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
Cardiac O2 supply and demand
-O2 supply: oxygenation of the blood
Blood flow
-O2 demand: ventricular wall tension
HR and contractility (increased by sympathetic stimulation Beta)
-Double product= HR x Systolic BP
-Triple product= systolic BP x HR x left ventricular ejection time
NB: increases in ventricular wall tension and marked increase HR may reduce blood flow
How common is angina
- Over 1.3 million sufferers in UK approximately
- Considered to affect 3.6% of males aged 55-64 years and 1.7% female. Age 65-74 Years 9% male and 5% female
- 40-50% of angina patient have silent ischaemia estimated that 60-70% of all ischaemic episodes are silent
- Diabetic are most likely to have a silent ischemia
Classification of angina
- Angina pectoris: angina of effort and/or emotion, most common form. Onset of pain is predictable
- Variant angina (prinzmetal angina): spasm of epicardial coronary arteries- due to electrical instability associated with atrial tone
- Unstable (crescendo) angina: due to break up of unstable plaques causing embolism or thrombosis. May precede AMI, symptoms are more severe are more severe and last longer, may occur at rest
Acute myocardial infarction
3 diagnostic factors- all ambiguous
Symptoms: prolonged severe chest pain; sensation of suffocation; nausea; dizziness; sweating
Signs: Dysrhythmias, ECG change, increased cardiac components in the blood
Silent AMI: estimated that 25% of non-fatal AMI are not recognised
Often serious AMI will show signs of previous silent episodes
ECG abnormalities
T wave inversion or elevation: denotes ischemia
ST segment elevation: denotes myocardial injury
Q wave abnormalities: deep often broad wave usually >25% of following R wave, denotes infarction
Non-ST segment elevation ACS is less serious. There may be no other ECG changes and diagnosis by symptoms and cardiac cell markers in blood
Acute myocardial infarction: early stages
- 23% sudden death before hospitalisation another 13% die during admission
- Irreversible damage to the cardiac muscle occurs within 6 hours- but still some benefit upto 12 hours
- SPEED IS VITAL
- Defibrillators are now common in many public spaces
- With treatment around 5% die in the first year, then 5% per year indefinitely. Prognosis linked to degree of necrosis measure by: troponin; T elevation and ECG
Immediate complications 1
Acute left ventricular failure- and pulmonary oedema (renin). Lung signs- CXR, increased pulmonary wedge pressure, lung base crackles
CARDIOGENIC SHOCK: hypotension SBP <90, cold, clammy, cyanosed, hyperventilation, high shallow pulse, 90% mortality even with therapy
CARDIAC ARRHYTHMIAS: common extra ventricular beats, ventricular tachycardia, ventricular fibrillation, may also see atrial fibrillation, sinus tachycardia and heart block
Heart failure HF
- Congestive heart failure CHF: the heart is unable to pump sufficiently to maintain blood flow to meet the body’s demands
- Left ventricular failure (right side failure is different)
- Most associated with decreased ejection fraction (can be due to decreased diastolic filling)
- Also called chronic heart failure, congestive cardiac failure
Heart failure
About 1 million suffers in England
Generally progressive condition
Main causes: hypertension, cardiomyopathy (infection, genetic, medication
rhythm disturbance
Symptoms- breathlessness on exercise and incapacity
Signs- LVH, decreased ejection volume and fraction, increased venous pressure, changes in echocardiography
New York classification (angina)
Class I: no limitation is experienced in any activities
Class II: slight, mild limitation of activity; the patient is comfortable at rest or with mild exertion
Class III: marked limitation of any activity; the patient is comfortable only at rest
Class IV: any physical activity brings on discomfort and symptoms occur at rest
Stroke act FAST
Face
Arms
Speech
Time
Cerebrovascular accident (CVA)
HAEMORRHAGIC STROKE 15%: usually due to rupture of an aneurysm, linked to BP. Charcot-Bouchard related to hypertension; Berry not related to hypertension
THROMBOTIC STROKE 85%: consequences of atherosclerosis. Hypertension a major risk factor but no invariable relationship. Transient ischemic attack (TIA): common in hypertension are probably also secondary to atherosclerosis
Aneurysms
Aortic: dissecting and abdominal -incidence of dissecting directly related to BP. If it bursts it is fatal
Charcot-Bouchard: micro aneurysm (<1mm) of small perforating arteries mainly in basal ganglia and sub-cortical region. Related to age and hypertension
Berry: defects development of defects in circle of Willis in the brain
Definition of HTN
Stage 1
-Clinic BP is 140/90 mmHg or higher
-Ambulatory BP monitoring or home BP monitoring average is 135/85 mmHg or higher
Stage 2
-Clinic BO 160/11 mmHg or high AND
-ABPM or HBPM daytime average is 150/95mmHg or higher
Sever HTN
-Clinc BP is 180mmHg or higher
-Clinic diastolic BP is 110mmHg or higher
Acute coronary syndromes (ACS)
- Unstable angina
- NSTEMI
- STEMI
