Cardiac Chapters Flashcards
What is preload? What is another name for it?
Preload is the heart’s working volume. How much the ventricles have to pump with each beat.
End-diastolic pressure.
What factors increase preload?
Preload is affected by:
- Circulating blood volume (less volume = less preload, more volume = more preload)
- Venous constriction - constricted blood vessels allow blood to return to the heart quicker. Dilated blood vessels, such as from nitroglycerin, can slow blood return to the heart and decrease preload
- Body position - laying flat or raising the legs can increase blood return from the lower extremities causing an increase in preload.
- Intrathoracic pressure - decreased intrathoracic pressure allows venous blood to return easier. Increased intrathoracic pressure, such as with high levels of PEEP, can decrease venous return and therefore decrease preload.
- Heart rate - tachycardia can cause a drop in preload by not allowing the ventricles to fully fill.
What is afterload? Left ventricle VS right ventricle.
Afterload is the resistance the heart has to push against to eject blood. The left ventricle’s afterload is the systemic arterial blood pressure. The right ventricle’s afterload is the pulmonary arterial pressure.
What factors or conditions increase afterload?
Afterload is affected by:
- Vasoconstriction/ vasodilation - also referred to as systemic vascular resistance. Vasoconstriction increases SVR which increases afterload. Vasodilation does the opposite.
- Aortic stenosis - narrowing of the aortic valve which increases the afterload
- Arteriosclerosis - stiffening of the arteries. Decreased arterial compliance reduces the give which increases afterload
- Pulmonary HTN - increases the afterload placed on the RV
What is cardiac contractility? How does it affect CO?
The ability of the heart to change its force of contraction independent of changes in preload and afterload. Cardiac contractility affects CO largely by influencing the stroke volume. When the heart muscle beats with more force, it increases the stroke volume which increases the cardiac output.
Normal CO?
Normal SV?
Normal CO is 4.6L to 6L in a resting adult.
Normal SV is around 70mL per beat.
Describe the path of blood through the heart and lungs
- Blood returns to the heart via the inferior vena cava and the superior vena cava into the right atrium.
- The right atrium pushes blood through the tricuspid valve into the right ventricle.
- The right ventricle pushes blood through the pulmonic valve into the pulmonary artery.
- The pulmonary artery takes blood into the lungs where, through capillaries, gas is exchanged.
- Now oxygenated, the blood travels out of the lungs via the pulmonary vein and into the left atrium.
- Blood then passes from the left atrium into the left ventricle via the mitral valve.
- Blood is ejected from the left ventricles through the aortic valve into the aorta to the systemic circulation.
How does the autonomic nervous system affect cardiovascular function?
On a surface level - the ANS can alter HR and cardiac contractility. It can also affect the vascular tone.
How does the different parts of the ANS affect cardiac function?
Parasympathetic - the vagus nerve is in charge of parasympathetic stimulation of the heart. Vagal stimulation results in slowing of the heart rate via the release of acetylcholine.
Sympathetic - controlled by the reticular formation in the brain stem. Increased sympathetic activity results in an increase in heart rate and the force of contractions.
How does the ANS affect blood vessels?
The sympathetic NS is in ultimate control of blood vessel dilation and constriction. Some blood vessels have vasodilator and vasoconstricting fibers.
What neurotransmitters are mainly used to effect the ANS?
Acetylcholine for parasympathetic
Norepinephrine for sympathetic
What is blood pressure? Systole Vs Diastole.
What determines blood pressure?
How is blood pressure regulated by the body? Fast VS slow.
Blood pressure is the force exerted on the blood vessels. Systolic blood pressure measures force exerted during systole, when the blood has just been forcefully pumped from the left ventricle into the systemic circulation. Diastolic blood pressure is a measure of the blood pressure at its lowest, relaxed state.
Blood pressure regulation is largely determined by the ANS and the kidneys. Neural control has a quick effect on blood pressure while hormonal control takes a longer time to get up and moving.
In circumstances of low blood pressure, the baroreceptors located throughout the body (aortic arch is one) will detect this decrease in pressure.
Neural control of the blood pressure
Controlled by the sympathetic/parasympathetic nervous systems which make up the autonomic nervous system.
This is a quick/short-term change in blood pressure that is brought about through communication between baroreceptors/chemoreceptors - brainstem - PNS (vagus and glossopharyngeal nerves) / or SNS - to the SA and AV node. Commonly referred to as the baroreflex.
