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

LSS 1 - Thorax anatomy, Respiratory and Circulatory system > CVS Lecture 19/20 - Pathophysiology of Heart Failure and Integration of CVS responses -Systems Review > Flashcards

Flashcards in CVS Lecture 19/20 - Pathophysiology of Heart Failure and Integration of CVS responses -Systems Review Deck (39)
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1
Q

What is the definition of HF?

A

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

2
Q

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

A

Kidneys as they won’t be sufficiently perfused

3
Q

What is the prevalence and incidence of HF?

A

P=22M worldwide, I=2M annually

4
Q

What are the main causes of HF?

A

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

5
Q

What are the types of cardiomyopathy?

A

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

6
Q

What is happening to HF cases?

A

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

7
Q

How does myocardial remodelling occur (diagramatic)?

A

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

8
Q

What is cardiomyopathy?

A

Heart disease in absence of known cause

9
Q

What is hypertrophic CM well known for?

A

Commonest cause of young athletes dropping dead

10
Q

How common is CM?

A

Occurs in 5% of HF popn

11
Q

What are the causes of Dilated CM?

A

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

12
Q

What are the causes of restrictive CM?

A

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

13
Q

What are the causes of death in HF?

A

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)

14
Q

Why is adrenaline secreted during HF?

A

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

15
Q

Why does the kidney retain water and salt during HF?

A

So that Renin-Angiotensin System is switched on

16
Q

Which vasoconstrictors are produced during HF?

A

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

17
Q

What are the most effective drugs in HF?

A

Beta blockers - block sympathetic drive

18
Q

What do other drugs do in HF?

A

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

19
Q

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

A

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

20
Q

What are the important inflammatory markers for all cell types?

A

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

21
Q

What is the prognosis of HF?

A

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

22
Q

What are the signs and symptoms of HF?

A

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

23
Q

What does HF x-ray look like?

A

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

24
Q

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

A

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

25
Q

How does HF progress?

A

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

26
Q

What are the syndromes of HF?

A

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

27
Q

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

A

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

28
Q

What do you do if pulm oedema?

A

Give diuretics to remove fluid in lungs

29
Q

What are the key investigations for HF?

A

ECG, coronary angiography, 2D echocardiogram, MRI scanning

30
Q

How do we manage a patient with HF?

A

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

31
Q

What are the objectives when treating CHF?

A

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

32
Q

What common drugs are used to treat HF?

A

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

33
Q

What are possible treatments for severe HF?

A

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

34
Q

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

A
35
Q

How is blood flow redistributed?

A
36
Q

How does the body make up for low venous return?

A
37
Q

How is volume replaced synthetically?

A

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

38
Q

How does the CVS integrate with other systems?

A
39
Q

How does the respiratory system integrate with CVS?

A

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

Decks in LSS 1 - Thorax anatomy, Respiratory and Circulatory system Class (27):