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