MID 2: CARDIO Flashcards

1
Q

Varicose veins

A
  • a vein in which blood has pooled, producing distended, tortuous and palpable vessels
  • blood moves towards the heart in one-way valves in the veins. When the valves become weakened or damaged, blood can collect in the veins. This causes the veins to become enlarged
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2
Q

Varicose veins: Caused by

A
  • trauma to the saphenous veins (a large, subcutaneous, superficial vein on the leg) results in damage to one or more valves
  • blood is not being moved back to heart- gravity is pulling it back down
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3
Q

Varicose veins: Risk factors

A
  • age
  • female gender
  • family history
  • obesity
  • pregnancy
  • DVT (deep vein thrombosis)
  • previous leg injury
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4
Q

Chronic venous insufficiency

A

inadequate venous return over a long period

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5
Q

Chronic venous insufficiency: Caused by

A
  • valvular incompetence
  • damages to venous due to trauma or previous DVT
  • obesity
  • high pressure in venous over a long period (due to sitting or standing for long periods, pregnancy)
  • family history
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6
Q

Chronic venous insufficiency: Risk factors

A
  • sitting or standing for long periods
  • lack of exercise
  • smoking
  • history of DVT
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7
Q

Chronic venous insufficiency: Manifestations

A
  • edema to lower extremities- can extend to knees
  • hyperpigmentation of skin of feet and ankles (brown-coloured skin, often near the ankles)
  • tight feelings in your calves or itchy
  • pain when walking that stops when you rest
  • varicose veins
  • painful leg cramps or muscle spasms
  • venous stasis ulcers which might be hard to treat
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8
Q

Thromboembolus (DVT)

A
  • thrombus: blood clot that remains attached to a vessel wall
  • thromboembolus: detached thrombus
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9
Q

Thromboembolus (DVT): Caused by

A
  • venous stasis (veins can not send the blood from your legs back to your heart)
  • venous endothelial damage
  • hypercoagulable states
  • orthopedic surgery/trauma
  • spinal cord injury
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10
Q

Thromboembolus (DVT): Manifestations

A
  • leg pain- starts in calf, cramping
  • red or discoloured skin on the leg
  • feeling of warmth on leg
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11
Q

Atherosclerosis

A
  • arteriosclerosis: abnormal thickening and hardening of the vessel walls
  • form of arteriosclerosis- thickening and hardening caused by accumulation of lipid-laden macrophages in the arterial wall
  • leading cause of cerebrovascular diseases and coronary artery disease
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12
Q

Atherosclerosis: Risk factors

A
  • consumption of high fat food and cholesterol causing increase in LDL (low density lipoprotein, “bad cholesterol”)
  • hypertension
  • smoking
  • obesity (inhibits the oxidation of LDL)
  • diabetes
  • hyperlipidemia
  • insulin resistance
  • infection
  • periodontal disease
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13
Q

Atherosclerosis: Manifestations

A
  • Partial vessel occlusion can result in transient ischemic events- when exercising or stress
  • As lesion becomes complicated- creation of a thrombosis may result in total obstruction of an artery → ischemia → significant pain and tissue infarction if tissues reperfusion is not done immediately
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14
Q

Hypertension

A
  • Consistent elevation of systemic arterial BP
  • Prevalence higher in those of African descent and in those with diabetes
  • Silent killer
  • Primary- no known cause (idiopathic); 92-95% of population
  • Secondary- caused by a systemic disease process that raises peripheral vascular resistance or cardiac output e.g. renal vascular or parenchymal disease, adrenal tumors; 5-8% of population
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15
Q

Hypertension: Risk factors (for primary hypertension)

A
  • High sodium intake
  • Natriuretic peptide abnormalities: substances made in the heart, high level of it seen in heart failure, involved in the long-term regulation of sodium and water balance, blood volume and arterial pressure, 2 major pathways of natriuretic peptide actions: (1) vasodilator effects, (2) renal effects that leads to natriuresis (sodium excretion) and diuresis
  • Inflammation
  • Obesity
  • Insulin resistance
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16
Q

Hypertension: White coat syndrome

A
  • Anxiety when in hospital
  • Temporary hypertension
  • Have patient take BP at home or an automated BP without a physician present
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17
Q

