Week 3 (ch. 12 CVS Disorders) Flashcards
Heart function
The pump for both systems and pulmonary circulations
Left ventricle: anatomy and function
LV is thicker
Eject blood into extensive systemic circulation
How many valves in the heart?
4 valves - ensure one way blood flow
Describe the conduction system of the heart
- Ensure both atria and ventricles contract as desired for efficient filling and emptying
- originates at SA node
- conduction impulses produce electrical activity picked by up electrodes = electrocardiography
- abnormal variations (arrhythmia or dysthymia) may indicate acute problems
Cardiac Control Center: where is it location?
Medulla of the brain
Cardiac Control Center: function
Controls heart rate and force of contraction
Baroreceptors
Detect change in BP
Cardiac Control Center: what does it response through and how
SNS
- increased HR (tachycardia) and contractility
- any stimulation of the SNS (stress, fever, exercise, pain)
PSNS
- decrease HR (bradycardia)
Coronary Circulation: Right and left coronary arteries —> part of what
Systemic circulation
- many small branches extend from these arteries to supply the myocardium and endocardium
** cardiac muscles requires constant supple of o2 but have limited storage ability. Any BF interference affects heart function
Coronary Circulation: Right and left coronary arteries —> where are they
They branch off aorta immediately distal to the aortic valve
Left coronary artery divides into what
Left anterior descending or inter-ventricular artery, Left circumflex artery
Right coronary artery branches into what?
Right marginal artery, Posterior inter-ventricular artery
What is the cardia cycle coordinated by?
Conduction system
Systole: cardiac contract
Diastole: cardiac relaxation
Describe how heart moves through ventricles and atria, starting with Atria relaxed, filling with blood
- Atria relaxed, filling with blood (diastole?)
- AV valves open
- Blood flows into ventricles
- Atria contract, remaining blood forced into ventricles (systole?)
- Atria relax
- Ventricles contract
- AV valve closes
- Semilunar valves open
- Blood into aorta and pulmonary artery
- Ventricles relax
Heart sounds: “lubb-dub”
Heart with stethoscope
“Lubb” = closure of AV valves, ventricular systole
“Dub” = closure of semilunar valves, ventricular diastole
Heart sounds: murmurs - cause
Caused by incompetent valves or hole in septum
Heart sounds: pulse
Indicates heart rate
Pulse deficit
Difference in rate between apical and radial pulses
What is BP
Pressure of blood against the systemic arterial walls
What does BP depend on
Cardiac output and peripheral resistance
Peripheral resistance
Force opposing blood flow
Systolic pressure
Diastolic pressure
Higher number
- pressure entered by blood when ejected from LEFT VENTRICLE
Lower number
- pressure that is sustained when ventricles are relaxed
Pulse pressure
Difference between systolic and diastolic BP
Does LOCAL vasoconstriction affect systemic BP
No
Changes in blood pressure: sympathetic branch of ANS
Describe how this changes blood pressure
Increased output —> vasoconstriction and increased BP
Decreased output —> vasodilation and decreased BP
BP is directly proportional to what
Blood volume
Changes in blood pressure: hormones - which ones and their impact on BP
- Antidiuretic hormone
- increased BP - Aldosterone
- increases blood volume
- increases BP - Renin-angiotensin-aldosterone
- vasoconstriction
- increases BP
Diagnostics: Electrocardiography
Initial diagnosis and monitoring of dysrhythmias, myocardial infarction, infection, and pericarditis
Diagnostics: Ausculation
Determines valvular abnormalities or abnormal shunts of blood that cause murmurs
Diagnostics: Echocardiography (echo)
Used to record heart valve movements, blood flow, and cardiac output
Diagnostics: exercise stress tests
Used to assess general CV function
Diagnostics: Chest X-Ray films
Used to show shape and size of heart
Diagnostics: Cardiac catheterization
Measures pressure and assesses valve and heart function
- determines central venous pressure and pulmonary capillary wedge pressure
Diagnostics: Angiography
Visualization of blood flow in the coronary arteries
Can complete corrective treatment procedures
Diagnostics: Doppler studies
Assess blood flow in peripheral vessels
Record sounds of blood flow or obstruction
Diagnostics: Blood tests
Assess levels of serum triglycerides, cholesterol, sodium, potassium, calcium, other electrolytes
