Cardiac 1 Flashcards
What is the formula for cardiac output
Cardiac output = stroke volume x heart rate
Define Stroke Volume and list the factors which determine it
Volume of blood in ml/beat that is pumped out of the heart in one minute
Determined by preload, afterload and contractility
Describe Preload
Volume and pressure inside ventricle at end of diastole
What are key factors influencing Preload?
Venous return and total circulating volume
Venous return is dependent on blood volume and flow through the venous system and the AV valves
Also affected by arterial contraction, resistance from valves, ventricular compliance, and heart rate
Provide examples of conditions that affect Preload
Venous tone: vasoconstriction (increased preload) and vasodilation (decreased preload) Ex. allergic reactions and some drugs.
Circulating blood volume: preload is decreased by a decrease in total circulating volume (hypovolemia) Ex. blood loss, dehydration. Hypervolemia increases preload.
Atrial contraction: If Atria can’t pump blood efficiently the volume of blood that enters the ventricles will decrease resulting in lower preload Ex. atrial arrhythmias
Resistance from valves: Inflow resistance – narrowing of atrioventricular valves: tricuspid and mitral valve stenosis = decrease ventricle filling = decrease preload. Outflow resistance – narrowing of aortic and pulmonic valves = stenosis = decrease ventricle emptying = increase preload
Ventricular compliance (distensibility – the ability to stretch): decreased compliance decreases preload Ex. myocardial infarction, cardiomyopathy, chronic heart failure, ventricular hypertrophy. Increased compliance increases preload Ex. dilated cardiomyopathy
Heart rate: tachycardia = decreased ventricle filling time = decrease preload
Describe Afterload
Resistance against which ventricles have to pump to eject blood to produce cardiac output
What are key factors influencing afterload?
Systemic vascular resistance, aortic pressure, valve disease, blood viscosity
Provide examples of conditions that affect Afterload
Systemic Vascular Resistance (SVR): Hypertension – increased TPR means that afterload is chronically elevated
Aortic pressure - Vessel diameter: anything that reduces the diameter of the blood vessel (Ex. vasoconstriction, thickening) will increase afterload. Anything that increases vessel diameter (Ex. vasodilation) will decrease afterload
Valve Disease: Any condition of the aorta that may cause increased resistance to left ventricular ejection will increase afterload Ex. aortic stenosis. Mitral regurgitation = blood leaks back into the left atrium = decreases stress on the left ventricle wall = decreases afterload
Blood viscosity: determined by assessing a patient’s hematocrit. Blood that is viscous (high hematocrit) is sluggish and more resistant to flow = increased afterload. Less viscous or thin blood(low hematocrit) = little resistance to flow, decreases afterload
What is Heart Failure?
Failure of the heart to pump sufficient blood to meet the metabolic demands of the tissues.
Injuries to myocardium cause loss of functioning muscle, compensatory mechanisms lead to long term adverse effects
Identify contributing factors for congestive heart failure
Incomplete emptying – caused by inotropic injury (systolic failure)
Incomplete filling – caused by compliance issue (diastolic failure)
Usually a combination of both types of failure, resulting of back-up of blood throughout the system
Incidence higher in women, chronic hypertension, obesity, left ventricular hypertrophy, cardiomyopathy, excessive alcohol use, end-stage COPD, valvular disorders, anemia, renal failure, AF, CAD and diabetes
Describe chronic venous insufficiency
Venous insufficiency = blood flow interruption in the venous system due to valve incompetence, reflux and/or venous obstruction
Chronic venous insufficiency is when there is the inadequate return over time.
List Signs and Symptoms of chronic venous insufficiency
lower extremity edema, hyperpigmentaion of limbs, hemosiderosis (brown discoloration), achy pain, pruritis, varicose veins, venous ulcers, thickened skin
Which valves are the AV valves and which structures are they between?
Tricuspid valve - On right side of heart between right atria and right ventricle
Bicuspid valve/Mitral valve – on left side of heart between left atria and left ventricle
Which valves are the semilunar valves and which structures are they between?