Hypotension

A
  • Can happen when there is one or a combination of the following factors: decrease in blood volume, vasodilation
  • Decrease in cardiac contractility
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18
Q

Hypotension: Caused by

A
  • Pregnancy, due to an increase in demand for blood from both mother and the growing fetus
  • Large amounts of blood loss through injury
  • Impaired circulation caused by heart attacks or faulty heart valves
  • Weakness and a state of shock that sometimes accompanies dehydration
  • Anaphylactic- a severe form of allergic reaction
  • Infections of the bloodstream
  • Endocrine disorders such as diabetes, adrenal insufficiency and thyroid disease
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19
Q

Hypotension: Manifestations

A
  • Fatigue
  • Lightheadedness
  • Dizziness
  • Nausea
  • Clammy skin
  • Depression
  • Loss of consciousness
  • Blurry vision
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20
Q

Orthostatic hypotension

A
  • On moving from sitting to standing, or from lying down to standing, gravity acts on the vascular system which reduces the volume of blood returning to the heart and blood pools in the leg. The lower venous return reduces the volume of blood that is available to pump out of the heart, which causes a drop in cardiac output and a momentary drop in BP
  • Normal compensation for position changes: decrease in intrathoracic pressure causes stimulation of baroreceptor- increase heart rate through increase the sympathetic outflow and decrease the parasympathetic outflow, closure of valves in venous system causes maintaining more blood in right heart, contraction of leg muscles causes more blood return to heart
  • Reflex mechanisms are inadequate
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21
Q

Aneurysm

A
  • Dilation or outpouching of a vessel wall
  • True aneurysm- all 3 layers of the arterial wall
  • False aneurysm- occurs when a blood vessel wall is injured and the leaking blood collects in the surrounding tissue leading to an extravascular hematoma
  • Dissecting aneurysm- splits the vessel wall along the length of the vessel
  • Most common types of aneurysm: abdominal aortic aneurysm (AAA) and thoracic aortic aneurysm (TAA)
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22
Q

Aneurysm: Risk factors

A
  • Genetic and environmental
  • Smoking and diet- aortic aneurysms
  • Atherosclerosis plaque erodes the vessel wall
  • Hypertension contributes to increases stress of vessel wall
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23
Q

Aneurysm: Manifestations

A
  • Depends on location
  • Can be asymptomatic until they rupture- then severe pain and hypotension
  • Thoracic- dysphagia, dyspnea- bulge affects surrounding tissue
  • Femoral aneurysm- if it affects circulation- ischemia to lower limbs
  • Cerebral- increased ICP- signs of stroke
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24
Q

Embolism: Caused by

A
  • Dislodged thrombus
  • Bolus of air- IV lines, chest trauma
  • Amniotic fluid forced in to bloodstream by intra-abdominal pressure during delivery
  • Trauma of the long bones
  • Subacute bacterial endocarditis or abscess
  • Foreign body introduced through IV or arterial lines
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25
Q

Embolism: Manifestations

A
  • Ischemia or infection in tissue distal to obstruction→ organ dysfunction and pain
  • Life threatening depending on location: In coronary artery → causes MI, Cerebral artery → causes stroke, Pulmonary artery → causes pulmonary emboli
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26
Q

Peripheral vascular disease

A
  • Atherosclerotic disease of arteries in limbs
  • Gradual- pain with ambulation
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27
Q

Intermittent claudication

A

Muscle pain- Normally pain free but with increase activity the vessels cannot handle the increased blood flow required by the body

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28
Q

Buerger’s disease

A
  • Formation of thrombus in peripheral arteries
  • Associated with smoking, stroke and joint pain
  • Permanent occlusion causes collateral vessels to develop but are inadequate- not quick enough, lower blood volume
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29
Q

Buerger’s disease: Diagnosis

A
  • <45 years of age
  • Smoker
  • Evidence of peripheral ischemia
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30
Q

Reynaud phenomenon disease

A
  • Attacks of vasospasm in the small arteries and arterioles of fingers (less common toes)
  • Primary- vasospastic disorder with unknown origin
  • Secondary- associated with systemic diseases e.g. lupus
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31
Q

