Cardiovascular Disorders Flashcards
How do you measure cardiac output
Cardiac output = HR x stroke volume
Stroke volume is how much blood is moved with each beat
Central Venous Pressure - how do we measure it and what can it tell us?
Central Venous Pressure can be measured with a central line.
It goes into the Right Atrium
It also can tell us what the preload might be
In sepsis, the CVP gets low because of decreased preload
Normal is between 8-12mmHg
What is wedge pressure and how is measured?
Filling pressuring in the left atrium
It is measured with a pulmonary catheter
Helps determine functionality of the Mitral valve
What happens during diastole?
The filling of the ventricles with the opening of the tricuspid valve (RV) and the mitral valve (LV)
What happens during systole?
The contraction of the ventricles with the opening of the aortic valve (LV) and the pulmonic valve (RV)
Mean arterial pressure
Mean arterial pressure (MAP) is the average pressure exerted on the arteries and serves as a surrogate for measuring afterload, which is the pressure against which the LV must eject blood.
MAP = (2XDBP + SBP)/3
What does aortic stenosis sound like?
Systolic, “blowing”, rough harsh murmur at 2nd right ICS, usually radiating to the neck
Remember that it radiates to the neck**
What does mitral stenosis sound like?
Loud S1 murmur, low pitched, mid-diastolic; apical “crescendo” rumble
How does an ACE-I affect the Renin-Angiotensin-Aldosterone System (RAAS)
When BP falls, kidneys release Renin.
Renin cleaves Angiotensinogen into Angiotensin I which then works its way to the lung.
Angiotensin I is then cleaved into Angiotensin II by angiotensin converting enzyme (ACE).
Angiotensin II causes the blood pressure to rise.
When BP rises, the adrenals will retain salt. If BP gets too high, adrenals will release salt in order to release water in order to drop the BP
In an ACE-I, Angiotensin I is never converted into Angiotensin II so it cannot raise the BP.
AV Blocks
1st Degree: Prolonged PR interval always followed by QRS
2nd Degree Type 1 - Wenckebach: PR interval lengthens until a QRS is dropped
2nd Degree Type 2 - Mobitz: PR interval is usually normal however some P waves are not conducted and the beat is therefore dropped.
3rd Degree - Complete Heart Block: Para-systole, P waves and QRS are independent, wide QRS
Causes and treatment of hypertensive emergency
-Abrupt cessation of antihypertensives
-Cocaine or meth use (don’t use beta blockers with cocaine or meth - causes increase in BP)
-Pre-eclampsia or eclampsia
Treatment - Nicardipine infusion, Hydralazine or labetalol
-Or can restart home meds slowly
HTNsive Emergency defined as SBP>180 and DBP>120 with evidence of end organ damage.
-papilledema, proteinuria, hematuria, renal failure, AMS, EKG changes (ST depressions)
The 5 P’s of Peripheral Vascular Disease
Pallor
Poikilothermy (cold)
Parasthesias
Pulses (decreased)
Pain (claudicaton)
Management of an acute ischemic limb
Presentation: Cold, pulseless, cyanotic
Consult vascular surgery
Heparinize empirically
CT Angio to find where the occlusion is
Thrombectomy to remove if possible
Amputate if needed
Management of HLD
Statins - inhibit HMG CoA reductase - good at decreasing LDL
Fibrates - good for lowering triglycerides and increasing HDL
Niacin - lowers triglycerides, lowers LDL and increases HDL
What is a scoring measuring that can be used to determine risk for ACS?
HEART SCORE
History
EKG
Age
Risk Factors
Troponin
0-3 is low risk
4-6 is medium risk and should consider observation
7-10 is high risk and should observe and treat
Three types of Acute Coronary Syndrome
STEMI - ST elevations. Usually caused by a plaque rupture in one of the larger coronary arteries causing a clot
NSTEMI - EKG shows no ST elevations (could be ST depressions) but troponin is elevated. Could be caused by narrowing of a larger artery or occlusion of a smaller vessel
Unstable angina - Whereas most CAD causes symptoms during exertion, the symptoms will appear at rest.
When should not give Nitro during a STEMI
When ST changes are in the inferior leads (II, III and AVF) because it is R sided and thought to be more preload dependent. Nitro could drop preload.
Priorities for ACS
ASA 81mg chewed - makes platelets less sticky
Nitroglycerin 0.4mg SL every 5 minutes as needed for chest pain (except in inferior MI) - this will cause vasodilation and decrease BP to hopefully get blood passed the clot.
- Short half life. Can reverse with fluids
Oxygen if necessary
Morphine 2-4mg IV with caution
- Lowers anxiety and pain but can drop BP and preload
If STEMI - give heparin and revascularize with either PCI or thrombolytics
If NTEMI - give heparin, get ECHO and then consider coronary angiogram
What is the timeframe for PCI after onset of cardiac symptoms
within 3 hours
Otherwise you will need thrombolytics
When is CABG indicated?
If the CAD is noted to be affecting the:
left main coronary artery
Three major vessels (LAD, LCX, RCA)
Diffuse disease not amenable to PCI
Cardiogenic Shock: Causes, symptoms and treatment
Acute pump failure, usually by massive MI because a large enough portion of the heart does not move d/t ischemia
Signs and symptoms include: hypotension, pulmonary edema, tachyarrhythmia, oliguria, acidosis, and cyanosis
Largely fatal
Treatment includes:
Revascularization
Antiarrythmic agents
Vasopressors
VAD
Balloon Pump
Basics of how a Balloon Pump works
Utilized in cardiogenic shock and is a place holder for a CABG
Inserted through the femoral vein into the aorta
It will time itself with an EKG and inflate during diastole in order to push blood into coronary arteries and hopefully past occlusion
It deflates just prior to systole, helping to empty and suck out the LV
Creates a larger MAP
Differences in systolic and diastolic Heart Failure
Systolic Dysfunction: Failure of the heart’s pumping function - HFrEF
–Ejection fraction drops
–Increase in fluid to the lungs (crackles) because of LV backwards pressure
–results in fluid in the tissue because of RV backwards pressure into the vasculature causing dependent edema.
