Week 4: Cardiac

Question 1

What is the formula for cardiac output

Answer 1

Cardiac output = stroke volume x heart rate

Question 2

Define Stroke Volume and list the factors which determine it

Answer 2

Volume of blood in ml/beat that is pumped out of the heart in one minute

Determined by preload, afterload and contractility

Question 3

Describe Preload

Answer 3

Volume and pressure inside ventricle at end of diastole

Question 4

What are key factors influencing Preload?

Answer 4

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

Question 5

Provide examples of conditions that affect Preload

Answer 5

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

Question 6

Describe Afterload

Answer 6

Resistance against which ventricles have to pump to eject blood to produce cardiac output

Question 7

What are key factors influencing afterload?

Answer 7

Systemic vascular resistance, aortic pressure, valve disease, blood viscosity

Question 8

Provide examples of conditions that affect Afterload

Answer 8

ystemic 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

Question 9

What is Heart Failure?

Answer 9

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

Question 10

Identify contributing factors for congestive heart failure

Answer 10

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

Question 11

Describe chronic venous insufficiency

Answer 11

Venous insufficiency = blood flow interruption in the venous system due to valve incompetence, reflux and/pr venous obstruction

Chronic venous insufficiency is when there is the inadequate return over time.

Question 12

List Signs and Symptoms of chronic venous insufficiency

Answer 12

lower extremity edema, hyperpigmentaion of limbs, hemosiderosis (brown discoloration), achy pain, pruritis, varicose veins, venous ulcers, thickened skin

Question 13

Which valves are the AV valves and which structures are they between?

Answer 13

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

Question 14

Which valves are the semilunar valves and which structures are they between?

Answer 14

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

Question 15

Tricuspid valve – how many cusps? Location in heart? Supporting structures? Open or closed during systole/diastole?

Answer 15

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

Question 16

Bicuspid/Mitral valve - how many cusps? Location in heart? Supporting structures? Open or closed during systole/diastole?

Answer 16

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

Question 17

Pulmonic Valve - how many cusps? Location in heart? Supporting structures? Open or closed during systole/diastole?

Answer 17

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

Question 18

Aortic Valve - how many cusps? Location in heart? Supporting structures? Open or closed during systole/diastole?

Answer 18

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

Question 19

Outline the 5 phases of the cardiac cycle

Answer 19

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.

Question 20

What are the names of the three layers of blood vessels?

Answer 20

Tunica intima

Tunica media

Tunica externa (or adventitia)

Question 21

Which layer of blood vessels is primarily involved in vasoconstriction and vasodilation?

Answer 21

Tunica Media – this middle layer is made up of smooth muscle and elastic tissue and is responsible for vasoconstriction/vasodilation

Question 22

Describe the composition and role of the innermost layer of blood vessels. What is the name of this layer?

Answer 22

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.

Question 23

Describe the composition and role of the middle layer of blood vessels. What is the name of this layer?

Answer 23

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.

Question 24

Describe the composition and role of the outermost layer of blood vessels. What is the name of this layer?

Answer 24

tunica externa or adventitia (outermost/external): connective tissue, also contains nerves and lymphatic vessels. Thinner in arteries and thicker in veins.

Question 25

Where are baroreceptors found?

Answer 25

In blood vessel walls

Question 26

What are the two types of baroreceptors and their specific locations?

Answer 26

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

Question 27

What are the functions of Arterial Baroreceptors?

Answer 27

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

Question 28

What are the functions of Cardiopulmonary baroreceptors?

Answer 28

They regulate blood volume by influencing water and sodium excretion by the kidneys.

Question 29

Describe the general function of Chemoreceptors

Answer 29

Sense changes in blood composition

Question 30

What are the two types of chemoreceptors and what are their functions and locations?

Answer 30

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

Question 31

chylomicrons, chylomicron remnants, VLDL, IDL, LDL, HDL, and Lp (a) are classes of _____ .

Answer 31

Lipoproteins

Question 32

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?

Answer 32

HDL

Question 33

Describe the general function of lipoproteins

Answer 33

Lipid transport

Question 34

Describe the ways in which lipoproteins contribute to the development of atherosclerosis

Answer 34

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.

Question 35

List some non-modifiable risk factors for heart disease

Answer 35

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)

Question 36

List some modifiable risk factors for heart disease

Answer 36

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

Question 37

Define Pulse Pressure

Answer 37

The difference between systolic and diastolic BP

Question 38

What is a normal range for pulse pressure? What factors affect this value?

Answer 38

normal pulse pressure 40-50 mm Hg

value related to arterial wall stiffness and stroke volume

Question 39

Define Mean Arterial Pressure

Answer 39

the average pressure in the arteries during the cardiac cycle

MAP = Pd + 1/3(Ps-Pd)

Question 40

What is a normal range for MAP? What factors affect this value?

Answer 40

normal MAP 70-110 mm Hg

value related to the elastic properties of the arterial wall and volume of blood in arterial system

Question 41

What are the two types of receptors involved in the neural control of blood pressure?

Answer 41

Baro receptors and arterial chemoreceptors

Question 42

What is a condition that causes impairment of neural control of blood pressure?

Answer 42

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.

Question 43

What do the kidneys secrete in response to decreased BP, sympathetic nerve stimulation or GFR drops?

Answer 43

Renin

Question 44

Where is angiotensin made and where does it come into contact with renin to form angiotensin I?

Answer 44

Angiotensin is made in the liver and comes into contact with renin in the circulation to from angiotensin I

Question 45

What converts angiotensin I to angiotensin II?

Answer 45

Angiotensin converting enzyme (ACE)

Question 46

Describe the 4 pathways of Angiotensin II

Answer 46

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)

Question 47

Provide examples of micro and macro end organ damage from hypertension

Answer 47

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

Question 48

Define secondary hypertension

Answer 48

Occurs when hypertension is due to another medical condition or from taking a medication

Question 49

What percentage of HTN diagnoses are secondary hypertension

Answer 49

5-10%

Question 50

According to the text book, what are the 4 causes of primary hypertension?

Answer 50

1) renal vascular or parenchymal disease

2) adrenocortical tumors

3) adrenomedullary tumors (pheochromocytoma)

4) medications (oral contraceptives, corticosteroids, antihistamines)

Question 51

Define malignant hypertension

Answer 51

Rapidly progressive hypertension where diastolic pressure usually greater than 140

Causes end organ damage

Question 52

What are some causes of malignant hypertension

Answer 52

Can occur in primary hypertension

Other causes: complications of pregnancy, cocaine or amphetamine use, reaction to certain medications, adrenal tumours and alcohol withdrawal

Question 53

What are possible end-organ results of malignant hypertension?

Answer 53

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

Question 54

What is orthostatic hypotension?

Answer 54

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

Question 55

Why does orthostatic hypotension occur?

Answer 55

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)

Question 56

List potential risk factors for orthostatic hypotension

Answer 56

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.

Question 57

What is pericardial effusion?

Answer 57

Accumulation of fluid in the pericardial cavity, and occurs in forms of pericarditis

Question 58

What are the causes of pericardial effusion?

Answer 58

Idiopathic (20%)

Neoplasm

Infection

Question 59

What is Beck’s Triad?

Answer 59

Distant or muffled heart sounds, elevated jugular venous pressure, low BP

Question 60

What are signs & symptoms of pericardial effusion?

Answer 60

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

Question 61

What is cardiac tamponade and why is it dangerous?

Answer 61

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