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Theme 3 > How CVS fails > Flashcards

How CVS fails Flashcards

1
Q

Stroke: Ischaemic vs Haemorrhagic

A

rapid loss of brain function(s) due to loss of perfusion to part(s) of the brain

Haemorrhagic
Cerebral blood vessel rupture

OR

Ischaemic
Cerebral blood vessel blockage

Popularised symptoms: Face, Arms, Speech, Time
Treatment: Rehabilitation

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2
Q

Reasons why BV bursts

A 
Stresses
High pressure
High BP or Downstream blockage
Large diameter /  high wall tension
Low elasticity / low compliance 
Turbulent flow
Damage
Trauma
Eg Transluminal procedures (PCI)
Atherosclerosis
Diabetes
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3
Q

Aneurysm

A

Pathological, localized, blood-filled balloon-like bulge in the wall of a blood vessel. An aneurysm has a risk of rupturing, however, if it has not yet ruptured, an aneurysm does not necessarily cause symptoms.

Ruptured aneurysm = can lead to stroke or internal haemorrhage, and subsequent hypovolemic shock, leading to death.

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4
Q

Aortic dissection

A

Tear in the inner wall of the aorta that causes blood to flow between the layers of the wall of the aorta, forcing the layers apart. It can quickly lead to death, even with optimal treatment, as a result of decreased blood supply to other organs, cardiac failure, or rupture of the aorta. The risk of aortic dissection is increased with aortic aneurysms or high blood pressure

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5
Q

Vessel Wall Tension

A

Tension in a cylinder is the force (tangential to the circumference of the cross section) that is trying to rip the wall apart

In a cylinder it is proportional to P x radius (R in photo)

The larger the vessel, the greater the wall tension

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6
Q

Compliance (stretchiness)

A

The change in volume caused by a change in pressure

Thus: low compliance = a change in pressure results in very little change in volume

Double Arrow is pulse pressure

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7
Q

Blood flow

A

Laminar flow - Slower at edges. All in one direction
Laminar blood flow is athero-protective. The shear stress (ie forces “going sideways” in the direction of blood flow) diminishes coagulation and platelet adhesion, as well as reducing proliferation of endothelial cells and smooth muscle cells.

Turbulent flow (causes of)

  • High speed
  • Branching
  • Low viscosity

Turbulence caused by:

Junctions, Mixing & Obstacles

Atherosclerosis
Endothelial damage

Turbulent flow leads to leukocyte adhesion, platelet aggregation and smooth muscle cell proliferation — all of which contribute to atherosclerosis.

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8
Q

Endothelium activities

A

Blood vessel tone

- Local control of perfusion
 - Vasodilatation (Nitric oxide)

Fluid filtration
- Blood Brain Barrier, CSF, kidney (glomerulus), GI secretions

Haemostasis
- Esp. fibrinolysis

White Cell recruitment
- Atherosclerosis

Angiogenesis

Hormone trafficking – transcytosis (eg insulin)

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9
Q

Acute Myocardial Infarction

A

Aregion of heart tissue that is dying or dead - usually caused by a blocked coronary artery

Onset takes minutes – extremely painful *E
Reduces the capacity of the heart to pump

Large or multiple infarcts heart failure
AMIs can be fatal due to arrhythmia or HF

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10
Q

Atherosclerosis

A

A disease process

Results in “furring of the arteries”

Asymptomatic, but can lead to other disorders

Results from hyperlipidaemia, immune action, or unknown aetiology

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11
Q

Coronary Artery Disease

A

A disease process resulting in obstruction of the arteries supplying heart tissue

Symptoms: Angina or asymptomatic

Primary cause is atherosclerosis

Treat with: Drugs for hyperlipidaemia, angina or hypertension

Treat with: Stenting or surgically replacing clogged vessels

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12
Q

Plaque Rupture

A

When the fibrous cap of a plaque bursts open.

Atheromas are relatively safe, even if they occlude 50% of a vessel. However, if plaque rupture occurs in a coronary artery, a thrombus or embolism MI

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13
Q

MI: Sympathetic Activity

A

Sympathetic nervous system releases adrenaline and noradrenalin during acute MI

  - response to pain 
  - and to haemodynamic abnormalities

Sympathetic activity also helps to compensate during heart failure

Increases in: 
Rate
Contractility
Peripheral resistance
Risk of arrhythmia
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14
Q

Pulmonary Oedema

A

Fluid accumulation in lungs (esp alveoli) -> Impaired gas exchange & O2 diffusion lengthened

Caused by Left heart failure
- Damming of blood  hydrostatic pressure increase in pulmonary circulation

Symptoms: Dyspnoea / Orthopnoea / Hypoxia

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15
Q

Peripheral Oedema & Ascites

A

Ascites: Accumulation of fluid in the peritoneal cavity - many causes including heart failure

Peripheral Oedema: Swelling of tissues, esp ankles - many causes, esp chronic low output heart failure

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16
Q

Compensation

A

Maintaining homeostasis of a physiological function despite stressors or malfunctions – happens via endogenous physiological feedback

Eg: In heart failure, to maintain adequate cardiac output (despite cardiac damage), increase plasma volume + increase sympathetic activity

