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107 Cards in this Set

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Give the definition of heart failure.
The inability of the heart to meet the needs of the circulation, at rest and/or on exercise.

What are the 5 classic mechanisms of heart failure?


1. Systolic dysfunction (pump failure) - comes with diastolic dysfunction


2. Diastolic dysfunction (stiff heart)


3. Persistent tachycardia


4. Pericardial constriction


5. Chronotropic incompetence (the inability of the heart to regulate its rate appropriately in response to physiological stress

What does Laplace's law state?

Wall tension is inversely proportional to wall thickness. For example LV hypertrophy normalises regional wall stress.

What is the mechanism for coronary arterial flow?

Generated by the left ventricle itself through relaxation and diastolic suction.

What does aortic valve stenosis cause?

Increased afterload.

Define labels A - C.

Define labels A - C.


A - increased contractility


B - normal


C - heart failure

What chain of events does an increase in preload or afterload cause?

1. Hypertrophy/dilatation (Laplace law compensation)


2. Interstitial fibrosis (with subendocardial ischaemia)


3. Subclinical disease


4. Heart failure

What is the trigger for hypertrophy and fibrosis?

Larger and late systolic loading. It influences early diastolic filling and coronary suction.

Define labels A - L.

Define labels A - L.

A - Impaired LV function


B - Cardiac output and stroke volume


C - Neurohormonal activation


D - Systemic vascular resistance


E - Outflow resistance


F - Renal perfusion


G - Sympathetic stimulation, RAA and ADH


H - Sodium and water retention


I - Blood volume


J - Preload


K - Filling pressure


L - Ventricular dilatation and increased wall stress

What is the New York heart association functional classification?


A simple way of classifying the extent of heart failure.


1. No significant limitation, breathlessness only on marked exercise


2a. Breathless on moderate exercise


2b. Breathless on mild exercise


3. Breathless on minimal exercise


4. Breathless at rest

What are the cardinal symptoms of an elevated left atrial pressure?


Breathlessness on exertion


Orthopnoea (breathlessness when lying flat)


Paroxysmal nocturnal dyspnoea

What causes an elevated left atrial pressure?


An elevated LV diastolic pressure OR


mitral valve stenosis or regurg

What are the main causes of peripheral oedema (6)?


1. Fluid retention caused by neurohormonal activation (high aldosterone and ADH etc..)


2. Elevated central venous pressure/right atrial pressure due to RV diastolic dysfunction/right heart failure


3. Low serum albumin/low colloid osmotic pressure (eg. nephrotic syndrome, malnutrition, liver disease.


4. Venous disease, eg. deep vein thrombosis or varicose veins with incompetent valves.


5. Immobility


6. Elevated pelvic pressure/obstruction to venous return (eg. uterine or ovarian tumour or pregnancy)


What finding does this chest x-ray show?

What finding does this chest x-ray show?

Kerley B lines - due to fluid accumulating between the secondary lobules of the lungs, normally caused by pulmonary oedema due to heart failure.

What is BNP?

Brain natriuretic peptide. BNP is a substance secreted from the ventricles in response to changes in pressure that occur when heart failure develops and worsens.

What is the function of BNP?
The natriuretic peptides counteract the effects of renin secretion, causing a reduction of blood pressure and in extracellular fluid volume. Both BNP and atrial natriuretic peptide (ANP) are activated by atrial and ventricular distension due to increased intracardiac pressure. These peptides have both natriuretic and diuretic properties: they raise sodium and water excretion by increasing the glomerular filtration rate and inhibiting sodium reabsorption by the kidney.

When do you refer a patient directly for echocardiography who is breathless and suspected of having heart failure?


If they have a history of myocardial infarction.


If they have basal crepitations (pulmonary oedema - heart failure).


Is a male with ankle oedema.


If they don't have these, do a BNP test before echocardiography.

When is it appropriate to diagnose right sided heart failure? (signs)


When there is:


Signs of pulmonary hypertension;


Loud pulmonary second sound - P2


Parasternal impulse (RV hypertrophy)


Signs of high central venous/RA pressure;


Elevated jugular venous pressure


Signs of tricuspid regurg;


Pan-systolic murmur


High JVP


Enlarged pulsatile liver

How do you diagnose heart failure?

