Cardiovascular Disease (not PVD) and the medical/surgical management of CVD Flashcards
Characteristics of atherosclerosis
- lipid-laden plaques (lesions) affecting mod-lg size arteries
- thickening and narrowing of the intimal layer of blood vessels
- focal accumulation of lipids, platelets, monocytes, plaque, and other debris
Cardiovascular Disease: Risk factors- list of non-modifiable risk factors
age
family history
race
gender
Cardiovascular Disease: Risk factors- specific info on age
men > 45
women > 55
Cardiovascular Disease: Risk factors- specific info on family history
- cardiac event in 1st degree male relative < 55 or 1st degree female relative < 65
- risk increases further w/ younger age of onset, number of events, and how close genealogically the relative is
Cardiovascular Disease: Risk factors- specific info on race
African American
Cardiovascular Disease: Risk factors- specific info on gender
men > risk than pre-menopausal woman
after menopause risk is =
Cardiovascular Disease: Risk factors- list of modifiable risk factors
cholesterol diabetes diet hypertension obesity physical inactivity tobacco
Cardiovascular Disease: Risk factors- goals to reduce risk w/ cholesterol
- Total cholesterol <200 mg/dL
- LDL:<160mg/dL if at low risk for CVD, < 130 mg/dL if at mod risk for CVD, <100mg/dL if at high risk for CVD or have diabetes
- HDL > 40 mg/dL for men, > 50 mg/dL for women
- Triglycerides < 150 mg/dL
Cardiovascular Disease: Risk factors- goals to reduce risk w/ diabetes
HgA1C < 7%
Cardiovascular Disease: Risk factors- goals to reduce risk w/ hypertension
SBP <140 mmHg and DBP <90 mmHg
Cardiovascular Disease: Risk factors- goals to reduce risk w/ diet
low fat diet w/ balance of veggies, fruits, grains, and meats
Cardiovascular Disease: Risk factors- goals to reduce risk w/ obesity
- BMI 18.5 - 24.9 kg/m2
- waist for males < 40 in
- waist for females <35 in
Cardiovascular Disease: Risk factors- goals to reduce risk w/ physical inactivity
at least 30 min of activity 5-7 days/wk
Cardiovascular Disease: Risk factors- goals to reduce risk w/ tobacco
smoking cessation, regardless of time smoked, reduces risk
3 types of Acute Coronary Disease (ACD)
Angina pectoris Myocardial Infarction (MI) Heart Failure (HF)
General characteristics of ACD
- spectrum of clinical entities from angina to MI to sudden cardiac death
- imbalance of myocardial O2 supply and demand, causing ischemic chest pain
- may have no symptoms (more likely with diabetic) but present new pathologic Q wave on ECG
- subacute occlusions may have no symptoms
Angina Pectoris: What is Levine’s sign
pt. clutches fist over sternum
Angina Pectoris: general
- chest pain or pressure due to ischemia, may have levine’s sign
- imbalance in myocardial O2
- vasospasm (symptoms may be silent at rest)
Angina Pectoris: causes of myocardial O2 imbalances
exertion emotional stress smoking extremes of temp, especially cold overeating tachyarrhythmias
Angina Pectoris: 3 major types
stable angina
unstable angina
variant angina
Angina Pectoris: info about stable angina
- classic exertional angina occurring during exercise or activity
- occurs at predictable rate-pressure product (RPP = HRxBP)
- relieved w/ rest and/or nitroglycerin
Angina Pectoris: info about unstable angina pre-infarction, crescendo angina)
- coronary insufficiency w/out any precipitating factors or exertion
- chest pain increases w/ severity, frequency, and duration; refractory to treatment
- increased risk for MI or lethal arrhythmia
- pain is difficult to control
Angina Pectoris: inf about variant angina (Prinzmetal’s angina)
- caused by vasospasm of coronary arteries in the absence of occlusive disease
- responds well to nitroglycerin or calcium channel blocker long term
Angina Pectoris: symptoms in women
- sensation of discomfort
- crushing
- pressing
- bad ache
Angina Pectoris: general symptoms
- SOB
- fatigue
- diaphoresis
- weakness
Angina Pectoris: symptoms in older adults w/ atypical symptoms (absence of chest pain)
- dyspnea
- diaphoresis
- nausa and vomitting
- syncope
MI: what is it
prolonged ischemia , injury, and death of an area of the myocardium caused by occlusion of one or more coronary arteries
