CV day 2

"Life is just all about  problem based learning"

Today's learning issue:
Q1.5 years survival rate of heart failure=what kind of cancer 5 year survival rate?

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	Male	Female
Median survival rate	1.7 year	3.2 year
5-year survival rate	25%	38%
1-year survival rate	57%	64%

Kannel WB. Incidence and epidemiology of heart failure.Heart Fail Rev. 2000 Jun;5(2):167-73.

Source

Women	Pancreas	2%
	Lung	6%
	Oesophagus	8%
	Stomach	13%
	Brain	15%
	Multiple myeloma	22%
	Ovary	34%
	Leukaemia	36%
	Kidney	43%
	Colon	45%
	Rectum	48%
	NHL	52%
	Bladder	61%
	Cervix	68%
	Uterus	76%
	Breast	79%
	Hodgkin's lymphoma	83%
	Melanoma	90%
Men	Pancreas	3%
	Lung	6%
	Oesophagus	7%
	Stomach	12%
	Brain	13%
	Multiple myeloma	24%
	Leukaemia	38%
	Kidney	45%
	Rectum	45%
	Colon	46%
	NHL	51%
	Prostate	61%
	Larynx	67%
	Bladder	71%
	Melanoma	78%
	Hodgkin's lymphoma	84%
	Testis	95%

Male:

 Heart failure 5-year-survival rate:25%=Multiple myeloma 5-year-survival rate:24%

Female:

Heart failure 5-year-survival rate:38%=Leukaemia 5-year-survival rate: 36%

                                                           Ovary  5-year-survival rate: 34%

Q2:Cheyne-Stokes respiration in congestive heart failure.

It is likely that one or more of the following factors are likely to contribute to hyperventilation in congestive heart failure.

Hypoxaemia

Hypoxaemia may contribute to hyperventilation and Cheyne-Stokes respiration in congestive heart failure through peripheral chemoreceptor stimulation. However, in contrast to high altitude periodic breathing where hypobaric hypoxia stimulation of the peripheral chemoreceptors is likely to be responsible for the periodic breathing,24 hypoxia is thought not to be solely responsible for the development of Cheyne-Stokes respiration in patients with congestive heart failure for the following reasons. Hyperventilation, in the absence of hypoxaemia, has been shown to trigger central apnoeas during non-REM sleep induced by either mechanical hyperventilation in normal subjects31 or by arousal induced hyperventilation in Cheyne-Stokes respiration3 and idiopathic non-hypercapnic central sleep apnoea.32 Furthermore, supplemental oxygen has been shown to attenuate rather than abolish Cheyne-Stokes respiration in patients with congestive heart failure.33-36

Increased pulmonary vagal afferent traffic

Increased pulmonary vagal afferent nerve traffic related to pulmonary venous congestion and pulmonary C fibre stimulation has been shown to induce rapid shallow breathing and hyperventilation in animal studies.37-40 In humans with congestive heart failure, those with Cheyne-Stokes respiration have a significantly greater pulmonary artery pressure (mean 34 mm Hg) than those without Cheyne-Stokes respiration (mean 21 mm Hg).6 Moreover, there is a significant inverse correlation between awake pulmonary capillary wedge pressure (PCWP) and awake PaCO ₂.6 Finally, there is a tendency for the analogous condition high altitude periodic breathing to occur in patients with associated high altitude pulmonary oedema,41 so Cheyne-Stokes respiration with congestive heart failure is associated with increased pulmonary artery pressures, but whether this is a cause and effect relationship remains to be seen.

Increased sympathetic activity

Heistad et al reported a 20% increase in minute ventilation 10 minutes after a six minute venous infusion of noradrenaline, an effect that could be blocked by prior treatment with propranolol.13 As increased circulating noradrenaline levels and hyperventilation occur in congestive heart failure,11 12 particularly in those with Cheyne-Stokes respiration, it is possible that peripheral chemoreceptors bathed in noradrenaline, or possibly central sympathetic activation related to spontaneous arousals, precipitates Cheyne-Stokes respiration. Upper airway collapse towards the end of the central apnoea, known to occur in Cheyne-Stokes respiration,42 may also cause arousal from sleep and thereby hyperventilation.3 32

Q3:
Resistent Hypertension
-經過同時使用三種不同機轉的藥物治療，且達適當劑量還無法控制。
Refractory Hypertension
-BP remain 140/90(160/90 for >60 y)
-not secondary HTN
-maximal dose for 2 Different mechanism drugs
Urgent Hypertension
-severe elevation of BP
-without targeted organ dtsfunction
Emergency Hypertension
-severe elevation of BP(>180/120)
-evidence of targeted organ damage
Pseudo-resistent Hypertension
-lack of BPcontrol with appropriate treatment