HYPERTENSION(HTN)

 CONSIDER YOU ARE LEADING A HAPPY AND RISK FREE LIFE IF YOU DO NOT HAVE THE ABOVE WORD IN YOUR LIFE.

INTRODUCTION

HYPERTENSION IS THE NUMBER ONE HEALTH RELATED RISK FACTOR IN INDIA 

• IT HAS THE LARGEST CONTRIBUTION TO BURDEN OF DISEASE AND MORTALITY
• CONTRIBUTES TO AN ESTIMATED 1.6 MILLION DEATHS IN INDIA
• DUE TO ISCHEMIC HEART DISEASE OR STROKE
• 57% OF DEATHS RELATED TO STROKE AND 26% OF DEATHS RELATED TO CORONARY ARTERY DISEASE ARE DUE TO HYPERTENSION

DEFINITION

A VERY BEST DEFINITION FOR HTN IS 

LATERAL PRESSURE EXERTED BY THE COLUMN OF BLOOD ON THE VESSEL WALL MEASURED IN mmHg

SO BLOOD PRESSURE =CARDIAC OUTPUT*PERIPHERAL VASCULAR RESISTANCE(PVR)

EQUALS TO =(STROKE VOLUME *HEART RATE)*PVR

WHICH EQUALS TO=(END DIASTOLIC VOLUME-END SYSTOLIC VOLUME) *HEART RATE)*PVR)

• BP IS DETERMINED BY  
• PRE LOAD (EDV)=VOLUME OF BLOOD IN VENTRICLE AT END OF DIASTOLE
• AFTERLOAD(PVR)=RESISTANCE AGAINST WHICH VENTRICLE HAS TO PUMP BLOOD
• MYOCARDIAL CONTRACTILITY 
• VENOUS RETURN

BLOOD PRESSURE REGULATION AND DIVERSE INFLUENCES ON CARDIAC OUTPUT

• CARDIAC OUTPUT IS INFLUENCED BY TWO THINGS 
• BLOOD VOLUME&CARDIAC FACTORS
• IN BLOOD VOLUME 

1. SODIUM
2. MINERALOCORTICOIDS
3. ATRIAL NATRIURETIC PEPTIDE

CARDIAC FACTORS

1. HEART RATE 
2. CONTRATILITY

PERIPHERAL RESISTANCE GOVERNED BY 3 FACTORS

1. HUMORAL FACTORS 
2. NEURAL FACTORS
3. LOCAL FACTORS

HUMORAL FACTORS

CONSTRICTORS

1. ANGIOTENSIN II
2. CATECHOLOMINES
3. THROMBOXANE
4. LEUKOTRIENES
5. ENDOTHELIN

DILATORS

1. PROSTAGLADINS
2. KININS
3. NITROUS OXIDE

NEURAL FACTORS

1. ALPHA ADRENERGIC ACTS AS  CONSTRICTORS 
2. BETA  ADRENERGIC ACTS AS DILATORS

LOCAL FACTORS 

1. AUTOREGULATION
2. pH 
3. HYPOXIA

TECHNIQUES TO MEASURE BP

                                                                

• BEST METHOD -OSCILLOMETRIC METHOD USING OMRON 907
• OSCILLOMETRIC BP APPARATUS(SPRINT TRAIL)
• 24 HOUR AMBULATORY BP MONITORING
• PALPATORY METHOD
• AUSCULTATORY METHOD
• ANERIOD SPHYGMOMANOMETER

KOROTKOFF SOUNDS

KOROTKOFF SOUNDS OR K SOUNDS ARE THE SOUNDS MEDICAL PERSONNEL LISTEN WHEN THEY ARE TAKING BLOOD PRESSURE USING A NON INVASIVE PROCEDURE

                                             

AUSCULTATORY GAP

AN AUSCULTATORY GAP IS A PERIOD OF DIMINISHED OR ABSENT KOROTKOFF SOUNDS IN THE ABOVE PIC WHERE THE SILENCE PHASE WHICH LEADS TO THE START OF NEW PHASE THIS GAP IS CALLED AS AUSCULTATORY GAP ,THE IMPROPER INTERPRETATION OF THIS GAP MAY LEAD TO BLOOD PRESSURE ERRORS