Pulmonic valve – on right side of heart, between right ventricle and pulmonary artery
Aortic valve – on left side of heart, between left ventricle and aorta
Tricuspid valve – how many cusps? Location in heart? Supporting structures? Open or closed during systole/diastole?
Three cusps
right side of the heart between right atria and right ventricle
When ventricles are relaxed (diastole), tricuspid valve is open and blood flows from higher pressure in the right atria to lower pressure in the right ventricle. During ventricular contraction (systole) the valve shuts to prevent backflow into the right atria.
Upper end attached to a ring in the heart’s fibrous skeleton, lower end attached by chordae tendineae to the papillary muscles of the myocardium
Bicuspid/Mitral valve - how many cusps? Location in heart? Supporting structures? Open or closed during systole/diastole?
Location: between left atrium to left ventricle
2 cusps
Beginning of ventricular systole = closes (1st heart sound (S1 “lub”))
Prevents backflow of blood from the ventricle to the L atrium
Closed during systole ; open during diastole
Chordae tendineae attaches the end of the lower margin of the valve leaflets to the papillary muscles (extension of the myocardium)
Papillary muscles – hold the cusps together, and downward at the start of ventricular contraction, preventing backward prolapse into the atria
Pulmonic Valve - how many cusps? Location in heart? Supporting structures? Open or closed during systole/diastole?
Three cusps
Located between right ventricle and pulmonary artery (the only artery that carries deoxygenated blood)
When right ventricle is relaxed (diastole) pulmonic valve is closed and when the right ventricle contracts (systole) pulmonic valve opens for blood to pump to the lungs.
There is no chordae tendineae attached to pulmonic valve, it arises from the fibrous skeleton
Aortic Valve - how many cusps? Location in heart? Supporting structures? Open or closed during systole/diastole?
Location: between left ventricle to aorta
3 cusps
Beginning of ventricular diastole = closes (2nd heart sound (S2 “dub”))
prevents backflow of blood from the aorta to the left ventricle
closed during diastole; opens during systole
Cusps arise from the fibrous skeleton
Outline the 5 phases of the cardiac cycle
Phase 1: Atrial systole- atria contract, pushing blood through open mitral and tricuspid valves from atria to ventricles. Semilunar valves closed during this phase.
Phase 2: Beginning of ventricular systole- Ventricles contract, increasing pressure within the ventricles. Tricuspid and mitral valves close causing first heart sound (S1)
Phase 3: Period of rising pressure- semilunar valves open when pressure in ventricles exceed that of arteries, blood begins flowing from ventricles into pulmonary and aortic arteries.
Phase 4: Beginning of ventricular diastole- pressure in relaxing ventricles falls below the pressure in arteries, causing semilunar valves to snap shut creating second heart sound (S2).
Phase 5: Period of falling pressure- blood flows from veins into relaxed atria. Tricuspid and mitral valves open when pressure in ventricles falls below that in the atria.
What are the names of the three layers of blood vessels?
Tunica intima
Tunica media
Tunica externa (or adventitia)
Which layer of blood vessels is primarily involved in vasoconstriction and vasodilation?
Tunica Media – this middle layer is made up of smooth muscle and elastic tissue and is responsible for vasoconstriction/vasodilation
Describe the composition and role of the innermost layer of blood vessels. What is the name of this layer?
tunica intima (innermost/intimal): single layer of endothelial cells with important roles in coagulation, antithrombogenesis, and fibrinolysis. Also involved in immune system function, tissue, and vessel growth.
Describe the composition and role of the middle layer of blood vessels. What is the name of this layer?
tunica media (middle/medial): smooth muscle layer and elastic tissue. Thicker in arteries and thinner in veins. Large arteries close to the heart have more elastic tissue to allow for stretch during systole and recoil during diastole. Medium and small arteries farther from the heart have more muscle fibre which supports blood flow via vasoconstriction and vasodilation.
Describe the composition and role of the outermost layer of blood vessels. What is the name of this layer?
tunica externa or adventitia (outermost/external): connective tissue, also contains nerves and lymphatic vessels. Thinner in arteries and thicker in veins.
