Hypertension, ischaemic heart disease and cardiac failure Flashcards

1
Q

What is hypertension?

A

High blood pressure
Pulmonary= low pressure circulation, systemic= high (common)
Can occur in either or both circulations

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2
Q

What is the equation used for blood pressure?

A

BP= cardiac output x peripheral resistance

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3
Q

What are the classifications of systemic hypertension?

A

Primary vs secondary (based on cause)

Benign vs malignant (based on clinical presentation)

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4
Q

What is systematic hypertension?

A

Sustained resting blood pressure above certain level
140/90 mmHg (depends)
Diastolic pressure determines severity

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5
Q

What are the percentages of classification by cause?

A

Primary= 90% (idiopathic= unknown)
Secondary= 10%
-90% due to renal disease
-10% other causes especially endocrine disease

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6
Q

What are the risk factors for systemic hypertension?

A

Genetic susceptibility
High salt intake
Chronic stress (excessive sympathetic activity)
Abnormalities in renin/ angiotensin- aldosterone
Obesity
Diabetes mellitus
(careful clinical assessment- test the urine!)

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7
Q

Causes of secondary systemic hypertension

A

Renal disease- chronic renal failure polycystic kidneys
Endocrine- pituitary (ACTH), adrenal cortex= glucocorticoid, mineralocorticoid, adrenal medulla= catecholamines
Drug treatment= steroids
Coarctation of aorta

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8
Q

What is the difference between benign and malignant hypertension?

A
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
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9
Q

Where are-organ effects acting on?

A

Heart
Kidney
Brain
Vessels (including retina)

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10
Q

What are the end-organ effects of the heart?

A

Left ventricular hypertrophy- fibrosis, arrhythmias
Coronary artery atheroma
Ischaemic heart disease
Cardiac failure

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11
Q

What are the end-organ effects of the kidneys?

A

Nephrosclerosis (drop- out of nephrons = vascular narrowing, proteinuria, chronic renal failure)
Malignant hypertension is associated with acute renal failure

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12
Q

What vascular changes lead to benign and malignant hypertension?

A

Benign= acceleration of atherosclerosis, intimal proliferation and hyalinisation f arteries and arterioles
Malignant hypertension= fibrinoid necrosis

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13
Q

Describe ischaemic heart disease

A

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)

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14
Q

What is coronary artery disease?

A

Coronary blood flow is normally independent of aortic pressure, initial response to narrowing is compensation
over 75% occlusion leads to ischaemia

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15
Q

What are the causes of coronary artery disease?

A

Atheromatous coronary artery disease= progressive stenosis, haemorrhage into a plaque, thrombosis
Emboli (inflamed aortic valve- endocarditis)
Vasculitis

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16
Q

What is a myocardial infarction?

A

An area of necrosis of heart muscle resulting from reduction (usually sudden) in coronary blood supply

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17
Q

What are the causes of MI?

A

Coronary artery thrombosis
Haemorrhage into a coronary artery plaque
Increase in demand in the presence of ischaemia

18
Q

What are the clinical features of MI?

A

Central crushing chest pain

Features of heart failure

19
Q

How is an MI diagnosed?

A

Clinical history
ECG changes
Blood markers- enzymes (creatine kinase), other proteins (troponin)

20
Q

What are the macroscopic and microscopic changes after up to 18 hours after onset of symptoms?

A

None

21
Q

What are the macroscopic and microscopic changes after 24-48 hours after onset of symptoms?

A
Macro= pale, oedematous muscle
Micro= oedema, neutrophil infiltration, necrosis of myocytes
22
Q

What are the macroscopic and microscopic changes after 3-7 days after onset of symptoms?

A
Macro= yellow, rubbery centre with haemorrhagic border
Micro= obvious necrosis and inflammation- early granulation tissue
23
Q

What are the macroscopic and microscopic changes after 1-3 weeks after onset of symptoms?

A
Macro= infarcted area paler and thinner than unaffected ventricle
Micro= granulation tissue then progressive fibrosis
24
Q

What are the macroscopic and microscopic changes after 3-6 weeks after onset of symptoms?

A
Macro= silvery scar becoming tough and white
Micro= dense fibrosis
25
Q

Describe right coronary artery obstruction

A

Inferior infarction
ECG changes in leads 2,3 and aVF
Can involve posterior septum
30% of cases

26
Q

Describe circumflex artery obstruction

A

Lateral infraction
ECG changes in leads 1 and aVL and lateral chest leads V4-6
20% of cases

27
Q

Describe left anterior descending artery obstruction

A

Artery of sudden death
Anterior infarction
ECG changes in anterior chest leads
50% of cases

28
Q

What are the complications, interval and mechanisms of acute MI?

A

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

29
Q

Continued complications, interval and mechanisms of acute MI

A

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

30
Q

Causes of chronic ischaemic heart disease

A

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

31
Q

What is cardiac failure?

A

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

32
Q

What is acute heart failure?

A

Rapid onset of symptoms, often with definable cause (MI)

33
Q

What is chronic heart failure?

A

Slow onset of symptoms, associated with ischaemic or vascular heart disease (for example)

34
Q

What is acute-on-chronic heart failure?

A

Chronic failure becomes decompensated by an acute event

35
Q

What are the causes of heart failure

A
  • 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
36
Q

Examples of valvular heart disease

A

Bicuspid aortic valve

Senile calcific stenosis

37
Q

Describe Left Ventricular failure

A

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

38
Q

Describe right ventricular failure

A

Causes= secondary to left ventricular failure

Related to intrinsic lung disease- ‘cor’ pulmonale (chronic obstructive pulmonary disease- COPD)

39
Q

What are the clinical features of forward failure?

A

Reduced perfusion of tissues

Tends to be more associated with advanced failure

40
Q

What are the clinical features of backward failure?

A

Due to increased venous pressures
Dominated by fluid retention and tissue congestion- pulmonary oedema (left ventricular failure), hepatic congestion and ankle oedema (right)

41
Q

What are the clinical features of left ventricular failure?

A

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

42
Q

What are the clinical features of right ventricular failure?

A
Ankle swelling
Hepatic congestion (may be painful)