CVS Flashcards
Clinical approach to “sympathetic crashing acute pulmonary edema”
1) Nitrates (hydralazine is also an option, but it is less titratable and less predictable)
2) PEEP/NIPPV
3) Diuretics (IV Lasix)
4) Beta blocker (if HR > 150)
5) Transition to long-term antihypertensive (ie. labetalol and hydralazine)
Clinical approach to “symptomatic bradycardia”
1) Atropine
2) Pacing (Transcutaneous or TVP)
3) Chronotropy (epinephrine, dopamine, isoproterenol)
4) Calcium (if secondary to hyper-kalemia)
5) Insulin (for beta blocker/CCB overdose)
how to manipulate pulmonary vascular resistance to “unload the right ventricle”
- maintain SpO2 >92% (Hypoxic pulmonary vasoconstriction is to be avoided)
- Avoid excessive PEEP. PPV/PEEP is transmitted to the pulmonary circulation, adds to afterload. Unless patient is refractory hypoxemia d/t ARDS and needs to be oxygenated
- Avoidance of hypercapnea. CO2 increases pulmonary arterial pressure and RV afterload
- Pulmonary vasodilators (nitric oxide, prostacycline, bosentan, sildenafil, milrinone, levosimendan)
Target electrolyte levels in the setting on an AMI
- iCa+ > 1.0 mmol/L (Low serum calcium is independently correlated with LV systolic dysfunction in CAD patients with and without AMI)
- K+ 3.5-4.5 mmol/L (in setting of ACS, hypokalemia defined as potassium levels <3.5 is associated with ventricular arrhythmias)
- Mg+ >1.0 mmol/L (low serum Mg levels may be associated with cardiac arrhythmias and sudden death. Magnesium has antiarrhythmic effects)
NSTEMI treatment pathway
- “Dual anti platelet therapy” (ASA + P2Y12 inhibitors)
- Statin therapy (atorvastatin)
- Beta blockade (metoprolol)
- Nitrates (NTG)
- Systemic anticoagulation (heparin/LMWH)
- Maintain normoxia (SpO2 >90%)
- Optimize electrolytes (target normal range)
treatment pathway for tamponade
- Optimize preload with a fluid bolus (remember that tamponade is OBSTRUCTIVE and not cardiogenic shock. obstructive shock patients are preload dependent d/t elevated RV afterload
- Augment rate: Allow tachycardia (in your CO equation your preload/afterload/contractility are all fucked so if you want to maintain MAP you’ll have to keep the HR a little bit higher)
- Improve Forward flow: Levophed (if they are in shock you’ll have to support their hemodynamics with vasopressors. levy is 1st line)
- Remove effusion: pericardiocentesis
CO goals in aortic stenosis
- preload high (force blood through the tiny little hole)
- afterload normal
3.HR low (prevent pulmonary edema/back flow) - contractility high (force blood out)
CO goals acute aortic regurgitation and acute mitral regurgitation
- afterload low
- HR high (dont allow backfill)
- contractility high (force blood out)
- PPV or Intubation
CO goals acute mitral stenosis
- preload normal (Phenylephrine or vasopressin)
- afterload normal
- HR low (prevent pulmonary edema/back flow) [Esmolol or amiodarone]
- contractility normal
CO goals aortic stenosis
- give fluids/Avoid preload-decreasing drugs
- Vasopressors for cardiogenic shock (Phenylephrine or vasopressin)
- sensitive to both bradyarrhythmia and tachydysrhythmias (Treat both aggressively)
ACS treatment pathway
- Dual antiplatelet therapy (Aspirin + P2Y12 inhibitor)
- Anticoagulant (UFH/enoxaparin/fondaparinux)
- Oxygen (sats >94%)
- Rate control (Metoprolol)
- Analgesia (NTG, opioids)
- Statin therapy
- Reperfusion (TnK or PCI)
- Angiotensin-converting enzyme inhibitors
- Optimize electrolytes (target normal range)
PULMONARY EDEMA + SHOCK (“wet and cold” Cardiogenic Shock) treatment algorithm
- IV/O2/Monitor
- Differentiating the shock (pump failure vs mechanical complications)
- optimize the MAP (Norepinephrine +/-
Inotropic agent) - “fix the lungs” (CPAP/NIPPV/Intubation)
- differentiate + optimize volume status (fluid bolus vs lasix)
- consider inotrope for HFrEF/shitty contractility (dobutamine/epi)
- treat underlying etiology
- mechanical circulatory support
treatment goals for acute cardiogenic shock
- Address the underlying cause of shock
- If shock is from pump failure, patients are frequently extravascularly fluid-overloaded but intravascularly volume-depleted
- Fluid challenges in 250-mL isotonic crystalloid boluses with frequent re-assessment of intravascular volume status
- if patient is still hypotensive post fluids, start an adrenergic agonist (norepinephrine)
- Dobutamine is a good option for inotropy when the primary mechanism of shock is poor cardiac contractility. Patients may still require levo for hemodynamic support
treatment goals for Hypertensive acute decompensated HF
- Treatment should be targeted to afterload and preload reduction
- Afterload can be reduced with a number of medicines, including nitrates and ACE inhibitors
- Nitrates are first line, with NTG being the most common
- loop Diuretics can be used in intravascularly volume-overloaded patients for preload reduction (Lasix)
- Check and replenish electrolytes, particularly magnesium and potassium (arrhythmias)
treatment for cardiogenic shock patients who are “warm and wet”
- Fix lungs (CPAP/BIPAP)
- Fix perfusion (Norepinephrine +/- inotrope)
- Determine volume status and address