CVS Lecture 19/20 - Pathophysiology of Heart Failure and Integration of CVS responses -Systems Review

Question 1

What is the definition of HF?

Answer 1

Syndrome which arises when the heart is unable to maintain an appropriate BP without support

Question 2

What is the major organ involved in HF (apart from heart)?

Answer 2

Kidneys as they won’t be sufficiently perfused

Question 3

What is the prevalence and incidence of HF?

Answer 3

P=22M worldwide, I=2M annually

Question 4

What are the main causes of HF?

Answer 4

Arrhythmias (tachycardia), valve disease (regurgitation), pericardial disease (heart can’t pump efficently), Congenital heart disease (holes/misconnections), Myocardial disease (e.g CHD)

Question 5

What are the types of cardiomyopathy?

Answer 5

Dilated CM, Hypertrophic CM, Restrictive CM, Arrhythmic RV CM

Question 6

What is happening to HF cases?

Answer 6

50% of MI survivors develop HF, so deaths due to HF are increasing

Question 7

How does myocardial remodelling occur (diagramatic)?

Answer 7

When infarct occurs, fibrous thin tissue expands, so no contraction in that tissue, then there’s late ventricular enlargement as the myocardial tissue thins due to cell slippage and there’s thinning of fibrous tissue

Question 8

What is cardiomyopathy?

Answer 8

Heart disease in absence of known cause

Question 9

What is hypertrophic CM well known for?

Answer 9

Commonest cause of young athletes dropping dead

Question 10

How common is CM?

Answer 10

Occurs in 5% of HF popn

Question 11

What are the causes of Dilated CM?

Answer 11

Idiopathic, genetic, infectious: HIV, mycobacteria; toxins and poisons: Alcohol (myocardial depressant), cocaine; drugs (chemotherapeutic agents); metabolic disorder: nutritional and endocrine deficiencies; collagen disorder, AImmuneCM, peri-partum CM, neuromuscular disorders

Question 12

What are the causes of restrictive CM?

Answer 12

Heart is restricted so can’t dilate normally, ejection fraction can be preserved but diastolic dysfunction present - associated with hypertrophy and scleroderma and inflitrative disorders: amyloidosis and sarcoidosis

Question 13

What are the causes of death in HF?

Answer 13

Progression of HF - ^ myocardial wall stress, retention of Na and H2O; sudden death - opportunistic arrhythmia; cardiac event (MI), other CVD event, non-CVD causes (pneumonia)

Question 14

Why is adrenaline secreted during HF?

Answer 14

Body believes it’s bleeding to death so sympathetic drives switches on, ^ noradrenaline

Question 15

Why does the kidney retain water and salt during HF?

Answer 15

So that Renin-Angiotensin System is switched on

Question 16

Which vasoconstrictors are produced during HF?

Answer 16

Endothelin-1, VP, Renin/Ang, Neuropeptide Y

Question 17

What are the most effective drugs in HF?

Answer 17

Beta blockers - block sympathetic drive

Question 18

What do other drugs do in HF?

Answer 18

ACE inhibitors block RAS, Aldosterone receptor antagonists block aldo receptors which are high in HF

Question 19

What are some diagnostic tests that can be done to check for HF?

Answer 19

Atrial natriuretic peptide (ANP are raised if impaired heart-released from atria) and troponin I and T

Question 20

What are the important inflammatory markers for all cell types?

Answer 20

IL-1b, IL-6, TNFalpha which are taken up by liver and C-reactive protein, fibrinogen and serum amyloid A are released

Question 21

What is the prognosis of HF?

Answer 21

5-yr mortality rate 50%, survival following diagnosis: men 1.7y, women 3.2y

Question 22

What are the signs and symptoms of HF?

Answer 22

FATIGUE , orthopnea > Paroxysmal Nocturnal Dyspnoea, ^ HR (maintain CO), weak pulses, ^ Venous pressure, peripheral oedema (Na, H2O retention), crepitations, hepatomegaly and ascites

Question 23

What does HF x-ray look like?

Answer 23

^ cardio-thoracic ratio -> heart should NOT be >50% thorax width

Question 24

What is the NY heart association classification of functional capacity for patients with HF?

Answer 24

Reason: so you can tell patient has improved - 1=basically no symptoms and 4=patient can’t get out of chair FUNCTIONAL CLASSIFICATION

Question 25

How does HF progress?

Answer 25

1) loss of myocardium, BP falls 2)progression and suddenly drops off 3) sudden decline can occur in weeks/months but leads to death

Question 26

What are the syndromes of HF?

Answer 26

Acute HF (pulm oedema), Circulatory shock (cardiogenic shock), chronic HF

Question 27

What will the patient present with if blockage in coronary artery?

Answer 27

Heart muscle dies so look very sick, tachycardic, sweating, sitting upright, very breathless, coughing up frothy sputum

Question 28

What do you do if pulm oedema?

Answer 28

Give diuretics to remove fluid in lungs

Question 29

What are the key investigations for HF?

Answer 29

ECG, coronary angiography, 2D echocardiogram, MRI scanning

Question 30

How do we manage a patient with HF?

Answer 30

Establish HF, Determine aetiology, ID concomitant disease relevant, assess severity of symptoms, predict prognosis, anticipate complications, choose appropriate treatment, monitor progress and tailor treatment

Question 31

What are the objectives when treating CHF?

Answer 31

Prevention of myocardial damage and reoccurrence, relieving symptoms and signs, and prognosis - reduce mortality

Question 32

What common drugs are used to treat HF?

Answer 32

Diuretics, ACE inhibitors, beta blockers, Aldosterone antagonists, digoxin, devices (cardiac resynch, implanted cardioverter defib)

Question 33

What are possible treatments for severe HF?

Answer 33

IV drugs (diuretics, nitrates, DA), fluid control (dialysis), Devices (ICD, intraaortic balloon pump, ventricular assist), surgery (valve surgery, cardiomyoplasty, transplant)

Question 34

How does the body bring BP up from low central venous pressure?

Answer 34

Question 35

How is blood flow redistributed?

Answer 35

Question 36

How does the body make up for low venous return?

Answer 36

Question 37

How is volume replaced synthetically?

Answer 37

Crystalloid solutions -> isotonic NaCl soln, ringer’s lactate. Colloids -> increased plasma oncotic pressure, remain in intravascular space for hours. Blood products -> packed RBC, fresh frozen plasma, whole blood crossmatched

Question 38

How does the CVS integrate with other systems?

Answer 38

Question 39

How does the respiratory system integrate with CVS?

Answer 39

Chemoreceptors are chemosensitive cells and sensitive to O2 lack, CO2 excess or H+ excess -> chemoreceptors are located in carotid bodies, and aortic arch -> activation of chemosensitive receptors results in excitation of vasomotor centre which increases SNS activity and increases BP -> CV responds to respiratory needs