Where is the cardiovascular control center? Parasympathetic effects VS sympathetic effects. How are these effects transferred throughout the body?
Located in the brainstem.
Parasympathetic effects (activation), cause a slowing of the heart via release of acetylcholine. Parasympathetic effects are transferred from the brainstem to the heart via the vagus nerve.
Sympathetic effects (activation) result in an increase in heart rate, increased contractility, and vasoconstriction. The SNS brings about these effects via the neurotransmitter norepinephrine.
Increased cardiac contractility = ?
Higher stroke volume which leads to higher CO
What are baroreceptors? Where are they located?
Baroreceptors are stretch receptors located in the aortic arch and the carotid sinus, among other places. These stretch receptors determine the degree of stretch placed on the arteries which correlates to the blood pressure. This degree of stretch is passed along to the brainstem which brings about appropriate changes via the parasympathetic and sympathetic pathways.
Baro-reflex. Describe how it works for both hypertension and hypotension.
A short-term reflex initiated by the baroreceptors located in the aortic arch and the carotid sinus. Detection of HTN or hypotension are quickly communicated with the brain stem.
During acute hypertension the brain stem activates the parasympathetic nervous system via the vagus and glossopharyngeal nerves to reduce the heart rate which lowers the BP via reducing the CO. Ach is the neurotransmitter used to achieve this.
During acute hypotension the brain stem receives input from the baroreceptors that tells it the blood pressure is low. The brain stem activates the SNS via norepinephrine to increase the HR, increase cardiac contractility, and constrict blood vessels all of which work to increase the blood pressue.
What are chemoreceptors? Where are they? How does this affect the blood pressure?
These are monitors in the same location as the baroreceptors, the aortic arch and the carotid sinus. Chemoreceptors detect changes in blood oxygen, pH, and Co2 levels. Chemoreceptors primary function is to adjust respiratory volume, but since reduced blood oxygen also induces SNS vasoconstriction, it raises blood pressure.
What is in control of the long-term hormonal control of blood pressure?
The Renin-Angiotensin-Aldosterone system.
What is renin? Where does it come from? What stimulates it’s release? What does it do?
Renin is released from the kidneys (specifically the juxtaglomerular cells) when a drop in BP or when there is a decrease in circulating volume or sodium. Renin activation is communicated with the kidney when these factors are detected by the baroreceptors. Renin converts Angiotensinogen into Angiotensin 1.
What is angiotensin 1? What happens to it?
Angiotensin 1 is an inactive circulating plasma protein that becomes activated by renin. Upon activation, angiotensin 1 enters the lungs where angiotensin converting enzyme (ACE) converts angiotensin 1 into angiotensin 2.
What is ACE? Where is it located and what does it do?
Angiotensin converting enzyme. This enzyme is located in the lungs and converts angiotensin 1 into angiotensin 2.
What is angiotensin 2? What effects does it have on the blood pressure and circulation?
Angiotensin 2 is a hormone that causes both short and long-term effects on circulating volume and blood pressure.
Short-term effects - strong vasoconstriction of arteries. This increases the PVR which increases the blood pressure.
Long-term effects - Reduces sodium excretion by increasing sodium reabsorption by the proximal tubules of the kidney. Water follows sodium, so this effectively increases the circulating volume which increases the SV which increases the BP. It also stimulates the release of aldosterone from the adrenal medulla and Vasopressin from the pituitary gland.
Juxtaglomerular cells
These are cells that are found in the kidneys and are responsible for release of renin when decreased BP, circulating volume, or sodium is detected.
What two hormones are stimulated by angiotensin 2? Where do these hormones come from?
Aldosterone (adrenal medulla) and Vasopressin (ADH) from the pituitary gland
What is Vasopressin? AKA? What does it do?
Vasopressin is also known as antidiuretic hormone. It is released from the posterior pituitary gland when stimulated by angiotensin 2. Vasopressin works to increase the circulating volume by retaining more water in the collecting ducts of the kidneys.
What does aldosterone do?
Aldosterone works to increase circulating volume by causing sodium and water retention in the kidneys.
What is pericarditis? What are the types of pericarditis?
Pericarditis is inflammation of the pericardium. The pericardium is the double walled, fluid filled sac that surrounds the heart.
Types - dry, effusion with purulent, serous, or hemorrhagic exudate.