Reynaud phenomenon disease: Diagnosis

A
  • Vasospastic attacks
  • Change in skin colour and sensation
  • Causes pallor, numbness, sensation of coldness
32
Q

Coronary artery disease: Modifiable risk factors

A
  • Dyslipidemia: Low-density lipoproteins (LDL) need to stay low and high density lipoproteins (HDL) need to stay high, cholesterol in arteries, uncontrolled hypertension, stress
  • hypertension
  • Cig smoking: Generating free radicals, contributes to atherogenesis- formation of fatty plaques
  • Diabetes mellitus: Insulin will not work properly, increase inflammation and thrombosis, damage to endothelium and thickening of vessel walls
  • Obesity and sedentary lifestyle
  • Atherogenic diet: High in protein, cholesterol and saturated fats , Low fruit and vegetables
33
Q

Coronary artery disease: Non-modifiable risk factors

A
  • age
  • gender: Assigned male at birth are at greater risk, after menopause- women increased risk
  • family history: genetics
34
Q

Myocardial ischemia: Diagnosis

A
  • Increased heart rate
  • ECG- needs to be done with patient is exercising
  • Extra heart sounds- gallops or murmurs
  • Impaired left ventricular function (echocardiography)
  • Symptoms of pulmonary congestion (SOB, wheezing, dyspnea)- left-sided heart failure
  • Normal heart electric cycle
35
Q

Angina

A
  • Substernal chest discomfort
  • Sensation of heaviness or pressure
  • May radiate to neck, lower jaw, left arm and shoulder
  • Pallor, diaphoresis, dyspnea
  • Women- atypical chest pain
36
Q

Stable angina

A
  • Vessels coated with plaque- stiff and full
  • If they relax and destress to open up vessels it can go away
  • When increasing demand or stressed
  • Chronic coronary obstruction
  • Gradual narrowing- stable plaques
  • Activated by physical exertion or stress- narrowing does not allow enough coronary blood flow
37
Q

Stable angina: Manifestations

A
  • Substernal chest discomfort
  • Pain due to ischemia is when body use anaerobic metabolism and build up of lactic acid
38
Q

Stable angina: Risk factors

A
  • Uncontrolled diabetes, dyslipidemia, obesity
  • Hypertension
  • Increased LDLs (low density lipoproteins)
  • Decreased HDLs (high density lipoproteins)
  • Sedentary lifestyle
  • High BMI
  • Genetics
39
Q

Unstable angina

A
  • Unpredictable
  • Not totally blocking off artery- but potential could and then become a myocardial infarct
  • Can occur at rest
40
Q

Prinzmetal angina

A
  • E.g. cocaine users
  • Not predictable, can occur at rest (at night)
  • Does not progress to heart attack (benign condition)
  • Not from blockage but from spasm
  • Vasospasm of coronary arteries with or without atherosclerosis
  • Decreased vagal activity, hyperactivity of the SNS
  • Can cause dysrhythmias
  • Treated with long-term medication - calcium channel blockers
41
Q

Silent angina

A
  • Asymptomatic- does not present as typical angina (do not sense having it)
  • Common in people with diabetes
42
Q

Silent ischemia

A
  • Not typical symptoms
  • Increased risk for cardiac event- because not feeling/seeing the warning signs
43
Q

Silent ischemia: Caused by

A
  • Diabetes mellitus
  • Surgical denervation during CABG
  • Cardiac transplant
  • Previous MI- local nerve injury
  • Mental stress
44
Q

Silent ischemia: Manifestations

A
  • Fatigue
  • Dyspnea
  • Feeling of unease
45
Q

Myocardial infarct (MI)

A
  • Cardiac cells can withstand ischemic conditions for about 20 minutes before hypoxic injury causes cellular death and tissue necrosis
  • Prolonged ischemia causing irreversible damage to the heart muscle
  • Clot remains, vessel occluded for longer period of time
  • MI involves the left ventricle → pulmonary venous congestion
  • MI involves the right ventricle → increase in system venous pressures
46
Q

MI: Diagnosis

A
  • History exam
  • ECG results
  • Troponin levels- Troponin I and Troponin T
47
Q

Non-STEMI

A
  • Damage is limited to myocardium directly below the endocardium
  • ST wave depression and T wave inversion
48
Q