MI: precipitating factors
- atheroscleroic heart disease w/ thrombs formation
- coronary vasospasm
- embolism
- cocaine use
MI: 3 zones of infarction
- zone of infarction
- zone of injury
- zone of ischemia
MI: info about zone of infarction
consists of necrotic, non-contratcile tissue
electrically inert
on ECG- pathological Q waves
MI: info about zone of injury
area immediately adjacent to central zone
tissue is non-contratcile
cells undergoing metabolic changes
electronically unstable
on ECG- elevated ST segments over injured area
MI: info about zone of ischemia
outer area
cells undergoing metabolic changes
electronically unstable
on ECG- inverted T waves
MI: Infarction sites
transmural
non-transmural
MI: Infarction sites- transmural
full thickness of myocardium
often a ST elevated (STEMI) or Q wave MI
MI: Infarction sites- non-transmural
sub-endocardial, sub-epicardial, intramural infarctions
Non-St elevated MI (NSTEMI) or non Q-wave MI
MI: sites of coronary occlusion
- Inferior MI, R ventricle infarction, disturbances in upper conduction system: R coronary artery
- Lateral MI, ventricular ectopy: circumflex artery
- Anterior MI, disturbances of lower conduction system: L anterior descending artery
MI: what happens w/ impaired ventricular function
- decreased stroke volume, cardiac output, and ejection fraction
- increased end diastolic ventricular pressures
MI: What happens when there is electrical instability
arrhythmias, present in injured or ischemic areas
Heart Failure: general summary
clinical syndrome where heart is unable to maintain adequate circulation of blood to meet the metabolic needs of body
Heart Failure: 3 types
L sided heart failure (CHF)
R sided HF
Biventricular HF
Heart Failure: L sided heart failure (CHF)
characteriszed by:
-pulmonary congestion, edema, and low cardiac output due to back up of blood from L ventricle to L atrium
and lungs
-due to insult to L ventricle from myocardial disease
-excessive workload of heart ( HTN, valvular disease, and congenital defects)
- cardiac arrhythmias or heart damage
-
Heart Failure: R sided HF
characterized by:
- increased pressure load on R ventricle
- mitral valve disease
- chronic lung disease (cor pulmonale)
- hallmark signs are jugular vein distention and peripheral edema
Heart Failure: Biventricular HF
- severe LV pathology producing back up into the lungs
- Increased PA pressures
- RV signs of HF
Heart Failure: associated symptoms
muscle wasting
myopathies
osteoporosis
Heart Failure: s/s of pulmonary congestion - L ventricle failure
dyspnea, dry cough
orthopnea
paroxysmal nocturnal dyspnea (PND)
pulmonary rales, wheezing
Heart Failure: s/s of pulmonary congestion - R ventricle failure
dependent edema
weight gain
ascites
liver enlargement (hepatomegaly)
Heart Failure: s/s of low cardiac output - L ventricle failure
- hypotension
- tachycardia
- light headedness, dizziness
- cerebral hypoxia- irritability, restlessness, confusion, impaired memory, sleep disturbances
- fatigue, weakness
- poor exercise tolerance
- enlarged heart on x-ray
- S3 heart sound, possibly S4
- murmers of bi and/or tricuspid valve regurgitation
Heart Failure: s/s of low cardiac output - R ventricle failure
-anorexia, nausea, bloating
-cyanosis (nail beds)
-R upper quadrant pain
-jugular vein distention
-R S3 heart sounds
murmers of pulmonary or tricuspid insufficiency
Heart Failure: what is HF compensation and how is this done
- heart returns to functional status w/ reduced CO and exercise tolerance
- Physiologic compensatory mechanisms are SNS stimulation, LV hypertrophy, anaerobic metabolism, cardiac dilation, arterial vasoconstriction
- medical therapy used to assist compensation
Heart Failure: cause for sudden death
significant ischemia or ventricular arrhythmia
Medications: list of medications used for management of CVD
ACE inhibitors Angiotension II receptor blockers Nitrates Beta-adrenergic blocking agents Calcium channel blocking agents Antiarrhythmics Digitalis Diuretics Aspirin Tranquilizers Hypolipidemic agents
Medications: ACE inhibitors
- inhibit conversion of Angiotension 1 to Angiotension 2
- decreases sodium retention and peripheral vasoconstriction in order to decrease BP
