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103T3- Physiology of the cardiovascular system. Principles of pathlogy, diagnosis and treatment of cardiovascular diseases > Failure of the cardiovascular system > Flashcards

Failure of the cardiovascular system Flashcards

1
Q

Describe what can happen if blood pressure is too high/

A

Hypertension, leads to vessel damage and heart damage

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2
Q

Describe what can happen if blood pressure is too low

A

Hypotension leads to syncope and shock

Shock- Occurs in critically ill people. Medical emergency as poor blood flow around the body. Categorised as SBP<90mmHg. Affects cerebral and kidney function

Treatment: aggressive IV fluids, oxygen and airway maintained.

Syncope- insufficient perfusion to the brain, causes fainting. Can occur in healthy people

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3
Q

What is meant by valve prolapse?

A

Valve leaflets are forced, by back pressure, to invert themselves in a backwards orientation .

\/ –> /\

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4
Q

Describe what angina pectoris is. Treatment?

Possible treatment for MI?

A

Its a symptom of over exertion of damaged heart tissue. It doesn’t necessarily occur during exercise. Nitrates for acute onset and longterm treatment resembles that for CAD.

Aggressive reperfusion of damaged tissue quickly.
Morphine
Oxygen
Nitrates
Aspirin
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5
Q

Describe Chronic low output heart failure and the differences in Right and Left CLOHF

A

Usually due to large or numerous infracts
Poor 5 year survival rate

Left
Causes respiratory problems due to backlog in pulmonary system. Left atrium becomes full earlier on and increased hydrostatic pressure leads to congestive HF.
Fluid leaks into lungs (Pulmonary oedema)
Dyspnoea, orthopnoea, paroxysmal nocturnal dyspnoea
Hypoxia in brain causes encephelopathy, irritability, loss of attention, restlessness, stupor & coma

Right
Leads to systemic problems as blood gets backed up to the body
May be caused by left HF
Causes include shunt, hypoxia
Peripheral oedema due to increased venous pressure.
Jugular venous distention

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6
Q

Describe cardiogenic, distributive and hypovolaemic shock.

A

Cardiogenic shock refers to a decreased ability of the heart to pump blood which causes low CO leading to critically poor perfusion.

Distributive shock occurs in distributing vessels(arteries). The blood vessels are too wide so pressure is too low to transport blood as in anaphylaxis.

Hypovolaemic shock occurs in loss of blood. Total plasma volume is low, low venous return and low vessel pressure as in haemorrhagic shock

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7
Q

Consider treatment for cardiac maladies.

Briefly describe the action of ACE Inhibitors and give an example.

A

There function is to decrease cardiac output.

Decrease plasma fluid and vasodilation which causes decreased blood pressure.

Used in hypertension and congestive heart failure

E.g. Ramipril

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8
Q

Consider treatment for cardiac maladies.

Briefly describe the action of diuretics and give an example.

A

There function is to decrease cardiac output by increasing the production of urine.

Decrease plasma fluid which leads to decreased venous pressure.

E.g. Bendroflumethiazide, Indapamide, Furosemide

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9
Q

Consider treatment for cardiac maladies.

Briefly describe the action of beta blockers and give an example.

A

There function is to decrease cardiac output.

Cause vasodilation of arteries which decreases pressure.

Used in hypertension and arrhythmia.

E.g. Bisoprolol, Propranolol

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10
Q

Describe decompensated heart failure.

Consider fluid overload, damming, positive feedback and oedema.

A

Decompensated HF causes the kidneys to overcompensate by retaining more fluid which leads to fluid overload.

The heart is unable to cope with the hypervolaemia so theres a damming effect in veins alongside high hydrostatic pressure this leads increased back pressure which further damages the heart.

There is a positive feedback mechanism involved in this process which causes fast deterioration of the heart.

In extreme cases, capillaries leak into tissues and lungs causing oedema. This reduces gas exchange at the lungs.