• UNDERESTIMATION OF SYSTOLIC BLOOD PRESSURE
• OVERESTIMATION OF DIASTOLIC BLOOD PRESSURE
• COMMONLY SEEN IN HTN
• DISTURBANCE OF FLOW OF BLOOD IN ARM

                                                                             

 BLOOD PRESSURE GUIDELINES

THE  GUIDELINES  ARE VERY MUCH IMPORTANT BECAUSE OF THESE GUIDELINES WE TREAT A PATIENT ACCURATELY AND IN CORRECT PROPOSITIONS

AS OF NOW THE EUROPEAN SOCIETY OF CARDIOLOGY  2018 NEW GUIDELINES 

                                                            

JOINT NATIONAL COMMITTEE(JNC-8) GUIDELINES IN INDIA

FACTORS LEADING TO HYPERTENSION

TWO FACTORS 

ENVIRONMENTAL

             +

GENETIC 

• IN THIS TAKING ENVIRONMENTAL FACTORS

MOST IMPORTANT RISK FACTOR OR STRONGEST INDEPENDENT RISK FACTOR BEYOND ANY DOUBT IS OBESITY (WEIGHT GAIN)AND MANY A TIME  PART OF YOUR METABOLIC SYNDROMES

APART FROM OBESITY THERE ARE FEW MORE INDEPENDENT RISK FACTORS AMONG WHICH IS MUCH ACCEPTED THEORY WHICH IS DIET 

• DIET WHICH IS HIGH IN SODIUM 
• DIET WHICH IS LOW IN K,Ca,Mg

STRESS IS ALSO A IMP FACTOR

PARTIAL LIST OF POSSIBLE CONTRIBUTING FACTORS 

• ALCOHOL CONSUMPTION
• DIET LOW IN VITAMIN D
• HIGH FRUCTOSE DIET
• LACK OF EXERCISE

GENETIC FACTORS

HEREDITARY 

WE SHOULD LOOK AT THE HISTORY OF PARENTS WHETHER ONLY ONE IS HAVING OR BOTH OF THEM AND WHICH GENE IS RESPONSIBLE FOR HTN

• EITHER PARENT IS HYPERTENSIVE  WHAT IS THE RISK OF HTN?
• THE RISK OF YOU GETTING HTN WOULD BE 10 -15%
• IF BOTH PARENTS ARE HYPERTENSIVE WHAT IS THE RISK OF HTN?
• THE RISK WOULD BE 30-40%
• SO THE GENE RESPONSIBLE FOR HTN IS ALPHA ADDUCIN GENE

PATHOPHYSIOLOGY OF HYPERTENSION

SO WE HAVE TWO TWO FACTORS GENETIC AND ENVIRONMENTAL FACTORS SO HOW THESE FACTORS CAUSE HTN WE WILL KNOW 

SO WHEN YOU SEE A PATIENT OR ASSES HIM YOU WILL COME TO KNOWN THE TYPE OF HTN HE HAS GOT 

• ONE IS VOLUME DEPENDENT HTN 
• SECOND ONE WOULD BE PRESSURE DEPENDENT HTN 

COMING TO THE VOLUME DEPENDENT HTN

SODIUM AND WATER IS MORE INTRAVASCULARLY SO PRESSURE IS MORE SO HTN 

IN PRESSURE DEPENDENT HTN THERE IS IRREGULAR OR DISTURBED AXIS BETWEEN RAS AND SYMPATHETIC SYSTEM 

SO WHAT IS ACTIVATING THESE? 

SO COMING TO VOLUME AND ALSO B2B WHICH IS BACK 2 BASICS 

WE KNOW BP=CO *PR

PRESSURE NATRIURESIS

UNDERSTAND THIS EVEN IF YOUR CO IS HIGH AS LONG AS KIDNEY IS NORMAL IT IS NOT POSSIBLE TO HAVE A SUSTAINED RISE IN BP

WHICH MEANS WHEN CO IS INCREASED =INCREASED RBF (RENAL BLOOD FLOW)=INCREASED RENAL MEDULLARY FLOW=WHICH INCREASES RENAL INTERSTITIAL HYDROSTATIC PRESSURE=INCREASED SODIUM AND WATER EXCRETION

