Cardiovascular Flashcards
Explain the physiological factors that determine arterial blood pressure and the mechanisms that maintain BP homeostasis (34)
Arterial blood pressure is the force exerted by blood on the arteries as it flows through - necessary to maintain proper perfusion.
Arterial BP = CO x TPR
Q = cardiac output = amount of blood pumped from left ventricle in 1 min. Q = SV x HR. SV - amount of blood leaving left ventricle in one contraction, HR - number of contractions in 1 min
TPR - total resistance to blood flow, caused by friction between blood and walls of vessels. Influenced by total vessel length (increase length = increased pressure), thickness of blood, vessel radius (can change based on information they receive from sympathetic nerve system
Both SV and HR are regulated by the cardiovascular centre found in the medulla oblongata. CV centre controls neural, hormonal and local feeback loops that regulate blood pressure. Receives input from higher brain centres and sensory receptors. Sends output to the heart via sympathetic and parasympathetic nervous system. HR and/ or SV can increase or decrease depending on the signals the heart receive based off the input by the higher brain centres and sensory receptors in the body. Increased exertion or feeling anxious/ worry can cause increased sympathetic nerve stimulation, leaving to increase SV and HR, increased Q and increased arterial pressure
Baroreceptors are pressure sensitive receptors that monitor the amount of stretch in major arteries. More flow = more stretch, increased stretch = increased pressure, this information is relayed to the CV via nerves.
Chemoreceptors monitor chemical responses/ changes in blood. Decreased O2, increased CO2 or H+ stimulates the chemoreceptors to send impulses to the CV centre. Other CV centre inputs include - proprioceptors and nociceptors
Sympathetic nervous system excitation causes vasoconstriction in the gut blood vessels (increased vascular resistance), vasodilation in the skeletal vessels (decreased vascular resistance), net effect is vasocontriction
Hormones regular BP by altering Q and changing vascular resistance. Adrenaline and noradrenaline increase Q by increasing HR and contractability. ADH increased blood volume - reduced amount of water passed out by urine, causes vasocontriction in arteries. Both increase TPR
If BP decreases, receptors detect change and send signals to CV centre, causing increases in Q and increased TPR resulting in increased BP.
If BP increases, receptors detect change and CV centres cause decrease in Q and decreased TPR causing a decrease in BP
A 35-year-old man is admitted to hospital with medical shock - classify the different causes of shock
Cardiogenic (due to heart problems)
Hypovolemic shock (cause by too little blood volume
Anaphylactic shock (allergic reaction)
Septic shock (infection)
Neurogenic shock ( damage to nervous system)
Obstructive shock (obstruction in heart/great vessels)
Identify the causes of hypovolemic shock and explain the progressive signs and symptoms of shock at each stage (40)
STAGE 1:
- Volume of blood loss up to 15%
- HR is minimally elevated to maintain cardiac output caused by reduced SV
- No change in BP/pulse pressure/ resp rate
STAGE 2:
- Volume of blood loss from 15-30%
- HR and resp rate elevate, 100-120bpm / 20-24RR
- To maintain cardiac output from reduced SV, increase oxygen uptake to compromise for blood loss
- Pulse pressure begins to narrow - systolic BP may to unchanged - slightly decreased
- Less blood circulating, decreased blood viscosity, decreased BP
STAGE 3:
- Volume loss from 30-40%
- Drop in BP (due to less blood circulating, decreased blood viscosity, decreased BP)
- Changes in mental status occur (less blood circulating to the brain)
- HR and resp rate significantly elevated >120bpm to maintain cardiac output
- Urine output declines, greater water retention - from increased ADH production, helps to maintain BP
- Capillary refill delayed - blood takes longer to reach peripheral tissues (vasoconstriction of peripheral arteries to send more blood to the major organs/ systems, vasoconstriction helps maintain BP)
STAGE 4:
- Volume loss >40% total blood volume
- Hypotension with narrow pulse presence (less blood circulating, decreased viscosity, decreased BP)
- Tachycardia more pronounced
Increasingly altered mental status
- Urine output minimal/ absent
- Capillary refill is delayed
What does a physio need to consider when managing a patient presenting with symptoms of shock?
- Further medical assistance/ help
- Do not move the person unless there is danger
- Reassure the person
- CPR if necessary
- Do not give anything to eat or drink
- Position person on side in case of vomiting
- Identify the type of shock
Explain how right sided heart failure could be caused by COPD
COPD causes low oxygen levels from airway inflammation (chronic bronchitic) and damage to air sacs/ alveoli (emphysema)
- Reduced air into lungs + reduced gaseous exchange - less surface area from alveoli collapse due to loss of elasticity. Less O2 into blood - less ventilation. Creates V-Q mismatch.
