Studydroid is shutting down on January 1st, 2019



keywords:
Bookmark and Share



Front Back
What can cause hypovolaemia?
Haemorrhage, diarrhoea & vomiting, heat shock or excess sweating, burns, dehydration, excessive diuretics.
How much circulating volume can young healthy individuals lose and maintain normal blood pressure?
20-30%. Blood pressure is a poor indicator. Loss of greater volumes (or smaller volumes in people with poor CV reserve) can result in rapid, profound circulatory compromise and death.
What is the initial cardiac response to hypotension?
Circulating volume loss results in reduced venous return. Left shift along Frank-Starling curve- reduced SV/cardiac output (CO). Without other CV response, this will reduce BP.
What is the physiological response to a drop in circulating volume?
Drop in blood pressure stimulates baroreceptor activation, activating the sympathetic nervous system, raising blood pressure.
What does activation of the sympathetic nervous system do?
Neural and hormonal (catecholamine) induced vasoconstriction, especially in cutaneous, muscular and splanchnic beds (increased SVR). 
Steepens Frank-Starling response (inotropic response: increase CO).
Tachycardia (chronotropic response: increase CO).
Increased circulating Ang II and vasopressin
What other responses occur in circulatory volume loss mediated tissue hypoxia?
Causes acidaemia stimulating peripheral chemoreceptors. Stimulate increased respiratory rate (to blow off CO2) and increase sympathetic outflow.
What occurs to tissue fluid following circulatory volume loss?
Tissue fluid will move to the circulatory compartment (auto-transfusion) due to altered hydrostatic balance.
What does Angiotensin II and Vasopressin promote?
Promote renal sodium and water retention, attempting to restore circulating volume.
If hypovolaemia is profound and cannot be compensated for by endogenous response or medical intervention, what may happen?
Leads to a downward spiral. Hallmarks include reduced cardiac contractility through coronary hypoperfusion and acidosis. Neural hypoxia may alter sympathetic reflexes.
When does fluid overload develop?
Very unusual in healthy people, unless receiving overzealous fluid resuscitation. 
Patients with poor cardiac (renal and hepatic) reserve can develop it.
Severity of hypovolaemia. Cardiac reserve is 5L. Should learn this. Urine output is 0.5ml/hour/kg
Summary of circulatory volume blood loss.
Summary of blood loss. SVR: systemic vascular resistance. Epi: epinephrine (adrenaline), NE: norepinephrine (noradrenaline).
What occurs following uncompensated blood loss, potentially leading to death.
What signs might be expected in fluid overload in the systemic circulation?
Often due to overenthusiastic fluid administration. Oedema: ankle and sacral. Raised JVP. Ascites.
What signs might be expected in fluid overload in the pulmonary system?
Pulmonary oedema- basal crackles. Orthopnoea. PND-paroxysmal noctural dyspnoea.
What effect does volume depletion have on the Frank-Starling curve?
Decreaces preload so moves more towards the left of the curve. Administration of fluid shirts curve to the right.
What is the Bainbridge reflex?
Reflex that increases heart rate, thus cardiac output that is activated by atrial stretch- when blood volume is high
When is the Bainbridge effect demonstrated?
In fluid loss, treatment with IV fluid is used.
What can happen following treatment for blood loss with IV fluids if given too much?
Although BP improves, patient can become progressively SOB, tachypnoeic and hypoxic. LV is stretched, less compliant.
What happens when the LV becomes less compliant?
LV diastolic pressure increases; LA pressure rises, pulmonary venous and capillary pressures rise, alveolar capillary hydrostatic balance flips to favour outward movement of vascular fluid, pulmonary oedema develops.
What are hydrostatic forces?
Mechanical pressure of vessel vs. tissue. If increase BP, can push fluid out.
What are oncotic forces?
Total osmotic forces of vessel vs. tissue. If liver failure etc. can lead to reduced serum albumin, so lower oncotic pressure in vessels.
What do hydrostatic and oncotic forces favour?
Favours pulmonary oedema through. 1) Increased vessel pressure (e.g. Alveolar capillaries during acute fluid overload). 2) Reduced vessel oncotic force (e.g. low serum albumin). 3) Disrupted pulmonary capillary integrity e.g. ARDS (leaky vessels can't hold albumin/proteins, so water leaks out
What occurs in patients with poor cardiac reserve? Often seen in LV hypertrophy.
Have less favourable pressure-volume loops- are more sensitive to increases in LV diastolic pressure.
What can cause poor cardiac reserve?
LV hypertrophy, often associated with renal diseases. Less able to excrete fluid so more sensitive to overload.
Why does acute fluid overload present with pulmonary oedema?
Due to backup of fluid and as an acute response to this.
Why may systemic oedema occur without pulmonary oedema?
Take longer to accumulate, sign of chromic.
Why does pregnancy put demands on the cardiovascular system?
Supporting enlarging foetal and utero-placental circulation.
What does failure of the cardiovascular system in pregnacy lead to?
Foetal loss, intrauterine growth retardation, pre-eclampsia and maternal cardiac decompensation.
What additional cardiovascular challenges occur in normal pregnancy?
Labour, post-partum auto-transfusion, haemorrhage and twin pregnancy.
How is the increased cardiac output demand achieved in pregnancy?
Progressive increase, mostly in 1st trimester. Achieved through increase in stroke volume (1st trimester) and heart rate (1st and 2nd trimester).
What happens to cardiac output during labour?
Further marked increase during labour (>2x baseline). Cardiac output, stroke volume and heart rate do not normalise for 2 weeks post-partum.
What are the other cardiovascular changes during pregnancy?
Circulating volume increases by 40-50%. RBC volume increase by 30%, resulting in relative anaemia. (As blood plasma increases more than RBC) Fall in SVR with mild reduction in BP. Compression of IVC can impede venous return by feotus.
What drives the changes seen in cardiovascular system during pregnancy?
Oestrogens and progesterones; vasodilate (through reduced SVR and BP, and compensatory tachycardia), promote fluid retention (relative anaemia, increases CO- right shift Frank-Starling curve and Bainbridge reflex). Post-partum loss of caval compression and auto-transfusion blood/tissue fluid from uterine vasculature- increase CO.
How does the cardiovascular system adapt to changes in volume?
Frank-Starling and Bainbridge reflexes. Neuro-hormonal responses. Structural changes of cardiac remodelling- concentric =LV hypertrophy, Eccentric = LV dilatation. Remain reasonably misunderstood as no-one wants to study pregnant women.
LV end diastolic dimension (mm) in pregnancy
LV end systolic dimension (mm) in pregnancy
LV mass (g) change in pregnancy
Left atrial area (cm Sq) in pregnancy
Blood pressure isn't a great indicator or fluid status, what is a better indicator?
Urine output, cap refil, JVP, pulse. Tachycardic in hypotensive. Postural BP
What happens if you administer too much fluid to a patient?
Can overload the patient, pushing them over the plateau of Frank Starling curve. Leads to reduced contractility.
How long does it take the cardiovascular system to return to normal levels following pregnancy?
Around 2 weeks.
Why do pregnant women particularly get postural hypotension?
Vasodilatation in peripheries (decrease in SVR)- blood pools there rather than being forced out and up to brain.
What happens to cardiac output during pregnancy?
What happens to stroke volume during pregnancy?
What happens to heart rate during pregnancy?
What happens to the CO during labour?
x of y cards Next >|