Cardiology & Cardiovascular Disease
Disease of the arteries
Consistent elevation of systemic arterial blood pressure
Blood pressure= systolic/diastolic
Systolic= force/contraction 100-120mmHg
Diastolic= relaxation 60-80 mmHg
High bp → obstruction OR greater pressure when pumping
Common disorder that impacts 25% of the population; leads to major risk of atherosclerosis, CHF, and renal failure
Hypertensive bp → 130/80 or greater
2 types of HT: Primary/Essential HT or Secondary HT
Blood Pressure Category | Systolic (mmHg) | Diastolic (mmHg) |
---|---|---|
Normal | < 120 | < 80 |
Elevated (Pre-hypertension) | 120-129 | < 80 |
High blood pressure STAGE 1 | 130-139 | 80-89 |
High blood pressure STAGE 2 | 140 > | 90 > |
Hypertensive crisis (emergent) | 180 > | 120 > |
MOST COMMON TYPE OF HT
Problems lie in the blood vessels
Genetic and environmental factors; but, don’t know where the problem lies in the gene defects; usually runs in the family
Affects 92-95% of individuals with HT
Increase in age → wear & tear of heart and blood vessels in age
Family history → cultural/lifestyle
Race/ethnicity → African Americans at highest risk for hypertension
Sex → males at higher risk
All are ESSENTIAL, cannot be changed
High sodium intake → diet, H2O follows, increase in pressure
Inflammation
Obesity/weight gain
Insulin resistance
The 3 go hand in hand, diabetes and hypertension are usually seen together
Dyslipidemia → high cholesterol
Alcohol, smoking, prolonged/current stress → all cause vasoconstriction -
ASYMPTOMATIC, NO SYMPTOMS
Non-specific fatigue
Malaise
The body adapts
CBC
Kidney panel (BUN/creatinine)
Lipid profile
Urinalysis
EKG
ECG
With patients, you would measure a first time, have them come in again and measure again, and then make them come in a final time for 3 measurements in order to rule out hypertension; NEVER treat upon first reading
CONSERVATIVE = reducing the risks
Lifestyle changes
Low sodium diet
Weight reduction
Exercise
Decrease stress
Patient education
Medicines
Diuretics → African American community responds well to this treatment
ACE inhibitors
ARB
Calcium channel blockers
Beta blockers
HYPERTENSIVE CRISIS (malignant hypertension)
Retinopathy
Elevated BP
Nephrosclerosis
CHF, atherosclerosis, angina, MI
CVA
RAPIDLY PROGRESSES
180/>120
Life-threatening with organ damage
Don’t respond to medications
If they do survive, can lead to dialysis or coma
Systemic disease that raises peripheral vascular resistance or cardiac output
UNCOMMON
Usually caused by something else (ex: sleep apnea, renal artery stenosis, hypothyroidism)
Caused by atherosclerosis
Blockage of blood flow
Narrowing of coronary arteries leads to myocardial ischemia → MI
Form of arteriosclerosis
Presence of atheroma (plaque) in the large arteries
Cause of atheromas = damage
When atheromas break, causes an embolism/thrombus which can lead to a MI
Fatty streak is #1 sign of atherosclerosis and CAN be reversed
Related to diet, exercise, and stress
Genetic abnormalities
Family Hx
Age
Males (females protected by estrogen until menopause)
Hyperlipidemia
Obesity
Sedentary lifestyle
Cigarette smoking
Diabetes
Inflammation
Local, temporary deprivation of the coronary blood supply (O2) to meet myocardial needs → chest pain
Blockage (thrombus/embolus)
Occurs in different patterns
Recurrent, intermittent brief episodes of substernal chest pain
Pressure, heaviness, squeezing, burning or choking sensation
Triggered by physical or emotional stress
Lasts 1-5 minutes, relieved by rest or nitroglycerin
No cell death or necrosis
Physical exam is often normal in findings
Angina is a warning sign of progression of disease
CBC
EKG
Stress test (treadmill/nuclear)
ECG
CT scan & angiography
Cath lab
Relieve symptoms, and slow progression of disease by reducing complications (stop smoking, treat risks)
Nitroglycerin → decreases the demand for O2, reduces systemic resistance
Ranolazine → anti-anginal
Unstable angina = 1 foot into the heart attack door
REVERSIBLE MI
Myocardial infarction (MI) → acute process that is sudden and extended obstruction of the myocardial blood supply which causes myocardial cell death
Reversible myocardial ischemia without necrosis
Angina at rest
More frequent/severe and prolonged
Changed from usual pattern of angina
Longer in duration
Lower in threshold
DOES NOT RESPOND TO NITRO