- Low O2 levels cause a rise in BP in the arteries of the lungs, causing pulmonary hypertension. Pulmonary arteries constrict via hypoxic pulmonary vasoconstriction taking blood away from damaged alveoli creating a backlog of pressure from the capillaries into the right ventricles.
To keep pressure of the heart, the right side of the heart works harder to pump the blood through to the lungs. This causes increased strain on the right side of the heart - increased HR.
Cardiac hypertrophy can be seen over time, causing a reduction in chamber size, less filling capacity, decreased preload. This leads to a weaker contraction (starlings law) so a lower cardiac output.
Heart weakens over time and eventually leads to failure.
Explain why the clinical features of right-sided heart failure occur
Swelling/ Oedema in feet, ankles, legs:
- Pressure back up enters the vena cava and venous system after the right ventricle
- Pressure increases in the veins, blood builds up in veins as it cannot overcome the pressure to return to the heart
- To try and reduce BP, blood plasma diffuses into body tissues via osmosis
Fatigue:
- Decreased Q from R ventricle due to cardiac hypertrophy and weaker contraction
- Less blood pumped to lungs to undergo exchange
- In lungs, reduced O2 levels and less SA for gaseous change to occur, less O2 into blood
- Unable to supply the body with adequate O2 and nutrients to cope with metabolic needs
Increased prominence/ pressure in jugular vein
- Raised pressure backup from the arteries in the lungs enters the venous system after the right ventricle
- Increased pressure reaches jugular vein in neck
Liver swelling
- Pressure backup from the arteries in the lungs reaches the veins surrounding the liver
- Blood builds up in these veins - can’t overcome the pressure to return to the heart
- To try and reduce pressure, blood plasma diffuses into body tissues via osmosis
- Enters the liver, extra fluid causes swelling
Ascites - fluid build up in abdomen
- Pressure backup from the arteries in the lungs reaches veins surrounding the abdomen
- Swelling
What specific issues foes the physio need to consider when managing a patient with right sided heart tissue?
Fatigue/ exercise tolerance:
- Likely will be more susceptible to heart failure or COPD
Reduced mobility:
- Increased falls risk
- Potentially loss of proprioception due to swelling
- Reduced confidence due to knowledge of condition
Resting HR:
- Increased resting HR due to compensate lower SV
- More likely to reach max HR with less exertion
Education/ discussion:
- End of life options - poor prognosis, 50% die within 5 years of diagnosis
State 2 possible causes of left sided heart failure and explain how each of these could lead to left sided heart failure
Myocardial infarction (heart attack)
- Blockage in the coronary arteries due to blood clot
- Less oxygen reached myocardium
- Myocardium necrosis
- Weaker contractions of heart due to muscle cell death
- Remaining cells work harder to maintain optimal blood flow out of left ventricle - increased HR, eventually failure
Long term high blood pressure
- Prolonged hypertension promotes left ventricular hypertrophy because the heart has to work harder to pump blood
- Over time the heart muscle weakens and works less efficiently
- Increased HR to try and compensate for inefficient contractions
Explain why the clinical features of left heart failure may occur
Breathlessness
- Impaired gas exchange as lungs congested with oedema
- Backwards failure - blood backs up into veins in the lungs
- Pressure increases in blood vessels, fluid pushed into alveoli
- Reduced oxygen movement through lungs
- Increase RR to try to get more oxygen available to exchange to maintain bodily needs, leads to breathlessness
Sudden wakening at night with breathlessness:
- Increased sympathetic activation can bring on breathlessness
Increased RR - same as breathlessness
Cough:
- Lungs congested with pulmonary oedema (same steps as breathlessness)
- Triggers cough receptors
Shortness of breath when lying flat:
- Lung congestion with pulmonary oedema
Reduced mobility:
- perfusion therefore reduced muscle strength
- Think myocardium layer can’t efficiently pump blood from LV, less blood in circulatory system - forward failure.
- Less O2 and nutrients delivered to muscles
- Deconditioning from fatigue and breathlessness
Atrial fibrillation:
- Abnormal heath rhythm from irregular contractions causing forward failure
Hypertension:
- Increased ventricular pressure to help move blood forwards from ventricle to artery
Tachycardia
- Increased HR to compensate for reduced SV to maintain cardiac output
Reduced urine output
- Body holds onto more water to increase circulatory volume to increase venous return
- Improves preload of ventricles
- Improves contraction and Q as per Starlings Law
Weight gain
- Increased water retention
- Decreased activity
Crepitations on auscultation
- Fine crackles during breathing
- Due to fluid in airways blocking airflow
What does a physio need to consider when managing a patient with left sided heart failure?