Diagnostics: Arterial blood gas determination
Checks the current o2 level and acid-base balance
General treatment measures: dietary modifications
Decrease fat intake, general weight reduction, reduce salt intake
General treatment measures: regular exercise program
Increase HDL, lowers serum lipid levels, reduces stress level
General treatment measures: cessation of smoking
Decreases risk of coronary disease
General treatment measures: many different drug therapies
º vasodilators º beta-blockers º calcium channel blockers º digoxin º anti-hypertensive º adrenergic blocking o ACE inhibitors º diuretics º anticoagulants º cholesterol lowering
Coronary Artery Disease (CAD): what is the basic problem
Or Ischemic Heart Disease (IHD)
Or Acute Coronary Syndrome
Insufficient O2 for the needs of the heart muscles
- common cause of disability and death
- leading cause of death for men and women in US
Coronary Artery Disease (CAD)
Or Ischemic Heart Disease (IHD)
Or Acute Coronary Syndrome
What can it lead to
Heart failure
Dysthymias
Sudden death
Arteriosclerosis
General term for all types of arterial changes
- degenerative changes in small arteries and arterioles
- loss of elasticity
- lumen gradually narrows and may become obstructed
- cause of increased BP
Atherosclerosis
Presence of atheromas in large arteries
- plaques consisting of lipids, calcium, and possible clots
- related to diet, exercise, and stress
Lipids are transported in combination with what?
Proteins
Serum lipids: low density lipoprotein
Transports cholesterol from liver to cells
Major factor contributing to atheroma formation
Serum lipids: high density lipoprotein
Transports cholesterol away from the peripheral cells to liver
Catabolism in liver and excretion
- “good” lipoprotein
Atherosclerosis: risk factors
Non-modifiable = age, gender, genetics
Modifiable = obesity, sedentary lifestyle, smoking, diabetes mellitus, poorly controlled hypertension, combination of oral contraceptives and smoking
Atherosclerosis: diagnostic tests
Serum lipid levels (LDL and HDL)
Exercise stress testing (screening for arterial obstruction)
Nuclear medicine studies (determine the degree of tissue perfusion)
Atherosclerosis: treatment
Weight loss Exercise Diet Lower Na intake Stop smoking Control hypertension Control of primary disorder Antilipidemic drugs Surgical prevention (coronary artery bypass grafting)
Angina Pectoris
Chest pain; deficit of O2 to meet myocardial needs
- recurrent, intermittent brief episodes of substernal chest pain
- triggered by physical or emotional stress
- attacks vary in severity and duration but become more frequent and longer as disease progresses
Angina Pectoris: s/s and how is it relieves
S/s = pallor, nausea, diaphoresis (excessive sweating), chest pain
Relieved by rest and administration of coronary vasodilators
Angina Pectoris: describe the way chest pain may occur in different patterns
Classic or exertional angina Variant angina (vasospasm occur at rest) Unstable angina (prolonged pain at rest; may precede myocardial infarction)
Angina Pectoris: Treatment
Rest
Sit in upright position
Nitroglycerin (sublingual)
Check pulse and respiration
Administer O2
If patient known to have angina - second dose of nitroglycerin
Pt. Without history of angina - emergency medical aid
Myocardial infarction
Occurs when coronary artery is totally obstructed
- atherosclerosis is most common cause
- thrombus from atheroma obstructs artery
- vasospasm is caused in small %
- size and location of the infarction determine the damage
Myocardial infarction: signs
Feeling pressure, heaviness, or burning in chest - especially with increased activity
— sudden SOB, weakness, fatigue
— nausea, indigestion
— anxiety/fear
Pain may occur and, if present, is usually substernal, crushing, radiating
Myocardial infarction: diagnostics
Changes in ECG
Serum enzyme and isoenzyme levels
Serum levels of myosin and cardia troponin are elevated
Leukocytosis, elevated CRP and ESR common
Arterial blood gas measurements may be altered
Pulmonary artery pressure measurements are helpful
Myocardial infarction: complications
Sudden death
Cardiogenic shock
CHF
Rupture of necrotic heart tissue/cardiac tamponade
Thromboembolism causing CVA with left ventricular MI
Myocardial infarction: treatment
Goal: reduce cardiac demand O2 therapy Analgesic Anticoagulants Thrombolytic agents can be used
Medications are given to help treat Myocardial infarction along with secondary problems such as?