SO THE CONCLUSION IS AS LONG AS YOU HAVE FULLY FUNCTIONAL KIDNEY THERE IS NO WORD OF HTN

SO THIS VERY FAMOUS THEORY IS CALLED PRESSURE NATRIURESIS

SO NOW WE SHOULD BE MORE CONCERNED AND CAREFUL ABOUT ONE THING SEE WHEN WE HAVE NORMAL KIDNEY NO MATTER WHAT THE CO IS OUR KIDNEY HANDLES IT, SO NOW WHAT CAN CAUSE THE HTN, THE OTHER PRODUCT OF BP WHICH IS PR (PERIPHERAL RESISTANCE) COMES IN THIS SCENARIO

SO  ENVIRONMENT +GENETIC FACTORS CAN CAUSE TWO THINGS 

ENVIRONMENT              VASCONSTRICTION 

         +                      =             

GENETIC                            DEFECT IN SMOOTH MUSCLE PROLIFERATION

SO THESE TWO INCREASES PR PERIPHERAL RESISTANCE WHICH LEADS TO HTN

WHICH ARE CAUSED BY IMPAIRED RAS AXIS AND SYMPATHETIC SYSTEM

SO NOW LETS STUDY PERIPHERAL RESISTANCE INDUCED HYPERTENSION 

SO THESE ENVIRONMENTAL AND GENETIC FACTORS ACTS BY TRIGGERING SMOOTH MUSCLE PROLIFERATION.HOW? THESE RISK FACTORS CAUSE A ENDOTHELIAL INJURY OR IN OTHER WORDS PRODUCE A DYSFUNCTIONAL ENDOTHELIUM WHICH INCREASES SMOOTH MUSCLE PROLIFERATION INCREASES PR CAUSES HTN

SO WHICH IS MY PRESSURE DEPENDENT HTN IS DEPENDENT ON SMOOTH MUSCLE PROLIFERATION  WHICH IN TURNS DEPENDS ON DYSFUNCTIONAL ENDOTHELIUM 

SO ALL THE WAY LEADING TO HTN 

PATHOGENESIS OF BENIGN HTN

SO LETS STUDY WHAT HAPPENS ONCE WE HAVE HTN

SO THIS POISON WHICH IS HTN WILL FURTHER LEAD ON TO MORE ENDOTHELIAL DAMAGE =FURTHER EXTRA CELLULAR MATRIX =EXTRA SMOOTH MUSCLE PROLIFERATION =SO THIS IN THE VESSEL CAUSE TO CHANGE WHICH IS CALLED AS HYALINE ARTERIOSCLEROSIS =THIS MEANS YOUR VESSEL BECAME MORE STIFFER MORE HYALINE 

SO THE HYALINE ARTERIOSCLEROSIS IS CAUSED MAINLY BY BENIGN OR PRIMARY OR ESSENTIAL HTN

HYALINE ARTERIOSCLEROSIS HAVING THIS WILL LEAD TO WORSENING OF ATHEROSCLEROSIS WHICH IS IN 5% OF PATIENTS IT CAUSES RUPTURE OR EMBOLISATION OR EVEN MIGHT GO FOR CLOTTING IN SMALL VESSEL SO THIS CLOTTING IN SMALL VESSEL CAN LEAD TO A DANGEROUS CONDITION WHICH IS CALLED MALIGNANT HTN

                                                      

PATHOGENESIS OF SYMPATHETIC SYSTEM

SO THIS SYMPATHETIC SYSTEM CAUSES VASOCONSTRICTION=SO THIS VASOCONSTRICTION CAUSES ISCHAEMIC HEART DISEASE DUE TO HTN =TARGET ORGAN DAMAGE  WHICH IS LVH (LEFT VENTRICULAR HYPERTROPHY)

SO OVERACTIVITY OF SYMPATHETIC SYSTEM IS WHAT ACCTUALLY WE DONT WANT !!!!!!!!!

SO WHAT IS THE REASON FOR THIS OVERACTIVITY????????

