A1 Hypertension Flashcards
Role of the bronchial circulation
complementary to pulmonary circulation, supplying lung cells with oxygen and nutrients
BP is dependent on
- TPR
- CO (amount of blood ejected by heart each minute) (CO = HR x Stroke volume)
BP = CO x TPR
If arterioles are dilated what does that mean for BP
dilated - low resistance to flow: low peripheral vascular resistance –> low BP
Factors affecting
- arterial BP (6)
- systemic BP
- Stroke volume, Heart rate, Peripheral resistance, Elastic vessels, Blood volume, Ventricular ejection
- ANS (immediate), Renin-angiotensin system (slower/ long term reg), Local chemical mediators released from vascular endothelium
how do the following influence BP
- heart
- arteries
- veins
- acts mainly via β1 to increase cardiac contractility and HR = increased CO and BP
- SNS produces vasoconstriction via α1 (increases BP & afterload on the heart)
- SNS α1 results in venoconstriction (increases venous return to heart (preload), raises CO and increases BP)
explain RAS effect on BP
Na depletion –> kidneys release renin via SNS –> angiotensinogen converts to Ang I. ACE converts to Ang II = vasoconstriction
Renal medulla releases aldosterone = Na retention —> increases BP
role of endothelium derived Factors
describe
1. EDRFs
2. EDCFs
Modulation of vascular smooth muscle and vessel diameter
- NO, Prostacyclin, Hyperpolarising factor
- Endothelin (ET-1), Thromboxane A2 (TxA2)
Define
- Systolic pressure
- Diastolic pressure
- Pulse pressure
- Mean arterial pressure
- max arterial P reached during peak ventricular ejection
- min arterial P just before ventricular ejection begins
- difference between SP & DP
- average P in the Cardiac cycle
hypertension risk factors
- primary
- secondary
- obesity, lack of exercise, alcohol, non insulin-dependent diabetes, age
- initiated by other disease:
Aortic coarctation, Renal disease, Mineralocorticoid excess, Thyroid disease, Eclampsia
Anti-hypertensive drugs
describe drugs acting on SNS
- Beta blockers
(e.g. atenolol, propanolol)
Decrease CO, reduce renin production (reduce AngII), can indirectly cause vasodilation of peripheral arteries (CO feeds into BP)
((predominate effect on B1 heart (some extra effects via B2 by vasodilation)) - a-blockers
(e.g. prazosin (selective))
Block post-synaptic a1 = dilation of arteriolar resistance vessels and lower peripheral resistance. Also dilate venous capacitance vessels, reducing venous return and CO
describe drugs action of RAS
- ACE inhibitors (e.g. captopril)
- Ang II receptor antagonists (e.g. losartan)
selectively block AT1 receptors which mediate the vasoconstrictive effects of AngII
describe Vasodilators and give examples
- Diuretics (e.g. Thiazide)
Act at varying sites in the kidney to increase Na+ and water depletion = hypotensive effect. - Ca channel blockers (e.g. amlodipine)
Block Ca entry into vascular smooth muscle cells &/or cardiac muscle cells. Promotes relaxation of the muscle and vasodilation.
what antihypertensive drugs act at
- CNS
- Blood vessels
- Kidney
- heart
- B blockers, a2 agonists
- a1 blockers, Ca blockers, vasodilators, AT1 antagonists, ACE inhibitors
- diuretics, B-blockers, ACE inhibitors
- B-blockers
Define
1. Systemic hypertension
- usually asymptomatic and often diagnosed when patient presents with another condition
Define Pulmonary hypertension
common w/ COPD: pulmonary vasculature has been affected = increased vascular resistance
Have shortness of breath/ ~chest pain
Sustained increase in pulmonary vascular resistance –> progressive right HF