Hypertension, ischaemic heart disease and cardiac failure Flashcards
What is hypertension?
High blood pressure
Pulmonary= low pressure circulation, systemic= high (common)
Can occur in either or both circulations
What is the equation used for blood pressure?
BP= cardiac output x peripheral resistance
What are the classifications of systemic hypertension?
Primary vs secondary (based on cause)
Benign vs malignant (based on clinical presentation)
What is systematic hypertension?
Sustained resting blood pressure above certain level
140/90 mmHg (depends)
Diastolic pressure determines severity
What are the percentages of classification by cause?
Primary= 90% (idiopathic= unknown)
Secondary= 10%
-90% due to renal disease
-10% other causes especially endocrine disease
What are the risk factors for systemic hypertension?
Genetic susceptibility
High salt intake
Chronic stress (excessive sympathetic activity)
Abnormalities in renin/ angiotensin- aldosterone
Obesity
Diabetes mellitus
(careful clinical assessment- test the urine!)
Causes of secondary systemic hypertension
Renal disease- chronic renal failure polycystic kidneys
Endocrine- pituitary (ACTH), adrenal cortex= glucocorticoid, mineralocorticoid, adrenal medulla= catecholamines
Drug treatment= steroids
Coarctation of aorta
What is the difference between benign and malignant hypertension?
Benign= slow changes in vessels and heart with chronic and end-organ dysfunction Malignant= rapid changes in vessels with acute end-organ dysfunction/ blood pressure tends to be higher
Where are-organ effects acting on?
Heart
Kidney
Brain
Vessels (including retina)
What are the end-organ effects of the heart?
Left ventricular hypertrophy- fibrosis, arrhythmias
Coronary artery atheroma
Ischaemic heart disease
Cardiac failure
What are the end-organ effects of the kidneys?
Nephrosclerosis (drop- out of nephrons = vascular narrowing, proteinuria, chronic renal failure)
Malignant hypertension is associated with acute renal failure
What vascular changes lead to benign and malignant hypertension?
Benign= acceleration of atherosclerosis, intimal proliferation and hyalinisation f arteries and arterioles
Malignant hypertension= fibrinoid necrosis
Describe ischaemic heart disease
Blood supply to the heart is insufficient for its metabolic demands
Deficient supply- coronary heart disease, reduced coronary artery perfusion (shock, severe aortic valve stenosis)
Excessive demand- pressure overload (hypertension, valve disease)/ volume overload (valve disease)
What is coronary artery disease?
Coronary blood flow is normally independent of aortic pressure, initial response to narrowing is compensation
over 75% occlusion leads to ischaemia
What are the causes of coronary artery disease?
Atheromatous coronary artery disease= progressive stenosis, haemorrhage into a plaque, thrombosis
Emboli (inflamed aortic valve- endocarditis)
Vasculitis
What is a myocardial infarction?
An area of necrosis of heart muscle resulting from reduction (usually sudden) in coronary blood supply
What are the causes of MI?
Coronary artery thrombosis
Haemorrhage into a coronary artery plaque
Increase in demand in the presence of ischaemia
What are the clinical features of MI?
Central crushing chest pain
Features of heart failure
How is an MI diagnosed?
Clinical history
ECG changes
Blood markers- enzymes (creatine kinase), other proteins (troponin)
What are the macroscopic and microscopic changes after up to 18 hours after onset of symptoms?
None
What are the macroscopic and microscopic changes after 24-48 hours after onset of symptoms?
Macro= pale, oedematous muscle Micro= oedema, neutrophil infiltration, necrosis of myocytes
What are the macroscopic and microscopic changes after 3-7 days after onset of symptoms?
Macro= yellow, rubbery centre with haemorrhagic border Micro= obvious necrosis and inflammation- early granulation tissue
What are the macroscopic and microscopic changes after 1-3 weeks after onset of symptoms?
Macro= infarcted area paler and thinner than unaffected ventricle Micro= granulation tissue then progressive fibrosis
What are the macroscopic and microscopic changes after 3-6 weeks after onset of symptoms?
Macro= silvery scar becoming tough and white Micro= dense fibrosis
Describe right coronary artery obstruction
Inferior infarction
ECG changes in leads 2,3 and aVF
Can involve posterior septum
30% of cases
Describe circumflex artery obstruction
Lateral infraction
ECG changes in leads 1 and aVL and lateral chest leads V4-6
20% of cases
Describe left anterior descending artery obstruction
Artery of sudden death
Anterior infarction
ECG changes in anterior chest leads
50% of cases
What are the complications, interval and mechanisms of acute MI?
Sudden death- within hours- often ventricular fibrillation
Dysrhythmias- first few days- abnormal electrical activity
Persistent pain- 12 hours to a few days- progressive necrosis (extension)
Angina- immediate or delayed (weeks)- ischaemia of non-infarcted cardiac muscle
Cardiac failure- variable- ventricular dysfunction, dysrhythmias
Continued complications, interval and mechanisms of acute MI
Mitral incompetence- first few days- papillary muscle dysfunction, necrosis
Pericarditis- 2-4 days- inflammation of the pericardium producing sharp chest pain
Cardiac rupture- 3-7 days- weakening of wall by necrosis
Mural thrombosis- 1 week or more- abnormal endothelial surface
Ventricular aneurysm (may rupture)- 4 weeks or more- stretching of newly formed scar tissue
Causes of chronic ischaemic heart disease
Chronic angina (exercise induced chest pain)
Heart failure (related to reduced myocardial function)
Usually widespread coronary artery atheroma
Areas of fibrosis often present in the myocardium
What is cardiac failure?
Failure of the heart to pump sufficient blood to satisfy metabolic demands
Leads to under perfusion which causes fluid retention and increased blood volume
Systemic and pulmonary
What is acute heart failure?
Rapid onset of symptoms, often with definable cause (MI)
What is chronic heart failure?
Slow onset of symptoms, associated with ischaemic or vascular heart disease (for example)
What is acute-on-chronic heart failure?
Chronic failure becomes decompensated by an acute event
What are the causes of heart failure
- Pressure overload= hypertension (pulmonary or systemic), valve disease (aortic stenosis)
- Volume overload= valve disease (aortic incompetence)
- Intrinsic cardiac disease= ischaemic heart disease, primary heart muscle disease, myocarditis, pericardial disease, conducting system disorders
Examples of valvular heart disease
Bicuspid aortic valve
Senile calcific stenosis
Describe Left Ventricular failure
Dominates hypertensive and ischaemic heart failure
Causes pulmonary oedema with associated symptoms
Leads to pulmonary hypertension and eventually right ventricular failure
Combined- congestive cardiac failure
Describe right ventricular failure
Causes= secondary to left ventricular failure
Related to intrinsic lung disease- ‘cor’ pulmonale (chronic obstructive pulmonary disease- COPD)
What are the clinical features of forward failure?
Reduced perfusion of tissues
Tends to be more associated with advanced failure
What are the clinical features of backward failure?
Due to increased venous pressures
Dominated by fluid retention and tissue congestion- pulmonary oedema (left ventricular failure), hepatic congestion and ankle oedema (right)
What are the clinical features of left ventricular failure?
Hypotension
Pulmonary oedema- paroxysmal nocturnal dyspnoea (severe shortness of breath and coughing that generally occur at night), orthopnoea (breathlessness lying flat), breathlessness on exertion, acute pulmonary oedema with production of frothy fluid
What are the clinical features of right ventricular failure?
Ankle swelling Hepatic congestion (may be painful)