Only relieved with time
Requires aggressive treatment
Heart attack
Atherosclerosis most common cause
Thrombus from atheroma may obstruct artery; size and location determines damage
The irreversible death (necrosis) of heart muscle secondary to prolonged lack of O2 supply (ischemia)
Occurs when coronary artery is totally obstructed → necrosis
Severe chest pains
Intense lasting for 30-60 minutes
Radiating pain to neck, shoulder, jaw, and LEFT arm
Levine sign → clenched fist over the heart (seen mainly in women)
Epigastric → belly pain, not life threatening but MI can mask as belly pain
Nausea & vomiting from pain as a sympathetic response
Diaphoresis
Dyspnea → SOB
Fatigue & malaise
TROPONIN LEVELS
CK-MB isoenzymes if troponin test not an option
CBC
Comprehensive metabolic panel
Lipid profile
12 Lead EKG
ST segment depression, T wave inversion or ==ST segment elevation ==
ECG
CT/MRI (waste of time & $$)
Angiography
Oxygen therapy to reduce cardiac demand
Aspirin
Nitroglycerin → vasodilator
Morphine → relieves pain, lowers stress, vasodilates blood vessels which increases blood flow
ACE inhibitors
Beta blockers
Calcium channel blockers
Thrombolytic agents
Tissue plasminogen activator (once cleared for use)
Statins
Angioplasty & stents (only when troponin levels are not lowering)
Coronary artery bypass surgery
External counter pulsation (ECP)
Sudden death
Cardiogenic shock
CHF
Rupture of necrotic heart tissues/cardiac tamponade (increases mortality or CVA risk)
Thromboembolism causing a CVA w/LVMI
Vasospasms
Angina occurs at rest during sleep, and occurs in clusters
Does not develop during treadmill tests
No evidence of cardiac diseases or atherosclerotic heart disease
Occurs in younger people
More often seen in females than males
Reduced nitric oxide availability
Imbalance of sympathetic and parasympathetic systems
Increased alpha-adrenergic receptors activity
Nitroglycerin (acute attacks)
Calcium channel blockers (maintenance)
Inability of the heart to pump enough blood to meet the body’s needs → inadequate perfusion of tissues
Less filling of the heart (diastole)
Insufficient stroke volume (systole)
Can be left or right sided heart failure
Systolic dysfunction: inability to generate adequate cardiac output to perfuse tissues; EF <40%
Diastolic dysfunction: decreased compliance of left ventricle, abnormal relaxation
High output (other diseases cause heart to fail)
Both pumps fail = biventricular failure
Left sided HF = Lungs
CONGESTIVE HEART FAILURE (CHF)
Most common type of HF
Low cardiac output
Dyspnea (pulmonary congestion/edema)
“Left HF is a disease with symptoms”
Restlessness
Confusion
Orthopnea
Tachycardia
Exertional dyspnea
Fatigue
Cyanosis
Tachypnea
Blood-tinged sputum
Cough/crackles/wheezes
Paroxysmal nocturnal dyspnea
Right sided HF = Rest of the body
Most common cause is LEFT SIDED HF
Inability of the right ventricle to provide adequate blood flow at a normal venous pressure
“Right HF is a disease with signs”
Pedal edema
Fatigue
“Pitting” edemas
Ascites
Enlarged liver & spleen
Increased venous pressure
May be secondary to chronic pulmonary problems
Distended jugular
Weight gain
Anorexia/complaints of GI distress
Dependent edema
Normal heart function, something caused an increased demand, the heart can’t keep up
Inability of the heart to supply the body with nutrients, despite adequate blood volume and normal/elevated myocardial contractility
Causes include: severe anemia, hyperthyroidism, septicemia, and beriberi (B12 deficiency)
Cardiovascular system fails to perfuse tissues adequately
Manifestations often include feeling weak, cold, hot, nauseated, dizzy, confused, afraid, thirsty, SOB, hypotension, tachycardia, increased respiratory rate
Loss of blood or plasma
Blood vessels ⬇️
Blood pressure ⬇️
Heart workload ⬆️
Caused by hemorrhage, burns, dehydration, peritonitis, pancreatitis
Decreased pumping capability of the heart
Caused by MI of left ventricle, cardiac arrhythmia, pulmonary embolus
Vasodilation owing to loss of sympathetic and vasomotor tone
Caused by pain and fear, spinal cord injury, hypoglycemia (insulin shock)
Systemic vasodilation and increased permeability owing to severe allergic reaction
Caused by insect stings, drugs, nuts, and shellfish
Vasodilation owing to severe infection, often gram negative bacteria
Caused by virulent microorganisms or multiple infections