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11
Q

Define hypertension and describe some risks and causes of hypertension

A

Mismatch between blood volume and circulatory capacity

Asymptomatic

Risk of CHD and MI
Maybe secondary to kidney disease
Chronic hypertension can lead to aneurysm/stroke, MI, Kidney and/or heart failure, cardiac hypertrophy

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12
Q

Describe some causes of orthostatic hypotension

A

Low bp on standing
Dizziness or syncope

Causes: drugs, age and hypovolaemia

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13
Q

Describe cardiogenic shock

A

Compensatory mechanism include tachycardia tachypnoea. Failure to compensate leads to acidosis, low urine output, hypotension, confusion and syncope

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14
Q

Define stroke and its causes in terms of stress and damage.

A

Rapid loss of brain function due to loss of perfusion to part of the brain.
Haemorrhagic stroke occurs when cerebral blood vessel ruptures.
Ischaemic stroke occurs when cerebral blood vessel is blocked.

Stress: Hypertension, high wall tension, low compliance, turbulent flow

Damage: Trauma, atherosclerosis, diabetes

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15
Q

How can acute MI cause death?

A

Arrhythmia (electrical disorganisation) or HF

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16
Q

Describe some symptoms and causes of atherosclerosis

A

“Furring of the arteries”

Asymptomatic

Results from (1) Hyperlipidaemia (2) Immune action (3) Unknown aetiology

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17
Q

Describe some symptoms,causes and potential treatment for CHD.

A

Angina or asymptomatic

Causes: normally caused by atherosclerosis

Treatment:
Non-invasive- drugs for hypertension/hyperlipidaemia
Invasive- Stenting or surgical removal of clogged vessels

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18
Q

Define plaque rupture. What is the consequence?

A

When the fibrous cap of a plaque bursts open. In this event, the contents flood into the blood stream and act as a magnet for platelets.

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19
Q

Outline the sympathetic activity during MI

A
  1. SNS releases noradrenaline and adrenaline in response to pain and haemodynamic abnormalities
  2. This causes increased heart rate and increased contractility
  3. This causes increased peripheral resistance and increased risk of arrhythmia
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20
Q

Describe pulmonary oedema.

A

Cause: Left heart failure causes damming of blood which increases hydrostatic pressure in pulmonary circulation

Effect: Fluid accumulation in lungs leading to impaired gas exchange and the length of O2 diffusion is lengthened

Symptoms: dysponoea and/or orthoponoea which are both due to hypoxia

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21
Q

Describe the difference between peripheral oedema and ascites

A

Peripheral oedema is caused by high hydrostatic pressure. It is caused by low output heart failure. Ascites is the accumulation of fluid in the peritoneal cavity. It is also caused by heart failure

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22
Q

Describe the act of compensation in terms heart failure

A

Increased plasma volume
Increased sympathetic activity
= Starlings law

23
Q

Decompensation is a medical emergency. What is it?

A

The failure of the heart to maintain adequate blood circulation after long standing vascular disease.

24
Q

An example of compensation is cardiac remodelling. Describe it

Treatment

A

It involves growth of the pericardium either by hypertrophy or dilation. It is cause by injury in response to increased after load or preload.

If it continues it becomes pathological

ACE inhibitors (decrease water retention, decreased starlings law) or spironolactone

25
Q

Ventricular hypertrophy occurs in response to work e.g. athletes heart. Define the two types of ventricular hypertrophy

A

Eccentric
Dilation due to volume overload. Increased cell length and width (chamber dilation with increased ventricular pressure)

Concentric
Thicken due to pressure overload. Cross sectional areas of the myocytes increases. (augmented muscle may reduce cavity diameter)

26
Q

There are two hormones which are secreted to increase plasma volume. Identify and describe their action.

A

Aldosterone
Its a steroid hormone
Causes kidneys to reabsorb more NaCl which causes more water reabsorption, thus decreasing diuresis and naturiuresis.
Secreted from adrenal cortex

Anti-diuretic hormone
Its a peptide hormone
Causes kidneys to reabsorb more water, thus decreasing diuresis
Secreted from posterior pituitary but made in the hypothalamus

27
Q

Describe the link between diuresis and bp. How do diuretic drugs work

A

Decreased diuresis (water loss to urine) causes increases BP

Diuretic drugs antagonise (inhibit) these hormones thus causing increased fluid loss

28
Q

Angiotensin III is very important in increasing blood pressure. How does it work?

