Topic 8 - CVD 1 Flashcards
Hypertension
Constant elevation of systemic arterial BP, resulting from sustained ↑ in TPR, ↑blood volume or both
Risk factors
- age, race, stress, obesity, Na intake, excessive alcohol, low vit d, low k diet, chronic conditions
Consequences - chronic hypertension
- stiffness of arteries
- left <3 failure
- stroke
- kidney failure
- blindness
Types of Hypertension
Primary / essential / idiopathic - most common - combination of D+S hypertension Secondary - caused by underlying disease, e.g. renal Isolated S/D - only systolic/diastolic affected
ECG wave
P wave = atrial depol (atrial cont.)
- contributes to generation of AP
- movement of ions into cells and cell becoming +
QRS complex = ventricular depol (V systole)
- atrial depol also occurs here but is masked
T wave = ventricular repol
- membrane potential becomes -ve
Q-T interval = ventricular systole
Preload / EDV
workload imposed upon ventricle prior to contraction/systole
volume and pressure generated in the ventricle at the end of diastole
Causes lengthening of myocardial fibres
Frank-Starling mechanism
“within physiological limits, the force of contraction of the heart is directly proportional to initial length of muscle fibres”
Ability of heart to changes its force of contraction and therefore SV in response to changes in venous return
Afterload
The force required to eject blood from the heart
Impedance to ejection of blood varies depending on
- systemic vascular resistance
- ventricular wall tension
- Arterial Pressure
Arterial BP = CO x TPR
Measure AP during S or D
S = pressure during ventricular contraction
D = pressure during ventricular filling
Important AP is regulated to maintain tissue perfusion
- Effect of Cardiac Output
Q changes due to alterations in SV and/or HR
If Q ↑ = arterial blood volume ↑ = AP ↑
if Q ↓ = arterial BP ↓
- Effects of TPR
Resistance provided by the vascular system
Determined by changes in diameter of arterioles
VasoC = ↑ AP VasoD = ↓ AP
Constriction and dilation regulated by neural control
- baroR
- chemoR
- SNS innervates arteriole smooth muscle
- Effects of Hormones
- RAAS
renin secreted by kidneys in response to low Na
release of renin stimulated by ↓ in BP
renin acts on angiotensinogen to form angiotensin 1
Ag1 forms Ag2 by ACE = powerful vasocon
Release of aldosterone from kidneys - ADH
causes reabsorption of water by kidneys
secreted by PP into blood
potent vasocon (↑ TPR)
released in response to ↓ in plasma volume detected by baroreceptors
↑ blood plasma volume by ↑ permeability of kidneys at DCT so water is retained making urine concentrated