STEMI

A
  • Damage extends from endocardium to epicardium
  • ST elevation
  • Risk for serious complications
49
Q

Cardiomyopathies

A
  • Disease of the heart muscle that makes it harder for your heart to pump blood to the rest of your body
  • Dilated, hypertrophic, or restrictive
50
Q

Dilated cardiomyopathy

A
  • Ischemic heart disease
  • Impaired systolic function leads to increased intracardiac volume
  • Ventricular dilation
  • Reduced ejection fraction
51
Q

Hypertrophic cardiomyopathy

A
  • Thickening of septal wall
  • Muscle used too much, swollen too much
52
Q

Restrictive cardiomyopathy

A
  • Condition where the chambers of the heart become stiff over time
  • Though the heart is able to squeeze well, it is not able to relax between beats normally
53
Q

Cardiomyopathies: Caused by

A
  • Viral infection
  • Ischemia
  • Hypertension
  • May be idiopathic (cause unknown)
54
Q

Myocarditis

A
  • Inflammation of heart muscle (myocardium)
  • Usually caused by a viral infection
  • Can affect muscle and electrical system
  • Abnormal heart rhythms (arrhythmias)
55
Q

Valve dysfunction

A
  • Stenosis (valve not opening → pulmonary edema, cyanosis) or regurgitation of all your heart valves
  • Aortic or mitral regurgitation- inability of aortic valve to close properly or prolapse of mitral valve
  • Aortic stenosis- valve between left ventricle
  • Mitral stenosis- valve between left atria and left ventricle, most common in rheumatic heart disease
56
Q

Heart failure

A
  • Compensation mechanisms for decreased CO in cases of congestive heart failure include increased renin and aldosterone secretions
  • Unable to generate an adequate cardiac output
57
Q

Heart failure: Risk factors

A
  • Ischemic heart disease and hypertension
  • Valvular heart disease
  • Cardiomyopathies
  • Myocarditis
  • Congenital heart disease
  • Renal failure
  • Age
  • Obesity
  • Diabetes
  • Excessive alcohol use
58
Q

Left-sided heart failure

A
  • Heart failure with decreased ejection fraction
  • Ejection fraction < 40% - inability for the heart to perfuse tissues
  • Contractility is decreased- can happen in a MI, myocarditis, cardiomyopathies → stroke volume falling down and left ventricular end-diastolic volume increases (LVEDV) → stretching of the myocardium → dysfunction and decreased contractility
  • Sometimes it starts with increased afterload as a result of increased peripheral vascular resistance- seen with hypertension
  • Medications- interrupt the cycle (of decreasing contractility, increasing preload and increasing afterload → worsening of symptoms)
  • Pulmonary issues → lead to right ventricular failure= systemic issues
59
Q

Right-sided heart failure

A
  • Unable to pump blood effectively to the lungs, back of fluid in the vena cava- backed up into circulation
  • Can be acute or chronic
  • Caused by pulmonary hypertension
  • Can be caused by left ventricular failure
  • Symptoms depend on cause
  • Occurs without left ventricular failure in COPD cystic fibrosis
  • Pressure will rise in the systemic venous circulation → peripheral edema and hepatosplenomegaly
  • Systemic issues
60
Q

Shock

A
  • 3 types: hypovolemic, cardiogenic, distributive (neurogenic, septic and anaphylactic are distributive)
  • All cause vasodilation
  • All lead to impaired cellular metabolism
61
Q

Hypovolemic shock

A
  • Insufficient intravascular fluid volume (decreased by 15%)
  • Loss of whole blood- hemorrhage*- severe bleeding
  • Loss of plasma -burns
  • Loss of interstitial fluid- diarrhea, diuresis (diabetes insipidus), emesis
  • Low CO→ boosts cardiac output and tissue perfusion pressures
  • Liver and spleen release stored RBC and plasma
  • Aldosterone release- retention of sodium and water, ADH increases water retention (activation of RAAS)
  • As condition continues- compensation starts to fail
62
Q

Hypovolemic Shock: Manifestations

A
  • Mental status deterioration
  • Rapid and thready pulse but decreased BP
  • High systemic vascular resistance (trying to keep low volume central, thirst, oliguria, cold gray skin)
63
Q

