Cardiovascular Flashcards
Cardiac Output
CO = HR x Stroke Volume
The amount of blood that leaves the heart within one minute
Normal = 4-8 L/min
Cardiac output compensation
HR increases if stroke volume decreases
Stroke volume increases if HR decreases
Stroke Volume
SV = preload + afterload + contractility
Normal = 60-100 ml/beat
Preload
The volume of blood in the ventricle at the end of the diastole (heart is relaxed)
Preload contributing factors
Total volume and venous tone and location of blood in the body
Things that DECREASE preload: hypovolemia, arrhythmia, loss of atrial kick, venous vasodilation
Things that INCREASE preload:
- Right heart: Left ventricle failure, mitral valve disease, aortic valve disease, cardiac tamponade/effusion, volume overload, decreased compliance
- Left heart: Right ventricle failure d/t ischemia, increased pulmonary vascular resistance, cardiac tamponade/effusion, volume overload, left ventricle failure
- R ventricle pressure 2-6 mmHg
- L ventricle pressure 4-12 mmHg
Afterload
The amount of resistance the left ventricle must overcome to get the blood into the circulatory system/to create systole
Increased afterload = increased work of heart = increased myocardial O2 demands
Afterload contributing factors
Arterial tone, arterial constriction vs. dilation
Things that DECREASE afterload: vasodilation, sepsis, vasodilator therapies
Things that INCREASE afterload:
- Right heart: pulmonary htn, hypoxemia, pulmonary stenosis
- Left heart: Vasoconstriction, vasopressors, hypothermia, aortic stenosis
Contractility
The heart’s ability to squeeze/pump independent of preload and afterload
- Elasticity of the heart muscle itself
Reflected through ejection fraction (Normal = 55-65%)
Contractility contributing factors
Ventricle size, myocardial fiber stretch/shortening ability, calcium availability
Things that DECREASE contractility: Parasympathetic stimulation (rest and digest), negative inotropic therapies (beta blockers and calcium channel blockers), metabolic states (hyperkalemia, MI, acidosis)
Things that INCREASE contractility: sympathetic NS stimulation (fight or flight), Inotropic therapies (epinephrine, dopamine, digoxin, calcium), metabolic states (hypercalcemia)
Chest Pain PQRST
P - pain (description, pain level, activity at onset)
Q - quality of pain
R - radiation/relief
S - severity of symptoms
T - time (when did it start and how long has it lasted)
MI clinical manifestations
Angina
EKG changes
Dyspnea
pulmonary edema
Diaphoresis + pallor
Palpitations
Hypo/Hypertension
Nausea + vomiting
Decreased UO
Neuro disturbances
MI medical management
Platelet aggregation inhibitors: Aspirin, Plavix, Effient
Anticoagulants: Heparin, Angiomax
Percutaneous coronary intervention (PCI)
Coronary angioplasty - a minimally invasive procedure that can be used to treat a heart attack or other coronary artery disease
PCI patient management
ST segment monitoring
BP < 150/90
Assess puncture site frequently
Immobilize affected extremity
Monitor for retroperitoneal hemorrhage
Neurovascular and pulse checks of affected extremity
Monitor for postural tachycardia and/or hypotension, back and/or flank pain
Cardiogenic shock after MI
Clinical indications
- Tachycardia, tachypnea, hypotension
- Cool/Clammy skin
- Lethargy/Confusion/AMS
- Low UO (signs of hypoperfusion)
- Diminished bowel sounds
- Signs of R/L ventricular failure
Prevention/Treatment