Balance and mobility:
- Increased falls risk
Fitness/ exercise tolerance:
- Reduced Q that can’t be increased
- Pacing advise?
Positioning:
- Supine can worsen congestion
- Fluid in lungs?
Chest physio not indicated:
- Sputum caused by fluid - will reaccumulate if cleared
May require ambulatory O2
- Due to recued gaseous exchange
Mental status
Progressive disease
- Will worsen
Explain how the pathological changes of atherosclerosis give rise to the clinical features of Peripheral arterial disease (40)
Definition:
- Atherosclerosis is the accumulation and hardening of fatty plaques in the walls of arteires
- It occurs in vessels >/= 2mm, can happen anywhere
- Causes changes to tunica intima
- Reduces lumen size, reduces blood flow
Process:
- Damage is caused to the endothelium by high BP, toxins and/ or increased cholesterol levels
- LDLs move into tunica intima, causing the start of the inflammatory process
- Monocytes are attreatced to damage site, turn into macrophages, engult phagocytes via phagocytosis
- These macrophages die after filling, callef foam cells after death
- Cytokines are released upon death, attracting more monocytes
- Smooth muscle cells from tunica media move to tunica intima - plaque begins to form
- Collagen is secreted to form a fibroud cap - protecting contents of plaque from blood
- If plauqe breaks, platelets will clot and form a plug, restricting the lumen more
- A thrombus occurs if the plaque ruptures - able to dislodge and travel around the body
Peripheral arterial disease:
- Causes narrowing and blocking or arteries in the peripheral limb, most commonly atherosclerosis
- Clinical features:
- Intermittent claudication: reduced lumen size = reduced blood flow, less oxygen availble for use in exercise, can’t keep up with exercise intenstity, switches to anaerobic, metabolites cause pain
- Ulcers: reduced lumen size reduced blood flow to skin of peripheral limbs, causing cell death, ulcers form as a result of infarction
- Muscle weakness: Less oxygenated blood able to reach skeletal muscle, less energy available for use, weaker contractions produced
- Cold limbs: Reduced blood flow
- Discolourisation: Readuced blood flow, appears dull and pale
Poor nail growth: Reduced oxygenated blood and nutrient flow to the nails on peripheral limbs as a result of reduced lumen size, nails can’t grow/ repair properly
Explain how a diagnosis of Peripheral Arterial Disease might affect the selection and use of physiotherapy treatments for the lower limb (10)
- Avoid manual techniques as they may dislodge the thrombus, could lead to further and more severe problems e.g. coronary artery blocking = MI = potential death, or cerebral arteries = stroke
- Increased falls risk due to muscle weakness
- Likely will have a resting BP, use of exercises will increase BP further, level of exercise needs to be calculated and considered for patients with peripheral arterial disease
State the predisposing factors for Coronary Artery Disease, giving a brief explanation of how each factor increases the risk (20)
- Overweight: Excess weight can lead to extra fatty material in arteries, increased likelihood of atherosclerosis, linked directly with CAD
- Physical inactivity: Body doesn;t use it’s fat stores to create energy, causes fatty build up, atherosclerosis is more likely to happen, linked to CAD
- Unhealthy eating: intake of fatty foods, build up of fat in arteries, atherosclerosis more likely
- Smoking tobacco: Increases damage to endothelium (beginning stage in atheroscleosis)
- Age: Over time, arteries become less flexible, plaques can occur over time, normal aging also comes with increase BP, high cholesterol, diabetes and obesity
- Gender: Men are a higher risk that premenopausal women due to protective effects of oestrogen
Explain how the pathological changes of CAD may lead to signs, symptoms and clinical features (20)
Angina: too much plaque build up in coronary arteries, narrowed arteries block blood flow to heart muscle, chest pain
Pain in neck, left arm or back: Angina can radiate into these arease, due to position of heart
Shortness of breath: Narrowing of coronary arteries means less oxygenated blood reaches myocardium, increase RR to maximise O2 uptake, makes us feel short of breath
Fatigue: Heart received less O2 blood, less available energy, O2 blood pumped less efficiently, less O2 available for use
Heart attack: A fully blocked artery can cause a MI, heart cells cant receive O2 or nutrients and can’t have any waste products removed, heart will begin to die after 20 mins
Suggest how the physio may play a role in preventing CAD
Advice: stop smoking, balanced diet, alcohol consumption, recognition of early signs
Exercise: Cardiac rehab if suitable, promotes weight loss and tackles inactivity
Forces existing fat stoers to be used, less fatty build up
Strengthens heart muscles
Encourages lower levels of LDL and higher levels of HDL
