnea. As it occurs in the night, it is also called paroxysmal nocturnal dyspnea.

43. Fatigue (Weakness & Exercise Intolerance) O ccurs due to decreased cardiac output that causes tissue hypoxia. The exercise intolerance occurs due to decreased perfusion of skeletal muscles and decreased oxygen supply to meet the need of the body. Edema in the Dependent Parts Important feature of congestive cardiac failure. Ankle or pedal edema in Ambulatory patients Sacral edema in bed-ridden patients.

44. Mechanism of edema formation in heart failure

45. Hepatomegaly This occurs due to hepatic congestion. Tender hepatomegaly is an important feature of right ventricular failure (and also of congestive cardiac failure). Increased JVP Jugular venous pressure is elevated due to increased right atrial pressure. Raised JVP is a reliable sign of congestive cardiac failure. Ascites Accumulation of excess of free fluid in peritoneal cavity is called ascites. This occurs in advanced stage of heart failure.

46. (A) Increased jugular venous pressure (JVP) in a case of heart failure; (B) Note the prominent and engorged jugular vein on the right side of the neck

47. PHYSIOLOGICAL BASIS OF MANAGEMENT 1 . Rest : Adequate rest decreases venous pressure and congestion. 2. Diet: A salt restricted , but a normal caloric diet is prescribed for heart failure patients. Salt restriction decreases water retention. 3. Digitalis: Digitalis improves heart function by its positive inotropic effect. It increases myocardial contractility and therefore, cardiac output. Digitalis acts by inhibiting sodium potassium pump activity on the myocardial cells. Therefore, intracellular sodium increases, which is exchanged with extracellular calcium. This results in increased calcium concentration in the cell that increases myocardial contractility .

48. 4. Diuretics: Diuretics promote water excretion . By decreasing ECF volume, diuretics decrease venous return to the heart. This decreases load on the heart 5 . Vasodilators : Vasodilators decrease peripheral resistance (afterload). Therefore, cardiac output increases. 6. ACE inhibitors: ACE inhibitors prevent the formation of angiotensin II. 7. Angiotensin receptor antagonists: Angiotensin antagonist such as Losartan prevents the action of angiotensin on blood vessel. 8. Treatment for the primary cause: Removal of precipitating factors and correction of underlying cause of heart failure should be initiated along with other modalities.