Cardiovascular Pathology Flashcards
What is the pericardium?
Outer layer
Fixes the heart to the mediastinum
Provides barrier against infection
Provides lubrication for the movements of the heart
The visceral layer of serous pericardium is also called the epicardium
What is the myocardium?
Provides a scaffolding for the heart chambers
Essential for contraction and relaxation of the cardiac walls so that blood can pass between chambers
Allows electrostimulation conduction through it own tissues and into the endocardium
What is the endocardium?
Important role in heart genesis, valve and great vessel formation
Contains Purkinje fibres
Transmit electrical impulses
Provides a low friction lining reducing frictional damage to circulating cells and prevents valves sticking together
What are some cardiac disorders?
Ischaemic Heart Disease
Heart Failure
Cardiomyopathies
Rheumatic Heart Disease
Other Forms of Carditis
What are some vascular disorders?
Arteriosclerosis
Hypertension
Vasculitis
What is the systolic section of blood pressure?
Correlates to when the left ventricle contracts
Measuring the amount of pressure that is put under the arterial walls
We measure the pressure at the brachial artery
What is the diastole section of blood pressure?
When the ventricle is filling
The large arteries are elastic & can stretch, and then they snap back but they continue to propagate blood through
so diastolic shows how well your large arteries recoil (how elastic they are)
What are the Limitations when taking BP in a healthcare setting?
White coat syndrome
Mask syndrome – BP goes down in front of the health care practitioner.
Best practice, on going BP at home when relaxed
What is normal Blood pressure?
Normal 120/ 80
Can have healthy people in and around those values
But population wise:
if elevated over 120/80 over a period of time hypertensive
If decreased under 120/80 over a period of time hypotensive
What are the two types of hypertension?
Primary (essential)
Secondary (due to something else)
What is primary hypertension?
most common type - 90– 95% of cases
As we age, our BP increases
Unsure what causes this.
Known as the silent killer as it is asymptomatic. A high cause of death.
50% of adults in the US have hypertension – 50% of those, don’t know they have it.
The 50% that do know they have it, are being treated incorrectly it.
1 in 2 people with mismanaged hypertension will die of ischaemic heart disease
THIS IS WHY IT IS REALLY IMPORTANT TO CHECK IT!
What is the blood pressure equation?
BP = Cardiac Output X Peripheral Vascular Resistance
CO = how much blood leaves the heart per minute
Heart Rate: How many times does the heart beat per min (approx. 70)
Stroke Volume: how many litres (approx. 5l) pumped out
Increase HR or SV = Increase CO
Vascular Resistance = the diameter of the blood vessels.
If you narrow the diameter of a blood vessel – you increase resistance – you increase BP.
Everything works back to this formula! Remember this.
What is the Pathophysiology of (Primary)hypertension ?
The Sympathetic Nervous System
Kidneys & body Fluid - The Renin Angiotensin Aldesterone System
Vasculature
Sodium (ion) handling
All play a role in increasing blood pressure.
BP = Cardiac Output X Peripheral Vascular Resistance
What is the role of the sympathetic nervous system?
Has a role in the stress response – fight / flight
Release of adrenaline / noradrenaline – controlled by the hypothalamus
The SNS gets activated to keep you alive in that moment
Redirect blood
Increase blood
Breath more air in
Move blood to the muscles away from the skin
Dilate pupils to see
Hormones released in sympathetic response have an effect on blood vessels.
The SNS efferents target different organs
Heart – SA and AV nodes – speeds the heart rate up
Myocardium – increases the contractile force
Blood vessels – cause most arterioles to constrict
Adrenal glands – adrenaline release, which circulates around the blood stream and ramps up all of the above
Kidneys – causes them to release hormones
What are the kidneys role in blood pressure?
Kidneys get a 5th of blood volume every minute.