Where are baroreceptors found?
In blood vessel walls
What are the two types of baroreceptors and their specific locations?
Arterial and Cardiopulmonary
Arterial located in the aortic arch and carotid sinus
Cardiopulmonary locate in the low-pressure areas of the heart – right atrium, right ventricle and pulmonary vessels
What are the functions of Arterial Baroreceptors?
respond to blood pressure changes, sending information through the glossopharyngeal and vagus nerves to cardiovascular centers in the pons and medulla. High BP = vasomotor center stimulates parasympathetic nervous system and causes vasodilation. While cardiac control center inhibits sympathetic NS while stimulating PNS = decreased HR. These changes reduce the total peripheral resistance, HR and cardiac output which causes decreased BP
What are the functions of Cardiopulmonary baroreceptors?
They regulate blood volume by influencing water and sodium excretion by the kidneys.
Describe the general function of Chemoreceptors
Sense changes in blood composition
What are the two types of chemoreceptors and what are their functions and locations?
Peripheral and Central chemoreceptors
Peripheral chemoreceptors
are nerve cells found within the aortic arch and carotid arteries. Primarily sensitive to the concentrations of oxygen and secondarily sensitive, to the concentrations of CO2 and pH in the blood. When peripheral chemoreceptors detect low oxygen in the blood, they send information through the glossopharyngeal and vagus nerves to vasomotor and cardiac centers in the pons and medulla. These centers cause sympathetic stimulation which increases HR, total peripheral resistance and cardiac output, raising blood pressure.
Central chemoreceptors
found in the medulla and are more sensitive to concentrations of CO2, and low pH, which again, through the vasomotor center, stimulate sympathetic vasoconstriction raising blood pressure
chylomicrons, chylomicron remnants, VLDL, IDL, LDL, HDL, and Lp (a) are classes of _____ .
Lipoproteins
Of the 7 classes of lipoproteins, all but one are pro-atherogenic. What is the name of the one class of lipoproteins that is anti-atherogenic?
HDL
Describe the general function of lipoproteins
Lipid transport
Describe the ways in which lipoproteins contribute to the development of atherosclerosis
Short version: foam cell formation, which causes endothelial dysfunction, platelet aggregation and immune responses. This attracts even more lipoproteins and furthers plaque formation.
Long version:
Following their retention in the arterial wall, lipoproteins undergo modifications and trigger a series of maladaptive responses that accelerate further lipoprotein retention and cause further plaque progression
Aggregated lipoproteins are taken up by macrophages as well as vascular smooth muscle cells (in advanced lesions), leading to the formation of lipid-laden foam cells. This process is facilitated by modification of the LDL particle by non-oxidative alteration, oxidation, glycosylation, or glycooxidation
In addition to facilitating uptake by macrophages and ultimately foam cell formation, oxidised LDL particles promote atherosclerosis via endothelial dysfunction (due to impaired release of nitric oxide and increased endothelial production of oxygen free radicals), macrophage recruitment, enhanced platelet aggregation and thromboxane release (which contributes to vasoconstriction and intravascular thrombus formation), and increased apoptosis of smooth muscle cells and endothelial cells
Retained LDL particles promote inflammatory and immune changes via cytokine release from macrophages, promoting further recruitment of immuno-inflammatory cells (monocytes/macrophages, neutrophils, lymphocytes, dendritic cells)
Proatherogenic factors and enzymes that are released by monocytes/macrophages in the developing atheroma, including lipoprotein lipase and phospholipase-A2, induce the formation of proteoglycans with great affinity to atherogenic lipoproteins, promoting a vicious circle that leads to further lipoprotein retention and progression of atherosclerosis
At later stages of plaque development, proteases secreted by macrophages degrade the overlying fibrous cap rendering the plaque vulnerable to acute rupture, whereas procoagulant factors favour thrombus formation upon disruption of a thin-capped plaque.