Diastolic Dysfunction: Failure of the heart’s filling function - HFpEF
–EF is largely normal (50-65%)
–Inadequate stroke volume because of hypertrophy of the ventricular wall
Risk factors for Heart Failure
AsCVD
Viral infections of the heart muscle (myocarditis)
Severe ETOH use - ETOH cardiomyopathy
Arrhythmias
New York Heart Association Classes of Heart Failure
New York Heart Association Classes of Heart Failure:
Class I: No symptoms with any activity
Class II: Limitation only with strenuous exertion. No limitation with mild exertion
Class III: Limitation with exertion but no dyspnea at rest
Class IV: Dyspnea at rest
Treatment of CHF
Medications:
–ACE-I/ARB to stabilize remodeling and improve BP (ACE-I first line treatment)
–Digoxin for HR control
–Diuretics to help with fluid retention
Lifestyle modifications:
–Physical activity as tolerated
–Treat sleep apnea
–Weight reduction
–Sodium restriction (no more than 1500mg per day)
–Fluid restriction (no more then 1.5L per day for NYHA Class III and IV
Digoxin - How does it work and what does it treat?
Used to treat A-fib
Slows heart rate and increase the force of contraction
Very narrow therapeutic window so you need to check a level to avoid toxicity
–rapidly deadly, severe bradycardia and hypotension
Management of decompensated Heart Failure
Could present with severe hypoxia and/or hypo- or hypertension
Could happen over days to weeks and they could develop worsening edema.
Could happen very suddenly over minutes and cause flash pulmonary edema
–Sudden change in afterload
Treatment is ensuring adequate gas exchange (O2 BiPAP, CPAP, intubation) and afterload reduction (nitrates)
Lasix takes an hour or so to work and will not help with flash pulmonary edema
Hypertrophic Cardiomyopathy: Causes and treatments
Often genetic
Cardiac myocytes increase in size and therefore the ventricular wall increases as well
Often happens in athletes due to constant exertion
Can cause sudden death due to VT
Can present as diastolic heart failure
Treated with pure beta 2 antagonists - Atenolol
Takotsubo Cardiomyopathy
Broken Heart Syndrome
Transient condition which causes increased contraction at the LV base, ballooning of the LV apex, disordered response to catecholamine stress
Presents like CHF with systolic dysfunction but on EKG shows anterior STEMI but patent coronary arteries on cardiac cath
Usually results in a few days - can give metoprolol and consider balloon pump
Peripartum cardiomyopathy
Form of dilated cardiomyopathy that occurs during pregnancy for unknown reasons
Often confused with normal sxs of pregnancy (SOB, leg swelling) but progress to more overt signs of CHF (crackles on exam)
Treatment is to deliver the baby
Inflammatory myocarditis
Can be caused by infection
–Insect borne infections (Borrelia burgdorferi causes Lyme Disease or Trypanosoma cruzi which causes Chagas’ Disease - Central/South America)
–Parvovirus B19, Coxsackie
–Hypersensitivity after infection with Strep Pyogenes
Presents as CHF with systolic dysfunction
Treatment is focused on underlying causes - treating the infection
Alcoholic Cardiomyopathy
Caused by constant high intensity exposure to large amount of alcohol, causing myocardial cell death leading to dilated cardiomyopathy
Presents as CHF with systolic dysfunction
Most common in males ages 30-50 (not common for regular CHF to present in this age group)
Treatment focuses on cessation of ETOH
Mitral Stenosis: Causes, symtoms, treatment
Almost always caused by Rheumatic heart disease, which is a type II hypersensitivity reaction during the later phases of a strep pyogenes infection (strep or scarlet fever left untreated) which causes a thickened mitral valve, thickened chordae tendinae and hypertrophied left ventricle.
Sxs are that of CHF
Findings include diastolic murmur heard best at the apex with the bell and sometimes an S3
Often asymptomatic but for symptomatic disease, treatment is the same as CHF and AF (risk for arrhythmias)
Treated surgically with by valvuloplasty (percutaneous balloon) or mitral valve replacement
Aortic stenosis: Causes, symptoms, exam findings and treatments
Caused simply by aging in 50% of cases but also congenital bicuspid aortic valve, or rheumatic heart disease
Common symptoms are exertional syncope, angina, CHF
Exam findings reveal a loud murmur, usually @ RUSB, occasionally an S4 (Tennessee) and displaced PMI
Treatment is with long acting nitrites in order to reduce afterload.
Aortic valve replacement is generall the surgical treatment but sometimes can be done with TAVR
Aortic Regurgitation
Can be acute (endocarditis) or chronic (aging, Marfan’s syndrome, congenital bicuspid valve)
Sxs include that of CHF but frequently with a pronounced shock presentation
Water hammer pulse - high peak of systole and falls again, intense peaks.
Mitral regurgitation: Causes, sound, treatment
As with aortic regurg, can be acute (endocarditis) or chronic (aging, connective tissue)
Regurgitant jet - squirt of blood back into the LA. Can hear it when listening to the back.
Treatment of chronic MR is focused on afterload reduction (to lower LVEDP) but for acute MR, an IABP can be used for systolic unloading until the patient can be stabilized for emergency mitral valve repair
