52.5 Cardiovascular Regulation in Critical Illness Flashcards
(48 cards)
1
Q
What are the two main causes of cardiovascular failure?
A
- Heart failure
- Shock
2
Q
What are the four main types of cardiovascular shock?
A
- Hypovolaemic
- Cardiogenic
- Distributive (vasodilatory)
- Obstructive
3
Q
What is hypovolemic shock and what are the causes?
[IMPORTANT]
A
- Lack of perfusion of tissues caused by loss of fluid volume.
- Causes:
- Hemorrhage
- Diarrhoea/vomiting
- Third space losses (pancreatitis, burns) -> Fluid losses into spaces that are not visible
4
Q
What is cardiogenic shock and what are the causes?
[IMPORTANT]
A
- Lack of perfusion of tissues caused by decreased effectiveness of heart pumping.
- Causes:
- Reduced stroke volume in MI or myocarditis
- Bradycardia
- Tachyarrhythmias (when the heart rate is too fast for the heart to refill between strokes)
- Acute valve rupture
5
Q
What is distributive shock and what are the causes?
[IMPORTANT]
A
- Lack of perfusion of tissues caused by systemic vasodilation.
- Causes:
- Sepsis
- Anaphylaxis
- Neurogenic causes (epidural anaesthesia/spinal injury)
6
Q
What is obstructive shock and what are the causes?
[IMPORTANT]
A
- Lack of perfusion of tissues caused by mechanical obstruction of inflow or outflow from the heart.
- Causes:
- Cardiac tamponade
- Pulmonary embolism
- IVC obstruction (e.g. thrombus)
7
Q
Describe the symptoms of hypovolaemic shock on various organs.
A
- Type II Myocardial infarction -> Due to hypoperfusion, anaemia, increased coagulability and increased metabolic demand of the heart as it tries to compensate.
- Acute tubular necrosis
- Multi-organ failure
Shock is a downwards spiral since the effects and some compensatory mechanisms reinforce the problem of decreased oxygen delivery to tissues.
8
Q
Summarise the main treatments for hypovolaemic shock.
[IMPORTANT]
A
- Treat underlying cause
- Fluid resuscitation
- Colloid or crystalloid solution is usually sufficient if mild shock
- Blood infusion required if severe shock
- Major haemorrhage protocols (used if more than 50% blood lost in 3 hours)
- Guided administration of RBC, plasma and platelets in the correct ratio
- Bleeding control techniques
9
Q
What is the difficulty with surgical intervention for hypovolaemic shock?
A
- Surgery requires general anaesthesia, which tends to depress the cardiovascular system, exacerbating the shock.
- Therefore, the patient usually needs to be stabilised before surgical intervention.
10
Q
What is the body’s response to cardiogenic shock?
A
- The response is similar to in hypovolaemic shock, since the arterial baroreceptors detect the low pressure and there is the baroreflex
- The RAAS and sympathetic nervous system lead to vasoconstriction, fluid retention (at the kidneys) and cardiovascular remodelling in the long term
- This helps to increase cardiac output due to increased cardiac filling, but it causes the heart to have to work more against the increased fluid, which can exacerbate the problem
- However, natriuretic peptide release is triggered by stretch of the atria -> This leads to countering of the damaging effects of the shock
11
Q
What are the clinical signs of cardiogenic shock?
A
- Left sided -> Pulmonary oedema
- Right sided (or both sides) -> Jugular vein distension
12
Q
Summarise the approach to treating cardiogenic shock.
A
- Treat underlying cause (frequently a heart attack)
- Improve oxygenation
- High flow O2
- Continuous positive airway pressure
- Invasive ventilation via endotracheal tube
- Either:
- Reduce fluid retention if the patient is ‘falling off’ the Frank-Starling curve -> Increases cardiac output
- Loop diuretics (furosemide)
- Infuse fluid if hypovolaemic -> Increases preload and therefore cardiac output
- Reduce fluid retention if the patient is ‘falling off’ the Frank-Starling curve -> Increases cardiac output
- Either:
- Reduce afterload (if there is sufficient blood pressure to sacrifice) -> This increases cardiac output by shifting the Frank-Starling curve upwards
- Nitrates (as blood pressure allows)
- ACE inhibitors or angiotensin receptor blockers
- Use vasoconstrictors (if hypotensive) -> This maintains pressure
- Reduce afterload (if there is sufficient blood pressure to sacrifice) -> This increases cardiac output by shifting the Frank-Starling curve upwards
- Improve cardiac contractility
- Inotropes: Dobutamine, Milrinone, Levosimendan
- Mechanical haemodynamic support (i.e. mechanically supporting the heart)
- Intra-aortic balloon pump use
- Others: Impella, Tandem Heart, Extracorporeal membrane oxygenation (ECMO)
(CHECK when fluid infusion/retention and vasoconstriction/dilation are used)
13
Q
Summarise the contradictory treatments for cardiogenic shock. Explain why each may be used.
