BP = CO x PVR

CO = HR X SV

Cardiac Output

How would you reduce CO?

Herat Rate, Contractility, Filling Pressure

reduce HR, contractiilty, and venous return (blood volume) *Diuretics*

Peripheral Resistance (PVR)

How do you reduce PVR?

Arterial Diameter, Arterial Length, Elasticity (decreases with age)

Vasodilation: CNS action and relax musculature on vessels

Renin from the kidney increases angiotensin II

angiotensin II produces aldosterone in the adrenal gland

aldosterone holds onto Na+ and blood volume will increase

Alpha 1 vascular receptors

Beta 1 cardiac receptors

Blood Pressure Falls

Kidney releases renin... which produces angtiotensinogen --> angiotensin I --> angiotensin II --> tells the adrenal gland to produce aldosterone which raises blood pressure 

Causes Vasoconstriction

Triggers aldosterone production and release

natural mineralocorticoid

helps with Na+ and fluid retention

cardiac growth factor: ventricular size and strength*

Sympathetic receptor blocker

Renin-Angiotensin-Aldosterone inhibitor

Reduce Blood volume via diuretics

related closesly to lipid metabolism

especially cholesterol

lipid collects in the intima

Exogenous: dietary consumption and absorption

Endogenous: production of cholesterol in the liver

macromolecule consisting of lipid and specialized protein

- cholesterol has to be carried in the blood by a carrier

Transporter of Endogenous cholesterol

Lowering LDL = reduces risk of atherosclerosis

Reverse cholesterol transport

removes LDL- cholesterol and TG

HIGH HDL= reduced risk

however drugs which raise HDL don't seem to reduce risk

weight loss and ex. raise HDL

produce macrophages and oxidize LDL 

triggers an inflammatory response making it harder for LDL to get in so it accumulates on the outside

Unifying theme in the pathogenesis of the disease

inflammatory markers correlate with risk : C-reactive protein (Crp)

MI and Strokes are caused by plaque ruptures

athermous plaque

MI and Strokes are caused by plaque ruptures

athermous plaque

HMG - CoA Reductase inhibitors

*STATINS*

Statins

What are the adverse effects?

What is the double edged sword problem with statins?

Reduce endogenous cholesterol synthesis

Lowers LDL levels and reduces risk of heart disease

Liver damage, Muscle damage (myopathy and rhabdomyolysis)

don't do it during pregnancy or in children/teens

Statins cause muscle weakness which results in reduced activities = decrease HDL levels

PCSK 9 Inhibitor

produce lower levels of LDL than statins

sub cu injections every 2 weeks

Systolic of >130

Diastolic >80

especially in pt. with diabetes

rare tumor of adrenal medulla or sympathetic ganglia

- secretes high levels of NE

they are sweaty and anxious

- severe headaches, diaphoresis, palpitations, tremor, anxiety

Usually "silent killer"

- headaches, malaise, fatigue, complications

1. Reduce CO

- block beta 1 sympathetic action, reduce blood volume

2. Reduce peripheral vascualr resistance

- block alpha 1 sympathetic action and dilate vasculature

Lower blood volume

- loop diuretics

K+ sparring

Reduce peripheral vascular resistance

Ca++ channel blockeres

arterial and venous

Reduce blood volume and peripheral resistance

ACE inhibitors

Aldosterone antagonist

Renin inhibitor

ORTHOSTATIC HYPOTENSION

BP changes dramatically with change in position

Toxicity and side effects from drugs

typically due to vessel stenosis or occlusion

Vasospasm

Pump Failure

*Key= oxygen transport*

Low Cardiac output

Dyspnea

Orthopnea

Edema

- acute coronary syndromes

-Stable angina pectoris

- Congestive Heart failure

STEMI (elevated ST segments MI)

NSTEMI (non-elevated ST segments MI)