Medication to treat:
Dysrhythmias, hypertension, CHF
Cardiac Dysrhythmias (Arrhythmias)
Deviations from normal cardiac rate or rhythm
- reduces the efficiency of the hearts pumping cycle
- many types of abnormal patters exist
Cardiac Dysrhythmias (Arrhythmias): cause
Electrolyte abnormalities, fever, hypoxia, stress, infarction, infection, drug toxicity
Cardiac Dysrhythmias (Arrhythmias): diagnostics
Electrocardiography (ECG/EKG) - for monitoring the conduction system
- detects abnormalities
Cardiac Dysrhythmias (Arrhythmias): SA node symptoms
Bradycardia, tachycardia, sick sinus rhythm
Cardiac Dysrhythmias (Arrhythmias): Atrial symptoms
Premature atrial contraction, atrial flutter, atrial fibrillation
- most common
Cardiac Dysrhythmias (Arrhythmias): Atrioventricular
Heart blocks
- 1st degree, 2nd degree, 3rd degree
Cardiac Dysrhythmias (Arrhythmias): Ventricular
Bundle branch block, ventricular tachycardia, ventricular fibrillation, premature ventricular contractions
Cardiac Dysrhythmias (Arrhythmias): Asystole
Cardiac arrest
- no conduction, flat ECG
- immediate loss of consciousness
Cardiac Dysrhythmias (Arrhythmias): treatment
Determine cause
- fix electrolyte imbalance
- drug therapy changes (i.e., change drug dose of certain medication)
- antiarrhythmic / antidysrhythmic drugs
- pace maker
What are examples of anti-arrhythmic drugs
Beta-adrenergic blockers
Calcium channel blockers
Digoxin
In what type of arrhythmia would a defibrillator placement be useful for
Ventricular fibrillation
What arrhythmia’s require pacemaker
SA nodal problems
CHF: what is it?
Heart is unable to pump sufficient blood to meet metabolic demands of the body
Usually a complication fo another cardiopulmonary condition
CHF how does it happen in the heart?
One side usually fails first and the other side follows
- left sided CHF / right sided CHF
CHF: what happens when the heart cannot maintain pumping capability
Cardiac output (stroke volume) decreases
Backup and congestion develop as coronary demands for O2 and glucose are not met
- output from ventricle is less than the inflow of blood
- congestion in venous circulation draining into the affected side of the heart
CHF: s/s
Forward effects (similar with failure on either side)
- decreased blood supply to tissues (general hypoxia)
- fatigue and weakness
- dyspnea and SOB
- decreased cell function
- mild acidosis develops
CHF: compensation mechanisms
Tachycardia Cutaneous and visceral vasoconstriction Daytime oliguria (low urine output)
CHF: Left-sided failure s/s
Dyspnea and orthopnea
- develop as fluid accumulates in the lungs
Cough
- d/t fluid irritating the respiratory passages
Paroxysmal nocturnal dyspnea
- indicates the presence of acute pulmonary edema
- usually develops during sleep
- excess fluid in lungs frequently leads to infections such as pneumonia
CHF: left sided failure is related to what?