Triad of symptoms seen with pericarditis? Describe why these occur.
- Chest pain
- Pericardial friction rub
- ECG changes - stereotypical results are global ST elevation
This triad of symptoms occur due to inflammation pushing and restricting the normal heart function. The worse the inflammation, the more restricted the heart’s normal activities are.
How does pericarditis pain present? What helps relieve the pain?
Pericarditis pain presents as abrupt sharp pain that is felt mainly in the precordium area. It can radiate. The pain is worsened with coughing, deep breathing, and changing positions.
Tripod position (leaning forward) can typically relieve some of the pain.
What increases the risk for pericarditis? What is the most common causes?
- Male between the ages 20-50.
- Autoimmune disease - lupus, RA
- Uremia or dialysis treatment
- MI
- Recent cardiac surgery
- Most common cause is viral infection (coxsackieviruses and echoviruses)
How is pericarditis treated?
- Pericardiocentesis if there is tamponade or the patient is symptomatic
- NSAIDs - to inhibit the inflammation
Rheumatic heart disease
1. What is it?
2. What are the common signs and symptoms?
Rheumatic heart disease is an autoimmune condition that can develop after someone has developed rheumatic fever from group A strep infection.
Common S&S include:
- Fever - unusually high grade fever
- Joint pain - migrating polyarthritis
- Carditis - pericarditis, myocarditis.
- Mitral regurgitation
- AF
- Heart failure
- Nodules (collagen)
- Erythema marginatrum
What is Rheumatic fever? Who is most commonly affected?
An autoimmune condition that develops 2-4 weeks after infection with group A streptococcus (typically throat infection).
Children are most commonly affected, ages 5-15 years old. More prevalent in developing countries where treatment for streptococcus is less common.
What is the most serious aspect of rheumatic fever - rheumatic heart disease?
Rheumatic fever can develop into rheumatic heart disease which can potentially lead to life long heart valve issues. These heart valve issues can lead to heart failure down the road. The most common valve issue is mitral regurgitation.
Signs and symptoms of mitral regurgitation.
How is this murmur heard?
SOB, fatigue, palpitations, swelling, heart murmur.
Mitral regurgitation is a systolic murmur described as holosystolic or pansystolic, sounds described as whooshing or blowing.
What is erythema marginatum? What is it associated with?
Raised, red, and well-defined lesion with pale center. This is one of the classic signs of rheumatic fever.
Stenosis VS insufficiency (regurgitation)
Stenosis is the narrowing of the valve opening and the inability of the valve leaflets to open fully. This results in reduced blood flow leaving with each contraction and increased afterload. This can negatively affect the heart chambers over time. Stenosis is always a disease of time. Calcification or bacterial vegetation are two possible culprits.
Insufficiency is the inability of the heart valves to fully close. This allows blood to back flow which can negatively affect the heart’s functioning.
Right VS Left Heart Failure
1. Common causes?
Right heart failure is most commonly caused secondary to left heart failure. It can also be caused by pulmonary HTN, PE, ASD, VSD, chronic lung disease.
Left sided heart failure is most commonly associated with systolic dysfunction. It can result from left sided valvular dysfunction such as mitral regurgitation and aortic stenosis.
What are the signs and symptoms of left sided heart failure? Describe the pathophysiology behind these symptoms.
Left sided heart failure results in less blood being pushed forward from the left side. Blood then backs up into the pulmonary circulation. As more and more blood is backed up, it increases the pressure in the pulmonary system and can cause a fluid shift from the veins/arteries and into the interstitial space. This fluid impairs gas exchange and is known as congestion or pulmonary edema.
Signs and symptoms:
- SOB
- Cough (pink frothy sputum)
- Increased PAP
- Crackles or rales on auscultation
- Orthopnea - laying flat decreases gas exchange and makes it difficult to breath
- Fatigue - a reduction in blood moving forward due to decreased CO
- Weak - less blood moving forward
- Lethargic - less blood moving forward
- Decreased UO - less blood moving forward throughout the systemic circulation triggers the RAAS system to hold on to more fluid and sodium which causes less UO
What are the signs and symptoms of right sided heart failure? Describe the pathophysiology behind these symptoms.
Right sided heart failure results when the right ventricle is unable to pump sufficient blood through to the pulmonary system and to the left side of the heart. This causes a backup of blood into the systemic circulation.