Due to this, very suited to constantly check how much blood pressure is in the system and how much blood volume is being moved around
If it senses a change in BP, the kidneys respond - The Renin Angiotensin Aldosterone System
Main function of kidneys is to filter blood, and to do this, it needs a lot pressure to force plasma out of the blood to do its main filtration job.
If they can’t filter, the metabolites sit and accumulate in the body which can become toxic > death.
The kidneys respond to a drop in blood volume (reduced blood volume, reduced GFR)
Kidneys respond by releasing by renin.
What is the The Renin Angiotensin Aldosterone System ?
The kidneys respond to a drop in blood volume (reduced blood volume, reduced GFR)
Kidneys respond by releasing by renin.
Three ways in which renin is released.
The pressure within the afferent blood arterioles has dropped, the granular cells within the blood vessels release renin.
- A drop in blood volume causes a reduced GFR= there will be slow movement through the nephrons.
So more time to reabsorb sodium back into the body through the tubules of the nephron
Therefore by the time the sodium reaches the very end of tubules, the sodium will be low as a lot of it has had time to be reabsorbed back into the body.
Therefore the macular denser cells which detect low sodium in the end of the tubules cause a release of renin.
Sympathetic NS can innervate granular cells to release renin.
Now renin is released and circulates around the body and comes across angiotensinogen (ogen – inactive) which is released from the liver.
When Renin interacts with angiotensinogen, it activates it angiotensin 1
Angiotensin 1 circulates in the blood until it reaches the lungs, where it meets the enzyme ACE.
Ace converts Angiotensin 1 into Angiotensin 2
Angiotensin 2 is one of the most potent vasoconstrictors of the body.
If you constrict blood vessels, you increase BP
Outcome of this system
Angiotensin 2
can further stimulate the nervous system – leading to further BP increase.
Travels to the Blood Brain Barrier, at the 3rd ventricle Angiotensin 2 can cross and stimulate the Sympathetic Nervous System.
Also releases aldosterone from adrenal glands.
Aldosterone causes reabsorption of sodium back into the body, and then water follows, so then you increase blood volume
At the Hypothalamus
Causes release of vasopressin – ADH
ADH reabsorbs back into the body (increasing blood volume, increasing BP).
What are the 3 ways renin is released?
The pressure within the afferent blood arterioles has dropped, the granular cells within the blood vessels release renin.
A drop in blood volume causes a reduced GFR= there will be slow movement through the nephrons
Sympathetic NS can innervate granular cells to release renin
What affects the vasculature and therefore the BP?
Anything that narrows the lumen will cause an increase in BP:
Ageing – elasticity reduces, replaced with collagen type tissue.
Atherosclerosis – can be both a cause of high BP and an effect.
Obesity
Smoking
There is also Local control
What is sodium handling?
Sodium in the body is an ion (Na+ )
The body is predominantly made up of water, so due to the charge of ions, wherever sodium goes, water follows.
If an individual eats a lot of salt, a lot of water will be pulled with it into the body which causes:
Blood volume to increase, which causes BP to increase
Our bodies can mostly adapt and excrete out excess sodium.
Some people are salt sensitive, and their BP rises significantly with increase in salt - salt reduction diet intervention.
Salt sensitivity is present in 50% of primary hypertensive people
25% of people of normal tensive people – are salt sensitive.
Salt sensitive people – don’t have as adaptive vascularity can’t change blood vessels diameter quickly.
For most people this is transient, but if you’re salt sensitive, it will take a bit longer to respond to this.
No objective measure for this – hence why its primary hypertension, and generally advise people to reduce salt.
What are the risk factors for primary hypertension?
Modifiable:
Stress
Obesity
Smoking
Physical Inactivity
Increased salt consumption
Non- Modifiable
Genetics
Low income countries or low socio economic income homes
What is secondary hypertension?
Has a cause
If you remove the cause, BP reduces.
Causes are grouped as:
Renal
Endocrine
Other
sleep apnoea
pregnancy
Drug induced
What are the renal causes of secondary hypertension?
