Hypertension, heart failure and coronary heart disease Flashcards

1
Q

What is hypertension?

A

A blood pressure being higher than normal-changes often but optimal tends to be <120 <80

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2
Q

How large is the blood pressure problem?

A

It is the leading cause of death in the world

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3
Q

What is ambulatory blood pressure?

A

Its the blood pressure that can be measured by a cuff-often 5-10mmHG lower than clinically determined
Current practice aims around 120mmHg

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4
Q

How does blood pressure change with age?

A

Systolic BP rises with age by Diastolic does not-and lowers very slowly
but BP going higher is normal-and sign of health because heart is healthy

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5
Q

What is pulse pressure?

A

Pulse pressure is difference between SBP and DBP

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6
Q

What are the relations between blood pressure and mortality?

A

There is no threshold-even at SBP 110 is a risk factor to death-but as you rise in BP, exponential increase of death
Even with perfect health-cant get rid of problem, only reduce it-people will still be suceptible

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7
Q

What is primary hypertension?

A

Primary-identifiable causes, such as renal diseases, tumours, contraceptives, rare genetic causes -about 5-15% of hypertensions (pretty rare more or less)
Single gene causes are even rarer (monogenic)-often sodium channels
Complex polygenic-more common

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8
Q

What is the secondary hypertension?

A

Idiopathic-no cause

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9
Q

What are the links between blood pressure and genes?

A

Twin studies show that 30-50% of BP changes can be due to SNP’s-but we havnt identified that many
monogenic are rare-most are small genes with small effects, and interact with sex, and etc

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10
Q

What are the signs of established hypertension?

A

It describes high BP for a long time-often with higher TPR, lower arterial compliance, but normal CO, blood volume-but can have shifts in volume location (lower venous compliance)

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11
Q

What causes TPR modification in hypertension?

A

MAYBE-vasocontricion on the short term

Maybe structural narrowing, remodelling and loss of capillaries?

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12
Q

What is isolated systolic hypertension

A

SBP >140 and BP<90 -not to do with TPR, but only arterial compliance lower-reflexion of the wave on the solidified arteries

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13
Q

What are the 2 main causes of hypertension?

A

The kidney is thought to have a major role in creating and maintaining hypertension. PSNS and SNS also seem to have a role in early hypertension
Kidney is a major regulator of sodium/water/ecf regulator-if you transfer a diseases kindey to another mice, its BP rises=recall it also damages it

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14
Q

What damages can hypertension cause?

A

Increase risk of CHD, Stroke, arthermatous didease, heart failure, atrial fibri, dementio, retinopathy

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15
Q

How does hypertension affect the heart?

A

A high arterial BP means the heart has to beat against a larger afterload-more likely to fail. But also larger thicker left wall to push out = second main cause of heart failure (on the rise) 2-3x increase

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16
Q

How does hypertension affect large arteries and vessels?

A

It causes a thickening of the media of the arteries-proliferation of SMC and activation of endothelia
Can also cause aneurysm-as tension rises, the wall weakens-expands and as it expands, the pressure on it increases => blood vessel burst (actual rare-strokes are embolism not aneurysm)

17
Q

How does hypertension affect the eye and microvasculation?

A

eye-Thcikening of the small atries wall, vasospasm, impaired perfusion and leakage into tissue -pretty rare
For microcirulation-tickening of th wall and lowering of microvascular-less perfusion and increases resistance

18
Q

What are main treatments of hypertension

A

Diet and lifestyle modification
ACE inhbitors-stop from angiotensin to become angotension II => less ADH, aldosterone and tubular sodium reabosrption-less water retention
also causes less constiction and SNS exitation
Angiotensin inhbitors do the same
Diuretics- only rare for people in hypertensive crisis-Thiazides-do not work because of diuretics but does that-we dont know how it reduces TPR, but it works
beta blockers-rare for hypertension-block heart B1 receptors to reduce Cardiac output, and Kindey B1-reduce renin
Calcium channel blocks-matter in SMC and cardiomycoties=>reducing the amount of Ca in cells reduces the contraction of these cells=> reduces contractility (and some reduce rate of condution, beating weaker and slower

19
Q

How would you describe cardiac output?

A

Volume of blood that leaves either side of the hear-usually in the context of the left ventricule
Influenced-by preload, afterlaod and cardiac contractility
measured as strove volume x Heart rate
inadequate in heart failure

20
Q

How would you describe ejection fraction? How do you measure it?

A

Stroke volume is End diastolic volume-End systolic volume-and the ejection fraction is SV/End diastolic volume
above 55% is normal
under to 45 is reduced, 30-44 is moderatly reduced, and <30 is severly reduced
measured in echocardiograms

21
Q

Define heart failure

A

inability of the heart to keep up with demand-inadequate perfusion of ograns-lead to congestrion in lungs and legs-lots of symptoms and signs
looking at echocardiograms-usually heart has tachycardia-not beating as well-spastic
Walls are thinner

22
Q

What are the 3 types of heart failure comparaison?