1. Look for clinical symptoms and signs - decreased CO, increase in filling pressure, increased BNP, breathless etc.


2. Reduced systolic AND diastolic function - decreased ejection fraction, decreased long axis function, increased LA volume.


3. Reduced exercise capacity and functional reserve


4. Inefficient ventriculo-arterial coupling

What is hypertrophic cardiomyopathy?

A condition causing increased wall thickness that is not explained solely by loading conditions. Wall thickness greater than or equal to 15mm

Define labels A and B on the histology.

Define labels A and B on the histology.


A - hypertrophic cardiomyopathy


B - Normal

How does HCM affect the physiology of the heart?


It causes:


Asymmetric septal hypertrophy


Chamber stiffness - diastolic dysfunction


Blood demand/supply mismatch


Outflow tract obstruction


Mitral valve abnormalities


Arrhythmias - atrial and ventricular

Briefly explain how HCM causes mitral valve abnormalities.

Due to the ventricular septum hypertrophying the mitral valve presses against it causing obstruction to blood flow. So blood leaks back through the mitral valve - mitral regurg. Systolic anterior motion occurs.

What are the different ways in which HCM can present itself?


No symptoms.


Sudden death (triggers arrhythmias) - young adults and athletes.


Dyspnoea - diastolic dysfunction, AF, mitral regurg, dilated CM, LV outflow tract obstruction


Syncope - arrhythmia, baro-reflexes, LVOT obstruction


Angina - Microvascular disease, ventouri effect

What is the venturi effect?

When fluid has to go through a stenosis its pressure decreases.

What causes HCM?

Abnormalities in the genes that code for the heart muscle (sarcomeric proteins). This causes myofibre disarray, this causes the muscle to grow abnormally thick. It is an autosomal dominant condition.
What do the arrows show on this ECG?

What do the arrows show on this ECG?

Dagger Q waves.
What are the abnormalities you see on the ECG of someone with HCM?
Asymmetrical septal hypertrophy produces deep, narrow (“dagger-like”) Q waves in the lateral (V5-6, I, aVL) and inferior (II, III, aVF) leads.

What do these MRI's show?

What do these MRI's show?

Varying degrees of fibrosis in HCM.

How do you treat LVOT obstruction in HCM?


AVOID:


Dehydration and vasodilators.

Why can't you use vasodilators like verapamil to treat LVOT?

It worsens the LVOT obstruction - increases systolic anterior motion - leads to elevated LA and LV pressure - increases mitral regurg - decreases CO resulting in pulmonary oedema.

What medical treatments are used for LVOT obstruction?


Non-dilating beta blockers.


Beta blocker and disopyramide


(anti-arrhythmic sodium channel blocker class 1).


Verapamil and diuretics with caution.

What surgery is used to treat LVOT obstruction?

Myomectomy - the resection of excess muscle and tissue. Performed when the patient is on bypass - difficult.

Myomectomy - the resection of excess muscle and tissue. Performed when the patient is on bypass - difficult.

What other procedure can treat LVOT obstruction?

Alcohol septal ablation - injection of absolute alcohol into a carefully selected blood vessel of the heart. The alcohol kills a segment of muscle tissue that is interfering with the flow of blood out the heart.

Alcohol septal ablation - injection of absolute alcohol into a carefully selected blood vessel of the heart. The alcohol kills a segment of muscle tissue that is interfering with the flow of blood out the heart.

What is dilated cardiomyopathy?

A condition characterised by cardiac enlargement with reduced systolic function ,absence of primary valve disease, and non-significant coronary artery disease.

What are the causes of DCM?


Idiopathic


Infective - viral myocarditic, HIV


Toxins - alcohol, steroids, drugs


Neuromuscular disease


Storage disease


Arrhythmia - tachycardia induced


Endocrine - thyroid disorders

Anaemia

What are the treatments for DCM?