Starling’s Law

17
Q

Decompensated Heart Failure definition

A

A medical emergency
the failure of the heart to maintain adequate blood circulation, after long-standing (previously compensated) vascular disease.
Respiratory distress

18
Q

Cardiac Remodelling

A

Growth of Cardiac Muscle
-> changes in shape, size, function

Caused by injury:
MI, hypertension, valve disease
Response to increase afterload or preload

The result is Hypertrophy or Dilation

Compensatory (initially) -> pathological (later)

Treatments that inhibit: ACE inhibitors or spironolactone

19
Q

Spironolactone

A

An aldosterone antagonist -potassium-sparing diuretics,

Used primarily to treat heart failure, ascites in patients with liver disease, low-renin hypertension, hypokalemia, secondary hyperaldosteronism (such as occurs with hepatic cirrhosis).

Inhibits the effect of aldosterone by competing for intracellular aldosterone receptors in the kidneys’ cortical collecting duct. This decreases the reabsorption of sodium and water, while decreasing the secretion of potassium. This will result in fluid loss and lower blood volume (hence it works as a diuretic); this will decrease afterload, and it should reduce pathological remodelling.

20
Q

Ventricular Hypertrophy

A

Response to work

Athlete’s heart

Eccentric - dilate due to volume overload

Concentric - thicken due to
Pressure overload

21
Q

Antidiuretic Hormone (ADH)

A 
Also called vasopressin
Causes kidneys to reabsorb more water
Decreases Diuresis
From Posterior Pituitary
Peptide
22
Q

Aldosterone

A

Causes kidneys to reabsorb more NaCl (and thus more H2O)
- Directly decreases natriuresis which decreases diuresis

From adrenal cortex
Steroid

23
Q

Decreased Diuresis

A

Increased blood pressure

Diuretic drugs antigonise these hormones leading to fluid loss

24
Q

Angiotensin II (AII) Increases Pressure

A

Vasoconstriction

Increased fluid retention
Increase aldosterone secretion by adrenal cortex
Increases Na+ retention
Increases ADH secretion by posterior pituitary

Contributes to ventricular hypertrophy + remodelling

25
Q

3 main types of diuretics

A

Thiazide & thiazide-like

  • Eg: indapamide
  • Blocks reabsorption at DCT

Loop

  • Eg: furosemide
  • Blocks reabsorption in thick Loop

K+ sparing

  • Eg: spironolactone
  • Inhibits aldosterone receptors in cortical collecting duct
26
Q

Heart Failure Definitions

A

Chronic low output heart failure

Cardiac output is low, usually due to accumulated damage to the heart
Chronic condition with poor 5 year survival rate
Often abbreviated simply as “heart failure”
There is also high output heart failure

Decompensated heart failure
Medical emergency, —> rapid death if not treated

27
Q 
Heart failure (chronic low output): 
Left vs. Right Side
A

Heart does not pump sufficient blood

Left Heart failure: respiratory symptoms
Right heart pumps into lungs but left atrium is too full
Increase hydrostatic pressure in pulmonary circulation

“Congestive” Heart Failure: pulmonary vasculature is congested
In extreme: Fluid leaks out of blood vessels and into lungs

Right Heart Failure: systemic symptoms
Increase central venous pressure  peripheral oedema (or ascites)

Reduced cardiac output
Sympathetic activation (compensates by  Increase HR and PR)
28
Q

Heart Failure: Symptoms & Signs

A

Fatigue - Esp. during exertion

Peripheral Oedema

Dyspnoea

  • Orthopnoea
  • Paroxysmal nocturnal dyspnoea
29
Q

Cardiogenic Shock

A

Critically low perfusion due to low cardiac output
Medical emergency, usually fatal

Insufficient perfusion of tissues, esp. the heart
Progresses by positive feedback

Definition of shock includes SBP < 90 mmHg *E
Treatments: Aggressive intravenous fluid AND Oxygen + airway maintained

30
Q

Homeostasis for low Cardiac Output

A

Increase sympathetic activity

- Increase heart rate
 - Increase heart contractility
  - Vasoconstriction

Kidney accumulates fluid the slower response

  • Decrease glomerular filtration rate
  • Increase Central Venous Pressure
  • Icrease venous return & preload
31
Q

Low output state vs low volume state

A

Heart Failure (or Infarct)
Normal pressure (increased vascular resistance)
Ends with shock
Rare before age 50

Haemorrhage
Loss of fluid leads to loss of pressure
Ends with shock
Any age (due to trauma)

32
Q

Decompensated Heart Failure

A

The kidney increases plasma volume to compensate for poor perfusion of renal tissue
The kidney responds as if it is a haemorrhage
This leads to Fluid Overload

The heart is unable to pump the extra fluid
Fluid damming leads to increased venous hydrostatic pressures
Increased back pressure further damages heart
Positive feedback loop —> rapid deterioration

The capillaries leak fluid into tissues (eg lungs and ankles)

The lungs CANNOT exchange O2 and CO2

33
Q

Low Output HF Treatment Goals

A

Prevent acute decompensated heart failure

Counteract cardiac remodelling

Minimize symptoms

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