Kidney requires enough BP to maintain GFR
Chronic Kidney disease (reduction in GFR causing release of renin)
renal artery stenosis can’t bring blood to the whole kidney – again releases renin
What are the endocrine causes of secondary hypertension?
A Primary aldosteronism (tumor)– Aldosterone enhances Na reabsorption at the distal tubule
Cushings – cortisol released from the adrenal glands. Cortisol is a stress hormone and stimulates SNS and therefore increases BP.
Hyperthyroidism/ hypo: T3/ T4 have a role in enhances in the sympathetic nervous system. Too much, more sensitive to BP- increases heart rate contractibility, increase HR and CO = high BP
Hypo – the opposite. Vasoconstriction of blood vessels.
Adrenal hyperplasia – tumour on medulla- causes release of adrenaline
Tumour in parathyroid gland – calcium homeostasis. If blood calcium is low, parathyroid is released. Helps reabsorption of Ca from bone, and reabsorption of calcium in intestines and kidneys (with vitamin D). Increased Ca2+ has an effect on the heart – increased contractibility o the heart and constricts the blood vessels.
What are the other causes of secondary hypertension?
Sleep apnoea
Periods of decreased ventilation whilst sleeping e.g. obstructive or central.
The body will generally wake up, so you have poor quality of sleep.
Activate the SNS more often, no longer getting restorative sleep as much
Pregnancy
General blood volume increase
Hormonal effect from being pregnant has an effect on edema (more fluid on the body)
Drug induced
Cocaine – increase BP, has an effect on increasing adrenaline SNS effect
Herbal remedies – St. John’s Wart.
NSAIDs – block prostaglandins (chronic use)
Anti depressant. – which increase serotonin or noradrenaline
Decongestants.
Long standing hypertension is a risk factor for the brain. How?
haemorrhagic stroke (long term stress, effects the tissue composition, where it branches is the weakest point)
small vessel haemorrhages in the brain
retinal changes – vision changes
Long standing hypertension is a risk factor for the heart. How?
Ischaemic heart disease (MI)
Cardiomegaly / hypertrophy of cardiac muscles
Long standing hypertension is a risk factor for the kidneys. How?
Nephropathy – remodelling kidney changes due high BP, leads to kidney failure.
Long standing hypertension is a risk factor for the arteries. How?
AAA – Abdominal Aortic Aneurysm
Dissecting Aneurysm- high pressure blood shears between the two layers of the blood vessels (tunica / media)
Peripheral Vascular Disease – significant atherosclerotic plaque – stops perfusion into the legs
Carotid changes – atherosclerosis at bifurcation.
What is Edema?
Accumulation of excess fluid in tissues is termed edema
Under normal circumstances on a small amount of interstitial fluid leaks which is removed by lymphatic vessels.
Excess fluid leaks from capillaries in 3 main circumstances:
Increased hydrostatic pressure in vessels (heart failure)
More fluid leaves capillaries with reduced plasma oncotic pressure (hypoproteinemia)
More fluid leaves capillaries if vascular permeability is altered (allergic reaction liberating histamine, acute inflammation)
What are the Two important types of edema due to cardiac failure?
Increased hydrostatic pressure in the pulmonary vascular bed
Due to left sided heart failure
- Subcutaneous edema
Increased hydrostatic pressure in the systemic venous
system
Due to right sided heart failure.
What are the risk factors of Atherosclerosis?
Hyperlipidaemia
Hypertension
Diabetes mellitus
Cigarette smoking
Family history
In Atherosclerosis, what are the 3 types of lesions?
Fatty streak (small, intracellular fat , innocuous)
Atheroma (raised, lipid centre, dangerous)
Fibrous plaque (intimal scar, innocuous)
What are fatty streaks?
Almost all children older than 10 in developed countries have fatty streaks, with coronary fatty streaks beginning in adolescence.