Diuretics


Beta blockers


ACE inhibitor or angiotensin receptor blockers


Aldosterone antagonists


Heart rate reduction


Resynchronised pacing


Defibrillator


LVAD (artificial heart pump)


TRANSPLANT

How do neuromuscular diseases cause DCM?

 


In Duchenne and Becker muscular dystrophies, abnormal amounts of dystrophin in cardiac myocytes lead to their necrosis and fibrosis with resultant cardiomyopathy. Symptoms of congestive heart failure, such as dyspnea, fatigue, orthopnea, and edema, are seen with varying frequency. The development of symptoms is modulated by the level of neuromuscular disability that may mask symptomatic heart failure and the degree of cardiac involvement, which generally progresses over time.

What is dystrophin?
A rod-shaped cytoplasmic protein, and a vital part of a protein complex that connects the cytoskeleton of a muscle fibre to the surrounding extracellular matrix through the cell membrane.

How do NMD patients present with DCM?


Fatigue


Tachycardia,


S3 heart sound


Orthopnoea


Nocturnal dyspnoea


Dependent oedema


Syncope


Elevated JVP


Bi-basal crepitations

What is ARVC?

Arrhythmogenic right ventricular cardiomyopathy.

A condition mainly affecting the right ventricle(butcaninvolveLV:15%)characterised by fibro-fatty infiltration, ventricular dilatation, and hyper-trabeculation. Usually presents with arrhythmia.


What can you see in this image (1 thing)?

What can you see in this image (1 thing)?

Hyper-trabeculation.

What are the ECG abnormalities in ARVC?


EPSILON WAVE - a small positive deflection buried at the end of the QRS complex


T-wave inversions in V1-3


Prolonged S wave upstroke in V1-3


Localised QRS widening


Possibly V-tach


What do the arrows show?

What do the arrows show?

The epsilon wave.

What do the arrows show on the echo?

What do the arrows show on the echo?

Hyper-trabeculations.

What is RCM?

Restrictive cardiomyopathy -

a condition characterised by normal cardiac size, reduced systolic function, and bi-atrial dilatation. Usually resulting from myocardial infiltration. Sarcoidosis and fibrosis normally occur. Caused by amyloidosis (excess depositions of the amyloid proteins).

What are the ECG features of RCM?


Low voltage QRS complexes


Non-specific ST segment and T wave changes


Bundle branch blocks


AV blocks


Irregular rhythm

What is an emerging therapy for heart failure?
IRON - want to raise haemoglobin.

What structural interventions are available to heart surgery patients?

Angioplasty


Revascularisation (bypass)


Cut out scar tissue - reduce LV wall cavity


Corcap procedure (shower cap over heart) - limits the expansion of an aneurysm


Myoplasty - release latissimus dorsi and wrap around heart, turbo charges ventricle muscle


Mitral valve surgery - annulus rings or MV clips between valve leaflets (reduces regurg)


LVAD

What is an LVAD?

A LV assistance device stitched into the apex of the heart. It sucks blood from the LV and pumps it into the aorta. It's a continuous flow device - the flow isn't pulsatile anymore its continuous. So you are only eligible for this if you are waiting for a heart transplant.

What is resynchronisation therapy?

This resynchronises LV contractions. Pacing wires are put in the heart and connect to a pacemaker. This forces wall areas to contract together. The wires go through the coronary sinus in the right atrium then into the LV. Improves LV end-systolic volume and ejection fraction.

What is an ICD?

Implantable cardioverter defibrillator - anyone who has had a heart attack and has an ejection fraction of 30% is eligible. The worry is inappropriate shocks. Can cause VT storm - inappropriate shock, heart rate increases, another shock is given - vicious cycle.

Define labels A - D.

Define labels A - D.

A - None


B - Diuretics and vasodilators


C - Fluids


D - Diuretics, vasodilators and inotropes (increase contractility of the heart

Define labels A - N.

Define labels A - N.


