Cardiac problems - health & disease Flashcards

1
Q

What is shock

A

Any situation in which a reduction of blood flow to the organs and tissues damages them

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2
Q

What is hypovolemic shock?

A

A decrease in blood volume secondary to hemorrhage or loss of fluid other than blood

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3
Q

What is low-resistance shock?

A

This is due to a decrease in total peripheral resistance secondary to excessive release of vasodilators, as in allergy or infection

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4
Q

Cardiogenic shock

A

This is due to an extreme decrease in cardiac output from any variety of factors (eg MI)

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5
Q

How can venous pooling leading to reduced BP

A
  • Venous pooling due to gravity = increased hydrostatic pressure in legs when a person is standing pushes outward on highly distensible vein walls, causing distension. some blood from capillaries goes to the expanding veins rather than returning to the heart. (increased capillary pressure also causes increased filtration)
  • this means there is a reduced venous return
  • reduced end-diastolic pressure
  • decreased stretch of ventricles
  • reduction of SV, CO, BP

(reduced BP does then trigger baroreceptor reflex so the affect doesn’t last long)
gentle leg contractions produce intermittent, complete emptying of deep leg veins

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6
Q

What happens to blood flow during exercise and how?

A
Increased blood flow to 
-working skeletal muscles
-heart
-skin if heat needs to be dissipated 
Decreased flow to:
-kidneys
-abdominal organs

This is due to arteriolar vasodilation

  • local metabolic factors mediate vasodilation in skeletal and smooth muscle
  • in the skin vasodilation is achieved mainly by decreased sympathetic stimulation to the skin
  • arterial vasoconstriction also occurs in the kidneys and abdominal organs due to increased symp stimulation

there is a net decrease in peripheral resistance this is due to the huge dilation of the muscle arterioles

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7
Q

What is the effects of mild upright exercise? eg jogging

A
  • Increased skeletal muscle blood flow
  • Increased meal arterial pressure
  • Increased systolic pressure
  • Constant diastolic pressure
  • Reduced total peripheral resistance
  • Increased CO (due to increased HR and SV)
  • Increased HR (due to decrease parasymp to SA and increased symp)
  • Increased SV (due to increased venticular contractibilty)
  • Increased (small increase) end-diastolic ventricular volume (due to increased filling, starling mechanism=increased SV)
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8
Q

What factors promote venous return during exercise?

A
  1. Increased activity of skeletal muscle pump
  2. Increased depth and frequency of inspiration (resp pump)
  3. Symp mediated increase in venous tone
  4. Greater ease of blood flow from arteries to veins through the dilated skeletal muscle arterioles
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9
Q

How do control centres in the brain affect the body during exercise?

A

“Exercise centres” in the brain produce the primary outflow of symp and parasym outflow to the body
-descending pathways go to appropriate autonomic preganglionic neurons (symp to skeletal muscles, kidneys and abdominal organs) (parasym to skin increases dilation)

  • Once exercise is underway or during intense exercise local chemical changes activate chemo receptors.
  • Afferent input from these receptors goes to the medullary cardiovascular centre and facilitates the output reaching the autonomic neurons from higher brain centres
  • This results in further increase in HR, myocardial contractility, and vascular resistance in nonactive organs
  • Meachanoreceptors in active muscles are also activated and provide input to medullary cardiovascular centre.
  • Baroreceptors react again causing a further increase in BP (they respond as though BP has decreased due to a ‘resetting’ as excecise begins’)
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10
Q

What differences occur during weight-lifting as opposed to jogging?

A

-high-force, slow-shortening velocity contractions
same -CO, BP increase and arterioles undergo vasodilation

differences - once contracting muscles exceed 10-15% of their maximal force the blood flow to the muscle is greatly reduced because the muscle are physically compressing the blood vessels that run through them. So cardiovascular changes are ineffective -contractions can only be maintained briefly before fatigue kicks in.
-total peripheral resistance is increased due to the compression, this leads to an increase in mean arterial pressure during contraction.
(frequent exposure can cause maladaptive changes to the left ventricle including wall hypertrophy and diminished chamber volume)

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11
Q

What is maximal oxygen consumption?