It consists of aggregates of foam cells, which are lipoprotein-loaded macrophages.
Fatty streaks may also include T cells, aggregated platelets, and smooth muscle cells.
It is the precursor lesion of atheromas.
What is Atheroma?
Atheroma is an accumulation of degenerative material in the intima of an artery wall.
The material consists of mostly macrophage cells, or debris, containing lipids, calcium and a variable amount of fibrous connective tissue.
It develops in areas of turbulent flow due to increased hydrostatic pressure at that point, whereas it is not seen in low pressure systems such as the Pulmonary artery or vein
What are Aneurysms?
Change in the structure of the tunica media may result in loss of elasticity of the vessel wall.
Major factor in the pathogenesis of aneurysm formation.
Mainly occurs in large arteries affected by severe atherosclerosis,
Abdominal aorta
An aneurysm which continues to grow in size, will cause progressive weakening of the artery wall.
The larger the aneurysm becomes, the greater the risk of rupture.
This requires surgical intervention
Prevention of a rupture is the most important goal in medical therapy
Shapes of aneurysms can be described as..?
Fusiform
bulges or balloons out on all sides of the blood vessel.
usually due to atheroma
often below renal arteries; may affect iliac arteries
Saccular
E.g. Berry Aneurysm in the circle of Willis.
bulges / balloons out on one side
Pseudoaneurysm
aka False aneurysm
Not an enlargement of any of the layers of the blood vessel.
May be as a result of prior surgery.
Blood fills between the layers of the blood vessel wall creating a pseudo aneurysm.
What is a dissecting aneurysm?
An aneurysm that occurs with a tear in the artery wall that separated the 3 layers of the wall
(rather than ballooning out the entire wall)
What are the causes of aneurysms?
Multifactorial reasons which lead to the breakdown of structural proteins in the artery walls which provide support and stability to the vessel wall.
Atherosclerosis plays an important role in aneurysm formation
risk factors associated with atherosclerosis
e.g. male, genetics, hyperlipidemia, hypertension, smoking, diabetes, obesity.
What are some specific causes of aneurysms related to their location?
Abdominal Aortic Aneurysm (AAA)
Atherosclerosis
Genetic
Giant Cell Arteritis
Cerebral Aneurysms
Hypertension
Atherosclerosis
Head Trauma
Iliac Artery Aneurysm
Atherosclerosis
Pregnancy
Post lumbar / Hip surgery
Femoral / Popliteal Aneurysm
Atherosclerosis
Trauma
What is Thrombophlebitis?
acute inflammation of veins which triggers a thrombus
Caused by:
bacteria
parasite
physical / chemical stimuli
Superficial thrombophlebitis – visible, localised swelling, erythema
What is Deep vein thrombosis?
Deep vein thrombosis – global swelling but no localised erythema visible due to thrombosis within muscle compartment
What are varicose veins?
Not primarily inflammatory
Abnormally dilated veins
Sites for varicose Veins:
Legs
Osoephagus
Testes, Vuvla,
perianal (haemorrhoids)
What is pericarditis?
Inflammation of the pericardium
Causes:
Infective – Bacterial or Viral
immune-mediated
Chest trauma e.g. RTA
Ischaemic – e.g. following a trans-mural MI causing an inflammatory pericarditis +/- effusion
Resolution may result in:
Constrictive pericarditis - Fibrosis, Fusion + Occasionally calcification
or
Cardiac tamponade – too much fluid in the pericardial space
Both conditions can lead to cardiac failure
What is Cardiomyopathy?
Disease of the myocardium
Inherited or acquired
3 main types:
HOCM (Hypertrophic obstructive cardiomyopathy) – 1 in 500
DCM (Dilated cardiomyopathy) - 50% inheritance (inherited + acquired types)
ARVC (Arrthymogenic right ventricular cardiomyopathy) - rare
What are the causes of Acquired Cardiomyopathy?