A
Fluid management:
- Fluid infusion
- Most of the fluid enters the venous circulation and therefore increases preload
- This increases cardiac output
- Reducing fluid retention (loop diuretics)
- This is used if the patient is ‘falling off’ the Frank-Starling curve
- In these situation, further increases in preload decrease cardiac output because the heart cannot mobilise all of the blood supplied to it
Vascular control:
- Vasodilation (nitrates, ACE inhibitors, ARBs)
- Reduces afterload, which increases cardiac output by shifting the Frank-Starling curve upwards
- This is useful, but can only be done if there is sufficient arterial blood pressure to sacrifice
- Vasoconstriction
- Increases arterial blood pressure
- But also increases afterload, which reduces cardiac output
14
Q
Summarise how you can think of the shock and its treatments using Guyton diagrams.
[CONCEPTUALLY USEFUL]
A
- Fluid infusion (which mostly enters the veins) or venous vasoconstriction (i.e. decreased capacitance) lead to a shift to the right of the Pmcf, which consequently shifts the venous and arterial lines
- Arterial vasoconstriction leads to increases in TPR, which decreases the gradient of the arterial and venous lines (no change in Pmcf though)
- When both happen at the same time (i.e. both arterial and venous vasoconstriction), the two effects are combined and so the lines shift to the right but the gradient decreases
- Decreased afterload (e.g. due to arterial vasodilation) shifts the Frank-Starling curve upwards
15
Q
Describe the diagnosis and treatment for distributive shock caused by sepsis.
A
Diagnosis:
- ABCDE
- Blood cultures
Treatments:
- Oxygen supply
- IV fluids
- Broad spectrum antibiotics
- Vasopressors
- Steroid -> Support vasoconstriction, but weaken the immune response against the infection
- Manage coagulation
16
Q
Describe the treatment for distributive shock caused by anaphylaxis.
A
- Remove trigger
- Lay down
- Adrenaline (“epipen”)
- Oxygen delivery
- IV fluids
- Chlorphenirame
- Hydrocortisone
17
Q
What are the symptoms of chronic ischaemic heart failure?
[IMPORTANT]
A
- Tiredness and lethargy (caused by reduced perfusion of tissues, and by acidaemia)
- Breathlessness, particularly on exertion and (in the case of left ventricular failure) on lying flat
- In the case of right ventricular failure, dependent oedema (i.e., usually ankle oedema)
18
Q
What are some clinical signs of heart failure?
[IMPORTANT]
A
- Reduced systemic arterial pressure
- Increased heart rate
- Apex beat displaced to the left (left ventricular dilation)
- Pulmonary oedema
And if there is right ventricular failure:
- Raised jugular venous pressure
- Dependent oedema (venous congestion in dependent areas, plus reduced oncotic pressure as resulting from fluid retention by the kidneys)
19
Q
Summarise in general what causes chronic ischaemic heart failure.
A
- Chronic ischaemic failure may occur in isolation, or may be an end point of other diseases, such as hypertension.
- When it apparently occurs in isolation, the underlying pathology is usually some form of obstruction to the blood supply of the myocardium.
20
Q
List some causes of chronic ischaemic heart failure.
[IMPORTANT]
A
- Coronary atherosclerosis
- Small vessel disease (occlusion of small and medium arteries supplying the myocardium)
- Ventricular hypertrophy (in response to hypertension or valve disease, but increasing metabolic demand)
- Atrial fibrillation (there is a correlation between atrial fibrillation an heart failure, but it is not certain which is the primary event)
- Anaemia (decreased oxygen delivery)
21
Q
How are natriuretic peptides involved in heart failure?
A
- Atrial natriuretic peptide (ANP, released mainly from the atria) and B-type natriuretic peptide (BNP, released mainly from the ventricles) are released in response to myocardial stretch.
- Blood levels of both are elevated in chronic failure, and BNP is used clinically as a measure of the severity of the failure.
- Both are weak angiotensin antagonists so they should be capable of counteracting the progression of heart failure. It is a mystery why this effect is so small.
22
Q
Describe the principles of treating chronic ischaemic heart failure.
A
- It is usually difficult to treat the underlying cause of chronic ischaemic heart failure.
- The exceptions are treating anaemia or surgical interventions (for valve disease or large-vessel coronary atherosclerosis)
- In the majority of cases the aim of medical therapy is to relive the symptoms and, where possible, to slow the progression of the disease.
23
Q
What are some targets of treatments for heart failure?
A
- Should increase cardiac contractility without increasing oxygen demand (or, alternatively, it should increase oxygen delivery through obstructed blood vessels)
- Should maintain systemic arterial pressure without increasing peripheral resistance
- Should reduce ventricular dilation without reducing arterial pressure and without reducing venous return too much
- Should reduce oedema without dehydrating the patient, and without triggering the RAA axis
However, these are all very difficult to achieve, so the drugs tend to have significant side effects.