A

This is when oxygen consumption increases till it reaches a point where it fails to increase despite an increase in work load, after this point has been reached work can be increased and sustained only briefly by anaerobic metabolism.

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12
Q

What limits maximal oxygen consumption (or V0 max.)

A

1) Cardiac output
2) The respiratory systems ability to deliver oxygen to the blood
3) The exercising muscles’ ability to use oxygen

for most people (except highly trained atheletes) CO is the limiter (HR increases until it reaches a maximum)

  • rapid heart rate which decreases diastolic filling time
  • inability of the peripheral factors favouring venous return to increase filling further during short time avalible
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13
Q

What can change v0 max?

A

A person’s physical activity

  • prolonged bed rest may decrease by 15-25%
  • intense training may increase by 15-25%

Increased SV and decreased HR = same CO

1) increased ventricle size and hypertrophy
2) increased number of blood vessels in skeletal muscle which permits increased muscle blood flow and venous return
3) also increases concs of oxidative enzymes and mitochondria in the exercised muscles = this increases muscle endurance but does not affect V0max as it was not limiting it to start with

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14
Q

What is Ventricular hypertrophy?

A

Ventricular hypertrophy is the thickening of the ventricular walls (lower chambers) in the heart. Although left ventricular hypertrophy is more common, enlargement can also occur in the right ventricle, or both ventricles.

-Healthy cardiac hypertrophy (“athlete’s heart”) is the normal response to healthy exercise or pregnancy, which results in an increase in the heart’s muscle mass and pumping ability.

-Unhealthy cardiac hypertrophy (pathological hypertrophy) is the response to stress or disease such as hypertension, heart muscle injury (myocardial infarction), heart failure or neurohormones. Valvular heart disease is another cause of pathological hypertrophy.
pathological hypertrophy also leads to an increase in muscle mass, but the muscle does not increase its pumping ability, and instead accumulates myocardial scarring (collagen). In pathological hypertrophy, the heart can increase its mass by up to 150%.

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15
Q

What does ageing affect the heart’s performance?

A
  • Decrease in max heart rate

- increased heart stiffness that decreases rapid filling during diastole

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16
Q

What is hypertension?

A

Chronically increased blood pressure - above 140/99 mmHg

-huge PH issue 26% of worldwide population

17
Q

How does hypertension lead to heart failure?

A
  • The left ventricle must chronically pump against an increased arterial pressure (afterload) it develops an adaptive increase in muscle mass called left ventricular hypertrophy.
  • This hypertrophy helps to mantain the heart’s function as a pump, however over time changes in the organisation and properties of myocardial cells occur = results in diminished contractile function and heart failure
  • Hypertension also increases chances of atherosclerosis, heart attacks, kidney damage and strokes
18
Q

What is primary/secondary hypertension

A

Primary hypertension is when hypertension of uncertain cause is diagnosed - 90% of all cases (often reduced artial radius causing increased resistance)

Secondary hypertension - when there is an indentified causes of hypertension.
-Often damage to the kidneys can lead to renal hypertension, this is when excess renin release leads to excessive concs of angiotensin II and decreased urine production, this results in excess ECF volume.
Some are genetically predisposed to excess renal Na+ reabsorption - these patients respond well tolow-sodium diets and use of diuretics
-Hyper secretion of cortisol of thyroid hormone can lead to chronic hypertension
-Oral contraceptives, and non steroidal anti-inflammatory drugs
-Sleep apnea (abnormal night breathing pattern) can also lead to hypertension

19
Q

What lifestyle choices are likely to lead to hypertension?

A
  • Obesity and insulin insensitivity
  • Chronic high salt intake
  • Smoking
  • Excess alcohol consumption
  • Diets low in fruit, veg and whole grains
  • Diets low in Calcium and Vit D
  • Chronic stress
  • Excess caffeine consumption
  • Maternal smoking
  • Low birth-weight
  • Not being breast fed as an infant

D.A.S.H - dietary approaches to stop hypertension showed success in low-salt diet

20
Q

What is heart failure?