A

Left vs right, chronic vs acute, normal ejection fraction vs abnormal

23
Q

Describe left vs right heart failure

A

Left heart failure-dysfunction with filling or ejection=>the blood backs up and leads to congestion-this then leads to pulmonary hypertension and blockage-breathless, coughing, wheezing, diziness, cyanosis
Right heart failure-also filling or ejection (right ventricule)-can be caused by increase in afterload of pulmonary circulation (caused by left heart failure)-ahrder to eject against it =>often secondary to left hear failure

24
Q

Describe Acute vs chronic heart failure

A

Chronic-more common-slow onset-due to infection, pulmonary embolism, MI or surgery
acute-similar symptoms, but rapid onset

25
Q

Describe Heart failure with reduced vs preserved ejection faction

A

HFrEF (reduced)-abnormal systolic function (unable to pump blood into aotra)-can be due to impaired conctration (damaged mycoye), or valve problems (stenosis)
HFpEF-abnormal diastolic function-normal contractio, but impaired relaxation or filling-SV down by EF normal or up. Because EDV reduced, reduced SV is masked

26
Q

List the main causes of Heart failure?

A

valve diseases- hardening of the ventricular or ejecting valves (unable to take blood or eject it)
Ischemid heart disease-narrowing or cornary arteries-ischemia-less of the heart has to perform harder-cycle of worsening
MI-significant occlusion-less cardimyocytes, less strengths-less ability to pump
Hypertension-increase afterload means heart has to pump harder-so increase cardiomyocyte means thciker walls-less blood comes in ans less is ejected
Dilated cardiomyopathy-walls of ventricule is thinner-dilate the ventricule=>more blood in it but not enough force to push it out (systolic dysfunciton)
Hypertrophic cardiomyopathy-similar to hypertension-less blood coming in
Main causes-coronary artery disease (34%), hypertension and cardiomyopathy (15% each), myocarditis and neoplasia (10% each)

27
Q

What are the clinical features of a patient with heart failure?

A

patient will have breathlessness, fatique, orthopnoae (when lie down betterà, dynspnea in sleep, anorexia, weight loss
=>tachycardia, reduced pulse volume, pitting oedoma, scites
can Xray for large heart, ECG (tachy), angiograms, execise test and BNP
Main causes are breathlessness and fluid overload

28
Q

What is JVP? Pitting oedema? and ascites? how does it relate to Heart failure?

A

JVP-jugular vein pulse-as increased pressure to the right side, pressure backs up to systemic veins-especialy jugular (pulsing)
Pitting oedema-especially in lower extremities-as conngestions increases, fluid exits where is can (hight hydrostatic)-pit effects of physical depressed-no bounce back of skin, idents visible after pushing
Ascites-fluid accumulates in peritoneal cavity-large stomach
ALL 3 are HALLMARKS OF HEART FAILURE

29
Q

What is BNP? B-typpe natruiretic peptide? relate to heart failure?

A

When myocytes stretch they release BNP-and that tends to act to reduce sodium excretion (less aldosterone, vasodilation, reduced sodium, inhbit renin to reduce pressure (normally reduce blood pressure)
hallmark of heart failure, as the heart is strethcing to try and keep up

30
Q

What are the lifestyle treatment for heart failure?

A

Lifestyle-always remember weight loss, exercise, stop smoking and less aclohol-all conservative treatments-what patient can do themselves

31
Q

What are medication for heart failure?

A

Similar to hypetension-ACE inhibiors (stop angiotensin II, and aldostrone)
B blockers-heart slows down-needs less energy and lower BP
Diruetic-get rid of excess fluid, pressure goes down
usually in that order-this helps reduce the load on the heart, and beta blockers allow energy savings
But if still symptomatic-sacubtril/vastrane- (vasatrane) bind aldosterone, and (sacubitril) inhbits enzyme that breaks down BNP
Cardiac resynchonistion therapy-allow heart to beat more efficiently

32
Q

What are nonpharmalogical management techniques of heart failure?

A

Fluid control (dyalisis), devices (aortic baloons, resynchonisation, total artificial hearts) surgical (coronary bypass graft, valve surgery, transplant

33
Q

Recall the law of Laplace

A

Wall stress-pressure x radius / 2 wall thichness
So in hypertrophy, wall stress goes down-but there is less palce so no good
but aim of therapy is usually reducing that wall stress
dilated cardiomyopathy-wall thick down-so high wall stress

34
Q

What are neural and hormonal responses (normal and pathophysio) to heart falure?
What is BNP? B-typpe natruiretic peptide? relate to heart failure?

A

normal-positive BNP and reduce the load
Patho-as heart not beating well, reduced perfusion which activated Renin AI, AII aldo (RAAS) apthway, increasing sodium intake and water intake-and BP

35
Q

What is the progression of heart failure like?

A

Diagnosis-then will get worse (mild, severe, death)
can get rare sudden death
Any other coronary events are bad too
quality of life is poor, life expentancy is down-tired all the time, even at rest (and breathless