Cardiovascular Flashcards
When does myocardial perfusion occur?
Diastole
Coronary perfusion pressure
CPP = DBP - PAOP
60-80 mmHg
Preload
-Stretch on the myofibrils at the end of diastole prior to ejection
-Affected by ventricular volume & pressure at the end of diastole
Right heart - CVP or Right atrial pressure (RAP) 2-6 mmHg
Left heart - PAOP 6-12 mmHg
PAOP
6-12 mmHg
closely correlate with LVEDP or PA diastolic pressure
PAOP should not be higher than PA diastolic - check position (should be in Zone 3)
Factors that increase PA systolic
“Lung problems”
pulmonary hypertension
COPD
ARDS
PE
Factors that increase PA diastolic
“Heart problems”
cardiac tamponade
LV failure
Mitral valve disease
Factors that increase PAOP
Left-side heart dysfunction
Mitral stenosis/insufficiency
Cardiac tamponade
Constrictive pericarditis
LV failure
Volume overload
High PEEP (if PEEP>10, PAOP will be inaccurate)
Increased preload
Causes: HF, hypervolemia, bradydysrhythmias
Tx: diuretics, vasodilators (nitro, morphine, nitroprusside, CCBs), ACE inhibitors, ARBS
Decreased preload
Causes: hypovolemia, vasodilation, increased intrathoracic pressure, high PEEP, cardiac tamponade, RV infarct, tachydysrhythmias, afib
Tx: volume - NS, LR, colloids, blood products
Increased/decreased contractility
Increase - SNS stimulation, sympathomimetics (epi, dopamine, dobutamine)
Decrease - Myocardia infarction/ischemia, cardiomyopathy, acidosis, hypoxemia, drugs (anesthesia, barbituates, beta blockers, CCB, antidysrhythmics)
Tx to increase - positive inotropes (digoxin, dobutamin, dopamin)
Afterload
-Pressure that the ventricle must pump against in order to open the semilunar valve
-Affected by vascular resistance, diameter of the ventricular vessels, and volume and viscosity of blood
-Left heart: SVR 900-1400
-Right heart: PVR 100-250
Increased afterload
Causes: SNS stimulation, vasopressors, HTN, aortic valve disease/stenosis, coagulopathy
Tx: systemic vasodilators (Nitroprusside, nitroglycerin, hydralazine, CCBs, ACE inhibitors, ARBs, PDE inhibitors - Milirone); IABP; pulmonary Vasodilators (Oxygen, aminophylline, CCBs, NO, sildenafil - PDE 5 inhibitor)
Decreased afterload
Causes: Hypotension, vasodilation (e.g., shock)
Tx: Vasopressors (norepinephrine, phenylephrine, dopamine, vasopressin)
I, aVL, V5, V6
Lateral wall
LCA (left circumflex artery)
II, III, aVF
- Inferior wall
- RCA (right coronary artery)
- AV node involvement –> dysrhythmia (bradycardia, AV blocks - 1st degree & 2nd degree type I - Wenckebach)
- Check for RV involvement by doing (Rt ECG): avoid nitrates and morphine if confirmed d/t hypotension and give volume
V1
Ventricular septum
V2, V3, V4
Anterior
V1-V4
- Anterior/septal
- Most dangerous MI b/c can lead to possible HF & cardiogenic shock
- LAD (left anterior ascending artery) - supplies bundle of his and bundle branches
- Heart blocks (2nd degree type II, 3rd degree, BBB) - prepare to emergently pace!
- New loud murmur, suspect ventricular septal rupture or papillary muscle rupture
CVP/RAP
right atrial pressure
2-8 mmHg
right ventricle preload
Elevated - fluid overload
Central venous oxygen saturation/ScvO2
>70%
Regional reflection of blood oxygenation from the head and upper torso
Slightly higher than SvO2 as it has not mixed with the venous blood from the coronary sinus
PA pressure (PAP)
Systolic: 15-30
Diastolic: 8-15
“Quater over dime” 25/10
Mean (MPAP): 9-18
>25 mmHg with normal PAOP –> pulmonary hypertension
PA occlusive pressure (PAOP)
6-12 mmHg
Lt arterial pressure
LV preload
Closely correlates with LVEDP or PA diastolic
Elevated PAOP –> left heart failure
Cardiac output/index
4-8 L/min
Cardiac index 2.5 - 4.3 L/min/m^2
CO may be normal when pt is tachycardic w/ low SV as a compensation
Stroke volume/index
50-100 mL/beat
SI 35-60 mL/beat/m^2
PA waveform
a - left atrial contraction
c- Closure of mitral valve
v- left ventricular systole; passive left atrial filling during atrial diastole
A large “V” wave indicates an increase in left ventricular pressure (e.g., mitral regurgitation)
Mixed venous oxygen saturation (SvO2)
60-75%
True mixed venous O2 saturation
Global balance btw DO2 & VO2
Only obtained from a PA catheter
Normal oxygen extraction ratio (O2ER) = 25-30%; 70-75% oxygen still bound to Hgb and returns to the right side of the heart
Increase in SvO2
- Increased O2 supply/delivery
- Decreased demand: anesthesia, sedation, paralysis, hypothermia
- Decreased extraction at tissue level: early sepsis, cyanide toxicity
Left shift on oxyhemoglobin dissociation curve
“sticky” hgb to O2, alkaLOsis (high pH), hypothermia, decreased 2,3 DPG
Decrease in SvO2
- Inefficient O2 supply/demand
- Increased metabolic needs: sz, restlessness, shivering, hyperthermia
Right shift
“less affinity” hgb for O2, acidosis (low pH), muscles, increased temperature, increased 2,3 DPG
Intra-aortic balloon pump
- Treats refractive cardiac failure and cardiogenic shock until surgery
- Increases/augments diastolic BP
- Improves coronary blood flow
- Improves CO up to 15%
- Requires arterial line and EKG signal for time of cardiac cycle
- Inserted via femoral artery and tip rests in the descending aorta.
- Avoid occluding subclavian, carotid, and renal arteries.
Inflates at the beginning of the diastole when the aortic valve closes at dicrotic notch to augment diastolic filling and coronary blood flow.
Deflates before the beginning of the systole R-wave of ECG or upstroke of arterial pressure wave
- Sudden loss of aortic pressure reduces afterload –> lowers heart work to push blood thus myocardial O2 demand.
Contraindications: aortic valve insufficiency/regurgitation, aortic aneurysms, suspected aortic dissection.
Variant (Prinzmetal) Angina
- Vasospastic angina - spasms in coronary arteries
- Usually during rest; at the same time every day
- Results from cold weather, stress, med, smoking, cocaine
-Relieved with CCBs, nitrates
-Dx with provocative testing & ECG