EX: Captopril (Capoten), Enalopril (Vasotec), Lisinopril (Zestril)
Medications: Angiotension II receptor blockers
- blocks binder of angiotension 2 at the tissue/smooth muscle level, decreasing BP
Ex: Losatan (Cozaar)
Medications: Nitrates
- decrease preload through peripheral vasodilation
- reduce myocardial O2 demand
- dilate coronary arteries & improve coronary blood flow
Ex: Nitroglycerin
Medications: Beta-adrenergic blocking agents
- Reduce myocardial demand by reducing HR and contractility
- control arrhythmias and chest pain
- reduce BP
Ex: Atenolol (Tenormin), Metoprolol (Lopressor), Propranolol (Inderal)
Medications: Calcium channel blocking agents
- inhibit flow of calcium ions
- decrease HR
- decrease contractility
- dilate coronary arteries
- reduce BP
- control arrhythmias and chest pain
Ex: Diltiazem ( Cardizem), Amlodipine (Norvasc)
Medications: Antiarrhythmics
- alter conductivity
- restore normal heart rhythm
- control arrhythmias
- improve CO
Ex: Quinidine, Procainamide
Medications: Digitalis
- increases contractility and decreases HR
- mainstay in the treatment of CHF
Ex: Digoxin
Medications: Diuretics
- decrease myocardial work (reduce preload and afterload)
- control HTN
Ex: Furosemide (Lasix), Hydrochlorothiazide (Esidrix)
Medications: Aspirin
- decreases platelet aggregation
- may prevent MI
Medications: Tranquilizers
decreases anxiety, sympathetic effects
Medications: Hypolipidemic agents
- reduce serum lipid levels when diet and weight reduction are not effective
Ex: Cholestyramine (Questran), Covastatin ( Mevacor), Simvastin (Zocor)
Activity restrictions for acute MI
- Activity can be increased once acute MI has stopped (peak in cardiac troponin levels)
- Activity should be limited to 5 METs or 70% of age predicted HR max for 4-6 weeks following MI
Activity restrictions for Acute HF
- O2 demand should not be increased in pt.s in acute or decompensated HF
- Once medically managed and no longer display signs of acute decompensation, activity may be increased while monitoring hemodynamic response to activity.
List of surgeries for CVD
- Percutaneous Transluminal Coronary Angioplasty (PTCA)
- Intravascular Stents
- Coronary Artery Bypass Graft (CABG)
- Transplantation
- Ventricular Assist Device
What’s up with the Percutaneous Transluminal Coronary Angioplasty (PTCA)
- Under fluoroscopy, surgical dilation of a blood vessel using a small balloon tipped catheter inflated inside the lumen
- Relieves obstructed blood flow in acute angina or acute MI
- Improves coronary blood flow, improves L ventricular function, and provide anginal relief
Tell me about Intravascular Stents
- an endoprosthesis (pliable wire mesh) implanted post-angioplasty to prevent re-stenosis and occlusion in coronary or peripheral arteries
- often coated w/ medication to prevent thrombosis
The what and why of the Coronary Artery Bypass Graft (CABG)
- surgical circumvention of the obstruction in the coronary artery using an anastomosing graft (saphenous vein, intermal mammary artery)
- multiple grafts may be necessary
- Improves coronary blood flow, improves L ventricular function, and provide anginal relief
Why resort to using Transplantation
used in end-stage myocardial disease such as cardiomyopathy, ischemic heart disease, and valvular heart disease
3 types of transplantation
heteroptics
orthotopic
heart and lung transplantation
What is heteroptic transplantation
involves leaving the natural heart and piggy- backing the donor heart
What is orthotopic transplantation
involves removing the diseased heart and replacing it with a donor heart
What is the heart and lung transplantation
involves removing both organs and replacing them with donor organs
Major problems post-transplantation
rejection
infection
complications of immunosuppressive therapy
Ventricular Assist Device. Go!
- implanted device (accessory pump) that improves tissue perfusion and maintains cardiogenic circulation
- used w/ severely involved patients such as cardiogenic shock unresponsive w/ meds, severe ventricular dysfunction
What is thrombolytic therapy
- given for acute MI
- meds activate body’s fibrinolytic system, disolve clot, and restore coronary blood flow
Ex: streptokinase, TPA, urokinase
