Other references Flashcards
Berk BC et al (2007)
Hypertensive heart disease:
HTN most common cause, LV hypertrophy but maintains systolic function. chamber stays the same size and diastole affected. Fibrosis is key with increase myofibroblasts
Beevers G (2001)
HTN pathophysiology:
CO increases early but main changes are increases in TPR by constriction of arteriole VSMCs. RAAS may be low in black people so isnt the cause. transplanted kidney experiment. Endo dys is irreversible and important. HTN is protrombotic and polygenetic.
Foex P et al (2004)
Paper on HTN treatments: Diretics, BBs, CCBs, ACEis, ARBs and alpha1 blockers
Hunter et al (1992)
Heart changes in pregnancy:
CO changes due to fast increase in SV and slower increase in HR. Big increases in labour and baseline returned to at around 2 weeks. LV mass and thickness increases and tae longer to correct. Increase venous return and vascular resistance drop. COntractility increased.
Savu O et al (2012)
Pregnancy heart changes eccentric hypertrophy and LV strain
Wust et al (2012)
Increased mitochondrial volume with training
Hoppeler et al (1985)
Capillary: fibre ratio improves with training
Harrington D et al (2001)
Improving cardiac function does not improve exercise tolerance
Anker et al (1997)
Skeletal muscle severely wasted in HF
Sabbah HN et al (1993)
Fibre type switch in HF to fast-twitch anaerobic fibres
Meyer et al (2001)
Respiratory weakness in HF associated with increased mortality
Witte et al (2004)
Airway resistance in HF leads to asthma like tendency
Witte et al (2003)
Higher frequency of ventilation in HF and higher sensation of breathlessness
NICE guidelines 2011
Hypertension treatments
ATLS 2008
Guidelines on hypovolemic shock