A
  1. Causes vasoconstriction
  2. Increasing fluid retention by increasing aldosterone and ADH secretions and Na+ retention

It contributes to remodelling and and ventricular hypertrophy

29
Q

Describe the Renin-angiotension-aldosterone system (RAAS)

A

Angiontensinogen is made and secreted into the blood stream by the liver.

The enzyme Renin (from the kidney) catalyses a reaction that converts angiotensinogen into Angiotensin 1

Angiotensin 1 is converted to Angiotensin 3 by ACE (from lungs)

Angiotensin 3 the secretes aldosterone which increases fluid retake in the kidneys by increasing uptake of NaCl

30
Q

Diuretic drugs prevent starlings law by decreasing BP as they cause fluid loss in urine. State the diuretic drugs which have an effect on:

a) Proximal convoluted tubule
b) Loop of Henle
c) Distal convoluted tubule
d) Collecting duct

A

a) Thiazide e.g. Indapamide (blocks reabsorption)
b) Furosemide (blocks reabsorption)
c) Thiazide
d) Spironolactone (K+ sparing diuretic, inhibits aldosterone receptors)

31
Q

Valve disease can be caused by fibrosis, calcification dilation. Describe the 4 broad causes of valve disease.

A
  1. Degenerative
    Most common in aortic valve>mitral valve. Ageing pop
  2. Rheumatoid
    Poorer demographics, children and young adults, post street rheumatic fever. Mitral >Aortic
  3. Infective
    Bacterial, fungal and -ve cultures. Immunocompromised individuals. Equally common in all valves
  4. Congenital
    Low proportion. Any valve
32
Q

Describe aortic stenosis

A

Causes: congenital, degeneration (>60yo), rheumatic (<60yo).

Symptoms due to obstruction of flow. Ventricle hypertrophies in order to force blood pass obstruction: syncope, angina and dyspnoea. Extreme cases fatigue and death

Sound: crescendo murmur

33
Q

Describe aortic regurgitation

A

Causes: Congenital, Rheumatic damage, Endocarditis, Aortic dissection/dilation (loss of support by pap muscles and chordae tendon), Marfans

Consequences: Volume overload as blood reenters ventricle from aorta during diastole, LV dilation, decompensation, high volume circulation which can lead to pulmonary oedema as hypertension in pulmonary circulation.

Symptoms : asymptomatic, chest pain, breathlessness, syncope, fulminant pulmonary oedema.

Sound: diastolic murmur

34
Q

Describe mitral regurgitation

How does chronic MR differ to acute MR?

A

Causes: 1. Valvular (e.g. prolapse, infection,degeneration) 2. chordae/papillary rupture 3. Dilation

Consequences: Volume overload in LV causes increased filling of LA during systole. Pressure overload of right heart causes right hypertrophy. LV dilation. Decompensation may lead to pulmonary oedema.

Symptoms: breathless, lethargy, palpitations (a.fib), peripheral oedema, chest pain.

Sound: pan systolic murmur

In chronic cases more blood reenters LA the aorta causes the LA to dilate but pressure is less than in acute cases

35
Q

Describe mitral valve prolapse

A

Initially closed during systole but eventually prolapses into LA due to abnormal supportive apparatus causing regurgitation.

Sound: Mid systolic click (prolapse), Late systolic murmur (blood flows into LA after intial regurgitation)

36
Q

Descrive mitral stenosis

A

Causes: rheumatic, congenital, storage diseases, malignancy, previous endocarditis, mitral valve calcification, systemic disease

Consequences due to lung/Right heart: breathlessness & congestion due to back pressure due to failure of LA to eject blood. Consequences due to LV: function only disturbed when atrial contractility lost or right heart pressures high.

Symptoms: haemoptysis, palpitations, systemic emboli, dysphagia

Sound: mid-diastolic rumbling murmur, snap, loud first heart sound

37
Q

Which tests/assessments might you order for a patient with suspected valve disease?

A

Auscultation, echo, HISTORY

Exercise test, stress echo, MRI, multislice CT, cardiac catheterisation

38
Q

Describe the surgical and minimally invasive repair options available for valve disease

A

Valve repair, valve replacement (mechanical, biological)

Percutaneous: BAV- balloon aortic vavulopasty, TAVI-transcatheter aortic valve implantation

39
Q

Describe what CVD is and its epidemiology

A

Cardiovascular disease includes coronary heart disease, cerebrovascular disease and peripheral vascular disease.