A

Heart failure is when the heart fails to pump an adequate cardiac output
2 main categories, although many people have elements of both
1) those with diastolic dysfunction (problems with ventricular filling)
2) those with systolic dysfunction (problems with ventricular ejection)

  • Reduced CO of heart failure triggers the arterial baroreceptor response - this results in
    1) Increased HR
    2) Increased total peripheral resistance due to symp activation of the arterioles, and increased conc of angiotension II and vasopressin
  • These responses are effective at increasing CO for a while however maintained chronically they result in fluid retention and expansion of ECF volume
  • increased total peripheral resistance due to increase symp neurons and increased conc of angiotension II and vasopressin makes the heart work even harder
21
Q

What causes diastolic dysfunction (within heart failure)

A

The wall of the ventricle has reduced compliance

  • Its abnormal stiffness results in a reduced ability to fill adequately during diastole.
  • This results in reduced end-diastolic volume
  • This results in reduced SV (Frank-starling)
  • So cardiac output is reduced and it not adequate to supply to body with oxygenated blood

-Usually due to chronic systemic hypertension, this results in hypertrophy that makes the ventricle stiff and less able to expand

22
Q

What causes systolic dysfunction (problems with ventricular ejection) -within heart failure

A

Systolic dysfunction results from myocardial damage, often due to a MI.

  • A decrease in cardiac contractibility resulting in a lower stroke volume at any given end-diastolic point
  • This manifests as a decrease in ejection fraction
  • The ventricle does not hypertrophy but end-distolic volume does increase
23
Q

Why does increased venous pressure cause edema?

A

The capillaries drain via venules into the veins.

  • So when venous pressure increases the capillary pressure also increases and causes increased filtration of fluid out of the capillaries and into the interstitial fluid.
  • Thus most of the fluid retained by the kidneys ends up as extra interstitial fluid not extra ECF = swelling of feet and legs
24
Q

What does failure of the left ventricle result in?

A

Pulmonary edema

  • accumulation of fluid in the interstitial spaces in the lungs or air spaces themselves
  • this impairs pulmonary gas exchange
  • This is because the left ventricle fails to pump blood to the same extend as the right ventricle, so blood volume in all the pulmonary vessels increases
  • This increases the capillary pressure causing filtration to occur faster than lymphatics can remove the fluid
25
Q

Why is Pulmonary edema often worse at night?

A

During the day, because of the patients upright position fluid accumulates in the legs.
When the patient lays down at night the fluid is slowly absorbed back into the capillaries thereby expanding the plasma volume and precipitating the development of pulmonary edema

26
Q

What can heart failure be treated?

A
  • Treat the hypertension with drugs (diuretics, b-adrenergic receptor blockers, ca2-channel blockers, ACE inhibitors)
  • Heart transplant
27
Q

What is hypertrophic cardiomyopathy?

A
  • Increased thickness of heart muscle, in particular left ventricle wall and inter ventricular septum
  • Genetic
  • Often leads to heart failure
  • There is also a disruption in the order of myocytes and conducting cells within the walls

-The thickening of the septum interferes with the ejection of blood through the aortic valve, particularly during exercise which can prevent CO from increasing sufficiently for the body’s needs
-May experience angina as the heart doesn’t get enough blood
-Disruption of conducting cells can lead to fatal arrhythmias
-Many people have no symptoms and so it can go undetected till it reaches a fatal stage
(often why young athletes can die unexpectedly-OTH)
-treatment -drugs to prevent arrhythamias, surgical repair of the septum and valve, or heart transplantation

28
Q

Explain what happens in Coronary heart disease, and the accociated symptoms

A

Coronary heart disease

  • changes in the heart’s arteries cause insufficient blood flow (ischemia) to the heart
  • this can result in an myocardial infarction of heart attack
  • many patients suffer angina attacks before suffering from a heart attack

Symptoms:
prolonged chest pain, often radiating to left atm
nausea, vomiting, sweating, weakness, shortness of breath

-Some specific cardiac muscle proteins leak into the blood when the muscle is damaged - these can be detected in order to diagnose CHD - often the myocardial-specific isoform of the enzyme creatine kinase and cardiac troponin.