Disease of the arteries
Consistent elevation of systemic arterial blood pressure
Blood pressure= systolic/diastolic
Systolic= force/contraction 100-120mmHg
Diastolic= relaxation 60-80 mmHg
High bp → obstruction OR greater pressure when pumping
Common disorder that impacts 25% of the population; leads to major risk of atherosclerosis, CHF, and renal failure
Hypertensive bp → 130/80 or greater
2 types of HT: Primary/Essential HT or Secondary HT
Blood Pressure Category | Systolic (mmHg) | Diastolic (mmHg) |
---|---|---|
Normal | < 120 | < 80 |
Elevated (Pre-hypertension) | 120-129 | < 80 |
High blood pressure STAGE 1 | 130-139 | 80-89 |
High blood pressure STAGE 2 | 140 > | 90 > |
Hypertensive crisis (emergent) | 180 > | 120 > |
MOST COMMON TYPE OF HT
Problems lie in the blood vessels
Genetic and environmental factors; but, don’t know where the problem lies in the gene defects; usually runs in the family
Affects 92-95% of individuals with HT
Increase in age → wear & tear of heart and blood vessels in age
Family history → cultural/lifestyle
Race/ethnicity → African Americans at highest risk for hypertension
Sex → males at higher risk
All are ESSENTIAL, cannot be changed
High sodium intake → diet, H2O follows, increase in pressure
Inflammation
Obesity/weight gain
Insulin resistance
The 3 go hand in hand, diabetes and hypertension are usually seen together
Dyslipidemia → high cholesterol
Alcohol, smoking, prolonged/current stress → all cause vasoconstriction -
ASYMPTOMATIC, NO SYMPTOMS
Non-specific fatigue
Malaise
The body adapts
CBC
Kidney panel (BUN/creatinine)
Lipid profile
Urinalysis
EKG
ECG
With patients, you would measure a first time, have them come in again and measure again, and then make them come in a final time for 3 measurements in order to rule out hypertension; NEVER treat upon first reading
CONSERVATIVE = reducing the risks
Lifestyle changes
Low sodium diet
Weight reduction
Exercise
Decrease stress
Patient education
Medicines
Diuretics → African American community responds well to this treatment
ACE inhibitors
ARB
Calcium channel blockers
Beta blockers
HYPERTENSIVE CRISIS (malignant hypertension)
Retinopathy
Elevated BP
Nephrosclerosis
CHF, atherosclerosis, angina, MI
CVA
RAPIDLY PROGRESSES
180/>120
Life-threatening with organ damage
Don’t respond to medications
If they do survive, can lead to dialysis or coma
Systemic disease that raises peripheral vascular resistance or cardiac output
UNCOMMON
Usually caused by something else (ex: sleep apnea, renal artery stenosis, hypothyroidism)
Caused by atherosclerosis
Blockage of blood flow
Narrowing of coronary arteries leads to myocardial ischemia → MI
Form of arteriosclerosis
Presence of atheroma (plaque) in the large arteries
Cause of atheromas = damage
When atheromas break, causes an embolism/thrombus which can lead to a MI
Fatty streak is #1 sign of atherosclerosis and CAN be reversed
Related to diet, exercise, and stress
Genetic abnormalities
Family Hx
Age
Males (females protected by estrogen until menopause)
Hyperlipidemia
Obesity
Sedentary lifestyle
Cigarette smoking
Diabetes
Inflammation
Local, temporary deprivation of the coronary blood supply (O2) to meet myocardial needs → chest pain
Blockage (thrombus/embolus)
Occurs in different patterns
Recurrent, intermittent brief episodes of substernal chest pain
Pressure, heaviness, squeezing, burning or choking sensation
Triggered by physical or emotional stress
Lasts 1-5 minutes, relieved by rest or nitroglycerin
No cell death or necrosis
Physical exam is often normal in findings
Angina is a warning sign of progression of disease
CBC
EKG
Stress test (treadmill/nuclear)
ECG
CT scan & angiography
Cath lab
Relieve symptoms, and slow progression of disease by reducing complications (stop smoking, treat risks)
Nitroglycerin → decreases the demand for O2, reduces systemic resistance
Ranolazine → anti-anginal
Unstable angina = 1 foot into the heart attack door
REVERSIBLE MI
Myocardial infarction (MI) → acute process that is sudden and extended obstruction of the myocardial blood supply which causes myocardial cell death
Reversible myocardial ischemia without necrosis
Angina at rest
More frequent/severe and prolonged
Changed from usual pattern of angina
Longer in duration
Lower in threshold
DOES NOT RESPOND TO NITRO
Only relieved with time