Signs and symptoms:
- Increase in CVP
- Increased fluid in the systemic circulation results in a fluid shift into the interstitial space, this manifests as peripheral edema, ascites.
- Anorexia, GI distress, and weight loss - symptoms are caused by discomfort from excess fluid
- JVD
- Hepatosplenomegaly - fluid backing up into the liver and spleen
A patient with heart failure is experiencing activity intolerance and signs of decreased tissue perfusion. What heart failure?
Left sided - from decreased CO
What are the most common causes of acute heart failure?
Acute heart failure is most commonly caused by MI, pulmonary embolism, endocarditis, myocarditis, arrhythmias, acute uncontrolled hypertension
Acute heart failure syndromes.
- How are these patients treated?
These are the sudden, new symptoms of heart failure or the gradual worsening of existing heart failure to the point where they need emergent treatment. These life threatening symptoms are almost always due to accumulation of pulmonary congestion.
Acute heart failure syndrome patients are treated by elevating the
- HOB
- Diuretics can be used to improve dyspnea and oxygenation by removing excess fluid from the lungs. Diuretics can also reduce peripheral edema and improve GI symptoms experienced with R sided HF.
- Assist devices can be used to bridge patients between complete heart failure and heart transplantation.
- Supplemental oxygen
- Vasopressors/ inotropes
Treatment for warm and dry heart failure.
Rest and sedation
Treatment for warm and wet heart failure? What is going on here?
Diuretics and vasodilators
Wet - pulmonary congestion
warm - without hypoperfusion
Treatment for cool and dry heart failure? What is going on here?
Volume and pacing
Cool - signs of hypoperfusion
Dry - no pulmonary congestion
Treatment for cold and wet heart failure?
What is going on here?
Inotropic support
Vasodilation
IAMP
Surgery
Cold - hypoperfusion
Wet - pulmonary congestion
How is chronic heart failure managed? Lifestyle changes.
8 of them
- Exercise - prescribing an appropriate amount of exercise for the patient can keep the heart working.
- Diet:
- Fluid restriction can be used to minimize swelling and pulmonary edema
- reduced sodium can manage fluid retention which affects swelling and pulmonary congestion
- heart healthy diet - vegetables, fruits, whole grains, lean meats. Stay away from sugars and red meats. - Weight management - obesity places a greater strain on the cardiac system
- Checking weight gain/loss at the same time every day
- Keeping up with blood pressure and intake/output logs
- Not smoking
- Limiting alcohol
- Reducing stress - can increase workload of the heart via catecholamines.
What pharmacologic options are there for management of heart failure? When to choose one over the others?
- Diuretics - these are frequently used in the care of patients with heart failure to reduce swelling and pulmonary congestion.
- ACEI - these medications block the RAAS which in turn reduces the amount of fluid and sodium the body retains. This is beneficial for heart failure patient because their biggest problems are related to excess fluid. A dry, non-productive cough is one of the biggest draw backs for prescribing ACEI.
- Digoxin - digitalis. An oral inotrope. Increases the heart’s contractility while also reducing the heart rate to allow better ventricular filling.
- Aldosterone antagonists - block the effects of aldosterone which result in increased sodium and water retention.
- Beta Blockers - negative inotrope, short-term makes HF worse. Long-term improves symptoms and EF.
- calcium channel blockers - vasodilate, decrease afterload
- Nitrates - decrease preload
Cardiac cachexia
1. What is cachexia?
2. What causes it?
Cachexia is muscle wasting and malnutrition.
Cardiac cachexia is muscle wasting and malnutrition affecting the heart of people with serve heart failure.
Cardiac cachexia is thought to be a result of increased workload of the heart, decreased nutritional intake due to depression and feelings of fullness, and poor perfusion allowing the buildup of toxins.
What is cardiomyopathy?
Diverse group of conditions that affect the myocardium and result in mechanical or electrical impairment.
What is hypertrophic cardiomyopathy?
5 key points
Hypertrophic cardiomyopathy is an autosomal dominant disorder that affects the heart. Hallmark findings include:
- Left ventricular hypertrophy
- Thickening of the intraventricular septum
- abnormal diastolic filling
- cardiac arrhythmias
- and a possible intermittent outflow obstruction at the aorta
Who is at greatest risk for developing hypertrophic cardiomyopathy?
HCM is an autosomal dominant trait. People with a first degree relative are at highest risk.
The disease tends to present early in life. Children and young adults tend to be symptomatic with the disease.