There was a marker rise in 20th secntury
2nd biggest UK killer claiming 1/3 of lives
Risk factors include age, family history, obesity, diabetes and menopause. Left ventricular hypertrophy increases risk of coronary heart disease

40
Q

What are the clinical manifestations of ischaemic heart disease?

A

Could buy asymptomatic
Stabile angina
Acute coronary syndrome (e.g. unstable angina)

41
Q

When would you prescribe calcium inhibitors instead of beta blockers as treatment for heart failure, hypertension, tachyarrhythmias, and post-myocardial infarction?

A

In patients with COPD or asthma as these conditions are contraindications for the use of bb.

42
Q

Describe the pathological progression of atherothrombosis?

A 
Normal artery
Fatty streak
Fibrous plaque
Atherosclerotic plaque
Plaque rupture/fissure &amp;thrombosis
43
Q

How might incomplete occlusion of a coronary artery appear on an ECG?

A

ST depression
Variable T wave abnormalities
Normal ECG

44
Q

What is STEMI?

A

ST-elevate myocardial infarction

Persistent ST elevation> 20 minutes

45
Q

Describe what is meant by unstable angina?

A

Angina at rest > 20 minutes
New onset < 2 months
Normal cardiac biomarkers

46
Q

Suggest an effective surgical treatment for myocardial infarction

A

Coronary artery bypass surgery using internal mammary artery

47
Q

What are the stats considering heart failure?

A

In-hospital mortality- 9.4%
30 day post discharge- 6.1%
Overall 30 day mortality- 14.9%
Mortality is affected by ward on which you are admitted to.

48
Q

Which pathologies can cause heart failure, generally speaking?

A

Thyrotoxicosis, profound anaemia, pregnancy, Pagets disease, acromegaly and sepsis

49
Q

Low output heart failure can be subdivided into systolic and diastolic. Describe each

A

Systolic
Progressive deterioration of myocardial contractile function
Due to ischaemic injury, volume overload or pressure overload

Diastolic
Inability of there heart chamber to relax and expand and fill sufficiently during diastole to accommodate an adequate blood volume
Due to significant LV hypertrophy, infiltrative disorders, constrictive pericarditis, restrictive cardiomyopathy

50
Q

What are cardiomyopathies and what causes them?

A

Diffuse disease of the heart muscle leading to function impairment

Dilated cardiomyopathy
This is 50% heriditary
Other causes include pregnancy, muscular dystrophies, drug toxicity (herceptin), myocarditis

Restrictive cardiomyopathy
RARE. Main cause is amyloid

Heriditary hypertrophic cardiomyopathy

51
Q

Describe the pathophysiology of heart failure

A

Pump failure leads to decreased SV and thus decreased CO. Compensatory mechanisms aim to maintain arterial pressure and perfusion of vital organs. Via:

  1. Frank-starling mechanism: vasoconstriction, increased venous return, increased preload, heart stretch, enhanced contractions
  2. Cardiac remodelling
  3. Activation of neurohormonal system: noradrenaline, ANP/DCP, activation of RAAS
52
Q

Consider the compensatory mechanisms employed by the body to combat heart failure. What happens when the following are used in excess:

  1. Vasoconstriction
  2. Na+ and water retention
  3. tachycardia
A
  1. Increase resistance against which heart has to pump as increased preload increases afterload. This ultimately leads to decreased CO
  2. Increase fluid volume, which increases preload which could lead to too much stretch leading to decreased contractile strength and cardiac output
  3. Decreased diastolic filling time leads to decreased ventricular filling which leads to decreased SV and CO
53
Q

Describe Cor pulmonae

A

Right HF due to significant pulmonary hypertension due to increased resistance within the pulmonary circulation

Its causes include PE, COPD, Valvular disease
Effects liver and portal system

Clinical signs include 3rd heart around (S3), displaced apex due to LV enlargement, crackles, peripheral oedema, ascites, hepatomegaly, elevated jugular venous pressure

Clinical tests include CXR, ECG, Blood investigations, ECHO, cardiac mrs, CT, coronary angiography

103T3- Physiology of the cardiovascular system. Principles of pathlogy, diagnosis and treatment of cardiovascular diseases (11 decks)

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