Pulmonary congestion
CHF: right-sided failure is dependent on what
Edema in feet, legs, or buttocks
CHF: Right-sided failure s/s
- increased pressure in jugular veins —> distention
- hepatomegaly and splenomegaly —> digestive disturbances
- ascites (accumulation of fluid in peritoneal cavities; marked abdominal distention)
Acute right-sided failure: flushed face, distended neck veins, headache, visual disturbances
CHF: diagnostics
X-Ray —> shows cardiomegaly or fluid in lungs
Cardiac catheterization —> measures pressures in circulation
ABG (arterial blood gases) —> measures hypoxia
CHF: treatment
Treat underlying problem
Reduce workload of heart
Preventative measures (flu shot, pneumonia, vaccine)
Cardiac support (drug therapy)
Congenital Heart Defects (CHD): cardiac anomalies
Structural defects in the heart that develop during the first 8 weeks of embryonic life
Congenital Heart Defects (CHD): congenital heart disease
Valvular defects
Septal defects
Detected by the presence of heart murmurs
If untreated, child may develop heart failure
Congenital Heart Defects (CHD) may be what
Cyanotic or acyanotic, depending on the direction of shunting
Congenital Heart Defects (CHD): s/s
Pallor, Tachycardia, Dyspnea on exertion
Squatting position (toddlers / children) - appears to modify blood flow, makes more comfortable
Clubbed fingers
Intolerance for exercise and exposure to cold weather
Delayed growth and development
Congenital Heart Defects (CHD): diagnostics
Severe are often diagnosed at birth/in utero, others may not be detected for some time (I.e., murmur caught on assessment)
Congenital Heart Defects (CHD): examination techniques
Radiography Diagnostic imaging Cardiac catheterization Echocardiography Electrocardiography
Congenital Heart Defects (CHD): treatment
Surgical and medical
Rheumatic fever —> rheumatic heart disease: what is it and what does it involved?
Acute systemic inflammatory condition; abnormal immune function
- involved heart and joints
Rheumatic fever —> rheumatic heart disease: when can it occur
A. A few weeks after an untreated infection (usually group A beta-hemolytic Streptococcus)
— abnormal immune function
B. In children ages 5-15 y/o
Rheumatic fever —> rheumatic heart disease: long term effects
Rheumatic heart disease
May be complicated by infective endocarditis and heart failure in older adults
Rheumatic fever —> rheumatic heart disease: Acute stage
Pericarditis, myocarditis, endocarditis and incompetent heart valves
Rheumatic fever —> rheumatic heart disease: other sites of infection
Large joints, erythema marginatum, non-tender subcutaneous nodules, involuntary jerky movements of the face, arms and legs
Rheumatic fever —> rheumatic heart disease: s/s
Low grade fever Leukocytosis Malaise Anorexia Fatigue Tachycardia Murmur Epistaxis Abdominal pain
rheumatic heart disease: diagnostics
Elevated serum antibody levels
Heart function test
Electrocardiography
Antibody titer
rheumatic heart disease: treatment
Prophylactic antibacterial agents
Anti inflammatory agents
Subacute Infective Endocarditis
Defective heart valves invaded by Streptococcus viridans, normal flora
Acute Infective Endocarditis
Normal heart valves attacked by harmful organisms (I.e., staphylococcus)
- severe tissue damage
- difficult to treat
Subacute and Acute infective endocarditis: basic effects
Same regardless of organism
Subacute and Acute infective endocarditis: predispositions
Abnormal heart valves
Bacteremia
Reduced host defenses
Infective Endocarditis: s/s (overall for both types)
Low-grade fever, fever, fatigue
Anorexia, splenomegaly, CHF
Infective Endocarditis: subacute s/s
Insidious onset - increasing fatigue, anorexia, cough and dyspnea
Infective Endocarditis: Acute s/s
Sudden, marked onset - spiking fever, chills, drowsiness
Infective Endocarditis: diagnostics
Blood culture
Murmur
Transesophageal echo
Infective Endocarditis: treatment
Antimicrobial
Drug therapy to promote heart function
Pericarditis is usually what
Secondary to another condition classified by cause or type of exudate
Acute Pericarditis: what is it and what happens?