29
Q

What is ventricular fibrillation? How is it treated

A

-Sudden cardiac deaths during myocardial infarction are due mainly to ventricular fibrillation, an abnormality in impulse conduction triggered by the damaged myocardial cells
The abnormal conduction pattern results in uncoordinated ventricular contractions that are ineffective in producing flow

atrial fibrillation only causes minor cardiac problems, ventricular is usually fatal

30
Q

What is the treatment for ventricular fibrillation?

A

TREATMENT
-cardiopulmonary resuscitation, CPR, a repeated series of chest compressions often accompanied by mouth-to-mouth resuscitation, this circulates a small amount of o2 to vital organs
-defibrillation is then followed, this is when an electrical current is passed through the heart to halt the abnormal electrical activity that is causing the fibrillation
Automatic electronic defibrillators are found in most public places in order to do this.

31
Q

What is atherosclerosis?

A

atherosclerosis is a disease of the arteries that results in thickening of the arterial wall closest to the lumen with plaques made up of

  1. large numbers of cells, including smooth muscle cells, macrophages and lymphocytes
  2. deposits of cholesterol and other fatty substances, both within cells and extracellularly
  3. dense layers of connective tissue matrix

atherosclerosis reduces coronary blood flow

  • the deposits buldge into the lumen increasing resistance to flow
  • dysfuntional endothelial cells in the atherosclerotic area release excess vasocontrictors (eg endothelin-1) and less vasodilators (NO and prostacyclin)
  • these processes are progressive and can lead to complete occlusion
  • coronary thrombosis (clot formation) can cause total occlusion within the narrowed artery triggering a heart attack
32
Q

What lifestyle factors can increase the chance of atherosclerosis and coronary heart disease?

A
  • Smoking
  • High cholesterol diets and amino acid homocysteine
  • Hypertension
  • Diabetes
  • Obesity
  • Sedentary lifestyle (active lifestyle reduces risk of heart attack by 35-55%)
  • Stress
  • Menopause (incidence of heart attacks in very low until after menopause)
33
Q

Why is regular exercise protective against heart attacks?

A

It induces:

  1. decreased myocardial oxygen demand due to decreased resting heart rate and blood pressure
  2. increased diameter of coronary arteries
  3. decreased severity of hypertension and diabetes (two major risk factors of atherosclerosis)
  4. decreased total plasma cholesterol concentration and an increase in HDL cholesterol
  5. decreased tendency of blood to clot and improved ability to dissolve clots
  6. better control of blood glucose due to sensitivity to insulin
34
Q

Explain the relationship between alcohol and coronary heart disease

A

-Low doses MAY increase HDL conc and inhibit blood clot formation
-higher doses increases changes of cancer and cirrhosis of the liver and accidents
(14 units a week) = 6 pints of beer

35
Q

What drugs are used to prevent angina and MI?

What other treatments are possible

A

-Vasodilators
eg nitroglycerine - it is converted to NO in the body
-B-adrenergic receptors
reduces arterial pressure in people with hypertension
-prevent or reverse clotting
eg, aspirin
-Cholesterol
statins -interfers with cholesterol production

Coronary balloon angioplasty - threading a catheter with a balloon at its tip into the occluded artery and then expanding the balloon. This enlarges the artery and breaks up the abnormal tissue deposists

coronary stents - open narrowed or occluded arteries (stainless steel lattice)

coronary bypass - when a new vessel is attached to an area of occluded coronary artery, this new vessel is often a vein taken from somewhere else in the body

36
Q

What is a transient ischemic attack? TIA

A

a temporary reversible occlusion of oxygen to the brain, can be due to atherosclerotic cerebral vessels. can last minutes to hours.