Males are more likely to have HCM
Athletes and physically active individuals are more likely to be diagnosed with the disease because they are more likely to experience the symptoms related to the disease. As the heart experiences greater demands for CO, the LV hypertrophy, reduced diastolic filling, and possible intermittent outflow obstruction all work to reduce potential CO.
What is the greatest risk for hypertrophic cardiomyopathy?
Sudden death, typically happens in young adults during athletics events where cardiac demands are high
How can hypertrophic cardiomyopathy be detected in the clinic?
HCM can be detected through screenings of family history since it is a genetic disease. If a first degree relative had the disease then there is a higher chance of the individual having it.
Symptoms - chest pain, SOB, dizziness, syncope especially during physical activity is a red flag for younger people.
Evaluation of a heart murmur - best heard during systole as the intermittent outflow obstruction impedes normal exiting of blood from the aorta.
EKG changes
Patent ductus arteriosus
- What is the ductus arteriosus?
- What problems does a patent one present?
The ductus arteriosus is an opening found between in the pulmonary artery that allows blood to bypass the lungs during a fetus development. This closes spontaneously in 90% of term infants within the first 48 hours of life.
Patent ductus arteriosus is a congenital condition where the ductus arteriosus does not close after conception. This results in decreased blood flow entering the lungs and becoming oxygenated.
When is PDA typically found? Who is more likely to have it?
PDA is typically found fairly early in the child’s life. Symptoms such as trouble breathing (tachypnea or cyanosis), poor feeding (r/t SOB during feeds), heart murmur (machine like systolic murmur), and signs of heart failure.
Pre-term infants are more likely to have the disease. Term infants are less likely but would present with the same symptoms.
What is atrial septal defect? How does it affect blood flow? Murmur?
Atrial septic defect is an opening between the left and right atria. This opening allows blood from the higher pressure left atria to shunt into the lower pressure right atria. This results in less oxygenated blood passing on to the systemic circulation and also increases the workload of the RA and RV.
ASD murmur is caused by the increased blood volume placed upon the RV. The pulmonic valve is opened for prolonged periods of time to allow this blood to pass through, this creates a separation between the aortic and pulmonic portions of the S1.
What is a ventricular septal defect? How do VSD affect PVR?
VSD are abnormal openings between the left and right ventricles. Since the left ventricle is stronger than the right, there is a shunting from the left ventricle into the right ventricle.
The increased amount of blood contributed from the LV through the VSD into the right ventricle increases the amount of blood the pulmonary circulation has to handle. This can increase pulmonary vascular resistance which can eventually lead to pulmonary hypertension and R sided heart failure.
Eisenmenger complex
This is a syndrome caused by a long standing left-to-right shunt. VSD is a common cause.
The prolonged shunting causes increased pulmonary workload which can cause pulmonary hypertension. The pressure can become so great that it reverses the blood flow throughout the heart. A right to left shunt then appears.
This results in deoxygenated blood mixing with oxygenated blood and results in cyanosis.
What is tetralogy of fallot? Describe each of the four problems.
Tetralogy of fallot is a congenital heart disease that is characterized by four separate conditions.
1. Over riding aorta - the aorta is positioned over the VSD which allows oxygen-poor blood from the right ventricle to pass into the aorta and then to the systemic circulation leading to cyanosis.
2. Right ventricular hypertrophy - the presence of pulmonary stenosis causes increased workload for the RV. It becomes hypertrophied over time.
3. Pulmonary stenosis - narrowing of the pulmonic valve and the pulmonary artery results in increased workload for the RV and decreased blood making it to the heart to become oxygenated.
4. VSD - Hole in the wall between the two ventricles allows blood to pass from the high pressure LV into the RV. This further reduces the amount of oxygenated blood being sent out to the systemic circulation.
What causes cyanosis in children with tetralogy of fallot?
- VSD - decreased amounts of oxygenated blood are sent to the systemic circulation due to the L to R shunt.
- Pulmonary stenosis - reduced blood flow is seen passing from the RV into the pulmonary system due to this stenosis.
- Over riding aorta
What are tet spells?
Also known as hypercynaotic spells. Sudden episodes of severe cyanosis seen in children with tetralogy of fallot. Usually preceded by crying, agitation, feeding, physical activity, and bowel movements.
Assuming the knee-to-chest position can dramatically improve these symtpoms.