Simple inflammation of pericardium
- may be secondary
Effusion may develop
- large volume of fluid accumulates in pericardial sac
- leads to distended neck veins, faint heart sounds, pulsus paradoxus
Chronic Pericarditis: what is it?
Results from the formation of adhesions between the pericardial membranes
Chronic Pericarditis: what happens?
Limiting movement of the heart during systole —> reduced cardiac output
— inflammation or infection may develop from adjacent structurea
Chronic Pericarditis: s/s and cause
Fatigue, weakness, abdominal discomfort
Caused by systemic venous congestion
Pericarditis: general s/s
Tachycardia Chest pain Dyspnea Friction rub Distended neck veins Faint heart sounds Pulsus paradoxus (systole pressure drop by 10) Fatigue weakness abdominal discomfort
Pericarditis: treatment
Treat primary cause
How might you be able to diagnose Pericarditis
Fluid aspiration
Secondary hypertension
Results from renal, endocrine, or pheochromocytoma of adrenal medulla or SNS chain of ganglia
Secondary hypertension treatment
Treat underlying problem
Malignant hypertension
Hypertensive emergency
- extremely high
- organ damage
- CNS and renal system damage
Primary hypertension: cause
Idiopathic
Primary hypertension: values
140/90
Primary hypertension is what
Increase in arteriolar vasoconstriction
Primary hypertension: how does diastolic value increase (what causes it to increase)
**diastolic pressure indicates the degree of peripheral resistance and increased workload of left ventricle
There is an increase in arteriolar vasoconstriction
Decrease in diameter of arterioles - major cause in peripheral resistance - reduced capacity of system - increases diastolic pressure
Vasoconstriction leads to decreased blood flow through the kidneys - leads to increased renin, angiotensin, and aldosterone - leads to increased vasoconstriction further increasing BP
Primary hypertension: long term effects
Damage to arterial walls
- sclerotic (hard and thick) narrowing of the lumen —> can form aneurysm or reduced blood flow
Primary hypertension: areas frequently damaged
Kidneys, brain and retina
Retina: easily observed for sclerotic changes and rupture
Chronic Primary hypertension can lead to what?
Chronic renal failure Stroke d/t hemorrhage Loss of vision CHF Decreased life span
Primary hypertension: s/s
Asymptomatic early stage
Fatigue, malaise, morning headache
Primary hypertension: treatment
Lifestyle changes (decrease Na intake, weight, stress, fitness) Drug therapy (diuretics, ACE inhibitors, combination drugs)
Primary hypertension: compliance to treatment
Compliance is hard d/t lack of s/s
Primary hypertension: prognosis
Depends on treating underlying cause and constant control / compliance of treatments
Peripheral vascular disease is a what
Arterial disorder
Peripheral Vascular Disease: what is it
Disease in arteries outside the heart
Peripheral Vascular Disease: increased incidence with what
Diabetes
Peripheral Vascular Disease: common sites
Abdominal aorta
Carotid arteries
Femoral arteries
Iliac arteries
Peripheral Vascular Disease: diagnostic tests
Doppler studies and arteriography
Plethysmography - measures the size of the limbs and blood volume in organs/tissues
Peripheral Vascular Disease: s/s
Weakness of legs Intermittent claudication (leg pain) Associated with exercise Sensory impairment Weak peripheral pulses Skin: pallor/cyanotic, dry, hairless, toenails thick and hard
Peripheral Vascular Disease: treatment
- control BG
- control BMI
- reduce cholesterol level
- platelet inhibitors
- anticoagulant meds
- stop smoking
- exercise
- maintain dependent position for legs
- peripheral vasodilators
- observe skin for breakdown and treat prompts
Peripheral Vascular Disease: what is something to keep in mind with the skin