Takosubo/Broken Heart Syndrome
Follows acute physical or emotional stress in 85% of cases
Can cause fatal arrthymias/heart rupture
Myocarditis
autoimmune or viral
Ischaemic
Endocrine
Diabetic/hyperthyroidism
Poisons
chemotherapy, alcohol, drugs
What is Rheumatic Fever?
An autoimmune response to an untreated Strep A infections
Scarlet Fever, Strep Throat
Causes an inflammatory disease which can involve:
Heart, skin, joints and brain
The disease typically develops 2 – 4 weeks after a streptococcal throat infection.
the heart is involved in about half of cases
Damage to the heart valves is known as rheumatic heart disease
What is Chronic Rheumatic Heart Disease?
Subsequent changes in the heart: Thickening of valve cusp, especially along lines of closure
Fusion of commissures
Result is aortic stenosis, insufficiency or often both
Aortic stenosis> LV hypertrophy
Aortic insufficiency> LV hypertrophy and dilatation
Subsequent changes in the heart:
Predominantly left-sided valves (almost always mitral)
Mitral > Aortic > Tricuspid > Pulmonary
Mitral alone 48%, Mitral + aortic 42%
What is Myocardial Infarction?
Occlusion of a coronary artery leading myocardial hypoxia > cell death.
usually due to thrombotic occlusion of a coronary vessel
It is generally accepted that the cross sectional area of the coronary artery lumen must be reduced by > 75% to significantly affect perfusion.
underlying coronary artery disease
Coronary arteries are prone to atheroma due to their unique flow pattern of being empty during systole and filling in diastole. This spurt—flow pattern causes turbulence and arterial wall trauma.
causes a rapid drop in systolic function
Time from Onset Gross Morphologic Finding
18 - 24 Hours Pallor of myocardium
24 - 72 Hours Pallor with some hyperaemia
3 - 7 Days Hyperaemic border with central yellowing 10 - 21 Days Maximally yellow and soft with vascular margins 7 Weeks White fibrosis
What is the treatment for Myocardial Infarction?
Anti- coagulants
Stents fitted
What are examples are Ischaemic Heart Disease?
Angina Pectoris
Characterised by paroxysmal attacks of exercise related chest pain
Anterior chest pain usually
Caused by myocardial ischaemia
Stable Angina (typical)
Increases on exertion
Resolves completely with rest or vasodilators
Unstable Angina
Occurs at rest or minimal exertion and usually lasts more than 20 minutes.
Severe and of recent onset (i.e. within 1 month).
Occurs with a crescendo pattern (brought on by less activity, more severe, more prolonged or increased frequency than previously.
What is congestive heart failure?
Cardiac function is insufficient to pump blood at the rate required by the tissues in the body
Heart failure can also affect the kidney’s ability to dispose of Sodium & water > leading to edema.
As glomerular filtration rate decreases
Divided it into:
Left sided heart Failure
Right sided heart Failure
What are the 2 types of left sides heart failure?
Systolic Failure
aka Heart Failure with reduced ejection fraction
the left ventricle loses its ability to contract normally, & so can’t push enough blood out into circulation.
Diastolic Failure
aka Heart Failure with preserved ejection fraction
The left ventricle loses its ability to relax normally (because the muscle has stiffened) & therefore the heart is unable to properly fill with blood between each beat.
If fluid collects in the lungs, it can cause shortness of breath – particularly when a person is lying down
this is known as pulmonary edema.
What is right sides heart failure?
NB. Blood returns from the body to the heart via the right atrium > into the right ventricle.
The right ventricle then pumps back to the lungs.
Can occur as a result of left sided heart failure
When the left ventricle fails, increased fluid pressure is transferred back to the lungs – damaging the hearts right side.
When the Right side loses power, the blood backs up into the body’s veins
this causes swelling in the ankles and abdomen.