Cardiogenic Shock

A
  • Heart failure
  • Caused by myocardial dysfunction resulting in reduced CO and inadequate tissue perfusion
  • Decreased cardiac contractility and low cardiac output
  • Tissue hypoxia
  • Not able to pump blood out to body
64
Q

Cardiogenic shock: Caused by

A
  • Myocardial infarct- most common
  • Congenital heart anomalies
  • Cardiomyopathy
  • Myocarditis
  • Arrhythmias
  • Drug toxicity
65
Q

Cardiogenic shock: Manifestations

A
  • Widespread impairment of cellular metabolism
  • Dyspnea
  • Tachypnea
  • Venous and pulmonary edema
  • Dusky skin color
  • Hypotension
  • Oliguria (scanty/low urine)
  • Ileus (lack of movement in bowel)
66
Q

Neurogenic shock

A
  • Neural alteration of vascular smooth muscle tone
  • Caused by any factor that could stimulate parasympathetic or inhibits sympathetic stimulation of smooth muscle (damage/trauma to the spinal above the level of the 6th thoracic vertebra)
  • Widespread vasodilation
  • Overstimulation of parasympathetic
  • Under stimulation of sympathetic
  • Loss of muscular tone= relative hypovolemia
67
Q

Septic shock

A
  • Infection → bacteremia (bacteria in blood) → systemic inflammatory response syndrome- sepsis → severe sepsis (organ dysfunction) → septic shock → multiple organ dysfunction syndrome (altered organ function)- homeostasis cannot be maintained without intervention
  • Infectious organisms cause systemic inflammation, initiating a cascade of physiological responses- inflammatory mediators (cytokines), prostaglandins, nitric oxide → vasodilation, increased capillary permeability, microvascular thrombosis → DIC (disseminated intravascular coagulation), myocardial dysfunction and reduced CO
  • Tissue perfusion is inadequate
  • Relative or absolute adrenal insufficiency may develop, contributing to reduced SVR (systemic vascular resistance)
68
Q

Septic shock: Caused by

A
  • CA (community acquired) infections or HCA infections
  • Bacteria, fungus, virus
69
Q

Septic shock: Risk factors

A
  • Genetics
  • Chronic diseases
  • Immune deficiency state
70
Q

Anaphylactic shock

A
  • Immunological process
  • Severe reaction to an allergen causing an acute multisystem allergic reaction
  • Causes arterial and venous vasodilation, increased capillary permeability and pulmonary vasoconstriction → increased right ventricular afterload, reduce pulmonary blood flow, decrease left ventricular preload, reduce CO
  • Widespread hypersensitivity
  • Exposure to antigen
  • Immune and inflammatory response
  • Sudden onset- death imminent without intervention
71
Q

Anaphylactic shock: Manifestations

A
  • Anxiety
  • Dizziness
  • Difficulty breathing
  • Stridor(narrowing of airways)
  • Wheezing
  • pruritus(itching) with hives
  • Swollen lips and tongue
  • Abdominal cramping
72
Q

Congenital heart defects

A

In utero pressure of right and left sides of heart are equal- after birth- left side pressure increases closing the openings that are there to shunt blood flow from right to left for fetal circulation

73
Q

Ventricular septal defect (VSD)

A
  • Blood can travel across the hole from the left pumping chamber (left ventricle) to the right pumping chamber (right ventricle) and out into the lung arteries
  • If the VSD is large, the extra blood being pumped into the lung arteries makes the heart and lungs work harder and the lungs can become congested (high pressure in lungs)
  • Most common defect
  • Small VSDs= loud murmur, may close on their own
  • Large VSDs= pulmonary artery banding, relieve pressure and blood flow to the lungs, when older can have open heart surgery to close the hole
74
Q

Atrial septal defect (ASD)

A
  • Asymptomatic
  • Pulmonary over circulation and slow growth
  • Right ventricle becomes less compliant with age
  • May be closed surgically
75
Q

Patent ductus arteriosus

A
  • Failure of the fetal ductus arteriosus to close within 15 hours of birth
  • Ductus allows blood to detour away from the lungs before birth
  • Respirations- faster and harder than normal, audible murmur
  • Fatigue
  • Poor eating