Senior Consultant, Department of Nephrology & Urology Science, Kauvery Hospital, Salem, India
*Correspondence: Email: email@example.com
Pathophysiology of Hypertension
From our first-year physiology lessons we know that blood pressure is product of cardiac output and peripheral vascular resistance. Cardiac output is governed by volume status and heart rate. Peripheral Vascular Resistance is determined by vasoconstriction/vasodilatation of the blood vessels. Sympathetic nervous system and Renin Angiotensin Aldosterone System are the 2 main neurohumoral factors which determine all the above said factors. Renin is secreted from the juxtaglomerular apparatus of the kidney and activates Angiotensinogen secreted from the liver forming Angiotensin II and Aldosterone. Aldosterone and AT-II mediate salt and water retention (both) and vasoconstriction (AT-II). AT-II also increases sympathetic nervous activity. Apart from that afferent sympathetic activity from the kidneys is increased in patients with renal disease which in turn leads to increased efferent sympathetic activity. So, it’s important to understand that kidneys through Renin Angiotensin Aldosterone System (RAAS) plays a pivotal role in initiating and sustaining hypertension. Clinically speaking also kidney disease is both a cause and effect of hypertension whereas cardiovascular system is predominantly not a cause of hypertension but affected by hypertension. This basic understanding of physiology also helps us to understand the place of each antihypertensive and why RAAS blockade has gained prominence for treatment of hypertension.
Diagnosis of Hypertension
What’s new in hypertension guidelines starts with the way we record Blood pressure. All the new guidelines talk about standardised office BP measurement. This stresses on the following parameters:
Based on this standardised BP measurement ACC 2107 guidelines defines the following categories:
Confirmation of diagnosis requires:
International Society of Hypertension has come up with newer guidelines in 2020 which are far less stringent but I prefer ACC guidelines.
Treatment of Hypertension
When to treat?
Goal of Treatment
Which agents to use:
The preferred first line agents now would be ACE-I/ARB blockers (A), Long acting DHP Calcium Channel Blockers like Amlodipine (C) and Diuretics (D). The evidence for these drugs come from ASCOT and ACCOMPLISH trials.
In Stage 1, we can start with one drug either A or C. If BP not controlled then we add the second drug either A or C which was not used to begin with. Third step will be to add D.
In Stage 2, we start with A and C at low dose and titrate upwards. Third agent to be added will be a diuretic. If still not at target then add Mineralocorticoid Receptor antagonist.
Beta blockers are used preferentially in patients with AF and Fast ventricular rate, CAD, heart failure. In black’s better response is seen with diuretics and Calcium Channel blockers.
How to use ACEi-ARBs:
Hypertension in CKD
Goal of Hypertension therapy in CKD
From AASK, MDRD and SPRINT trial we have evidence that reducing BP to < 130/80 reduces mortality in CKD patients. It also retards progression of renal disease in proteinuric CKD patients. The current KDIGO guideline (2020) suggests target SBP of less than 120 in adult patients with CKD.
Agents of choice in CKD
Antihypertensives in CKD is based on presence or absence of proteinuria.
|Angiotensin inhibitors Diuretics- If GFR<30 then Loop diuretic or metolazone
|Diuretics if there is edema CCB or Angiotensin inhibitors
|Non DHP CCB like Diltiazem Mineralocorticoid antagonists Alpha blockers and others
|Mineralocorticoid antagonists Alpha blockers Others
All of us have to adopt standardised office BP measurements. Without standardisation, BP readings can vary hugely depending on how and where is it recorded making it impossible to compare and have uniform recommendations. Antihypertensive therapy and goals have changed in the last decade because of our understanding of the central role played by RAAS and publication of large randomised control trials.