Increased risk for ulcers or delayed healing (lack of blood flow)
If gangrene develops, amputation is required
Aortic Aneurism is what
Arterial disorder
Aortic Aneurism
Localized dilation and weakening of arterial wall
Aortic Aneurism: how does it develop
From a defect in the medial layer of the arterial wall
Aortic Aneurism: succular
Bulging wall on the side
Aortic Aneurism: fusiform
Circumferential dilation along a section of artery
Aortic Aneurism: dissecting aneurism
Develops when there is a tear in the intima of the wall and blood continues to dissect or separate tissues
Aortic Aneurism: etiology
Atherosclerosis Trauma Syphilis Infections Congenital defects
Aortic Aneurism: s/s
Bruit, pulse felt on abdomen
Usually asymptomatic until large or rupture
Bruit
Blowing sound heard on auscultation with stethoscope
Aortic Aneurism: what does rupture lead to
Moderate or severe bleeding, usually leading to severe hemorrhage or death
Aortic Aneurism: diagnostics
Ultra sound, radiography, CT, MRI
Aortic Aneurism: treatment
Maintain normal BP until surgical repair
Prevent stress, coughing, constipation, exertion
Varicose veins is what type of disorder
Venous disorder
Varicose Veins: what are they
Irregular, dilated, tortuous areas of superficial veins
Varicose Veins: predisposing factors
Genetics
Increased BMI
Parity
Weight lifting
Varicose Veins: in the legs (cause and appearance)
May develop from defect or weakness in vein walls or valves
Appear as irregular, purplish, bulging structures
Varicose Veins: treatment
Keep legs elevated, compression stockings
Avoid restricted clothing and crossing legs
Surgery
Thrombophlebitis is what type of disorder
Venous
Thrombophlebitis: what?
Development in inflamed vein (e.g., IV site)
Phlebothrombosis: what
Thrombus forms spontaneously without prior inflammation; attached loosely
Factors for thromus development
Stasis of blood or sluggish blood flow
Endothelial injury
Increased blood coagulability
Thrombophlebitis / Phlebothrombosis: s/s
Often unnoticed
Aching, burning, tenderness in affected legs
Systemic signs: fever, malaise, leukocytosis
Thrombophlebitis/Phlebothrombosis: complications
Pulmonary embolism:
- respiratory and cardiac complications
- sudden chest pain and shock
- life threatening
Thrombophlebitis/Phlebothrombosis: treatment
Exercise, elevate legs
Anticoagulant therapy
Surgical intervention
Hypovolemic Shock
Loss of circulating blood volume
Cardiogenic shock
Inability of heart to maintain cardiac output to circulation
Distributive, vasogenic, neurogenic, septic, anaphylactic shock
Changes in peripheral resistance leading to pooling of blood in the periphery
Shock: Compensation Mechanisms
- SNS and adrenal medulla stimulated
- increase HR, force of contraction, systemic vasoconstriction - Renin secretion
- increases vasoconstriction —> will decrease urine output - Increased ADH secretion
- will decrease urine output - Secretion of glucocorticoids
- Acidosis stimulates increased respiration
These are mechanisms to INCREASE BP
What happens with prolonged shock
Cell metabolism is diminished, waste is not removed, leads to lower pH
Shock: early s/s
Anxiety Tachycardia Pallor Light-headed Syncope Sweating Oliguria
Shock: complications
- Acute renal failure
- Shock lung (adult respiratory distress syndrome)
- Hepatic failure
- Paralytic ileus, stress or hemorrhage ulcers
- Infection / septicemia
- Disseminated intra-vascular coagulation
- Depressed cardiac function
Shock: Treatment
- Emergency treatment
- supine
- keep warm
- call for help
- administer o2
- determine underlying cause and treat it - Depends on cause/type of shock
- early stages of shock has good prognosis
- decompensated shock, mortality is increased, renal failure or DIC