A - Congestion of peripheral tissues


B - Dependent oedema and ascites


C - GI tract congestion


D - Liver congestion


E - Anorexia, GI distress, weight loss


F - Impaired liver function


G - Decreased cardiac output


H - Pulmonary congestion


I - Activity intolerance and signs of decreased tissue perfusion


J - Impaired gas exchange


K - Pulmonary oedema


L - Cyanosis and signs of hypoxia


M - Cough with frothy sputum


N - Orthopnoea


O - Paroxysmal nocturnal dyspnoea

What is dependent oedema?

Oedema in a dependent area such as a limb. Characterised by pitting and swelling.

Describe labels A - J.

Describe labels A - J.


A - High central venous pressure (backwards failure)


B - Drug therapy


C - Low cardiac output (forward failure)


D - High intra-abdominal pressure


E - RAS inhibitors


F - Diuretics


G - Low pressure in afferent arteriole


H - High pressure on bowman's capsule


I - Dilatation of efferent arteriole


J - Low urine output

When GFR decreases How does the kidney remedy this?

Increased sodium and fluid retention to increase blood volume to increase cardiac output to increase BP and so increase GFR. It also uses angiotensin II to vasoconstrict causing an increase in total peripheral resistance and an increase in BP.

How can CO be increased?


Fluid expansion of ECF -


Decrease in GFR


Excessive salt absorption by renal tubule


Activation or RAA

Sympathetic drive

How can CO be decreased?


Renal prostaglandins.


Nitric oxide (causing vasodilation)


Basically autoregulation

How does total peripheral resistance increase?

Vasoconstriction:


Activation of RAA


Sympathetic drive

Endothelium-derived peptide endothelin.

How does TPR decrease?


Vasodilation:


Renal prostaglandins


Renal kinins


NO

Platelet activating factor

Describe the pathogenesis of essential (no pathology) hypertension

1. Abnormally high sodium levels


2. ECF fluid expansion


3. Volume receptors in the atrium detect this


4. Feeds info to CNS


5. A natriuretic hormone secreted by the pituitary in the CNS - this is a sodium/potassium pump inhibitor


6. The NH inhibits the Na+/K+ in the smooth muscle of arterioles


7. this stops the movement of sodium out of the cell causing sodium excretion


8. It also stops the movement of calcium ions out of the muscle cells causing vasoconstriction.


9. This increases TPR and raises BP

What are the non-modifiable risk factors for hypertension?


Liddles syndrome: Genetic defect, malformation of sodium channels in the collecting duct.


Metabolic syndromes: Diabetes; sodium antiporter in the PCT is affected. Insulin upregulates sodium potassium pumps - increase in sodium reabsorption

What is the PATHOLOGY of hypertension?

It leads to structural changes in the terminal radiaii of the arterial tree. The smooth muscle layer (tunica media) is affected. Smooth muscle cell hypertrophy leads to luminal narrowing. The internal elastic lamina becomes re-duplicated and interrupted and hyaline. Degeneration may occur in focal areas of the media where a glassy eosinophilic material accumulates.

What can occur in malignant hypertension?

Lesions which lead to various grades of ischaemia in target organs; cerebellum, eyes, heart, kidneys and peripheral vessels.

How does PVD caused by hypertension affect the structure and physiology of the kidneys?


The glomerular basement membrane shrinks and can't filter, then, hypertrophic and hyaline changes (deposition- causing blood vessels to become rigid and poor blood flow to nephrons) in afferent arterioles lead to sclerosis of the glomeruli.


The tubules also become ischaemic and undergo atrophy and fibrosis. Eventually the kidney as a whole contracts with a finely scarred surface (nephrosclerosis).

How do NSAIDS cause kidney damage?

NSAIDs causesvasoconstriction in the kidneys - causes a reduction in GFR and vasoconstriction in afferent arterioles. This causes hypertension, arteriolar damage ischaemia and eventually renal disease.

What are the adrenal causes of hypertension?


Primary hyperaldosteronism (Conn's syndrome), or an adenoma secreting aldosterone.


Aldosterone increases potassium excretion in the DCT and increases sodium reabsorption in the collecting duct - water retention - CO goes up - hypertension - increases renal bicarb production from the potassium excretion, this increases plasma pH - hypokalaemia.

