Cardiovascular Patient Flashcards
Hypertension facts
-A sustained elevation of arterial BP above normal levels
-Generally involves elevation of both systolic and diastolic pressure
+SYSTOLIC: LV stroke vol, aortic capacity + ridgity but influenced by diastolic BP
+DIASTOLIC: peripheral resistance m, HR
-Prevalence in 2014 was 32% (male) and 27% female
-Progressive causing vascular damage
-A sign of disease not a single disease state
Clinical signs and symptoms
- In early stage this is asymptomatic
- The association of the following with hypertension is not proven: headache, tinnitus, dizziness, palpitations and nose bleeds
- There is a proven association between elevated BP and increased morbidity and mortality
Cardiovascular system consequences of hypertension
- Direct effect of increased pressure: damage to vessels and increased risk of haemorrhage
- Increased cardiac work- leads to HF
- Indirect effects- major factor for development of atherosclerosis: plaque formation and progression reduction in flow (CHD) and peripheral vascular disease (PVD)
- Thrombus formation and atherogenic stoke
Measurements of BP (non invasive)
- Sphygmomanometer- mercury instrument is gold standard
- Detect Korotkoff sounds with either a stethoscope or microphone
Other non invasive methods
-Aneriod sphygmomanometer- instruments with electronic pressure sensors
-Device using oscillometric methods (wrist, arm, finger devices)
-The oscillometer method relies on detection of variation in pressure oscillations due to arterial wall movement beneath an occluding cuff
+Empirically derived algorithms are employed to calculate systolic BP and diastolic BP and mean arterial pressure
+Manufactures develop their own algorithms by studying a population group and may validate the stated accuracy by performing clinical trials
Ambulatory BP measurement
- Provide data over 24 hours. Can be non invasive: useful for ‘white coat’ hypertension and when variability is suspected
- Nice guidelines recommends that diagnosis for hypertension should be made using 24 hour ambulatory BP monitoring (AMBP), this should be offered to anyone with BP over 140/90
BP pressure treatment targets
- Use clinical BP to monitor BP control
- Optimal clinical BP control is <140/90 mmHg
- In people with white coat effect- target Home BP average of <135/85 mmHg
- Review BP control at least annually once BP treatment is stable
Terminology
ARTERIOSCLEROSIS: hardening of the arteries. Medical hypertrophy. Symmetrical and uniform
ATHEROSCLEROSIS: related to hyperlipidaemia. Fatty fibrous plaques (atheromas) laid down on inner surface of the vessels (intima). Focal changes
THROMBOSIS: consequence of atherosclerosis. Thrombus (clot) formed on inner surface of vessels. May shed off small parts (thromboemboli), these can occlude vessels
Atherosclerosis
- Focal disease of large arteries (may be found in atria), High Pressure
- Doesn’t occur naturally in animals
- Plaques occur at sites of haemodynamic stress- increased endothelial cell turnover
- Endothelial damage is initiating event
Risk factors
4 non modifiable
* Account for 80% of elevated risk
- Family history of IHD or hyperlipidaemia
- Advanced age
- Male sex
- Ethnic group
- Dyslipidaemia*
- Cigarette smoking *
- Hypertension*
- Obesity and poor diet *
- Diabetes *
- Stress
- Sedentary lifestyle
- Poor diet
Endothelial phase
- Earliest detectable evidence of pathophysiology is endothelial dysfunction
- Asymptomatic
- Injury to endothelium causing the release of adhesion factors- attracts monocytes- activation and adherence
- Endothelial cells bind LDL with endothelial transport of lipids into intima
- Injured cells and monocytes generate free radicals and there is lipid peroxidation
- Lipids become oxidised (initially in the circulation later intima)
- Disruption of normal LDL receptors
Spreading damage
- Macrophages move from blood stream into the endothelial layer- large part of atheroma mass
- Macrophages engulf oxidised lipids and turn to lipid saturated foam cells
- Cytokines from endothelial cells, macrophage and platelets cause smooth muscle proliferation and deposition of connective tiss
- Fibrous material become dense fibre caps of connective material
- Underneath there is much looser combination of lipid or necrotic cells, with Ca buildup- sclerosis
Peripheral arterial disease (occlusive)
-Due to atherosclerosis: usually preferentially effects lower limbs.
+Peripheral Vascular Disease. Pain is termed intermittent claudication (IC)
-May effect the upper limbs, particularly in heavy smokers (Buergers disease)
Symptoms IC; cold; pain; gangrene
-Pronounced colour change: gangrene or sudden pain often indicate arterial occlusion due to thrombosis or embolism
Angina
- Pain of angina is described as tightness or gripping in chest
- Pain may also be described in the arm, neck, jaw, ear
- Often but not always associated with extertional breathlessness
- Symptoms not a disease- usually due to underlying atherosclerosis
- Need to distinguish from non cardiac cause of chest pain e.g. GI reflux, psychological pain
Prognosis- angina/ acute myocardial infarction
- Angina is caused when myocardial oxygen demands exceed myocardial O2 supply. Resting heart extracts 2-3 times as much O2 as other tissue, increased flow= increased supply
- Prognosis is related to severity of disease not symptoms
- Mortality for angina Pe tori’s is 4% per annum (20% if unstable)
- Pain for >30 mins indicated AMI
- Diagnosis is usually made on the basis of exercise ECG
- Pain relieved by glyceryl trinitrate GTN is usually angina