List some non-modifiable risk factors for heart disease
age (chronological and biological age)
biological sex (male)
family history of cardiovascular disease or familial hyperlipidemia (1st degree relative, F<65 years or M <55 years)
ethnicity (first nations, south Asians (Indian, Pakistani, Bangladeshi, or Sri Lankan))
CKD, chronic inflammatory disease (rheumatoid arthritis, psoriatic arthritis, systemic lupus erythematosus, vasculitis, HIV infection, hypertensive diseases of pregnancy, polycystic ovarian syndrome, gestational diabetes)
List some modifiable risk factors for heart disease
Smoking
diet (a diet rich in vegetables, fruits, legumes, nuts, whole grains, fish, and lean proteins with soluble and insoluble fiber has been consistently shown to be associated with lower mortality)
-physical activity/ sedentary behaviour (engaging in at least 150 minutes per week of accumulated moderate to vigorous- intensity aerobic physical activity is associated with reduced risk of CVD)
-body weight (excess body weight/ BMI/ waist circumference)- adults diagnosed as obese or overweight are at increased risk of CVD, HF, afib
-alcohol consumption- reduction in intake may lower BP. high blood pressure = CVD risk. Adapt health behaviours to reduce BP levels. Consider pharmacological management in addition to health behaviour changes.
-Diabetes mellitus- associated with 2-4 fold increase in CVD. Adherence to healthier behaviours in those with T2DM is associated with lower CVD risk.
-Lipid levels- high LDL, triglycerides are risk factors for atherogenesis. Maintain optimal lipid levels.
-psychosocial factors (stress, depression, anxiety)- strongly associated with adverse CVD outcome
-SES factors (income, level of education, employment)- may confer risk equivalent to traditional risk factors. Health education, community-based programs, and behavioural counselling are suggested to address the impact of these factors on CVD risk
-Medications- thiazide diuretics, beta blockers, and oral estrogens can cause changes in serum lipid concentrations. Atypical antipsychotics (i.e., clozapine, olanzapine) have been associated with weight gain, obesity, hypertriglyceridemia, development of DM
Define Pulse Pressure
The difference between systolic and diastolic BP
What is a normal range for pulse pressure? What factors affect this value?
normal pulse pressure 40-50 mm Hg
value related to arterial wall stiffness and stroke volume
Define Mean Arterial Pressure
the average pressure in the arteries during the cardiac cycle
MAP = Pd + 1/3(Ps-Pd)
What is a normal range for MAP? What factors affect this value?
normal MAP 70-110 mm Hg
value related to the elastic properties of the arterial wall and volume of blood in arterial system
What are the two types of receptors involved in the neural control of blood pressure?
Baro receptors and arterial chemoreceptors
What is a condition that causes impairment of neural control of blood pressure?
Obesity, adipokines and insulin-resistance. Adipokines are cytokines released by adipose tissue that can contribute to inflammation. These conditions can cause dysfunction in the sympathetic nervous system, or neurohumoral dysfunction.
What do the kidneys secrete in response to decreased BP, sympathetic nerve stimulation or GFR drops?
Renin
Where is angiotensin made and where does it come into contact with renin to form angiotensin I?
Angiotensin is made in the liver and comes into contact with renin in the circulation to from angiotensin I
What converts angiotensin I to angiotensin II?
Angiotensin converting enzyme (ACE)
Describe the 4 pathways of Angiotensin II
Acts directly on arterioles in kidneys to decrease GFR & increasing reabsorption of Na+
Stimulates the secretion of aldosterone from adrenal gland –> promotes renal sodium and water reabsorption & K+ secretion –> increased blood volume
Stimulates secretion of ADH from pituitary –> inc water retention in kidneys –> increased blood volume
Causes vasoconstriction by stimulating smooth muscle –> elevates the systemic blood pressure and restores renal perfusion (blood flow)
Provide examples of micro and macro end organ damage from hypertension
Myocardium
Micro = increased workload and decreased coronary blood flow
Macro = Lt. Vent hypertrophy, myocardial ischemia, heart failure
Coronary arteries
Micro = accelerated atherosclerosis (coronary artery disease)
Macro = myocardial ischemia, infarction, sudden death
Kidneys
Micro = reduced blood flow, increased arteriolar pressure, RAAS and SNS stimulation and inflammation
Macro = glomerulosclerosis and decreased glomerular filtrations, end-stage renal disease
Brain
Micro = reduced blood flow and O2 supply, weakened vessel walls, accelerated atherosclerosis
Macro = TIAs, cerebral thrombosis, aneurysms, hemorrhage, acute brain infarction
Eyes (retinas)
Micro = Retinal vascular sclerosis, increased retinal artery pressures
Macro = Hypertensive retinopathy, retinal exudates and hemorrhages
Aorta
Micro = weakened vessel wall
Macro = Dissecting aorta
Lower Extremity arteries
Micro = reduced blood flow and high pressures in arterioles, accelerated atherosclerosis
Macro = intermittent claudication, gangrene
Define secondary hypertension
Occurs when hypertension is due to another medical condition or from taking a medication
What percentage of HTN diagnoses are secondary hypertension
5-10%
According to the text book, what are the 4 causes of primary hypertension?