HERE ALSO WE HAVE MULTIPLE FACTORS BUT THE MOST IMPORTANT WOULD BE ENDOTHELIAL DYSFUNCTION

WHAT CAUSING ENDOTHELIAL DYSFUNCTION?

1. DYSLIPIDEMIA
2. DIABETES MELLITUS
3. OBESITY
4. SMOKING
5. OXIDATIVE STRESS

OUT OF ALL THESE THE ONE FACTOR WHICH IS VERY DANGEROUS AND CAN ALSO LEAD TO START OF ANOTHER PATHWAY AND COMPLICATES EVEN MORE WHICH IS.......

RENAL ISCHEMIA WHICH CAUSES OVERACTIVITY OF BETA 1 RECEPTOR WHICH IN TURN ACTIVATES RAS MECHANISM 

                                                            

PATHOGENESIS OF RENIN ANGIOTENSIN ALDOSTERONE PATHWAY( RAAS)

B2B BACK TO BASICS 

IN THIS MECHANISM LETS STUDY THE RECEPTORS ABOUT RENIN AND WHICH IS BETTER ACE INHIBITORS OR ARB^S

SO 3 STIMULI FOR RENIN RELEASE WOULD BE

1. PROSTAGLADINS 
2. BETA 1 RECEPTORS
3. DECREASED RENAL PERFUSION 

ANGIOTENSIN I IS CONVERTED TO ANGIOTENSIN II  BY THE ENZYME PRESENT IN VASCULAR ENDOTHELIUM OF LUNGS WHICH IS ANGIOTENSIN CONVERTING ENZYME KINASE II 

ANGIOTENSIN II IS A POWERFUL VASOCONSTRICTOR 

SO ANG II HAVE TWO RECEPTORS AT1 AND AT2

SO ON AT1 ALDOSTERONE ACTS AND CAUSES VASOCONSTRICTION INCREASES SODIUM AND WATER RESORPTION 

BUT IN RECENT STUDIES WE HAVE SEEN THAT THE SAME ALDOSTERONE ACTING ON AT2 WILL CAUSE VASODILATION ,NATRIURESIS,INHIBIT CELL GROWTH

SO COMING TO WHICH IS BETTER ACE INHIBITORS OR ARB^S 

WHEN YOU USE ACE INHIBITORS YOU COMPLETELY BLOCK ANG II WHICH BLOCKS BOTH AT1 &AT2 

BUT U WANT AT2 TO BE ACTIVE SO WHEN YOU USE ARB^S YOU CAN BLOCK AT1 AND GET GREAT RESULTS 

                                                      

CONSEQUENCES OF HTN

SEE WHEN WE HAVE HTN BY SOME HOOK OR CROOK OR BY SOMETHING YOU HAVE TO REDUCE IT WHY?

BECAUSE IT CAUSES TARGET ORGAN DAMAGE 

SO WHICH ORGAN STANDS FIRST IN THIS DAMAGE LIST IT WILL BE THE HEART 

AS STUDIED ABOVE IT CAUSES LVH LEFT VENTRICULAR HYPERTROPHY WHICH IN RETURN CAUSES DIASTOLE DYSFUNCTION AND BELIEVE ME THERE ARE NO DRUGS TO TREAT DIASTOLE DYSFUNCTION

NEXT WOULD BE BRAIN IT CAUSES STROKE AND MULTIPLE LACUNAR INFRACTS WHICH IS ALSO MAJOR CAUSE OF DEATH IN INDIA 

INFORMATION OF DRUGS USED IN HTN

COMPLETE MANAGEMENT WILL BE GIVEN IN THE NEXT ARTICLE NOW ONLY SUMMARY OF DRUGS USED IN HTN AND PREPARATIONS AVAILABLE AND SITE OF ACTION OF THE MAJOR CLASSES OF ANTIHYPERTENSIVE DRUGS WILL BE SHOWN

SUMMARY OF DRUGS USED IN HTN

                                                

PREPARATIONS AVAILABLE

                                                          

SITE OF ACTION OF THE MAJOR CLASSES OF ANTIHYPERTENSIVE DRUGS

                                                           

I HAVE TRIED MY LEVEL BEST TO COVER EVERYTHING PLEASE SHARE IT FOR MAXIMUM REACH 

THANKYOU