Requires aggressive treatment
Heart attack
Atherosclerosis most common cause
Thrombus from atheroma may obstruct artery; size and location determines damage
The irreversible death (necrosis) of heart muscle secondary to prolonged lack of O2 supply (ischemia)
Occurs when coronary artery is totally obstructed → necrosis
Severe chest pains
Intense lasting for 30-60 minutes
Radiating pain to neck, shoulder, jaw, and LEFT arm
Levine sign → clenched fist over the heart (seen mainly in women)
Epigastric → belly pain, not life threatening but MI can mask as belly pain
Nausea & vomiting from pain as a sympathetic response
Diaphoresis
Dyspnea → SOB
Fatigue & malaise
TROPONIN LEVELS
CK-MB isoenzymes if troponin test not an option
CBC
Comprehensive metabolic panel
Lipid profile
12 Lead EKG
ST segment depression, T wave inversion or ==ST segment elevation ==
ECG
CT/MRI (waste of time & $$)
Angiography
Oxygen therapy to reduce cardiac demand
Aspirin
Nitroglycerin → vasodilator
Morphine → relieves pain, lowers stress, vasodilates blood vessels which increases blood flow
ACE inhibitors
Beta blockers
Calcium channel blockers
Thrombolytic agents
Tissue plasminogen activator (once cleared for use)
Statins
Angioplasty & stents (only when troponin levels are not lowering)
Coronary artery bypass surgery
External counter pulsation (ECP)
Sudden death
Cardiogenic shock
CHF
Rupture of necrotic heart tissues/cardiac tamponade (increases mortality or CVA risk)
Thromboembolism causing a CVA w/LVMI
Vasospasms
Angina occurs at rest during sleep, and occurs in clusters
Does not develop during treadmill tests
No evidence of cardiac diseases or atherosclerotic heart disease
Occurs in younger people
More often seen in females than males
Reduced nitric oxide availability
Imbalance of sympathetic and parasympathetic systems
Increased alpha-adrenergic receptors activity
Nitroglycerin (acute attacks)
Calcium channel blockers (maintenance)
Inability of the heart to pump enough blood to meet the body’s needs → inadequate perfusion of tissues
Less filling of the heart (diastole)
Insufficient stroke volume (systole)
Can be left or right sided heart failure
Systolic dysfunction: inability to generate adequate cardiac output to perfuse tissues; EF <40%
Diastolic dysfunction: decreased compliance of left ventricle, abnormal relaxation
High output (other diseases cause heart to fail)
Both pumps fail = biventricular failure
Left sided HF = Lungs
CONGESTIVE HEART FAILURE (CHF)
Most common type of HF
Low cardiac output
Dyspnea (pulmonary congestion/edema)
“Left HF is a disease with symptoms”
Restlessness
Confusion
Orthopnea
Tachycardia
Exertional dyspnea
Fatigue
Cyanosis
Tachypnea
Blood-tinged sputum
Cough/crackles/wheezes
Paroxysmal nocturnal dyspnea
Right sided HF = Rest of the body
Most common cause is LEFT SIDED HF
Inability of the right ventricle to provide adequate blood flow at a normal venous pressure
“Right HF is a disease with signs”
Pedal edema
Fatigue
“Pitting” edemas
Ascites
Enlarged liver & spleen
Increased venous pressure
May be secondary to chronic pulmonary problems
Distended jugular
Weight gain
Anorexia/complaints of GI distress
Dependent edema
Normal heart function, something caused an increased demand, the heart can’t keep up
Inability of the heart to supply the body with nutrients, despite adequate blood volume and normal/elevated myocardial contractility
Causes include: severe anemia, hyperthyroidism, septicemia, and beriberi (B12 deficiency)
Cardiovascular system fails to perfuse tissues adequately
Manifestations often include feeling weak, cold, hot, nauseated, dizzy, confused, afraid, thirsty, SOB, hypotension, tachycardia, increased respiratory rate
Loss of blood or plasma
Blood vessels ⬇️
Blood pressure ⬇️
Heart workload ⬆️
Caused by hemorrhage, burns, dehydration, peritonitis, pancreatitis
Decreased pumping capability of the heart
Caused by MI of left ventricle, cardiac arrhythmia, pulmonary embolus
Vasodilation owing to loss of sympathetic and vasomotor tone
Caused by pain and fear, spinal cord injury, hypoglycemia (insulin shock)
Systemic vasodilation and increased permeability owing to severe allergic reaction
Caused by insect stings, drugs, nuts, and shellfish
Vasodilation owing to severe infection, often gram negative bacteria
Caused by virulent microorganisms or multiple infections