What happens to renin levels when there is poor perfusion to the kidney?

There is inappropriate release of renin - levels will stay elevated - elevated renin = elevated aldosterone - no inhibition - hypertension.

What tumour cause is there for hypertension?

A tumour in the phaeochromocytoma in the adrenal medulla would secrete catecholamines - causes hypertension.

What are the direct renal causes of hypertension?


1. RAA system in renal ischaemia due to renal vascular disease


Non-renin dependent mechanisms in renal parenchyma disease

What causes renin to be released?

Reduced blood flow to the kidneys.

What are the 2 forms of renal artery stenosis?


1. Fibromuscular dysplasia


2. Atherosclerosis

What signs point to renal artery stenosis?


The sudden appearance of hypertension in an older person.


The development of resistance to usual antihypertensive meds or abrupt deterioration in BP control in a patient with previously stable hypertension.

Severe hypertension in an older person associated with progressive deterioration of renal function.

What are the effects of renal parenchymal disease?


*Most common cause of secondary hypertension*


Early phases: may be loss of vasodilator substances generated normally by healthy renal tissue, leading to unopposed vasoconstriction.

Later phase: Retention of salt and water as a result of inadequate GFR leading to expansion of extraceullular fluid volume

What are the 3 fundamental features of heart failure?


1. Haemodynamic changes


2. Metabolic events


3. Neurohormonal changes

Define labels A - D

Define labels A - D


A - Decrease in renal perfusion and decrease in renal venous pressure


B - Decrease in renal function and adenosine release


C - Increase in sodium and water retention (diuretic resistance


D - Decreased cardiac performance


Define labels A - F

Define labels A - F


A - Fluid overload - furosemide treatment


B - Decrease in renal perfusion


C - Decrease in renal venous pressure


D - Interstitial fibrosis, tubular damage, nephron loss


E - Short term changes in renal function


F - Long term changes in renal function

What is a high dose of furosemide linked to?

Adenosine release leading to renin secretion and resultant decline in renal perfusion due to angiotensin II.

Which 2 haemodynamic changes increase serum creatinine levels.

Increased central venous pressure and/or intra-abdominal pressure.

How do the kidneys try to compensate for changes in haemodynamics?

The kidneys try to increase preload with volume expansion but over time the excessive volume expansion leads to higher blood pressure and increases in afterload.

What are the metabolic events associated with heart failure?


Impaired ATP generation - due to decreased blood flow - less ATP - changes in intracellular calcium - impaired ventricular performance.


Inflammation - due to damages in the cell's structure - causes neutrophil and complement activation - leads to myocardial cell death


Anaemia - associated with poor outcomes in HF and CVD

What occurs when Baroreceptors detect heart failure?

The sympathetic nervous system is activated - increased contraction of venous smooth muscle, vasoconstriction in skin, splanchnic circulation nd skeletal muscle - increased contractility of cardiac myocytes. Increased renin secretion from the juxtaglomerular apparatus.

Apart from sympathetic stimulation, what else does the JGA respond to?


Stretch in afferent arterioles - fall in renal afferent pressure in HF will increase renin production.

Sodium/chloride detector located in the macula densa.

What is the role of angiotensin II?

It indirectly increases sodium and water retention by causing the secretion of aldosterone. ATII normally exerts a negative feedback control on renin secretion via an ATI receptor in the JGA.

What is a problem with the RAA system?

If resultant expansion in blood volume by angiotensin II dosent generate an adequate arterial BP, you will not get the normal suppression of renin production and blood pressure will rise.

What role does ATII play in the development of cardiac pathology?


Overproduction of ATII contributes to a series of fibrotic changes in the heart.


It produces transforming growth factor, causes fibrosis, collagen deposition, ECM breakdown and eventually ventricular dilatation.


Define labels A - D.

Define labels A - D.


A - Decrease filtration pressure


B - Loss of nephron mass


C - Increase in S-creatinine and cystatin C


D - Albuminuria, markers of tubular injury

What does activation of the angiotensin II receptor AT1R cause?