UA (Unstable Angina) = pain @ rest 

Initial Event is usually plaque rupture

happens due to abrupt reduction in coronary blood flow

Atherosclerosis is usually present

1.1 mill per year 20-40% are fatal

Diagnosed by a comibnation of history in PE, EKG, and lab tests

*More common in early morning=Cortisol is increased in the morning (salt retaining), vasculature is more viscous 

pt. c/o of chest pain in midsternum

can radiate to left side or GI upset

up to 30% have no pain

- women more likely to have atypical presentation

- misdiagnosed as gastritis, peptic ulcer, esophageal reflux

P Wave = R/L atrium contracting and pushing blood into ventricles

QRS = blood into ventricle

T= resetting contraction

STEMI= transmural ischemia = involves full thickess of cardiac wall

NSTEMI= more common = *subendocardial rather than transmural*

Anticoagulation: Heparin, ASPIRIN

Rest, O2, sedation,

Reperfusion: PCI... catherization and thrombolytic therapy

*Catheraization PCI is preferred... needs to be EARLY treatment

O2, reduce O2 demand on myocardium

1. Cardiac arrhythmia: Ventricular fib

2. Massive infarction: cardiogenic shock

Stable Angina:brought on by stress or exertion, relieved by rest

Unstable: occurs with min activity or at rest

Variant (Prinzmetal's) = atypical characteristics extreme fatigue with minimal exertion

Stable Angina

What's the treatment?

- Caused by coronary atherosclerosis

unmet oxygen demand

vasodilate: Nitrate, Beta blockers, Ca++ channel blockers

Uses a catheter to dilate narrow areas

PTCA= percutaneous transluminal coronary angioplasty

Coronary Artery Bypass graft

- usually saphenous vein is used

CHRONIC

cardiac fxn is insufficient to meet metabolic and blood flow requirements

Ventricular Ejection fraction is reduced

Incidence is rising*

LVEF = (SV= EDV-ESV)/(EDV)

50-60% is normal

35-40% is CHF range

- Remodeling occurs with results in progressive Cardiomegaly

- overstretching of the myocardium= fluid overload, increased BP and more ischemia 

inability to sleep supine without dyspnea

graded as how many pillows

1. Reduce cardiac workload: control hypertension, reduce weight

2. Reduce blood volume: restrict Na and give DIURETICS = Lasix

3. Reduce/prevent cardiac remodeling: aldosterone antagonist

4. Treat hyperlipidemia = STATINS

5. Agents proven to improve survival: Beta blockers ONLY WHEN CHF IS STABLE and no pulm. edema

ACE inhibitor

- seen in young and healthy ppl

- usually follows a precipitating event (viral infection, pregnancy or delivery)

- severe cases may require cardiac transplantation

- Causes 2% of all cardiac diseases

- multifactorail inheritance

- allow significant amounts of blood to bypass the lungs

- blood is under oxygenated 

- results in cyanosis, stunting of growth and shortness of breath

*more common than valve defects*

Foramen Ovale does not close

- BP is very low in the atrium

- thromboplebitis= blood clots that form in legs or arms

- clot could go all the way to lung and cause a pulm. embolism

not a problem in utero

- after birth can lead to L ventricular being stronger and flow back into R Ventricle

Shunt that doesn't close

*we are loosing efficiency on both sides and less blood going to periphery* 

surgery or medications can close it 

High blood pressure before that point and low blood pressure after that 

- high BP in UE and low BP in LE

More common congenital shunt disease

R ventricular hypertrophy, R septal defect, Aorta is overriding, pulm stenosis 

venous thrombus that embolizes to a pulmonary aretry

70% of thrombus comes for large lower extremity vein... usually from pelvic or abdominal veins

Venous Stasis (hospitalized), Hypercoagulability, Vascular Injury

*Joint Replacement Procedures are susceptible**

Anticoagulant Drugs: Heparin, prevent new emboli

Thrombolytic Drugs: try to dissolve embolus

Surgery: filter in vena cava

limit immobolization, avoid hyper coagulable states, Prophylactic anticoagulation

- Aneurysm: swelling or distention of Arterial segment

AAA = Abdominal Aortic Aneurysm = most susceptible

Rupture = associated with weakness of wall and atherosclerosis = high mortality rate

and Dissection