1) renal vascular or parenchymal disease
2) adrenocortical tumors
3) adrenomedullary tumors (pheochromocytoma)
4) medications (oral contraceptives, corticosteroids, antihistamines)
Define malignant hypertension
Rapidly progressive hypertension where diastolic pressure usually greater than 140
Causes end organ damage
What are some causes of malignant hypertension
Can occur in primary hypertension
Other causes: complications of pregnancy, cocaine or amphetamine use, reaction to certain medications, adrenal tumours and alcohol withdrawal
What are possible end-organ results of malignant hypertension?
arterial pressure renders cerebral arterioles incapable of regulating blood flow to cerebral capillary beds = hydrostatic pressure causes vascular fluid to move into interstitial space.
if BP not reduced cerebral edema and encephalopathy increase until death occurs
End organ damage: include papilledema, cardiac failure, uremia, retinopathy and CVA
What is orthostatic hypotension?
Decrease in systolic BP of at least 20mmHg or a decrease in diastolic blood pressure of at least 10 mmHg within 3 minutes of moving to a standing position
Can be idopathic/primary, acute or chronic
Why does orthostatic hypotension occur?
Occurs when normal vasoconstriction responses and heart rate elevation responses to fluid shifts during standing are impaired
In other words, insufficient vasomotor compensation & neural reflex (ex. baroreceptors and closure of valves in venous system)
List potential risk factors for orthostatic hypotension
Men > women
Ages 40-70
Primary OH commonly affects older adults (18%) and is a significant risk factor falls or associated injury
acute OH causes: altered body chemistry, meds (antihypertensives or antidepressants), blood volume depletion, venous pooling, prolonged immobility 2/2 illness, starvation, physical exhaustion
Chronic OH causes: may be primary or secondary to a disease ex. adrenal insufficiency, Parkinson’s etc.
What is pericardial effusion?
Accumulation of fluid in the pericardial cavity, and occurs in forms of pericarditis
What are the causes of pericardial effusion?
Idiopathic (20%)
Neoplasm
Infection
What is Beck’s Triad?
Distant or muffled heart sounds, elevated jugular venous pressure, low BP
What are signs & symptoms of pericardial effusion?
Becks Triad (Distant or muffled heart sounds, elevated jugular venous pressure, low BP)–>Indicator of Cardiac Tamponade
Pulsus paradoxus (Exaggerated drop in BP 10 mm HG when you breathe in) *ominous sign of cardiac tamponade because it is showing impairment of diastolic filling of the left ventricle
Distant or muffled heart sounds
sinus tachycardia
Poorly palpable apical pulse
Dyspnea on exertion
Dull chest pain
What is cardiac tamponade and why is it dangerous?
Pressure exerted by the pericardial fluid eventually will equal diastolic pressure within the heart chambers, which integers with right martial filling during diastole.
The decrease in right atrial filling causes increased venous pressure, systemic venous congestion, and S&S of right ventricular failure (distention of jugular veins, Edema, hepatomegaly)
Decreased atrial filling→ decreased ventricular filling, decreased Stroke volume, reduced cardiac output=circulatory collapse can occur
