Systemic Arterial Hypertension Flashcards
Heart rate and stroke volume are affected by…
Autonomic balance from sympathetic and parasympathetic nervous systems
SNS affects forces of muscle contraction by extrinsic inotropy
Blood volume and venous return affect force of muscle contraction by intrinsic inotropy
Heart rate and stroke volume control cardiac output
Smooth muscle tone is affected by….
Noradrenaline, angiotensin II and other circulatory or locally acting hormones e.g. No, ET, PGs
Decrease in resistance causes a decrease in smooth muscle tone
Increase in resistance causes an increase in muscle tone
Definitions of hypertension
That level of blood pressure associated with increased risk of some adverse effect at some time
That level of blood pressure at which treatment will do more good than harm
Guideline blood pressure values- ideal, stage 1, stage 2 and severe
Ideal: <120/80
Stage 1: >140/90 (>135/85)
Stage 2: >160/100 (>150/95)
Severe: SBP > 180 or DBP > 110
Diabetic blood pressure and/or cases of renal insufficiency
High BP = >130/80
Essential (primary/idiopathic) hypertension
Hypertension of unknown cause, most common form (>90%)
Likely to be mulitfactorial and polygenic with gene/ environment interactions, possible factors predisposing to increased TPR are:
basal sympathetic drive/ emotional stress, salt-sensitivity, renin output
Secondary hypertension
Hypertension secondary to an identifiable physiological, pharmacological or structural cause
~5% of cases
Assessment and management of all cases of hypertension should exclude treatable causal conditions as far as possible
Isolated systolic hypertension
Particularly raised in systolic component, common with ageing
Accelerated (malignant) hypertension
Rapid phase of rise of BP to high levels, development of complications
Uncomplicated/ complicated hypertension
Describe whether or not there is end organ disease e.g. stroke, renal failure
Causes of secondary hypertension
Renal or renovascular disease, adrenal disease, pregnancy, idiopathic or iatrogenic Cushing’s syndrome
Renal or renovascular disease (constriction of vessels to renal tissue)- e.g. polycystic disease, renal artery stenosis
Adrenal disease- e.g. primary hyperaldosteronism (Crohn’s disease), phaeocromocytoma
Pregnancy- e.g. complex/ unknown aetiology, several forms, chronic, gestational, pre-eclampsia, transient
Idiopathic or iatrogenic
Cushing’s syndrome- incl. chronic glucocorticoid therapy
Causes of secondary hypertension
Sleep apnoea, thyroid and parathyroid disease, congenital structural abnormalities, many drugs
Sleep apnoea- related to obesity
Thyroid and parathyroid disease- hyperthyroidism
Congenital structural abnormalities- coarctation of the aorta
Many drugs- NSAIDs, COX2 inhibitors, cocaine, amphetamine, sympathomimetics, ketamine, oral contraceptive hormones, erythoropoietin etc.
Physiological basis of hypertension
MAP= CO x TPR
Majority of people with established hypertension do not have increased CO
Increased TPR is the major finding in most hypertensive patients
What initiates increased TPR in hypertension?
Environmental factors- responses to stress, dietary sodium, alcohol consumption, obesity
Genetic factors are multiple and not fully defined but strong familial and racial tendencies
Renal, neural, endocrine and structural factors could all contribute to increased TPR
Increased TPR maintained by medial hypertrophy in arterioles
Role of SNS/ stress
Exaggerated sympathetic outflow from nucleus tractus solitarius in response to repeated episodes of stress»_space;> medial hypertrophy of arterioles
Structural changes in the arterioles lead to non-reversible rise in TPR, maintaining and amplifying the hypertension
