Heart failure & effects of exercise on blood pressure and CO Flashcards
heart failure- what happens
- Heart is overfilled with blood (left ventricle) and is unable to compensate for the change in volume
-> Blood overflows back into lungs causing pulmonary complications - Also known as heart congestion or congestive heart failure
- Initially changes in volume can be compensated by increasing heart contraction (rate) and shifting the curve upward and to the left
- ! if the heart is failing the curve is depressed and moves into the decompensated
heart failure- what happens to starling curve
- describe graphs
- a higher central venous pressure produces a smaller CO
- higher end-diastolic volume is required for a given energy of stroke work
symptoms of heart failure
- Weaker pumping action of the heart
- Pulmonary oedema (heart isn’t able to circulate blood around properly-> smaller circuit -> gets clogged up)
- Coughing, tiredness, shortness of breath
- Swelling in veins above the heart (jugular vein in the neck) & excess fluid in extremities (ankles and legs)
causes of heart failure
a. High blood pressure (chronic overload)
- Resistance from stiff or constricted blood vessels forces the heart to work harder
b. Artery disease and a restriction in coronary blood supply
c. Myocardial infarction (heart attack) and the loss of functional heart tissue
- Damaged heart muscle from a heart attack weakens the heart-pumping power
d. Diseased valves (leaky or stiff)
- Valves that leak or don’t open wide enough interfere with blood flow through the heart so it can pump properly
e. Stiff heart muscle
- The chambers of the heart can’t fill up with enough blood if the heart muscle is stiff
treatment of congestive heart failure
Main approaches:
- Reduce work of the heart
- Reduces cardiac dilation
- Improve myocardial
contractility
-> Cardiac distension is reduced by reducing the plasma volume with diuretic drugs (frusemide)
-> Contractility is improved by cardiac glycolysis (digoxin) or beta1-adrenoreceptor antagonists (dobutamine)
-> Cardiac work is reduced by reducing arterial resistance with vasodilators
ACE inhibitors reduce water retention
- draw whats happening flowchart
Digoxin increases heart contraction by blocking a Na+/ K+ pump
- Increases in intracellular Ca2+ levels increase myocardial contractility
- Prolongs plateau phase of cardiac AP blocking Na+/K+ pump -> Na+ in cell
-> Increases in intracellular Ca2+ levels increase myocardial contractility - Beta-blockers inhibit beta adrenoreceptors that are responsible for increasing HR (-> contraction) and vasoconstriction
Beta1-adrenoreceptor antagonists increase myocardial contraction
- NA released by sympathetic nerve terminals increases heart contraction by activating beta1-adrenoreceptors in the heart
blood pressure
Blood pressure is higher in the arteries than in the veins
- Blood flows from the aorta to the veins and the driving force for blood flow is the difference between the arterial and venous pressures
blood flow
- dependent on pressure and resistance
Blood flow perfusion pressure/ vascular resistance - equation
Poiseuilles equation: R= 8nl/pir^4
R= hydraulic resistance
n= liquid viscosity
l= length of vessel
r= radius of vessel
blood pressure in systemic circulation
CO= volume of blood that flows around the systemic circulation per minute
Blood pressure= CO x total peripheral resistance (diameter)
Arterial blood pressure
- is pulsatile
- Systolic pressure occurs at the peak of ejection from the heart
- Diastolic pressure occurs at the end of diastole
- In healthy adults should be around 120 (systolic)/ 80 (diastolic) mmHg at rest
Control of vascular blood flow
Vasoconstriction: increase in vascular tension and resistance (smooth muscle contraction)
Vasodilation: reduction in vascular tone and resistance (smooth muscle relaxation)
Intrinsic mechanisms: autoregulation and myogenic response
Extrinsic mechanisms:
- Local hormones (prostaglandins, bradykinin, histamine) and chemicals (nitric oxide)
- Autonomic nervous system
Autoregulatory mechanisms allow blood flow to remain constant
Compare the transient blood flow in blue and steady state blood flow in red:
- Decreases in flow are countered by sm relaxation and dilation while high flow is countered with sm contraction and constriction
Sympathetic control of vascular blood flow
- Glossopharyngeal and vagus nerves terminate in the medulla (nucleus tractus solitarius)
- These neurons project to the spinal cord and activate the sympathetic preganglionic neurons
- Projections of the preganglionic neurons via the ventral roots to sympathetic postganglionic neurons
- Sympathetic activity releases NA and influences vascular tone
Noradrenaline acts at different targets
- Sympathetic activity activates b1-adrenoceptors (G-protein coupled) increases heart rate
- But b2-adrenoceptors (G-protein coupled) present in the arterioles of skeletal muscle causes vasodilatation
-> Generally sympathetic activity in vascular smooth muscle activates a1-adrenoceptors (G-protein coupled) and causes vasoconstriction
Cardiovascular effects of sympathetic stimulation (increased sympathetic drive)
look at notes
central control of blood pressure
- Baroreceptors-high pressure receptors in the aorta and carotid sinus
- Baroreceptors send afferent information to the nucleus tractus solitarus in the brainstem
Baroreceptors
in the aorta and the carotid sinuses
Baroreceptors: mechanoreceptors that sense the degree of stretch
- Afferents from the carotid sinus travel to the spinal cord via the glossopharyngeal nerve
- Afferents from the aorta travel to the spinal cord via the vagus nerve
- Low-pressure receptors exist in the heart atria and sense cardiac distension
- Baroreceptor firing increases when blood pressure rises: Increases in baroreceptor firing inhibits sympathetic activity to the heart & blood vessels -> lowers blood pressure ( Baroreceptor reflex)
Baroreceptors only provide short-term regulation (minutes)
- The threshold set point for triggering baroreceptor firing can rise (ineffective for long-term regulation of blood pressure)
- The threshold can be reset for certain activities, e.g. exercise
Postural hypotension-Baroreceptors reflex stabilizes the fall in blood pressure when posture changes (sitting -> standing) - If arterial BP is raised for 15 minutes, the threshold for triggering the baroreceptor reflex rises. Blood is now in the legs rather than the head. So you feel dizzy. Baroreceptors decrease firing to increase sympathetic activity and heart rate to restore blood pressure.
Retribution of CO in various tissues at rest during exercise
CO to skeletal muscle can rise from 0.75-1Lmin^-1 to 38 Lmin^-1
CO to the brain remains unchanged
CO to abdomen falls to 0.75 Lmin^-1
CO to kidneys falls to 0.5 Lmin^-1
Increases sympathetic activity and inotropy during exercise
- Increased stroke work for the same filling pressure (shift curve up and left)
- Increased stroke volume is achieved by more efficient emptying of the ventricles at the end of systole
Changes in blood flow to calf muscle at rest and during exercise
- Rhythmic changes in blood flow occur during muscle contraction and relaxation
- During muscle contraction, blood moves towards the heart aided by valves in the limb veins