24
Q
What are specific signs of right ventricular failure?
A
- Peripheral oedema
- Elevated JVP (jugular venous pulse)
25
What are specific signs of left ventricular failure?
- Pulmonary oedema --> trouble breathing
- Lateral displacement of apex beat
- Peripheral coolness
(worse than right ventricular failure)
26
Which is more common, left or right-sided heart failure?
Left
27
What are the main secondary effects of cardiac failure?
- Neuroendocrine activation: sympathetic outflow, angiotensin, aldosterone
- Cardiac remodelling: ventricular dilation, fibrosis
28
How can the underlying cause of heart failure be treated?
- Surgery - e.g. coronary bypass graft. Good for focal atherosclerosis
- Resynchronise the tissue - e.g. cardioversion, for bundle-branch block in cardiomyopathy
29
How can the symptoms of heart failure be treated?
- Remove excess fluid around lungs - relieve breathlessness
- Vasodilate - increase exercise tolerance
- Encourage rest - so less anaerobic metabolism
30
How can the secondary effects of heart failure be treated?
- Reduce sympathetic drive
- Reduce angiotensin activity
- Prevent fibrosis and remodelling
31
Overall, what are the principles of heart failure treatment?
Encourage vasodilation and increased inotropy of heart to increase cardiac output WITHOUT increasing oxygen demand
May also need added diuretics to reduce the increased systemic vascular resistance
32
What is the definition of shock?
A potentially fatal, pathophysiological disorder characterized by acute failure of the cardiovascular system to perfuse the tissues of the body adequately
33
What are the general characteristic signs of shock?
- Rapid and weak pulse
- Mean arterial pressure reduced or normal
- Pulse pressure reduced
- Rapid and shallow breathing
- Reduced urine output
- Reduced mental awareness or confusion
34
What are the physiological compensatory mechanisms in response the drop in CVP (central venous pressure) in shock?
- Increase in heart rate, so increase in peripheral resistance and arterial BP
- Venoconstriction - try to maintain venous return
35
What are the endocrine responses to shock?
- Reduced perfusion to kidneys --> RAA axis
-- Angiotensin II, aldosterone, sympathetic activity (adrenaline, noradrenaline)
- Vasopressin secretion
- Glucocorticoid secretion (stress response)
36
How does blood pH change in shock?
- Decreases --> metabolic acidosis
- Due to tissues being under-perfused so undergo anaerobic metabolism
37
This is a normal pressure-volume loop of a cardiac cycle. How does this change when shock occurs?
- Loop gets narrower
- Loop gets shifted to the left down the curve
38
What are EDPVR and EPSVR?
ESPVR = End-systolic pressure-volume relationship - maximum pressure that can be developed by the ventricle at any LV volume
EDPVR = End-diastolic pressure-volume relationship - passive filling curve for ventricle
39
Why does the P-V loop get narrower in shock?
There is vasoconstriction - means that there is increased afterload, so ESPVR is increased (increased maximum pressure produced by ventricle, to push harder against afterload)
40
Why does the P-V loop shift to the left in shock?
There is hypovolemia, so EDV (end-diastolic volume) is decreased - slips down the EDPVR curve (lower maximum passive filling value)
41
What is internal fluid transfusion?
When the hydrostatic pressure is so low in shock that the Starling's forces work in the opposite direction and there is actually a net absorption of fluid into the circulation
42
What are the long-term renal and biosynthetic responses to shock?
- Reduction in GFR
- Thirst
- RBC synthesis
- Hepatic albumin synthesis
43
What are the general principles of shock treatment?
- Identify early
- Rapidly stabilise patient (before going over tipping point)
- Treat underlying cause
- Continue monitoring and support in ITU/CCU
44
What are the techniques for bleeding control?
- Mechanical: tourniquets etc
- Salvage cells: blood transfusion
- Endovascular repair: stents/embolisation
- Surgical repair: suturing, grafts etc
45
What specific treatment may be used for a bleeding out patient?
Autotransfusion
Collect their own blood and transfuse back into the patient
46
This graph shows a normal venous return curve (Guyton's analysis). What happens to the curve when mean systemic pressure (Pms) decreases in shock? Why?
Curve shifts to the left, in a parallel manner
Venous return is impaired at any right atrial pressure as there is a systemic decrease in pressure
47
This graph shows a normal venous return curve (Guyton's analysis). What happens to the curve when arteriolar resistance (Rv) increases in shock? Why?
Curve shifts to left without moving the x-intercept - bc mean systemic pressure (Pms) is constant (i.e. with enough right atrial pressure, would be able to overcome the venous resistance to get back to normal)
48
What is the acute stress response to stress?