1. Dipsogenic response - thirst


2. Vasoconstriction (direct and through SNS)


3. Cardiac hypertrophy


4. Aldosterone secretion (sodium uptake)


5. GFR maintenance


6. ADH secretion from posterior pituitary

Give the mechanism of action for ACE inhibitors.


They work by occupying the active site region of ACE that would normally be taken up by ATI's proline.


The -COOH groups of the ACE inhibitor block the catalytic activity of the Zn2+ ion in the ACE active site. eg. ramipril

Give the mechanism of action for angiotensin receptor blockers.

ARBs are highly selective for AT1R and can shift the balance of which receptors ATII bind to. If AT1R are occupied by ARBs then ATII can bind to AT2R receptors instead. Activation of the AT2R receptors, tends to cause opposing effects to the activation of AT1R receptors. Eg. candesartan

Give the mechanism of action for digoxin.

Ca2+ regulates the extent of actin-myosin cross-bridge formation and hence muscle contraction. In HF more Ca2+ is needed. Digoxin blocks the myocyte's sodium potassium pump, this stops sodium leaving the cell and potassium entering. Because the conc of Na+ in the myocyte increases and so the sodium/calcium exchanger on the membrane FLIPS. Sodium is pumped out of the cell and calcium is pumped in. The increase in calcium allows ofr more actin-myosin cross bridges and causes calcium induced calcium release from the SR.

How is potassium balanced in the kidney?

The kidney controls sodium secretion, driven by Na+ currents in the principal cells found in the Collecting ducts.

Which diuretic can cause gynaecomastia?

Spironolactone.

How does acetazolamide act as a diuretic drug?

Inhibits carbonic anhydrase in the PCT.

What ECG change represents right atrial hypertrophy?

Peaked P wave - Longer and needs more electricity to activate the extra tissue.
What pathology does this ECG finding represent?

What pathology does this ECG finding represent?

Left atrial hypertrophy.
Define labels A - D and identify the pathology.

Define labels A - D and identify the pathology.


A - Lead 1: negative (deflection is down)


B - Tall R wave in V1


C - aVf: positive (normal)


D - Dominant S wave in V6


Pathology - RV hypertrophy

What is right axis deviation?

When lead I is negative and aVf is positive.
Define labels A - E and define the pathology.

Define labels A - E and define the pathology.


A - Lead 1 is positive (normal)


B - Tall R wave in aVl


C - Big R waves in V1, V5 and V6


D - aVf is negative (downward deflection)


E - Inverted T wave in V6, and in V5, lead 1 and aVl


Pathology - LV hypertrophy

What is left axis deviation?

When lead 1 is positive and aVf is negative.
Define labels A - D and define the pathology.

Define labels A - D and define the pathology.


A - No P waves


B - Fibrillatory waves


C - No isoelectric baseline


D - Depressed ST segment


Pathology - Atrial fibrillation

What is the S3 gallop sound?

The ventricles filling.

What are AGEs?


Advanced glycation end-products. High glucose levels increase the production of AGEs. These are normally excreted in urine but in people with diabetes AGE levels are 10x normal and they cant be excreted and they build up in blood vessel tissue.


They form bonds with many of the proteinspresent in the blood vessel walls, a process called glycosylation which ultimately damages arteries.


How does hyperglycaemia affect NO production and what are the effects of this?

It inhibits the production of NO in endothelial cells. This means endothelial cells can't vasodilate and the vessels are in a hyperconstricted state. The lumen decreases in size - angina symptoms and raises BP.


What other structural vascular change does hyperglycaemia cause?

Thickened basement membrane - permeability affected - large molecules like albumin that normally cant get through can. So urine microalbumin test - usually indicated for the detection of early nephropathy actually reflects the health of the entire vasculature. Also the thick BM means nutrient transport is impaired - poor exercise tolerance.

What is diabetic autonomic neuropathy?

Associated with impaired autoregulation of blood flow in a variety of vascular beds including the skin and heart.


Patients lack the normal cardiac flow reserve that is activated under conditions of increased demand for myocardial perfusion - high mortality rate.